Beruflich Dokumente
Kultur Dokumente
2. GENER AL EXAMINATION
1. Built 10 11. Skin and its Appendages 27
2. Body Proportions 14 12. Vertebral Column 31
3. Nutrition 14 13. Thickened nerves 32
4. Decubitus 15 14. Joints 32
5. Clubbing 15 15. Temperature 36
6. Cyanosis 16 16. Pulse 39
7. Jaundice 19 17. Jugular Venous Pulse (JVP) 43
8. Pallor 22 18. Blood pressure 46
9. Lymphadenopathy 23 19. Hypertension 48
10. Edema 25 20. Hypotension 53
3.ABDOMEN
4. RESPIRATORY SYSTEM
1. Proforma 122 10. Chronic Obstructive Pulmonary Disease
2. Examination 124 (COPD) (Emphysema and Chronic
Bronchitis) 168
3. Pleural Effusion 135
11. Pneumonia 172
4. Collapse / Atelectasis of Lung 143
12. Bronchiectasis 175
5. Pulmonary Fibrosis /
Interstitial Lung Diseases 145 13. Lung Abscess 178
5. CARDIOVASCULAR SYSTEM
1. Proforma 188 12. Cyanotic Congenital Heart Disease 243
2. Examination 189 13. Patent Ductus Arteriosis (PDA) 250
3. Rheumatic fever 203 14. Ventricular Septa! Defect (VSD) 252
4. Infective Endocarditis 205 15. Atrial Septa! Defect (ASD) 253
5. Ischemic Heart Disease 208 16. Coarctation of Aorta 255
6. Cardiac Failure 220 17. Aneurysm of Aorta 257
7. Mitra! Stenosis (MS) 225 18. Pericardia! Effusion 259
8. Mitral Regurgitation (MR) 232 19. Cardiomyopathy 260
9. Mitra! Valve Prolapse (MVP) 236 20. Fitness for surgery
10. Aortic Regurgitation (AR) 237 (Pre-operative Evaluation) 263
PART II-TABLE-WORK
7. MEDICAL EMERGENCIES
1. Cardiac Arrest 374 28. Acute Retention of Urine 395
2. Cardiac Failure 377 29. Acute Renal Failure (ARP) 395
3. Ischemic Heart Disease 377 30. Diabetic Ketoacidosis 396
4. Stokes Adams Syndrome 377 31. Hypoglycemia 397
5. Hypertensive Crisis 377 32. Respiratory Acidosis 398
6. Hypertensive Encephalopathy 378 33. Metabolic Acidosis 399
7. Shock 379 34. Respiratory Alkalosis 399
8. Anaphylactic Shock 380 35. Metabolic Alkalosis 399
9. Pulmonary Embolism and 36. Dehydration 400
Deep Vein Thrombosis 380 37. Hypernatremia 400
10. Hemoptysis 382 38. Hyponatremia 400
11. Bronchial Asthma 383 39. Hyperkalemia 401
12. Respiratory Failure 385 40. Hypokalemia 401
13. Tension Pneumothorax 386 41. Acute Hypercalcemia 401
14. Hematemesis 387 42. Amebic Dysentery 401
15. Acute Gastroenteritis / Food poisoning 388 43. Bacillary Dysentery 402
16. Acute Pancreatitis 389 44. Cholera 402
17. Hepatic Coma 389 45. Typhoid 403
18. Coma 390 46. Dengue 403
19. Meningitis 390 47. Leptospirosis 404
20. Cerebrovascular Diseases 391 48. Diphtheria 405
21. Subarachnoid Hemorrhage 391 49. Tetanus 405
22. Epilepsy 391 50. Rabies 406
23. Sickle Cell Crisis 393 51. Cerebral Malaria 406
24. Acute Hemolytic Crisis 393 52. Acute Poisonings 406
25. Aplastic Anemia 394 53. Organophosphorous Compound
26. Hemophilia 394 Poisoning 407
27. Renal Colic 394 54. Acute Alcoholic Intoxication 408
55. Barbiturate Poisoning 408 59. Snake Bite 410
56. Acute Salicylate Poisoning 409 60. Scorpion Bite 411
57. Carbon Monoxide Poisoning 409 61. Hyperpyrexia 413
58. Carbon Dioxide Narcosis 410 62. Drowning 413
8. ELECTROCARDIOGRAPHY
1. Introduction 415 6. Rhythm Disturbances 422
2. Normal ECG 415 7. Conduction Defects Atrioventricular
3. Waves and Complexes 416 Block (AV Block) 429
4. Myocardial Infarction 421 8. Effect of Drugs and Electrolytes 430
5. Ventricular Enlargement 421
9. RADIOLOGY
1. X-ray chest 432 5. Barium studies 443
2. X-ray Chest - Heart 437 6. X-ray of Bones 447
3. Plain X-ray Abdomen 438 7. X-ray Skull 452
4. Urogenital System 440
10. INSTRUMENTS
1. Endotracheal Tube 455 20. Urosac Bag 465
2. Tracheostomy Tube 456 21. Stomach Tube 466
3. Laryngoscope 457 22. Ryle's Tube (RT) or Nasogastric Tube 466
4. Oxygen Mask and Oxygen Cannula 23. Sengstaken Blakemore Tube (S.B. Tube) 467
(Nasal Prongs) 458 24. Infant Feeding Tube 468
5. Nebulizer Chamber 458 25. Record Syringe and Needle 469
6. Metered Dose Inhaler 458 26. B.D. Syringe and Needle 469
7. Spacehaler 459 27. Tuberculin Syringe 470
8. Rotahaler 459 28. Insulin Syringe 470
9. Nelson's Inhaler 459 29. Lumbar Puncture Needle 471
10. Ambu Bag (Self-inflating Ventillation Bag) 460 30. Cisternal Puncture Needle 471
11. Airway 460 31. Vim-Silverman's Needle 471
12. Mouth Gag 461 32. Menghini's Needle and Syringe 471
13. Tongue Depressor 462 33. Bone Marrow Aspiration Needle 471
14. Trocar and Cannula 462 34. Pleural Biopsy Needle 472
15. Asepto Syringe and Bulb 462 35. Trucut Needle 472
16. Simple Rubber Catheter 462 36. Southey's Tube and Needle 472
17. Foley's Self-retaining Catheter 463 37. Tourniquet 472
18. Malecot's Catheter 465 38. Venesection Needle 473
19. Condom Catheter 465 39. Scalp Vein Needle 473
40. Pleural or Ascitic Aspiration Needle 473 44. Clinical Thermometer 475
41. Intravenous Cannulas 45. Flatus Tube 476
(Venflow or Angiocath) 473 46. Proctoscope 476
42. Three Way 474 47. Stethoscope 477
43. I.V. Set 474 48. Central Venous Catheter 477
11. PROCEDURES
1. Transvenous Pacing 479 11. Ascitic Tapping 490
2. Cardioversion 479 12. Gastric Analysis 491
3. Lumbar Puncture 480 13. Glucose Tolerance Test (G.T.T.) 492
4. Cisternal Puncture 484 14. Intravenous Therapy 493
5. Liver Biopsy 484 15. Subcutaneous Infusions 495
6. Kidney Biopsy 486 16. Tracheostomy 495
7. Bone- marrow Aspiration 487 17. Oxygen Therapy 496
8. Pleural Fluid Aspiration 488 18. Enema 497
9. Aspiration ofPneumothorax Cavity 489 19. Parenteral Hyperalimentation 499
10. Pericardia! Aspiration 490
12. HEMATOLOGY
1. Blood Collection 501 11. Electronic Cell Counters 514
2. Preparation ofBlood 502 12. Red Cell Indices 514
3. Hemoglobin Estimation 505 13. Red Cell Morphology 515
4. Packed Cell Volume (PCV ) 507 14. Anemias 517
5. Erythrocyte Sedimentation Rate (E.S.R.) 507 15. Differential Leucocyte Count 522
6. Reticulocyte Count 509 16. Leukemias 525
7. Osmotic Fragility ofRBCs 510 17. Parasites in Blood 525
8. Total Red Cell Count 510 18. Multiple Myeloma 526
9. Total White Cell Count 511 19. Coagulation studies 526
10. Platelet Count 513 20. Normal Hematological Values 613
L_
15. DRUGS
1. Cardiovascular Drugs 557 5. Antibacterial Agents 585
a) Inotropic Drugs 557 a) Sulfonamides 585
b) Anti-arrhythmic Drugs 558 b) Quinolones 586
c) Anti-angina! Agents 560 c) Beta-lactams 586
d) Anti-hypertensive Agents 561 d) Macrolides 588
e) Anti-thrombotic Agents 566 e) Aminoglycosides 589
e) Heparins/Aprotinin 566 f) Tetracyclines 589
f) Diuretics 567 g) Chloramphenicol 590
2. Autonomic Nervous System 568 6. Anti-tuberculous Drugs 590
a) Catecholamines 568 7. Anti-leprosy Drugs 591
b) Cholinergic and Anti-cholinergic Agents 569
8. Anti-amoebic Drugs 592
3. Drugs in Respiratory Diseases 570
9. Drugs for Kala- azar 593
a) Anti-asthma Agents 570
b) Agents for Cough and Expectoration 572 10. Anti-malarial Drugs 593
c) Anti-allergic Drugs 572 11. Anti-helminthic Agents 594
d) Serotoninergic Agents 573 12. Anti-fungal Agents 597
4. Drugs in Central Nervous System 13. Anti-viral Agents 598
Diseases 573
a) Opioids 573 14. Anti-retroviral Agents for HIV Infection 599
b) Analgesics and Anti-inflammatory Drugs 574 15. Alcohol 601
c) Drugs in Migraine 576 16. Anti-malignancy Agents 601
d) Drugs in Gout and Arthritis 576
17. Hemopoietic Drugs 603
e) Anti-epileptic Drugs 577
f) Muscles Relaxants 579 18. Chelating Agents 604
g) Anti-psychotic Drugs 579 19. Drugs in Endocrine Disorders 605
h) Sedatives / Hypnotics 580 20. Drugs for Diabetes 607
i) Anti-depressants 582
21. Lipid Lowering Agents 608
j) Anti-parkinsonism Drugs 583
k) Drugs in Stroke 584 22. Gastro-intestinal Drugs 609
I) Drugs in Degenerative Brain Disorders 584 23. Electrolytes 611
25. Plasma Expanders 612
Dr. Hardik Shah Dr. Sunita Iyer Dr. Nikesh Jain Dr. Rajiv Shah
H
istory taking is an art, which a doctor learns with their time ofoccurrence, duration and results
over the years by repeated practice and ex should be noted. Childhood illnesses (eruptive
perience. History is the record of medical fevers, per tussis, influenza), tuberculosis,
events that have already taken place in the patient. diabetes, hyp ertesnion, asthma, heart disease,
Since every disease has a pattern of behavior, a good jaundice, joint swelling, etc. must be inquired into.
history combined with a sound knowledge of medicine Past injuries, accidents, operations or hospital
would help the doctor to judge the likely cause(s) that stay and blood transfusion history must also be
may be responsible for the patient's problems. In over noted in details.
80% cases the most likely diagnosis can be reached 5. Personal history: Patient's appetite, food habits,
by a proper history. On clinical examination, the type of diet, bowel and micturition habits, sleep
clinical state of the patient is determined at that given and addictions like alcohol, smoking, tobacco
time. However, nothing is usually known of the past chewing, charas, ganja, marijuana etc., must
problems. Hence, without an appropriate history, an be inquired into. Loss of appetite and weight
incorrect interpretation of the physical findings may may suggest an active disease process. Similarly
be made. E.g. a person has brisk reflexes and extensor improper sleep due to other symptoms would
plantar: a recent history of transient ischemic attack suggest that those symptoms require urgent
would suggest recent stroke, whereas an old history attention. Alcohol, tobacco, smoking and other
of stroke a few years ago would suggest residual effect intoxicants can adversely affect many systems
of a past stroke. in the body and the role of these substances in
A good history must record the following information the patient's problems can be easily judged by
in a systematic order. the history. E.g. alcohol may be responsible for
1. Biodataofthe patient: This should include name, liver cell failure and cirrhosis as well as acute
age, sex, address, occupation, religion and marital gastritis. Heavy smoking may be responsible
status of the person. for precipitating coronary artery disease or
hypertension in the young.
2. Complaintsofthepresentillness: The complaints
with which the patient has come should be 6. Family history: Any illness in the family must
recorded in chronological order and the duration be recorded. The state of health of parents, peers
should be noted. and children should be noted. If any member is
deceased, the cause of death should be noted.
3. Origin, duration and progress: Details of each
Some genetically transmitted diseases are:
symptom must be recorded separately. The mode
of onset, whether sudden or gradual, the duration a. X-linked recessive diseases (e.g. Duchenne
of each symptom and its progress and finally the muscular dystrophy, hemophilia, G6PD
present status of the symptom must be noted. deficiency, ichthyosis). Women are carriers
Associated symptoms must also be inquired into and do not suffer from the disease, whereas
and recorded. males suffer from the disease. Hence, in such
illnesses, the family history would suggest
4. History of past illness: Similar illness in the past
similar illnesses in the patient's brothers,
PRACTICAL MEDICINE
3 > Anorexia
in the parents since they may be heterozygous
and hence only carriers. However, history
of consanguineous marriage in the parents 1. Viral hepatitis including anicteric hepatitis
(marriage between cousins or brother and
2. Tuberculosis
sister or uncle and niece) may be present and
may be responsible for the homozygous state 3. Carcinoma of stomach and other malignancies
in the patient and thus the manifestation of 4. Endocrine diseases: Addison's disease,
the disease. panhypopituitarism
7. Menstrual and obstetric history: In females, 5. Chronic wasting diseases: Uremia, cirrhosis of
the date of onset of menstruation, date of last liver, chronic alcoholism, chronic smoking etc.
menstruation and the amount of blood flow, 6. Drugs: Digitalis, quinine, metronidazole, etc.
regularity and pain during menstruation should
be noted. In a woman who has conceived, details
of past abortions, premature births and normal 4 Fever
or abnormal deliveries should be noted.
(Refer Pg. 36: Temperature)
Some of the common symptoms which the patients
present with and their causes are given below:
5 > Chest Pain
1
- -
Weight
- Loss 1. Cardiac: Ischemic heart disease, pericarditis,
1. Caloric malnutrition: Fasting, inappropriate diet infective endocarditis, cardiomyopathy, valvular
heart disease, dissecting aneurysm of aorta, etc.
2. Infections (chronic): Infective endocarditis,
tuberculosis, amebic liver abscess, fungal 2. Respiratory: Pleurisy, pneumothorax, pulmonary
infections, H.I.V. infection, etc. embolism, pulmonary hypertension, malignancy
3. Acute infections: Viral hepatitis, typhoid, 3. Musculoskeletal: Rib fracture, vertebral collapse,
septicemia costochondritis, myositis of pectoral muscle, etc.
4. Malignancy 4. Functional
5. Malabsorption syndrome 5. Miscellaneous: Herpes zoster of intercostal
6. Endocrine diseases: Diabetes m ellitus, nerves, esophagitis, pancreatitis, peptic ulcer,
thyrotoxicosis, panhyp opituitarism, Addison's cholecystitis, splenic flexure syndrome, etc.
disease, etc.
7. Anorexia nervosa
2
( 1 > History Taking and Symptomatology
9 > Palpitations
2. Respiratory: Airway obstruction, bronchial
asthma, chronic obstructive lung disease,
pulmonary infections, pulmonary edema, 1. Physiological: Exercise, emotional or sexual
pulmonary embolism, bronchogenic carcinoma, excitement, etc.
pleural effusion, pneumothorax, etc.
2. Excessive tea, coffee, tobacco, alcohol
3. Cardiac: Acute myocardial infarction, valvular consumption
heart disease, left ventricular failure, congenital
3. Anxiety state
cyanotic heart disease, etc.
4. High output state: Anemia, beriberi,
4. Metabolic: Diabetes, uremia, hypokalemia
thyrotoxicosis, A-V fistula, Paget's disease, etc.
5. Neurological: Respiratory center depression as
5. Cardiac arrhythmia: Extrasystoles, paroxysmal
in syringobulbia, motor neuron disease, Guillain
tachycardia, atrial fibrillation, heart block, etc.
Barre syndrome, bulbar polio, myasthenia gravis
6. Drugs: Sympathomimetic agents, nitrates,
6. Psychogenic
overdose of digoxin or insulin
(For ATS Dyspnea Scale: Refer pg. 125)
7. M i s ce l l a n e o u s : P h e o c h r o m o c y to m a ,
(For NYHA Classification: Refer pg. 211) hypoglycemia, etc.
7>Coug�
-
h �-
- - -
� 1 O > si_n_co__.p_e___
1. Respiratory: 1. Vasovagal syncope
a. Laryngeal and pharyngeal infections and 2. Postural hypotension
neoplasms
3. Cardiac arrhythmia: Stokes Adam's syndrome
b. Tracheobronchial: Tracheobronchitis, bronchial
4. Stenotic lesions of the heart: Aortic stenosis,
asthma, bronchiectasis, bronchogenic
hypertrophic subaortic stenosis, pulmonary and
carcinoma, pressure over the trachea and
mitral stenosis, Fallot's tetrad, ball valve thrombus
bronchus from outside, aspiration, etc.
in left atrium.
c. Lung: Pneumonia, tuberculosis, lung abscess,
5. Cerebrovascular insufficiency: Vertebrobasilar
tropical eosinophilia, pulmonary edema and
insufficiency, carotid sinus syncope, etc.
infarction, interstitial fibrosis, etc.
6. Miscellaneous: Massive myocardial infarction,
d. Pleural: Pleural effusion, pneumothorax, etc.
pericardial tamponade, left atrial myxoma,
2. Cardiac: Left ventricular failure, mitral stenosis, micturition syncope, cough syncope, internal
aneurysm of aorta, etc. bleeding, etc.
3. Mediastinum: Enlarged lymph nodes, mediastinal
11 > Poli�u.:...:
tumors, etc.
4. Psychogenic ri-=- a____ _
_
5. Reflex: Wax or foreign body in the ear, subphrenic 1. Transient: Excessive water drinking, diuretic
or liver abscess, etc. therapy, cold weather, stress
2. Persistent:
a. Diabetes mellitus
3
PRACTICAL MEDICINE
13 > Frequency of
stones, tumors, tuberculosis, interstitial
nephritis, papillary necrosis, polycystic
Micturition and kidneys, etc.
Nocturia 2. Ureteric: Trauma, tuberculosis, stones, neoplasms
3. Bladder: Trauma, tuberculosis, stones, neoplasms,
1. Bladder: Cystitis, small contracted bladder,
cystitis, following cyclo-phosphamide therapy
tumors, vesicular calculus, cystocele
4. Urethral: Trauma, stones, foreign body, urethritis
2. Bladder neck: Incomplete evacuation due
to enlarged prostate or stricture of urethra, 5. Prostatic: Prostitis, neoplasms
incompetent internal urethral sphincter, ectopic 6. Systemic diseases: Diabetes, amyloidosis,
ureter collagen disease, DIC, etc.
3. Urethra: Urethritis, neoplasms, balanitis, stricture
17 > Anuria
of urethra, pinhole meatus, phimosis
4. Miscellaneous: Polyuria, psychogenic, pregnancy,
pressure from surrounding structures 1. Renal: Glomerulonephritis, pyelonephritis,
polycystic kidney, chronic renal failure,
23 > Eructation
or ovary.
8. Metabolic: Diabetes, uremia, porphyria, lead
poisoning, Henoch Schonlein purpura 1. Faulty dietary habits: Aerated water, chewing
9. Neurogenic: Herpes zoster, tabes dorsalis, etc. gum, mouth breathing, etc.
10. Functional 2. Addiction: Smoking, alcohol, betel nut, pan, etc.
3. Gastrointestinal: Gas tritis, peptic ulcer,
20 > Dysphag ia
hiatus hernia, cholecystitis, stones, irritable bowel
syndrome
1. Esophageal: Inflammation, webs, strictures, 4. Psychogenic: Anxiety, depression, etc.
tumors, achalasia cardia, spasm, hiatus hernia,
5
PRACTICAL MEDICINE
29 > Diarrhea
disease, motion sickness, radiation, etc.
4. Metabolic: Diabetes, alcohol, pregnancy,
hypercalcemia, Addison's disease 1. Osmotic: Laxative abuse, maldigestion of food
5. Toxic: Febrile illnesses (viral hepatitis), cholera, 2. Infections: Typhoid, cholera, amebiasis,
drugs (salicylates), corrosive poisons giardiasis, helminthiasis, H.I.V. infection, etc.
6. Functional 3 Endocrine diseases: Thyrotoxicosis, diabetes,
Addison's disease, etc.
26 > Hematemesis
4. Drugs: Thyroxine, prostigmin, ampicillin,
_ phenolphthalein, etc.
5. Anxiety: Irritable bowel syndrome, etc.
(Refer Pg. 387)
6. Miscellaneous: Malignant carcinoid syndrome.
27 > Consti
30 > Bleeding Per Rectum
1. Acute:
1. Anal: Fissure, fistula, foreign body, etc.
a. In t e s t i n a l o b s t r u c t i o n : Vo l v u! u s ,
intussusception, hernia, etc. 2. Rectal: Piles, proctitis, foreign body, neoplasms
3. Colonic: Bacillary and amebic dysenter y,
b. Acute abdomen: Appendicitis, salpingitis,
ulcerative colitis, carcinoma, polyps, diverticula,
perforation, colic, etc.
ischemia, irritant drugs, etc.
c. General: Septicemia
4. Hematological: Blood dyscrasias, anti-coagulant
2. Chronic: therapy, uremia, etc.
a. Faulty habits: Laxative abuse, prolonged travel,
> Jaundice
insufficient dietary roughage, etc.
b. Painful anal conditions: Piles, fissures, etc. 31
c. Organic obstruction: Carcinoma, diverticulum, (Refer Pg. 19)
strictures, etc.
32 > Epistaxi_s_
d. Adynamic bowel: Scleroderma, myopathies,
myotonia, etc.
e. Metabolic: Hypothyroidism, hypokalemia, 1. Hematological:
hypercalcemia, porphyria, lead poisoning a. Thrombocytopenia: ITP, leukemia, aplastic
f. Drugs: Atropine group, opium group, tricyclic anemia, etc.
antidepressants, coffee, etc.
6
( 1 ) History Taking and Symptomatology
35 Itching_
a. Infective fevers: Typhoid, malaria, measles,
viral infections, etc.
b. Hypertension 1. Skin disease: Scabies, candidiasis, psonas1s,
c. High altitude urticaria, pediculosis, allergic dermatitis, dry skin
d. Collagen disease: Pseudoxanthoma elasticum, 2. Systemic diseases:
Ehlers' Danlos syndrome, etc. a. Drug reaction
b. Senile purpura
33 > Bleeding'---
Gums
-
- -------
c. Infections: Enterobius vermicularis, hook
worm, tinea infections, hydatid cyst, etc.
1. Hematological: d. Endocr ine diseases: Diabetes mellitus,
a. Thromboc ytopenia: Leukemias, aplastic hyp othyroidism, hepatic diseases, obstructive
anemia, ITP, etc. jaundice, primary biliary cirrhosis, etc.
b. Qualitative platelet defect: Glanzmann's e. Renal diseases: Chronic renal failure, etc.
thrombasthenia, von Willebrand's disease, f. Blood diseases: Polycythemia vera, malignancy,
giant platelet syndrome, etc. Hodgkin's disease, myeloma, etc.
c. Coagulation disorders: Hemophilia, Christmas 3. Pregnancy
disease, vitamin K deficiency, afibrinogenemia,
36 > Hirsutism
anticoagulants, etc.
d. Miscellaneous: Hypersplenism, vitamin
B 12 deficiency, disseminated intravascular I. With virilization: Arrhenoblastoma, malignant
coagulation, etc.
adrenal tumors, congenital adrenal hyp erplasia,
2. Gum diseases: Gingivitis, periodontitis, herpes, testicular tumors, etc.
Vincent's infection
3. Systemic disease:
a. Scurvy
b. Drugs: Phenytoin therapy
c. Diabetes mellitus, Cushing's syndrome
d. Pregnancy
e. Henoch-Schonlein purpura
f. Connective tissue disease: Ehlers' Danlos
syndrome, etc.
7
PRACTICAL MEDICINE
37 > _&�necomastia_
8. Referred pain: Pancreatitis, retroperitoneal
tumors, cholecystitis, diverticulitis, retroverted
1. Physiological: During infancy and at puberty uterus, uterine prolapse, etc.
2. Refeeding: Recovery from wasting diseases 9. Spinal deformities: Kyphosis, scoliosis and
3. Testicular: Agenesis, orchitis, tumour, Klinefelter's lordosis
syndrome, etc.
4. Endocrine: Acromegaly, adrenal tumors, ectopic
hormone production, etc.
39 > Hiccoug<.:_h_____
5. Drugs: Digitalis, spironolactone, phenothiazine, 1. Metabolic: Uremia, diabetes
metoclopramide, cimetidine, etc. 2. Toxemia: Septicemia, high fever
6. Miscellaneous: Cirrhosis of liver, rheumatoid 3. Abdominal: Liver abscess, peritonitis, subphrenic
arthritis, leprosy, etc. abscess, etc.
4. Thoracic: Aortic aneurysm, mediastinal glands,
substernal goitre, etc.
5. Neurological: Encephalitis, meningitis, brain
tumour, etc.
6. Psychogenic: Hysterical, neurosis
7. Epidemic hiccoughs
40 > Headache
1. Intracranial:
a. Meningeal: Meningitis
b. Vascular: Intracranial aneurysm, malignant
hyp ertension, subarachnoid hemorrhage
c. Skeletal: Metastasis, Paget's disease, etc.
d. Space occupying lesion: Subdural hematoma,
tumors, granulomas, abscess
38 > Backache 2.
e. Post lumbar puncture
Extracranial
1. Physiological: Faulty posture, asthenic a. Vascular: Migraine, cluster headache, temporal
individuals, pregnancy arteritis, etc.
2. Trauma: Prolapsed intervertebral disc, b. Skeletal: Paget's disease, torticollis, etc.
lumbosacral strain
8
( 1 ) History Taking and Symptomatology
44 > Intermittent
a. External ear: Wax, polyp, foreign body, etc.
b. Middle ear inflammation
c. Internal ear: Meniere's disease, labyrinthitis,
Claudication
acoustic neuroma 1. Arterial: Atheroma, embolism, Buerger's disease
2. Systemic: Migraine, barotrauma, anemia, aortic 2. Systemic: Diabetes mellitus, syp hilis, anemia,
regurgitation, salicylates, quinine, etc. McArdle's disease, overexertion
43 > Cram�s
tube blockage
- --- ------ 5. Miscellaneous: Migraine, aura of epilepsy,
1. Idiopathic anemia, hypotension, head injury, etc.
2. Elect rolyte distur bances: Hyponatremia,
hyp ocalcemia, hypomagnesemia
For details refer to P.J. Mehta's "Common Medical Symptoms" 6th Edition, 2013
9
T
he general examination of the patient must 4. Metabolic: Marfan's syndrome, homocystinuria
be done systematically, noting the following: 5. Miscellaneous: Cerebral gigantism, etc.
Differential Diagnosis
1. Built 11. Skin, hair and nails
1. Constitutional: Usually in constitutional tall
2. Body proportions 12. Vertebral column
stature the parents are also tall. In all children
3. Nutrition 13. Thickened nerves whose parents or grand parents are also tall, a
4. Decubitus 14. Joints suspicion of a pathological disorder must be
5. Clubbing 15. Temperature raised. The child is otherwise normal. In boys
usually no treatment is required. In girls long
6. Cyanosis 16. Pulse
term estrogen could be used to suppress further
7. Jaundice 17. Jugular venous growth. However, because of its side-effects,
8. Pallor pulse & pressure usually it is avoided unless the predicted adult
9. Lymphadenopathy 18. Blood pressure height is more than 183 ems.
10. Edema 19. Respiration 2. Gigantism (Acromegaly!Hyperpituitarism): In
gigantism the patient is very tall but with normal
body proportions. However, the features are
1 > Built coarse with increased heel pad thickness. There
may be evidence of raised intracranial tension
Built is the skeletal structure in relation to age and and bitemporal hemianopia. Pituitary tumors
sex of the individual as compared to a normal person. need surgery.
Tall Stature 3. CerebralGigantism(Soto'ssyndrome): Children
with cerebral gigantism have a large elongated
A child is considered to be tall when the height is head, prominent forehead, large ears and jaws,
greater than 2 standard deviations above the mean elongated chin, antimongoloid slant to the eyes
for the age. Gigantism is the term applied when the and coarse facial features. They have subnormal
patient's height is greatly in excess of the normal for intelligence and impaired coordination. The cause
his age before fusion of epiphysis. There is no fixed is not known.
height to constitute a giant, but in adults, it is applied 4. Sexual Precocity and virilizing disorders: In
for individuals with a height of more than 6� ft. these children, acceleration of linear growth
Causes occurs simultaneously with signs of premature
sexual development or inappropriate virilization.
1. Simple or primary gigantism: Racial, familial or This disorder may be due to congenital adrenal
constitutional hyperplasia, adrenal tumor, gonadal tumor or
2. Endocrine: Hyp erpituitarism, hyp ogonadism premature secretion of gonadotropic hormones.
3. Genetic: Klinefelter's syndrome The bone age is usually advanced so that the adult
stature may be diminished.
{ 2 ) General Examination
Table 2.1 : Differential Diagnosis of Gigantism when Upper Segment = Lower Segment
Constitutional Hyperpituitarism Cerebral gigantism
1. Family history +
2. Obesity + +
3. Mental retardation +
4. Otherfeatures OfGigantism Macrocrania, large hands andfeet
5. Marjan 's syndrome: These patients are tall Short Stature (Dwarfism)
with long limbs, narrow hands, long slender
Dwarfism is the term applied when the patient's
fingers (arachnodactyly), hyperextensible joints,
height is 2standard deviations less than that for
dislocation of the lens, high arched palate,
his/her age and sex. Mid-parental height usually de
kyphoscoliosis, arm span greater than the height
termines the final height.
and the lower segmetnt more than the upper
segment. Causes
6. Homocystinuria: This condition resembles
1. Hereditary/Genetic
Marfan's syndrome. The differences are mentioned
in the table. 2. Chromosomal: Turner's syndrome (45XO),
Down's syndrome, Noonan's syndrome, etc.
7. Klinefelter's syndrome:
3. Constitutional growth delay
a. Lower segment more than the upper segment
4. Delayed puberty
b. Gynecomastia
5. Nutritional: Malnutrition, malabsorption, rickets
c. Small, firm testes, azoospermia
6. Endocrine: Growth hormone deficiency,
d. Chromatin (Barr) body usually present
hypopituitarism, hypothyroidism, excessive
(47XXY). Some may be chromatin negative.
androgens, Cushings syndrome, congenital
e. Mental retardation may be associated. adrenal hyperplasia
f. Associated with mongolism and leukemia. 7. Skeletal: Achondroplasia, spinal deformities,
g. Chronic pulmonary disease, varicose veins skeletal dysplasias
and diabetes are more common 8. Systemicdiseases: Renal tubular acidosis, uremia,
11
PRACTICAL MEDICINE
congenital cyanotic heart disease, cirrhosis of low hairline, square and shield-like chest, cubitus
liver, etc. valgus and mental retardation. Although short,
they grow at the rate of less than 4 cm each year
Differential Diagnosis with normal bone age and dental age but absent
1. Hereditary: In hereditary short stature there is pubertal growth spurt, so that during adolescence,
no endocrine abnormality. The bone age and the the skeletal age is delayed due to the absence of
dental age are normal. Although they are short, sex hormones (streak ovaries).
they grow at a constant rate of 4-5 ems a year and Giving them oxandrolone 0.15 mg/kg/day with
they have normal body proportions for age. This growth hormone from early adolescence till
may be either genetic (if there is a family history of puberty can increase the height. After the age of
short stature) or primordial (if there is no family 15 years cyclical estrogen replacement therapy
history of short stature). The latter may be due to in physiological doses is given for life. Growth
intrauterine growth failure or postnatal growth hormone replacement is recommended before
retardation. These children require no endocrine epiphyseal fusion.
treatment. 4. Hypopituitarism (including Growth Hormone
2. Constitutional growth delayand delayed puberty: deficiency): These children have the skeletal age
This disorder is common among adolescent boys. and the dental age delayed by more than 2 years.
There is no true endocrine deficiency. They grow The growth rate is less than 4 cm/year. The ratio
at a constant rate of about 4 cm a year but their of the upper segment and the lower segment is
bone age and dental age is delayed by about 2 normal. They have genetic defects (prop- I, pit
years. Often there is a history of delay in growth I gene deficiency). MRI shows hypoplastic or
and pubertal development in the father and other aplastic pitutaries. Growth hormone replacement
male relatives. is necessary.
If puberty does not occur spontaneously by 15 years 5. Hypothyroidism: These children have mental,
of age, it can be induced by testosterone enanthate dental and skeletal retardation since birth. There
250 mg IM once a month for 3 months. would be coarse dry skin and constipation. Their
3. Turner's syndrome (SHOX gene deficiency): body proportion is infantile i.e. upper segment
These children are girls who have agenesis of is more than lower segment. Lifelong thyroxine
their ovaries. The chromosomal pattern is 45XO. replacement is required.
They have a characteristically short webbed neck, 6. Achondroplasia: Achondroplastic dwarfs have
short limbs resulting in short stature. Hence,
Table 2.3 : Differential Diagnosis of Short Stature (Dwarfism)
Constitutional Hereditary Hypopituitarism Hypothyroidism Turner's syndrome
1. Family history + +
2. Birth wt. and height N ,I. N N ,I.
3. Pattern of growth Slow from birth Slow from birth Slow few months Slow from birth Slow from birth
4. Features Immature but Mature Immature Infantile Characteristic
later normal features
5. Bone age Slight delay N Progressive Marked N
retardation retardation
6. Dentition N N Delayed Delayed N
7. Mental status N N N Retarded Retarded/N
8. Puberty Later but normal N Delayed Marked delay Absent
eventually
12
( 2 ) General Examination
1. Vitamin A Carrot, Spinach, sweet Night Blindness, Bitot's spots 500 IU/kg/day I.M.
(5000 IU, 80001U potatoes, milk, liver and Xerophthalmia, Keratomalacia, Toxic effects: Painful bone
in pregnancy) fish liver oils Imperfect enamel formation. Exostosis, premature epiphyseal
Follicular hyperkeratosis of fusion. Pruritus, intracranial
skin hypertension, anorexia,
irritability, dry itchy skin, sparse
hair
2. VitaminD Milk butter, yeast, fish, Tetany and rickets in children 5001U/day
(4001U) liver oil, egg yolk, Synthesis Osteomalacia in adults Toxic effect: Anorexia,
in skin when it is irradiated vomiting, diarrhea, lassitude,
thirst, sweating and headache
5. Vitamin81 Whole grain, cereals, yeast, Anorexia and nausea, Dry & 100mg orally or IM
(Thiamine) beans, liver, meat, egg yolk wet beriberi, Wernicke's
(1-2mg/day) encephalopathy. Korsakoff's
psychosis
7. Nicotinic acid Rice, liver, brain, eggs, Erythema, Pigmentation, 500 mg orally.
(15-2 0mg) meat and yeast hyperkeratosis of skin, Toxic effects: itching,
seborrhea around the nose, flushing, amblyopia, liver
raw red tongue, diarrhea, dysfunction and hyperuricemia
dementia and paraplegia.
8. Pantothenic acid Whole grain, milk, eggs, Burning feet syndrome 4-10mg orally
(3-10mg) liver, kidney, meat
13
PRACTICAL MEDICINE
10. Inositol Green citrus fruits, grains, yeast. Not known in man. In animals
(not known) - alopecia, dermatitis and fatty
liver
14. Cyanocobala- Liver, Synthesized in colon Pernicious anemia, Glossitis, 100 mcg orally or IM
min but not useful to the host as Subacute combined degene
Vitamin 8 12 it is excreted and not ration of spinal cord.
(1 mcg) absorbed
3 > Nutrition
the lower segment is always less than the upper
segment. Their mental and dental ages are normal
and so are the endocrine functions. A normal person is well nourished as regards proteins,
7. Systemic diseases: Most chronic systemic diseases fats, carbohydrates, vitamins and minerals. Certain
can cause growth failure during childhood. These clinical signs help to diagnose deficiency of one or
illnesses can be recognized by their own specific more of these nutrients.
clinical features and growth failure is a secondary 1. Proteins: Hypoproteinemia causes rough skin
problem. and later edema of feet and brittle hair.
2. Fats: Fat malnutrition leads to cachexia with
ortions
hollowing of cheeks, loss of the shape of hips (due
to loss of fats), flat abdomen and absent fat over
Normally, in adults, the height of the person is equal the subcutaneous tissues of the elbows.
to the length of arm span. The upper segment (from 3. Carbohydrates: Carbohydrate malnutrition
vertex to the pubic symphysis) is equal to the lower is difficult to detect clinically because there is
segment (from pubic symphysis to the heel). gluconeogenesis from fats or proteins.
In infants, the upper segment is greater than the lower 4. Vitamins: These can be fat soluble (Vitamins A,
segment and the height is greater than the arm span. D, E, K) or water soluble (rest) and are discussed
This infantile type of body proportion persists in in the tables.
achondroplasia, cretinism and juvenile myxedema. 5. Minerals: Deficiency of two minerals can be
The reverse of infantile body proportion i.e. arm span diagnosed clinically. Iron deficiency causes
greater than height and lower segment greater than koilonychia and pallor whereas calcium deficiency
upper segment occurs in eunuchoidism, Marfan's causes tetany.
syndrome, homocystinuria, Klinefelter's syndrome
and Frohlich's syndrome.
14
< 2 > General Examination
5 > Clubbing
to chronic obstructive phlebitis
Grades
Definition I. Softening of nail bed
II. Obliteration of the angle of the nail bed
Clubbing is bulbous enlargement of soft parts of the
terminal phalanges with both transverse and longitu Ill. Swelling of the subcutaneous tissues over the base
dinal curving of the nails. The swelling of the terminal of the nail causing the overlying skin to become
phalanges occurs due to interstitial edema and dilation tense, shiny and wet and increasing the curvature
of the arterioles and capillaries. of the nail, resulting in parrot beak or drumstick
appearance (Figs. 2.1 & 2.2).
Causes IV. Swelling of the fingers in all dimensions associated
1. Pulmonary with hypertrophic pulmonary osteoarthropathy
causing pain and swelling of the hand, wrist etc.
a. Bronchogenic carcinoma, mesothelioma
and radiographic evidence of subperiosteal new
b. Lung abscess bone formation (commonly seen in bronchogenic
c. Bronchiectasis carcinoma, paraneoplastic syndromes).
d. Tuberculosis with secondary infection
Schamroth's Sign (Fig. 2.3)
e. Diffuse fibrosing alveolitis
Normally when two fingers are held together with
f. Empyema nails facing each other, a diamond-shaped space is
2. Cardiac seen at the level of proximal nail fold. This is lost in
a. Infective endocarditis case of clubbing
15
PRACTICAL MEDICINE
\
3. Platelet-derived growth factor causing
vasodilatation.
(a) Pseudoclubbing
___JI(��--=�:
In hyp erparathyroidism or leprosy excessive bone
resorption may result in disappearance of the ter
minal phalanges with telescoping of soft tissues and
a 'drumstick' appearance of the fingers resembling
clubbing. However, the curvature of the nail is not
(b) present.
: Fig 2.1 (a)& 2 1 (b) (a) Normal nail bed, Profile angle=
180°, (b). Severe clubbing- hypertrophy of soft tissues,
\
I_
__ Pr�file an_gle � � �0 _
°
---� 6 > �ianosis
DEFINITION: Cyanosis is a bluish discoloration ofthe
nails due to increased amount of reduced hemoglobin
(more than 5 mg%) in capillary blood.
Types
I. Central
II. Peripheral
III. Cyanosis due to abnormal pigments
No space
IV. Mixed
Space
Table 2.5 : Differences between Central
and Peripheral Cyanosis
Central Peripheral
16
....
N
'Y
"';:
c;".l
CYANOSIS
;:!
Warm extremities tongue Cold extremities, Only in upper limbs / Cold extremities 5·
and blue tongue ;:,
also cyanosed pink tongue lower limbs ::.
C;:
I�"" I Peripheral
Mixed
(See separate flow chart)
Cold Exposure Diarrhea Precordial pain, Local arterial Plethoric face I Acut!LVF I Mitral
I
Thrombophtebitis vomiting perspiration constriction
hemorrhage Stenosis
I
PDA with Transposition of PDA with reversal of
great arteries with reversal of shunt shunt
Preductal Coarctation
of Arteries
'""'
'-l
�
00
CENTRAL CYANOSIS
I
Abnormal Normal
globulin
I
globulin
�-�r
Hb-M Spectroscopy of Dry cough Hemoptysis Clubbing Following
disease Pleuritic Instrumentation
Fallot's Eisenmenger
chest pain
Tetrad Complex
Pul. Atresia Primary or
Secondary Pulmonary Pneumothorax Pulmonary Collapse
Right to Foreign Body
Band at Band at 618 Hypertension Embolism Stricture
Left Shunt
630mU mU
Methemoglobin Sulphemoglobin
Fibrosis Carcinoma m
0
R
zm
{ 2 ) General Examination
7 > Jaundice
D. Reynaud's phenomenon
III. Mixed
A. Acute left ventricular failure Definition
B. Mitral stenosis (leftatrial failure and peripheral Jaundice is a symptom complex which is characterized
vasoconstriction).
19
PRACTICAL MEDICINE
I. HISTORY:
1. Abdominal pain Absent Present Present in crisis
2. Pruritus Transient Marked Absent
3. Past history a) Contact with a) Pain (Stones) a) Of crisis
jaundice patient b) Weight loss (Neoplasm) b) Drugs, blood
b) Drugs c) Surgery (Stricture) transfusion etc.
II. EXAMINATION:
1. Tender liver May be present Absent Absent
2. Spleen May be present Absent Present
3. Gall bladder Not palpable Palpable if due to neoplasm Not palpable
4. Pallor Absent Present Present
II. INVESTIGATIONS:
1. Urine:
Bilirubin Present Present Absent
Urobilinogen Present Absent Present
2. Stools:
Sterocobilinogen Present Absent Present
3. Peripheral smear Leucopenia in Normal Reticulocytosis
infective hepatitis Spherocytosis
4. L.F.T.
a) Bilirubin ++ ++ +
b)Alkaline phosphate Raised Markedly raised Normal
c)SGO T Markedly raised Raised Normal
s. Barium meal and cholangiography Normal May reveal pancreatic growth Normal
6. RBC survival Normal Normal Decreased
20
< 2 > General Examination
RBC
0
�'>8oRES
1. Breakdown
phase
1
Free bilirubin
2. Conjugation
phase
"'--
Urobilinogen
4. Renal
excretion
phase
Stercobilinogen
Bilirubin Metabolism
s
1. Breakdown phase: Hemoglobin released
by breakdown of aged cells is broken
down into globin and heme in the
spleen. The heme is further broken into �
iron and bilirubin. Bilirubin attaches to
serum albumin and is transported to
the liver where it is taken up. Bilirubin
(unconjugated) bound to albumin cannot
be excreted by kidneys. 1l] .s
-t-� ...�
.!
Conjugation phase: In the liver, bilirubin t .a �
� bl) ...0
:=
.t
2. -
u.l
C.
O .D 1:1:l <
is separated from albumin and conjugated :=
to glucuronide by glucuronyl transferase. ...
C
"'... � ... ...
e' .gp:�
0 (U
.D "' � (U
u uZ
The conjugated bilirubin is water-soluble
"'
;,!: "'>
and can be excreted by kidneys. z U)
0
.. "'...."'
re-excreted (enterohepatic circulation).
ii "'
Unabsorbed sterco-bilinogen gives � ;a
brown color to the feces. ·a... ·s..
0
:9
(U
4. Excret i o n p h a s e : Ci r c u l a t i n g
2:l u.l
..s c:s :a
urobilinogen is carried to the kidneys
for excretion in the urine as urobilinogen.
21
PRACTICAL MEDICINE
2. Hemoglobinopathies:Sicklecellanemia, C. Cirrhosis
homozygous beta thalassemia, sickle 1. Portal
thalassemia, HbE thalassemia
2. Biliary
3. Enzyme deficiency (E6PD, pyruvate
3. Hemochromatosis
kinase).
IV. Obstructive (Surgical Jaundice- Post
4. Paroxysmal nocturnal hemoglobinuria
hepatic):
(PNH)
A. Extra-Hepatic:
B. Extra-Corpuscular Defects:
1. Inflammatory: Stone, stricture, parasites,
1. Infections: Malaria, Clostridium welchii
acute cholecystitis
2. Drugs: L. Methyl dopa, quinine,
2. Neoplastic: Carcinoma of the head of
phenacetin, sulfonamides
the pancreas; neoplasm of bile ducts,
3. Physical agents: Burns, Irradiation gall bladder and ampulla ofVater
4. Poisons: SnakeVenom, Favism 3. Congenital: Biliary atresia
5. Immunological: Mismatched blood B. Intra-Hepatic:
t r a n s fu s i o n , p a r o x y s m a l c o l d
1. Cholestatic phase of infective
hemoglobinuria, lymphoma, CLL, SLE.
hepatitis
6. Miscellaneous: Uremia, cirrhosis ofliver
2. Drugs: Steroids, chlorpromazine,
II. Congenital Hyperbilirubinemia PAS, sulfonamides, chlorpropamide
A. Unconjugated: tolbutamide, methyl testosterone,
1. Disturbance of bilirubin transport: erythromycin.
Gilbert's syndrome. 3. Pregnancy with cholestasis.
2. Disturbance of bilirubin conjugation:
Crigler Najjar syndrome.
B. Conjugated: Disturbance in excretion of
8 > Pallor
bilirubin: Dubin Johnson syndrome and Pallor is paleness ofskin and mucous membrane either
Rotor's syndrome. as a result of diminished circulating red blood cells or
III. Hepatocellular (Medical Jaundice-Hepatic) diminished blood supply.
A. Infections Causes
1. Viral hepatitis
I. Anemia
2. Weil's disease (Leptospirosis)
A. Hemorrhagic
3. Septicemia
B. Hemolytic
4. Malaria, Typhoid
C. Dyshemopoietic
B. Toxic
1. Deficiency ofiron, folic acid orVitamin
1. Anesthetic agents: Halothane, B 12
chloroform
2. Aplastic anemia
2. Anticoagulants: Phenindione
3. Systemic and infiltrative diseases
3. Anti-tuberculous drugs: Rifampicin,
4. Chronic infection
P.A.S., I.N.H., Thiacetazone
5. Pregnancy
4. Metals: Arsenic, mercury, gold, bismuth
6. Malignancies
5. Chemicals: D.D.T.
6. X-ray irradiations
22
{ 2 } General Examination
II. Vasoconstriction The supratrochlear lymph nodes are palpated on the
A. Shock : Hyp ovolemic / cardiogenic medial aspect of the arm between the groove ofbiceps
and brachialis muscle, an inch above the arm fold.
B. Exposure to cold
The inguinal nodes are examined in the supine position
C. Fright
with the thigh extended. Both the medial and lateral
D. Syncope and postural hypotension groups of lymph nodes are examined.
E. Arterial Occlusion Scalene nodes are present behind the sternomastoid
III. Cutaneous muscle and may be palpable. In suspected malignancy,
A. Thick skin and nails biopsy it taken from that area, even if the nodes are
B. Edema (edema causing diseases) not palpable.
23
PRACTICAL MEDICINE
24
< 2 > General Examination
3. Highly malignant tumor grows rapidly and Infectious Mononucleosis
invades the surrounding tissues.
1. Acute onset offever, chills, sore throat, headache,
Secondary Carcinoma malaise and tiredness occurs
1. The nodes are enlarged, irregular and fixed to all 2. The lymph nodes are enlarged, discrete and
structures including the skin. slightly tender affecting especially the cervical
and submandibular nodes.
2. It has stony hard consistency.
3. Non-tender splenomegaly may occur.
3. Primary growth may be detected.
4. Petechial rash may occur at the junction of soft
4. Patient may be cachectic and wasted.
and hard palate on the fourth day and may persist
Hodgkin's Disease for 3-4 days.
Affects young adolescent males. 5. Peripheral smear shows leucocytosis (absolute
1.
lymphocyte count more than 1500/cmm) with
2. Cervical glands are affected early but later all atypical lymphocytosis.
lymph nodes are involved.
6. Paul-Bunnel test may be positive in 1:32 dilution
3. Lymph nodes are elastic and rubbery, discrete or more usually in the first l O days.
and movable with little tendency towards matting,
softening or suppuration. HIV Associated Lymphadenopathy
4. Pressure symptoms: Edema, venous engorge l. Commonly called PGL or persistent generalised
ment and cyanosis of head and neck may occur lymphadenopathy.
due to pressure on the superior vena cava and the
2. Usually seen in stage of intermediate
bronchus by the mediastinal glands. Root pains
immune depletion following HIV infection
and paraplegia may develop due to pressure on
(Refer Pg. 113).
the spinal cord.
Hepatosplenomegaly and anemia occur.
> Edema
5.
6. Pel Ebstein's type of fever (recurrent bouts of 10
remittent fever) may occur.
Edema is the collection offluid in the interstitial spaces
7. Weight loss more than 10% of body weight and or serous cavities. It becomes evident only when 5-6
night sweats. liters of fluid has accumulated in the water depots.
8. Peripheral smear will show lymphocytosis and Pitting on pressure occurs when the circumference
eosinophilia. of the limb is increased by l 0%.
9. Lymph node biopsy will show Reed Sternberg's
Mechanism
cell.
One or more of the following factors may be respon
Non-Hodgkin's Lymphoma sible.
Similar to Hodgkin's lymphoma in clinical presenta 1. Increased capillary permeability when it is
tion except: damaged e.g. acute inflammation.
1. Enlargement of nodes in Waldeyer's ring and 2. Increased capillary pressure e.g. cardiac failure.
supratrochlear glands 3. Decreased osmotic pressure of the blood e.g.
2. Symptoms are less common hypoproteinemia.
3. Can be a manifestation of HIV infection 4. Damaged lymphatic drainage e.g. filariasis.
4. Diagnosis confirmed by histologicalexamination
Site
of the bone marrow.
Venous edema commonly occurs in the lower limbs
25
PRACTICAL MEDICINE
Differential Diagnosis
1. Cardiac
A. Congestive Cardiac Failure: The edema is
found on the most dependent parts ofthe body
as gravity plays an important part. Hence, in an
ambulatory patient edema is in the feet, ankles
and legs whereas in the recumbent patient it
is mainly over the sacrum, lumbar region and
Unilateral: genitalia. It is most marked in the evening.
A. Lymphatic: B. Left ventricular failure: Accumulation offluid
1. Filariasis in the lung occurs much earlier than edema of
the feet, resulting in dyspnea, cough and basal
2. Pressure by new growth, metastasis
rates.
3. Radiation
C. Pericardial effusion: Since there is obstruction
B. Traumatic: Bruises, sprains, fractures to the flow of blood into the right atrium,
C. Infections: Cellulitis, boils, carbuncle edema of feet may occur, but no edema of
D. Metabolic: Gout lungs occurs because the heart is able to pump
the little blood it receives into the lungs and
E. Venous: Venous thrombosis, varicose veins.
general circulation. It is associated with raised
F. Hereditary: Milroy's disease JVP, hepatomegaly and ascites.
26
( 2 ) Ge11eral Examination
Painless Paillful
Ons.et
I Involves only Part of the limb Involves the
From birth big toe with affected and whole limb
Late onset
Tophi painful
Milroy's ! Filjiasis !
Disease
I Glut I
Cellulitis
Linear and
streaks
I
Present Absent
Filariasis Venous
Thrombosis
27
�
BILATERAL EDEMA
Onset
With loss of With puffy face With Ascites Pitting Edema feet Generalised
weight, without any
Cachexia, Polyarthritis cause
Starvation
Hypertension Sudden onset Constipation Dialated veins JVP raised
Hematuria I Wheezing Itch- Rough skin over chest and Ascites JVP raised Idiopathic
Proteinuria ing Hoarse voice Hepat<>megaly Chest signs
abdomen
0
R
z
l
< 2 ) General Examination
11 > Skin and its occur in typhoid, syphilis and purpura. If they
are not generalized, they are called roseolar.
---- A��endag_e_s���- 2. Papules: (Raised tiny nodule < 5 mm): This
Examination of skin often gives important clues to may occur in measles, chickenpox, smallpox
local or systemic diseases. The following features and following drugs like sulfonamides.
should be noted: 3. Pustules: These are papules containing pus.
I. Color: It may be pale, flushed, cyanosed, yellow, 4. Nodules: (Large papules as solitary projection
etc. from the skin : 5 mm - 5 cm). This may occur
II. Pigmentation: Pigmentation may occur in several in erythema nodosum, leprosy, tuberculosis,
diseases. Some common medical conditions secondary syphilis.
associated with pigmentation are: 5. Vesicles: (small blisters < 5 mm). This may
1. Endocrine: Addison's disease, Cushing's occur in herpes, chickenpox and smallpox.
disease, thyrotoxicosis. 6. Bullae: Fluid-filled lesion > 5 mm.
2. Deficiency: Pellagra, Kwashiorkor, 7. Wheal: (Elevated patches on the skin with
megaloblastic anemia. centre paler than the periphery) Allergy.
3. Infections: Kala azar, chronic malaria, V. Neurocutaneous Stigmata (Phakomatoses)
secondary syphilis, tuberculosis, leprosy, HIV,
1. Cafe-Au-Lait spots:
etc.
Dark brown patches resembling coffee in
4. Metabolic: Hemochromatosis.
milk. They are considered significant if they
5. Skin disease: Neurofibromatosis, lichen are more than 5 in number or single one> 15
planus, acanthosis nigricans, etc. mm. They are seen in:
6. Miscellaneous:Malignancy, pernicious anemia, a. Neurofibromatosis (regular outline
exposure to sunrays or radiations. without deep indentations)
III. Hypopigmentation: Hypopigmented patches b. Albright's syndrome (irregular outline
may occur in leprosy, leukoderma, albinism, with deep indentations)
fungal infections of skin, etc.
c. Tuberous sclerosis
IV. Eruptions: Various types oferuptions may occur
Schwartz criteria for significant cafe-au-lait
as follows:
spots
1. Macules: (Not raised above the skin). This may
a. > 5 in number, more than 2 cm
29
PRACTICAL MEDICINE
I
t 30
( 2 > General Examination
I. Scoliosis
Scoliosis is an abnormal lateral curvature of the
spine.
Causes:
l. Congenital
2. Postural: Carrying heavy weight in one arm.
3. Compensatory: Reduced length of one lower
limb.
4. Reflex: To relieve pain as in sciatica or renal Normal Scoliosis Kyphosis Gibbus Lordosis
colic
Fig 215:VertebralColumn
5. Neurological: Poliomyelitis, syringomyelia,
muscular dystrophy, hereditary ataxia.
IV. Pes Cavus
6. Rickets
Pes cavus is the increased anteroposterior
7. Functional
curvature of the arch of the foot.
II. Kyphosis Causes:
Kyphosis is an abnormal anteroposterior l. Idiopathic
curvature of the spine with forward concavity 2. Spinocerebellar atrophy: Friedreich's ataxia,
and dorsal prominence. peroneal muscular atrophy
Causes: 3. Spinal cord disease: Poliomyelitis, spina bifida
L Congenital: Wedge shaped vertebra. 4. Cerebral palsy
31
PRACTICAL MEDICINE
14 > Joints
flaccid weakness in the upper limb and spastic
paraplegia (syringomyelia).
Causes of Arthritis
I. History
1. Onset Acute Arthritis
2. Pain and swelling in the joint 1. Traumatic
3. History of trauma, tuberculosis, typhoid, 2. Infection: Gonorrhea, septic, typhoid, bacillary
exposure to venereal disease, pneumonia, dysentery, rheumatic, Reiter's syndrome. etc.
bacillary dysentery, bleeding tendencies, renal
3. Gout
colic.
4. Scurvy
4. Family history of hemophilia, tuberculosis
gout, etc. 5. Hemophilia
6. Acute attacks in chronic arthritis
II. Examination of Joints
Chronic Arthritis
A. Inspection:
1. Joints affected I. Infection: Tuberculosis, syphilis, rheumatic
2. Position of the joint and fixed deformity 2. Collagen disease: Rheumatoid, SLE., Polyarteritis
3. Swelling nodosa
4. Signs of inflammation over the joint 3. Degenerative: Ankylosing spondylitis
5. Muscular wasting just above the joint 4. Neuropathic: Tabes dorsalis, syringomyelia
B. Palpation: 5. Miscellaneous: Hemophilia, gout.
L Local temperature Differential Diagnosis
2. Tenderness
3. Swelling-fluctuant or non-fluctuant Septic Arthritis
4. Bony components and its relation to the 1. Acute onset with symptoms of septicemia
joint
32
( 2 ) General Examination
2. A single large joint or multiple small joints are 2. Arthralgia and hydrarthrosis are seen in
involved secondary syphilis
3. Joints are painful, especially on movement 3. Gummatous arthritis occurs in the tertiary stage
Spontaneous dislocation and fibrous or bony
4. Rheumatic Arthritis
ankylosis may occur.
1. It is common between 5-25 years.
Tuberculous Arthritis
2. There may be antecedent Stre ptococcus
1. There is insidious onset. It commonly affects the hemolyticus infection
upper Jimbs in adults and lower Jimbs in children. 3. T he onset may be rapid with relapses and
2. Tuberculous focus may be present in the body remissions
3. Night starts due to involvement of the articular 4. Multiple joints are affected with fleeting arthritis
cartilage may occur 5. Affected joints may be painful, tender and swollen
4. Muscular deformity and wasting may be present 6. Other evidences of rheumatic fever: Carditis,
5. Rise of local temperature with a spongy feel of the chorea, rheumatic nodules and erythema
thickened synovial membrane may be present marginatum may be present
6. Restriction of movements is common 7. Elevated ESR, positive ASO titer and C reactive
7. Cold abscess and sinus may occur protein may be present
8. X-ray: Generalized decalcification, obliteration Rheumatoid Arthritis
of joint space with erosion of the articular ends.
Pathological dislocation and recalcification may l. It commonly affects women between 24-40
be present. years age
2, Characteristically it is bilaterally symmetrical,
Gonococcal Arthritis affecting the small joints of the hand or foot and
1. It occurs 3 weeks after the primary infection may spread to large joints
2. Onset is sudden, with fever 3. Periodic painful swelling ofthe joints with stiffness
and deformity ( e.g. ulnar deviation of the hand,
3. It may be monoarticular (knee or elbow) or
flexion deformity etc.) may occur
polyarticular and may be manifested by acute
arthralgia or acute arthritis (redness, heat and 4. Muscle spasm and muscle wasting may be present
edema) 5. Restriction of movement is common
4. Gonococci may be demonstrated in urethral 6. X-ray: Decalcification and diminished joint space
discharge. may be seen
Stilt's disease is juvenile rheumatoid arthritis with sple
Reiter's Syndrome
nomegaly and lymphadenopathy.
This is characterized by multiple acute arthritis, non·
gonococcal urethritis and often conjunctivitis. Osteoarthritis
33
l;,t,)
�
POLYARTICULAR ARTHRITIS
' I
Acute onset Insidious onset
H/o Injury Fever Fleet ing Large synovial Painful Young female Painful joint Young male,Lumbar Any age,
Malaise joint pains in joints affected infection &Swellings spine and sacro joint pain,
Sore throat young person with pain but Hormonal I H/o fever iliac joints Radiologal
no synovial involved, HLA changes
Traumatic
changes Fever, lymph
I I I thickening or adenopathy, handaffected
Hemato
B27 posit ive
Endocrine Malignancy
Rheumatic 1
Morming
logical
effusion
I I systemic
stiffness,
Viral arthritis
i nvolvement
Al and
hard chance dapsone, disease, fever,
12 weeks prior multiple embolic Distal inter Urethritis, con Following Rheumatoid
disease Gastrointesti-
to arthritis erythematous episodes uveitis phalangeal junctivitis, diarrhea
nal infection
nodules joint affected, Keratoderm ia,
like Yersinia,
Skin lesions .,'"T'h,g;,
Post- Secondary
I
Shigella
I endocardlitis
Infectiv,
Streptococcal 11 syphilis
�
Juvenile
�
Psoriatic Reiter's Postcolitis Post colitis
arthropathy Syndrome Arthropathy rheumatoid arthropathy
arthritis
R
)>
r
Ankylosing
:I
spondylitis
m
0
R
zm
( 2 ) General Examination
4. Pain restricts movements. Grafting may be felt
on passive movements
5. Heberden's nodes may be present.
6. X-ray: Diminished joint space with osteophytes
may be seen
Gout
1. It occurs usually in obese men between 25·40
years
-� �� .�
- "'
·-
2. There is asymmetrical affection of the big toe.
0
"'il .. Later other joints may be affected. Relapses and
e;,.. .c
t: remissions are common.
� e
0
"'
o:I
CII 3. There is sudden onset of acute agonizing pain
0 ::i::
usually at night
4. Initially the tissues around the joint are red,
swollen and edematous. Later, ligaments and bone
ends are infiltrated by the chalky deposits which
form tophi. If the skin over the tophi gives way,
i
·o·� C chalky discharge results.
""
V
0
� 5. Movements are painful. Muscles wasting may
8 V
... Q. occur later
"8 I>()
V C
Cl ::J 6. Serum uric acid is elevated
� :S
V
>
V
u..
Hemophilic Joints
l. It is common in young boys with positive family
history. It is a sex-linked recessive disorder
2. There is sudden painful bilateral hemorrhagic
effusion into the knee joints
3. Clotting time is increased, activated partial
thromboplastin time (APTT) is prolonged
and antihemophilic globulin (AHG) levels or
Christmas factor levels in blood are low
4. Ultimately chronic disabling arthropathy results
Neuropathic Joints
1. Osteoarthritis in the denervated joints (Tabes
dorsalis, syringomyelia, peripheral neuropathy)
2. There is little pain but marked destruction of the
bone.
Scurvy
1. It is common in malnourished children
2. There is painful swelling of the knee joint
3. Hemorrhages and petechial hemorrhages in
----
35
PRACTICAL MEDICINE
skin and at hair roots may occur which requires pneumonia, typhoid, urinary tract infection,
examination with magnifying glass. infective endocarditis, brucellosis, typhus, etc.
Ankylosing Spondylitis
1. It is common in boys between 15 25 years
in ::r,�
Temperature
' �:;:
ttenl
--:=:,¥.·. ,:=-�----
\··,. ..":°/� -
105 / .
104
••• �:.-::,... , Con. lrnuous
2. There is insidious, progressive involvement of
103 fever
spinal joints especially sacroiliac joint 102 -·· •• .... : .':. ·� ....
101 : ', ; •• .' ••
3. Movements of the joint are restricted due to 100 ,: ', / \ .: ':.. Intermittent
pain and stiffness. Later, there is kyphosis and ...... •• • •.... fever
36
( 2 } General Examination
3. Vascular: Acutemyocardial infarction, puhnonary 4. Fever with membrane in the throat: Occurs in:
embolism, pontine hemorrhage, etc. a. Diphtheria
4. Traumatic: Crush injury. b. Infectious mononucleosis
5. Immunological: C. Agranulocytosis
a. Collagen disease, SLE, rheumatoid arthritis. d. Moniliasis
b. Drug fever e. Vincent's angina.
c. Serum sickness 5. Fever with delirium: This is common in:
6. Endocrine: Thyrotoxicosis, Addison's disease. a. Encephalitis
7. Metabolic: Gout, porphyria, acidosis, dehydration b. Typhoid state
8. Hematological: Acute hemolytic crisis c. Meningitis
9. Physical agents: Heat stroke, radiation sickness. e. Pneumonia (especially in alcoholics and elderly
10. Mi scellaneous: Factitious fever, habitual people with dementia)
hyperpyrexia, cyclic neutropenia f. Hepatic encephalopathy
Special Types of Fever 6. PUO (Pyrexia of Unknown Origin)
a. Temperature > 101°F (38.3 °C) on several
Fever with rigors: This occurs in:
occasions.
a. Malaria
b. Duration >3 weeks
b. Kala azar
c. Duration > l week in hospital with failure to
c. Filariasis reach diagnosis.
d. Urinary tract infection, pyelonephritis Classification
e. Cholangitis a. Classical PUO (lymphoma, collagen
f. Septicemia vascular disease, abcess, TB, viral infection,
g. Infective endocarditis endocarditis)
h. Abscesses, any site b. Nosocomial PUO: hospitalized, no fever
i. Lubar pneumonia on admission (thrombophlebitis, catheter
infections, deep vein thrombosis, drug fever,
2. Fever with herpes labialis: Elevated body transfusion reaction)
temperature may activate the herpes simplex
virus and cause small vesicles around the angle c. Neutropenic PUO: Absolute neurophil count
of the mouth (herpes labialis). It occurs with: <500 (fungal infection, perianal infection)
a. Pneumonia d. PUO in HIV infection (TB, Pneumocystis
j iroveci, toxoplasma, cryptococcus, CMV, Non
b. Malaria Hodgkins Lymphoma).
c. Meningitis
Hyperpyrexia
d. Severe streptococcal infection
3. Fever with rash: This is seen in: Hyperpyrexia is said to occur when body temperature
is more than 10s·F.
a. Chicken pox
b. Small pox Causes
c. Measles 1. Tetanus
d. Rubella 2. Malaria
e. Typhus 3. Septicemia
g. Allergy 4. Heat Stroke
37
�
�
FEVER
r1-,
Without With
I
Abdominal
1
Headache,
I
Valvular lesion
I
Cough,
Abd. pain, Past
I
I
Hepato- Cough,
specific specific pain, Rose spots, Vomiting, Neck Petechiae, Clubbing, Loss of history Amebic, splenomegaly, Haemoptysis,
symptoms symptoms Bradycardia stiffness Palpable spleen Weight anorexia dysentery Lymphadenopathy Breathlessness
I Influenza
I
I I 1TypLid I I Meningitis I I Endocarditis I Pulmonary 11 Amebic liver
I Tuberculosis Lymphoma
I
Brucellosis
I Abscess I I Leukemia Other
Occupational
hazards
Other signs of Throat pain, Cough, Chest Rigors Rashes
Viremia, Progressive
weight loss, High
Difficulty in
swallowing
pain, Rusty
sputum I
H/o Drug Ingestion
I
Risk Behaviour
Tonsillitis
-
Pneumonia I
HIV Infection Pharyngitis Burning Micturition Present Absent
Diphtheria
Infectious Drug Allergy Measles
Mononucleosis , Chickenpox
1
Absent Present
Benefits of Fever
In some human diseases, fever is beneficial, e.g. wide·
spread cancer, neurosyphilis, chronic arthritis, etc.
Fever was often induced in these diseases by injection
of milk protein or BCG vaccine.
It has been suggested that fever is associated with release
of endogenous pyrogens, which activate the T cells and
thus enhance the host defense mechanism.
Harmful Effects
l. Hypercatabolism-nitrogen wastage and weight
loss.
2. Fluid and electrolyte imbalance· due to sweating.
3. Convulsions and brain damage
4. Circulatory overload, arrhythmias, etc.
Hypothermia
Hypothermia is decreased body temperature.
Causes
l. Endocrine: Hypothyroidism or myxedema,
hypopit uitarism (Simmonds cachexia),
hypoglycemia
2. Toxic: Alcoholic intoxication, barbiturate
poisoning, ketoacidosis
3. Exposure to cold
4. Autonomic dysfunction or dysautonomias
16 > Pulse
Definition : Pulse is a wave which is felt by the finger,
produced by cardiac systole travelling in the peripheral
direction in the arterial tree at a rate faster than the
column of blood.
tidal or percussion wave which is felt.by the palpating
A normal pulse wave is transmitted peripherally tak
finger. On the following downstroke there is a notch
ing 30 msec to reach the carotids, 60 msec to reach (dicrotic notch) followed by a wave (dicrotic wave)
the brachial artery, 80 msec to reach the radial artery both of which are not normally palpable.
and 75 msec to reach the femoral artery.
Pulse is assessed by:
The normal pulse has a small anacrotic wave on the
upstroke, which is not felt. This is followed by a big l. Rate (No. of beats/min)
-
39
PRACTICAL MEDICINE
4. Equality
5. Peripheral pulses (e.g. femoral, posterior tibial,
dorsalis pedis)
6. Radio-radial delay (pre-ductal coarctation
of aorta), radio-femoral delay (post ductal
coarctation of aorta) (Refer Pg. 255)
7. Apex pulse deficit (atrial fibrillation)
The normal pulse appears at regular intervals and
has a rate between 60-100 per min. There may be a
mild variation in the rate between the two phases of
respiration which is called sinus arrhythmia.
b. Regularly irregular (e.g. second degree II. Pulsus Bisferiens is a rapid rising, twice beating
heart block 3:2, 4:3, Wenkeback; Ventricular pulse where both the waves are felt during systole.
Bigemini or Trigemini). Here the percussion wave is felt first followed by
a small wave. It is seen in:
c. Irregularly irregular (e.g. atrial fibrillation,
ventricular or atrial ectopics) A. Idiopathic hypertrophic subaortic stenosis: Here
initially there is no obstruction to the outflow
3. Force, volume, tension
40
(2 > General Examination
s D s D
41
PRACTICAL MEDICINE
Causes Causes
A. Superior vena cava obstruction. A. Physiological
B. Lung conditions. l. Fever
I. Asthma 2. Chronic alcoholism
2. Emphysema 3. Pregnancy
3. Airway obstruction B. High output states or syndromes
C. Cardiac 1. Anemia
l. Pericardial effusion 2. Beriberi
2. Constrictive pericarditis 3. Cor pulmonale
3. Severe congestive cardiac failure 4. Cirrhosis ofliver
NB: If the thoracic cage is immobile as in 5. Paget's disease
ankylosing spondylitis, pulsus paradoxus does 6. Arteriovenous fistula
not occur.
7. Thyrotoxicosis
VII. Pulsus Bigeminus ( Coupling) is coupling ofthe
C. Cardiac lesions
pulse waves in pairs, followed by a pause.
1. Aortic regurgitation
Causes 2. Rupture of sinus of Valsalva into the
A. Alternate premature beats. heart chambers
B. A.V. block, every third sinus impulse being 3. Patent ductus arteriosus
blocked 4. Aortopulmonary window
C. Sinoatrial block with ventricular escape. 5. Bradycardia
6. Systolic hypertension
--
Fig 2 29 Puls us b1gem1nus
- - --- --------------
VIII. Thready Pulse: The pulse rate is rapid and the
pulse wave is small and disappears quickly. This
is seen in shock especially cardiogenic.
IX. Waterhammer Pulse is a large bounding pulse
associated with increased stroke volume of the
left ventricle and decrease in the peripheral
resistance, leading to a wide pulse pressure. The
pulse strikes the palpating finger with a rapid,
forceful jerk and quickly disappears. It is best
felt in the radial artery with the patient's arm
elevated. It is caused by the artery suddenly
emptying because some of the blood flows back
from the aorta into the ventricle.
42
( 2 ) General Examination
I
I
I
I
'
I
I
I
I I I y
- a wave
-
svc rium contractirig:
TV open
"»
-"
"'
cwave
Ventricle contracting
TV closed; bulging into RA
Usually palpation of Carotid Pulse gives better infor
mation about the character of pulse than peripheral
arteries like the Radial artery. However Pulses Alter
nans, Bisferiens and water hammer pulse are better
x wave (descent)
felt at the peripheral arteries. Atrium relaxing then
Apex Pulse Deficit fill ng; TV closed
43
PRACTICAL MEDICINE
THE 'Y' WAVE: The 'y' descent is produced by open 1. Appearance Better seen Better felt
ing of the tricuspid valve and subsequent rapid inflow than felt than seen
of blood from the right atrium to the right ventricle 2. Number of waves Multiple Single
leading to a sudden fall ofpressure in the right atrium 3. Pressure below the Obliterates the No change
which is reflected in the jugular veins. It corresponds angle of mandible wave
with the third heart sound. 4. Changes with Present Absent
The ascending limb of the 'y' wave is due to continu respiration and
ous diastolic inflow ofblood into the great veins, right change of position
atrium and ventricle, which are all in free communica
tion during diastole.
45
inn--
PRACTICAL MEDICINE
Kussmaul's sign: Normally inspiration lowers the Phase I: The first appearance of faint clear tapping
JV pressure giving an inspiratory collapse, because sounds (Thuds) which gradually increase in
intrathoracic pressure falls and there is increased intensity.
blood flow into the thorax. In contrast, when the Phase II: The softening of the sounds which may
intrapericardial pressure is raised as in constrictive become swishing or blowing.
pericarditis there is a paradoxical increase in JV pres
Phase III: The return of sharper softer sounds,
sure on inspiration. This is Kussmaul's sign.
which become crisper, but never fully regain the
Hepatojugular Reflux intensity of phase I sounds. Neither phase II nor
phase III has any known clinical significance.
Normally, when pressure is applied over the abdomen
• Phase IV: Distinct abrupt muffling of sounds,
(right hypochondrium) for 30 seconds, initially there is
a rise in JV pressure (due to increased venous return), which become soft and blowing.
followed by a fall (due to the capacity of normal myo • Phase V: The point at which all sounds disappear
cardium to accommodate the extra venous return). completely.
However, in early cardiac failure, even before jugular Phase I is taken as systolic pressure and phase V as
pressure is elevated, there is a sustained elevated pres diastolic pressure.
sure in the jugular veins (for more than a minute) on
pressure over the abdomen because the failing heart
cannot compensate for the extra venous return. This Systolic
is positive hepatojugular reflux. Phase I Thud
120 mmHg
There is no rise in jugular venous pressure on apply 110mmHg
ing pressure over abdomen in:
Phase II Blowing
l. Budd Chiari syndrome
100mmHg
2. IVC Obstruction
Phase III Softer sounds
Decreased venous pressure in seen in:
90mmHg
1. Shock
2. Dehydration Phase IV Muffling
Diastolic
46
....
( 2 } General Examination
---- -----------------,
5. To measure BP in the legs a thigh cuffcontaining arm must be horizontal with fourth intercostal
space at the sternum. In normal people there is
Mercury no significant difference in BP between supine,
..r--
sphy�momanomctcr
sitting and standing positions provided the
arm is supported at the heart level. Some anti
Mcasuring sc:alc
1 hypertensive agents cause postural hypotension
Jntlatablc ;;mprcssmg
bladder enclosed w11hm
and when this is expected, BP must be measured
inextensible cuff \
in both lying and standing positions.
6. Ifthe arm is unsupported, the patient will perform
isometric exercise, which may elevate the diastolic
BP by l 0%. This is especially so in hypertensive
patients on beta-adrenergic blocking agents. To
avoid this the arm must be supported.
lnflallon oolb
sphygmomanomc1cr 7. The BP may be higher in right arm by 2-10 mm
Hg. Most pressures in practice are measured on
Fig. 2 41 Blood Pressure Measurement the right arm. However if the BP is higher by 10
47
----
PRACTICAL MEDICINE
19 > HJ�ertension
mm Hg in one arm further measurements should
be made in the arm with the higher BP.
8. The cuff should be snugly fitted to the arm. A cuff Hypertension {HT) is the silent killer of mankind.
which is too tight may give a false lower blood Most sufferers (85%) are asymptomatic and hence
pressure and a loose cuff may give a false higher early diagnosis is a problem. The dividing line between
BP. normal and abnormal BP is arbitrary because BP is
9. Repeated inflation of the cuff may cause venous dependant upon many factors like age, race, sex, etc.
congestion of the limb and elevate both systolic
Definitions and Classification
and diastolic BP. To avoid this the cuff should
be inflated as rapidly as possible and deflated The definition ofhyp ertension is not universal because
completely between successive readings. At least normal BP varies. The Sixth Joint National Committee
15 seconds should be allowed between successive Criteria (JNC VII) classifies hypertension for adults
measurements. aged 18 years and older into the following stages:
I 0. Auscultatory Gap: Is the interval ofblood pressure Table 2.7 : JNC VII Criteria for
when the Korotkoff sounds disappear and then Classification of Blood Pressure
re-appear at a lower pressure during auscultatory Category Systolic Diastolic
method of measury B.P. This leads to errors of mmHg mmHg
underestimation of systolic BP or overestimation Normal <120 AND <80
of diastolic B.P. This can be avoided by doing the
Pre-Hypertension 120-139 OR 80-89
palpatory method first, followed by auscultatory
method. Hypertension
Stagel 140-159 OR 90-99
Unequal BP in two arms
Stage2 �160 OR �100
I. In normal individuals, BP may vary upto 10 mm
I. Target BP is< 140mmHg systolicand<90mmHg.
Hg in the two arms.
2. Supravalvular aortic stenosis (right sided higher For diabetics OR chronic renal failure BP should
BP) be:
3. Preductal coarctation ofaorta {right sided higher < 130 mmHg systolic; < 80 mmHg diastolic
BP) For diabetics WITH chronic renal failure BP
4. Unilateral occlusive disease of the arteries should be:
- Atherosclerosis, embolism, aortoarteritis, < 125 mmHg systolic;< 75 mmHg diastolic
thoracic outlet syndrome, etc. (BP will be low on 2. Hypertensive emergencies ( malignan t
the affected side) hypertension) are characterized b y severe
elevations in BP (> 180/120 mmHg) with
Conditions Diagnosed by Measuring BP
evidence of impending or progressive target
I. Hypertension organ dysfunction. They require immediate BP
2. Hypotension reduction. (e.g.pappiledema, retinal exudates,
retinal hemorrhages, nephropathy, hypertensive
3. Pulsus paradoxus
encephalopathy, intracerebral hemorrhage, acute
4. Pulsus alternans Ml, acute left ventricular failure with pulmonary
5. Coarctation ofaorta (Hypertension in upper limb, edema, unstable angina pectoris, dissecting aortic
hyp otension in lower limb) aneurysm, eclampsia).
6. Aortic incompetence (Hill's sign) 3. Hypertensive urgencies ( a c c e l e r a t e d
7. A u t o n o mic d y s fu n c t i o n - postural hypertension) are associated with severe
hyp otension. elevations in BP without progressive target
organ dysfunction (e.g. upper levels of stage II
48
< 2 > General Examination
hypertension associated with severe headache, 1. CVS: Increased myocardial work leads to
shortness of breath, epistaxis). Retinal damage concentric hyp ertrophy of left ventricle, angina
may be present but without pappiledema. pectoris and accelerated coronary arter y
4. Isolated systolic hypertension is systolic BP;;;: 140 disease. There is systolic as well as diastolic
mmHg and diastolic BP <90 mmHg. It is seen dysfunction.
predominantly in elderly due to arteriosclerosis. It 2. Kidneys: Progressive arteriosclerosis involves
may fluctuate from time to time, high in morning, both the efferent and afferent renal arterioles
lower at night. and capillaries of glomerular tuft. This leads
s. Pulse pressure = SBP • DBP (Normal 30-60 to compromise in renal function, shrinkage of
mmHg). kidney, proteinuria.
6. Mean BP= 2/3 DBP + 1/3 SBP. 3. CNS:Hyp ertension may cause micro-aneurysms
(Charcot-Bouchard aneurysms) which may
Labile hypertension: The patient is hypertensive at
rupture and cause cerebral hemorrhage.
one time and normotensive at another time.
Accelerated atherosclerosis may cause cerebral
White Coat Hypertension: The patient's BP is high thrombosis, embolism and infarction. Cerebral
when measured by a professional but is normal when arteriolar spasm may cause hypertensive
measured in casual circumstances (at home). It is encephalopathy.
diagnosed by 24-hour ambulatory BP monitoring.
Sites of hypertensive bleed are: cerebellum,
Causes thalamus, basal ganglia (putamen), pons.
1. Essential Hypertension 4. Fundus
Keith Wagner Classification
2. Renal
a. Acute nephritis Grade I: Mild generalized ar teriolar
attenuation.
b. Interstitial nephritis and pyelonephritis
Grade II: Deflection of veins at AV crossing
c. Polycystic kidneys (AV nicking) + marked generalized arteriolar
d. Renal artery stenosis attenuation.
e. Diabetic nephropathy Grade III: Grade II + copper wire + cotton
3. Endocrine: Pheochromocytoma, Cushing's woolspots + flame-shaped hemorrhages + hard
syndrome, thyrotoxicosis, myxedema exudate.
4. Neurological: Raised intracranial tension, lead Grade IV: Grade III + silver wire + papilledema.
encephalopathy, etc.
Symptoms
5. Pregnancy induced HT
The clinical features may be due to the elevated BP
6. Cardiovascular HT: Co-arctation ofaorta, aortic
regurgitation, arteriosclerosis itself, target organ involvement or due to underlying
disease, as in secondary hyp ertension.
7. Drugs: Glucocorticoids, OCPs, sibutramine,
cocaine, etc. Symptoms due to hypertension
8. Miscellaneous: Polycythemia, polyarteritis 1. Headache: This occurs usually in the morning
n o d o s a, o b s t r u c t i v e s l e e p a p n e a, hours. It is throbbing and usually frontal.
hyp ercalcemia
2. Dizziness: The patient feels unsteady
Effects of Hypertension 3. Epistaxis: This occurs due to increased pressure
The common organs damaged by long-standing causing rupture ofthe capillaries ofthe nose. The
bleeding would reduce the circulatingvolume, and
hypertension are heart, kidneys, blood vessels, retina
and central nervous system. lower the BP (Natures way oflowering the BP and
prevention of hemorrhage in the vital organs).
49
PRACTICAL MEDICINE
Symptoms due to Affection of Target 2. Puffy face, rough skin, obesity· Myxedema
Organs 3. Tremors, tachycardia, exophthalmos, thyroid
1. CVS: dermopathy and goitre- Hyperthyroidism
a. Dyspnea on exertion (incipient LVF) 4. Prognathism, dubbed hand, coarse features •
Acromegaly
b. Anginal chest pain (IHD)
5. Pigmentation - Neurofibromatosis
c. Palpitations
2. Kidneys: Hematuria, nocturia, polyuria 6. Radio femoral delay and collateral vessels over
the chest wall · Coarctation of aorta
3. CNS:
7. Weaker left radial - Preductal coarctation
a. Transient ischemic attacks (TIA or stroke)
with focal neurological deficit 8. Waterhammer pulse - Aortic incompetence
b. Hypertensive encephalopathy (headache,
vomiting, convulsions, unconsciousness, focal
neurological deficit)
c. Dizziness, tinnitus and syncope
4. Retina: Blurred vision or sudden blindness
Symptoms due to Underlying Diseases
1. Edema and puffy face - Acute nephritis
2. Weight gain, hirsutism and stria - Cushing's
syndrome
3. Weight loss, tremors, palpitations and sweating
- Hyperthyroidism/pheochromocytoma
4. Weakness - Primary hyp eraldosteronism
5. Joint pains, bronchospasm &peripheral vascular
disease symptoms - Polyarteritis nodosa
Signs
General Examination
1. Moon face, buffalo hump and truncal obesity -
Cushing's syndrome
Cardiovascular System
1. Cardiomegaly
2. Third and fourth heart sound gallop
3. Loud second heart sound
4. Early diastolic murmur - due to Al
so
( 2 ) General Examination
51
PRACTICAL MEDICINE
5. Limit of alcohol intake to < l ounce/day of Nifedipine was the commonest used calcium
ethanol {24 ounces beer, 8 ounces wine or 2 blocker. Now Amlodipine is replacing
ounces 100-proof whiskey) it. Felodipine, nicardipine, nitrendipine
6. Relaxation: Various forms of relaxation like and dinidipine are other useful calcium
yoga, biofeedback and psychotherapy lower blockers. These drugs are especially useful
BP, especially in those with sympathetic in elderly hypertensives. Flushing, headache,
palpitations, edema and hypotension may
7. Regular exercise
occur.
II. Pharmacological Treatment
4. ACE Inhibitors: Renin released from the
l. Diuretics: Oral diuretics were the most widely kidney acts on circulating angiotensinogen
used anti-hypertensive agents. They are to produce angiotensin [, which is converted
effective alone in 50% of mild hypertensives. to angiotensin II by converting enzyme.
Thiazides are very effective. They are well Angiotensin II is a potent vasoconstrictor and
tolerated and need to be given only once it stimulatesaldosterone, which retainssodium
a day. They enhance the potency of other and causes hyper-tension. ACE inhibitors
anti-hypertensives. They act by reducing act by inhibiting the converting enzyme
extracellular fluid volume and cardiac output preventing the formation of angiotensin II
and they help to counteract the hypertensive and lowering ofBP. They also act by reducing
effect of high salt intake. They can aggravate the degradation of bradykinin · a potent
diabetes by suppressing release of insulin vasodilator, which lowers the BP.
due to hypokalemia. Hyperlipidemia,
ACE Inhibitors cause regression ofventricular
hyperuricemia, hypokalemia, hyponatremia,
hypertrophy, attenuation ofreperfusion injury
hyp omagnesemia may occur. Now they are
induced ventricular arrhythmias, preload
usually used in combination therapy.
and afterload reduction and coronary vaso·
2. Beta blockers: Reduce cardiac output and dilatation. These drugs have no adverse effects
lower BP but raise the peripheral resistance oflipids, uric acid or glucose metabolism. They
on acute administration { which increases BP). lower the BP by 15-25% . Diastolic pressure
However, on chronic administration, BP falls is lowered more than systolic pressure.
to pretreatment levels. In mild to moderate Concomitant sodium restriction and diuretics
hyper-tension, it lowers the BP to less than further lowers BP by 15-25%.
90 mmHg in more than 50% patients. Drug
ACE Inhibitors are useful in renovascular
withdrawal, if needed, should be done slowly,
hyp ertension. High angiotensin II is however
or rebound hypertension may occur. They can
required to maintain adequate filtration
be combined with diuretics, calcium blockers,
pressure behind the stenotic lesion. ACE
ace inhibitors and vasodilators. They may
Inhibitors decrease the perfusion pressure and
precipitate bronchospasm, cardiac failure,
lead to azotemia. Thus, they are contraindicated
peripheral vascular disease, impotence and
in bilateral renal artery stenosis. These drugs
depression.
are useful in hyp ertensive diabetics because
3. Calcium Channel Blockers: Lower BP of neutral effect of carbohydrate metabolism.
by: In addition they decrease microalbuminuria.
a. N atriuresis and diuresis due to increased Captopril also improves insulin sensitivity.
GFR and decreased aldosterone It has a short duration of action and is used
b. Anti-angiotensin-11 effect for cardiac failure. Enalapril, lisinopril,
C. Direct negative inotropic effect which perindopril, ramipril, etc. are longer acting
lowers cardiac output ACE inhibitors and useful in hypertension.
Tissue specific ACE inhibitors like Quinapril,
d. Peripheral vasodilatation Ramipril, Perindopril, Fosinopril are available.
52
< 2 ) General Examination
5. Angiotensin II Blockers are useful in patients 2. Intravascular volume contraction: Hemorrhage,
with ACE Inhibitor-induced cough and in vomiting, diarrhea, burns, intestinal obstruction,
elderly hypertensives. Losartan, Irbesartan, peritonitis, etc.
Valsartan, Candersartan are available. 3. Anaphylaxis
6. Alpha Blockers: Adrenergic stimulation of 4. Gram negative septicemia
alpha-I receptors in the vascular smooth
muscles causes vasoconstriction and Clinical Features
hypertension. Alpha blockers attenuate I. Due to shock: Tachycardia, vomiting, fainting
vasoconstriction, and thereby decrease 2. Due to causative disease
vascular resistance and blood pressure. 3. In vasovagalattacks, hypotension with bradycardia
Prazosin was the first alpha blocker with 4. In postural hypotension, fall of BP occurs on
short duration of action. Terazosin and suddenly on assuming an erect posture from
doxazosin are longer acting, once a day alpha supine posture
blockers. The efficacy can be enhanced by
the concomitant use of diuretics. The most Treatment
dramaticadverse effect is the first dose postural l. Of the cause
hypotension/syncope.
2. Posture: The patient should be in lying position
Alpha blockers also have other beneficial with legs raised.
effects like lowering of lipids, regression 3. For vasovagal attacks: Atropine 0.6 mg IV
of left ventricular hypertrophy, enhancing
4. For anaphylaxis: Hydrocortisone hemi-succinate
insulin sensitivity (hence ideal for diabetic
I 00 mg IV, repeated as required
hypertensives) and relief of obstructive
5. For postural hypotension: This is best treated by
symptoms in benign prostatic hypertrophy.
advising the patients to assume the erect posture
7. Vasodilators: These drugs act on the arteriolar
slowly and to wear elastic stockings and abdominal
smooth muscles, causing vasodilatation and binder.
lowering of BP. However, reflex tachycardia
6. Vasoconstrictors: Dopamine, nor-epinephrine and
and increase in cardiac output limits its
ephedrine have been tried.
usefulness in severe coronary artery disease.
These effects can be reduced by combining 7. Salt: Adequate amount ofsalt (NaCl) in diet helps
hydralazine with beta blockers. Minoxidil to expand the plasma volume.
is the other vasodilator whose usefulness is 8. Fludrocortisone Acetate: (0.1 - 0.2 mg) causes fluid
limited due to hirsutism in females. Diazoxide retention and avoids postural fall of BP.
and nitroprusside are parenteral vasodilators
Chronic Hypotension
useful in hypertensive emergencies.
A number of healthy subjects have a systolic BP of
80-100 mm Hg, which is compatible with long life
20 > Hi�otension expectancy. 0nly some patients complain ofweakness,
lethargy, easy fatigability, dizziness and fainting on
Definition: Hypotension is diminished blood pressure.
assuming erect posture or standing inactive for long
This could be acute or chronic.
periods. This occurs due to interference with neural
Acute Recumbent Hypotension pathways between the vasomotor center and efferent
sympathetic nerve endings in the blood vessels and
Causes heart, so that the normal rise in cardiac output and va
soconstriction on assuming erect posture are abolished.
l. Cardiovascular: Acute myocardial infarction,
pulmonary embolism, dissecting aneurysm,
ventricular tachycardia, cardiac rupture
53
PRACTICAL MEDICINE
Causes Treatment
I. Cardiac:· l. Mechanical: Elastic bandages over legs, head up
a. Low output cardiac failure position in bed etc.
b. LV dysfunction 2. Volume expansion with high fluid and salt intake
c. Cardiac tamponade 3. Fludrocortisone supplement (0.01 mg/day)
d. Constrictive pericarditis 4. Drugs:
e. Tight mitral stenosis a. Sympathomimetics: Ephedrine, ampheta
mine, L-dopa
f. Left atrial myxoma
2. Supine hypotension of pregnancy b. Prostaglandin synthesis inhibitors like
indomethacin
3. Endocrine
c. Alpha 2 receptor agonists
a. Addison's disease
d. Partial Beta agonist (pindolol)
b. Myxedema
e. Erythropoietin
c. Hypopituitarism
f. Somatostatin analogue (octreotide) prevents
d. Serotonin secreting tumors splanchnic pooling after eating)
4. Neurogenic g. Midodrine for neurogenic causes
a. Diabetic neuropathy 5. Atrial pacing
b. Extensive lumbosacral sympathectomy
Shy-Drager Syndrome
c. Peripheral neuropathy
d. Tabes dorsalis This is chronic orthostatic hypotension with degenera
tion ofCNS, mainly involving extra-pyramidal tracts,
e. Syringomyelia, Multiple sclerosis
basal ganglia and dorsal nucleus of Vagus. These pa·
5. Chronic idiopathic orthostatic hypotension tients have intact peripheral autonomic nervous system
Chronic Idiopathic Orthostatic but are unable to activate it. (In primary autonomic
Hypotension insufficiency there is depletion of nor-epinephrine
in the peripheral autonomic ganglia). In both these,
This occurs due to primary autonomic insufficiency catecholamine blood levels do not rise on standing,
due to degeneration ofcentral or peripheral autonomic although it may be normal at recumbency in chronic
nervous system. It is common in the elderly who may orthostatic hypotension but reduced in primary au
develop syncope, hypotension, convulsions but no tonomic insufficiency.
tachycardia on standing. They may have associated
anhydrosis, loss of hair, diminished lachrymal and
salivary secretion, bladder atony and impotency.
54
1 > Proforma VIII. Eye : Kayser - Fleischer ring on slit lamp
Examination of cornea.
History IX. Miscellaneous: Bony tenderness, genitals.
2 > Examination
6. Full bladder: Tender, rounded, cystic
massmaybepalpableabovesymphysis
pubis, which may disappear after
A. Inspection micturition
The abdomen can be divided in to 9 regions by 7. Fatal new growth:
drawing 2 horizontal and 2 vertical imaginery a. Abdominal dullness overlying the
lines. The 2 vertical lines are drawn by joining growth
mid clavicular point to the mid inguinal point. b. In ovarian growth, the distance
The upper horizontal line is drawn at the lower between the umbilicus and
most bony point of the rib cage, usually the symphysis pubis is greater than
9th or 10th costal cartilage (Sub costal plane • that between the xiphisternum
corresponds to the body ofL3 vertebra). The lower and umbilicus
horizontal line is drawn at the upper border of
the tubercles of the iliac crests (Trans tubercular
plane - corresponds to the upper border of LS
vertebra). The 9 quadrants are shown in Figure.
I. Shape of Abdomen : The shape of the
abdomen in most normal persons with
normal musculature is scaphoid or boat
shaped i.e. the abdominal wall sinks slightly
within the bony margins of the abdominal
surface.
In every muscular person, the lateral
margins of the rectus muscle is visible in
the center. Usually the medial edges of both
the recti are contiguous. However they may
be separated as a congenital defect, after
pregnancy or with obesity and ascites. This
is called divarication of recti. Distension of
the abdomen occurs due to fat (obesity),
fluid (ascites), feces, flatus, fetus, full
urinary bladder and (fatal) new-growth. Fig 3 1 lnspect,onofAbdomen-9Quadrants
56
( 3) Abdomen
57
PRACTICAL MEDICINE
58
( 3 )Abdomen
therapy. When they first form, the striae are conditions, the patient complains ofsevere
reddish or pink. If the state of distension pain (e.g. appendicitis).
stabilizes or the cause regresses, the colour II. Guarding: Abdominal guarding is due to
fades to white. muscular contraction, which often occurs
B, Palpation as a part of the defense mechanism over
a tender region. If the patient is put in a
For palpation of the abdomen, the patient must comfortable position and his mind set at
lie on his back, shoulders raised slightly and legs rest by explaining that no undue pain will be
flexed to relax the abdomen. He should keep his caused by the examination, the abdominal
mouth open and breathe quietly and deeply. The muscles gradually relax.
abdomen is palpated with the flat of the hand III. Rigidity: Abdominal rigidity is due to
initially, but the fingers are used to locate the muscular contraction, which occurs as a
margins of any viscera or tumor. part of the defense mechanism over an
I. Tenderness: Tenderness is pain on pressure. inflamed organ. It cannot be voluntarily
It is commonly found in inflammatory relaxed. It occurs in the following:
lesions of the viscera and the surrounding 1. Perforation of a hollow organ
peritoneum.
2. Peritonitis
The site of tenderness often suggests the
diagnosis 3. Acute pancreatitis or cholecystitis
1. In the epigastrium - Peptic ulcer 4. Intestinal strangulation
2. In the right hypochondriurn - Hepatitis, 5. Thrombosis of superior mesenteric
cholecystitis artery
3. In the right iliac fossa - Appendicitis
6. Ruptured ectopic gestation
(Mc Burney's Point) 7. Twisted ovarian cyst or torsion of
4. Purely visceral pain such as gastric or fibroid
intestinal colic is not associated with Pancreatobiliary secretions are more
any tenderness. irritating to the peritoneum than bacteria
Rebound tenderness can be elicited by are, and so board-like rigidity suggests
exerting a firm pressure with the hand a chemical peritonitis most commonly
and releasing it. In deep seated, subacute from perforated gastric or duodenal ulcer.
Bacterial peritonitis rarely produces board
like rigidity until late. It usually causes
increased resistance to compression.
IV. Viscera
A. Liver: The patient must be lying in
the supine position with hip and knee
flexed, to relax abdominal muscles.
The examiner moves his right hand
from the right iliac fossa gradually
upwards until a sense of increased
resistance is noted. The size of the liver
must be recorded as fingerbreadths
or centimeters below right costal
margin. The liver edge is accurately
Fig 3 5 S1teoftendernessin I l) Hepat1t1sandcholecyst1t1s,
located by the fingertips. It is normally
(2) Peptic ulcer,(3)Append1c1t1s and (4) Col1t1s
59
PRACTICAL MEDICINE
60
( 3) Abdomen
61
PRACTICAL MEDICINE
62
( 3) Abdomen
D. Auscultation
Auscultation of the abdomen is done for the
following:
1. Peristalsis : These are intestinal sounds
generated by contractions of the muscular
walls of the gut and the resultant vibration
of the gut wall produced by movement of
a gas-fluid mixture through the gut. These
bowel sounds (peristalsis) persist in the
5. Tidal Percussion : The upper border of fasting state due to the presenceofintestinal
the liver can be accurately determined by secretions and swallowed air. Loud bowel
percussion. sounds (hyperperistalsis) accompanied
Liver Span: Percussion is started anteriorly by abdominal distension and crampy
in the right midclavicular line from second abdominal pain suggests partial bowel
intercostal space downwards and repeated obstruction. Absence of bowel sounds for
in the anterior, mid and posterior axillary at least 5 minutes strongly suggests bowel
lines and the scapular line posteriorly. atony or ileus. Borborygmi refers to audible
The normal liver dullness is in the fifth peristalsis which can be heard even without
space in the midclavicular, seventh space a sthethoscope.
in the anterior axillary and ninth space in 2. Arterial Bruit: These are variable harsh
the scapular lines. The normal liver span sounds in tempo with the pulse due to
in an adult as judged by liver dullness turbulence in arterial flow. This may
measures 10-12 cm in men and 8-11 cm occur by unusually acute angulations at
in women. The upper border of the liver arterial branch points, arteriosclerotic
may be percussed in the fourth or third plaques, extreme tortuosity of an artery,
compression ofan artery or massive blood
flow through very vascular tumors like
hemangioma or hepatoma. Bruits over
the liver suggests very vascular tumor like
hepatoma or angioma. Similarly, over the
spleen it suggests vascular tumor. Bruit
over the aorta, if soft, has no significance.
However a loud bruit suggests aortic
aneurysm, atherosclerosis or extreme
tortuosity of the aorta, Bruit over the
kidneys in the flanks suggests renal artery
stenosis.
63
PRACTICAL MEDICINE
3. Venous Hum: Venous hum is continuous, Small vessels in the skin associated with arterial spiders
softer and lower pitched than bruit. It have been compared to the silk thread in American
signifies portal systemic shunting ofvenous paper money. Therefore, the skin is called paper
flow when portal flow is obstructed. It money skin.
is usually heard over the liver area and
umbilicus. Causes
1. In alcoholics 5. Pregnancy
Fetor Hepaticus
2. Cirrhosis 6. Rheumatoid arthritis
Definition: This is the fecal smell of the breath similar
3. Viral hepatitis 7. Thyrotoxicosis
to that of a freshly opened corpse of a mouse.
4. Normal persons especially children
Mechanism: Normal demethylating process is inhib
ited by liver damage. Hence, methionine is converted Mechanism: The selective distribution of spider nevi
to methyl mercaptan, which gives the typical smell. is not understood.
1. Exposure of upper parts of the body to certain
Causes elements may damage the skin so that it is
I. Acute liver cell disease/failure: Poor prognostic susceptible to develop spider nevi when an
sign and often precedes coma. appropriate internal stimulus exists.
2. Extensive portal collateral circulation 2. Estrogen exce�s may be responsible. It forms
arterioles of the endometrium in uterus during
Spider Nevi pregnancy, which resembles spider nevi.
Synonyms: Arterial spider, Spider telangiectasis, Spider Significance : Appearance of fresh spiders suggests
angioma progression of liver damage. Spider nevi disappear if
Definition: An arterial spider is a central arteriole, liver function improves or blood pressure falls due to
from which numerous small vessels radiate resembling shock or hemorrhage.
a spider's legs. Palmar Erythema
Sites: Arterial spiders are found in the territory of the
Definition : Palmar erythema is bright red warm
superior vena cava. They are commonly seen on the
face, neck, forearm and shoulder. palms. The thenar and hypothenar eminences and
soles offeet are especially erythematous. The erythema
Appearance: They range in size from 3 to 15 mm in blanches on pressure.
diameter. They are pulsatile and blanch on pressure.
When the skin is stretched or compressed they fill Causes
from the centre to the periphery.
1. In alcoholics 6. Leukemia
2. Cirrhosis 7. Pregnancy
3. Viral hepatitis 8. Febrile diseases
4. Thyrotoxicosis 9. Familial
5. Rheumatoid arthritis
Significance : Palmar erythema is not so frequently
seen in cirrhosis, as are vascular spiders.
Asterixis (Flaps)
Definition : Asterixis are rapid flexion-extension
movements at metacarpophalangeal and wrist joints.
Therefore they are seen as a flapping tremor.
Fig. 3 18 Spider nevi
Significance : In liver disease, it indicates that the
patient is in hepatocellular failure.
64
( 3> Abdomen
3 > He�atomegalr____
B. Secondary
VII. Toxic: Alcohol, arsenic, phosphor ous,
Definition : Hepatomegaly means enlarged liver. An chlorpromazine
enlarged liver may not always be palpable if it is slightly
Painful Hepatomegaly
enlarged and a palpable liver is not always enlarged.
I. Cardiac failure
Causes
2. Viral hepatitis
I. Infective: 3. Hepatic amebiasis
A. Along the biliary tree: Cholangitis. 4. Pyemic abscess of liver
B. Along the portal vein: 5. Hepatoma
1. Amebiasis 6. Actinomycosis of liver
2. Schistosomiasis 7. Weil's disease (Leptospirosis)
3. Bacterial infections Pulsatile Liver: Tricuspid insufficiency
C. Along the hepatic artery: Bruit over the Liver
1. Bacterial: Typhoid, brucellosis, 1. Hepatoma
tuberculosis
2. AV malformation
2. Viral: Infective hepatitis, infectious
mononucleosis Differential Diagnosis
3. Spirochetal: Syphilis, Weil's disease I. Viral Hepatitis (Refer Pg. 71)
4. Protozoal: Malaria, kala azar A. Prodromal symptoms of gastrointestinal
5. Fungal: Actinomycosis, upset e.g. anorexia, abdominal discomfort
histoplasmosis B. Fever, malaise
6. Parasitic: Echinococcus C. Dark colored urine
II. Congestive: D. Jaundice on 3rd or 4th day
A. Cardiac failure E. Enlarged tender liver with mild intercostal
tenderness
B. Cardiomyopathy
F. Palpable spleen in 25% cases
C. Constrictive pericarditis
II. Amebic Liver Abscess
D. Budd Chiari syndrome
A. Moderate to huge, tender liver
III. Cirrhosis (in early stages)
B. Fever with rigors
65
b
PRACTICAL MEDICINE
C. Rt. upper abdominal tenderness VI. Hydatid Cyst
D. Blood and mucus in stools in the past A. The liver is non-tender(unlike liverabscess).
E. Shift ofliver dullness upwards Ifcyst is on the surface, rounded, localized,
F. Investigations-moderate leucocytosis, smooth swelling (unlike carcinoma and
diminished movements of diaphragm on syphilis) is present
screening, aspiration of anchovy sauce B. When the cyst is tense there may be a
material from liver with demonstration of hydatid th rill
trophozoites in it. C. No jaundice or splenomegaly is present
Ill. Pyemic Liver Abscess D. There is history ofcontact with dogs
A. Signs of septicemia E. Urticaria may be present if hydatid fluid is
1. High fever with rigors and profuse absorbed
sweating F. Investigations: Eosinophilia, positive
2. Anemia, tachycardia, leucocytosis, complement fixation test, calcification of
positive blood culture cyst wall demonstrated by radiology and
B. Local signs positive Casoni's test
1. Pain, tenderness, edema and redness VII. Congestive Hepatomegaly
over lower right intercostal spaces A. Slight to markedly enlarged, firm, smooth,
2. Marked tender hepatomegaly tender liver, pulsatile if there is tricuspid
3. Shift ofliver dullness upwards incompetence
IV. Malaria: (Refer Pg. 90) B. Other evidence of cardiac failure: Edema
A. Fever with chills and rigors, coming down offeet, raised JVP and ascites
with sweating. Paroxysms offever every 72 C. In severe cases, dyspepsia and jaundice
hours with Pl. malariae and 48 hours with D. Evidence ofcardiac lesion
the other types
VIII. Cirrhosis ofLiver: (Refer Pg. 82)
B. Splenomegaly, mild to massive, always
present when liver is enlarged Signs oflivercellfailure: Pa!mar erythema,
A.
spider nevi, gynecomastia, testicular
C. Anemia
atrophy, flapping tremors, ascites, jaundice,
D. Peripheral blood smear and bone marrow Dupuytren's contracture, parotid gland
show presence ofparasites swelling, alopecia, loss oflibido.
V. Kala Azar: (Refer Pg. 95) B. Evidence of portal hypertension:
A. Long continued fever Splenomegaly, ascites (out of proportion
B. Hepatosplenomegaly to edema of feet), hematemesis, dilated
C. Anemia, weight loss veins over chest well, bleeding per rectum
D. Dark pigmentation IX. Hemochromatosis
E. Demonstration of Donovan bodies in A. A triad ofcirrhosis, diabetes mellitus and
reticulo-endothelial cells e.g. in bone pigmentation ofskin may be present.
marrow, liver and spleen B. Ascites is rare
F. Serological tests - Napier's Aldehyde test, C. Cardiac complications may occur
Antimony, Brahmachari's and W.K.K.
D. Increased stores on iron in serum and
complement fixation test, immuno reticuloendothelial cells
fl uoscent. Antibody test, Indirect
Hemogglutination test and ELISA may be X. Malignancy
positive A. Markedly enlarged liver with upward
66
{ 3 } Abdomen
4 > S�lenomegal)!____
increase of liver dullness, a hard often
irregular. edge, with uneven knobby hard
nodules, sometimes umbilicated. Sudden Definition : Splenomegaly is an enlargement of the
enlargement of the nodule is due to spleen (Refer Pg. 55). The spleen has to be two and a
hemorrhage halftimes its normal size to become palpable; therefore
B. Pain in the hepatic region and over the an enlarged spleen is not always palpable. In ptosis of
right shoulder. Dragging and fullness in spleen, it is palpable, though not enlarged.
the right hypochondrium
Evidence of Enlargement of Spleen
C. Jaundice - deep yellow to deep olive green
1. Predominant left sided abdominal distension,
D. Cachexia, loss of weight, and dry shriveled
if massive splenomegaly
skin may be present
2. Splenic mass moves downwards on inspiration
E. Ascites and edema of legs may occur
3. A notch is felt on the anterior border
F. There may be evidence of primary or pre
4. Left abdominal pain if massive splenomegaly
existing cirrhosis
XI. Biliary Obstruction Causes
(Commonly due to gall stones):
I. Infective:
A. Deeper jaundice than in cirrhosis
A. Bacterial: Septicemia, SBE, typhoid,
B. History of colicky pain syphilis.
C. Clay-coloured stools with dark urine B. Viral: Infective hepatitis, infectious
D. Fever with rigors due to cholangitis mononucleosis
XII. Alcoholic Liver Affection: C. Protozoa/: M a l a r i a, k a l a azar,
A. Smooth, tender, enlarged and firm liver is trypanosomiasis
present. D. Fungal: Histoplasmosis
B. Right upper abdominal pain, anorexia, II. Congestive:
nausea and vomiting may occur. A. Suprahepatic:
C. There may be profound weakness, jaundice, 1. Congestive cardiac failure
spider nevi and palmar erythema.
2. Constructive pericarditis
XIII. Leukemias (Refer Pg. 102)
3. Budd Chiari syndrome
XIV. Hodgkin's Disease (Refer Pg. 107)
B. Hepatic:
XV. Amyloidosis
1. Cirrhosis
A. Evidence of chronic wasting disease
2. Schistosomiasis
B. Liver large, smooth, rubbery and non-
3. Sarcoidosis
tender
4. Congenital hepatic fibrosis
C. Jaundice, ascites and generalized edema
C. Intrahepatic: Portal vein thrombosis - Extra
D. Splenomegaly
hepatic portal HT.
E. Albuminuria (kidney affection) and
III. Blood Diseases:
diarrhea (gastrointestinal affection)
A. Polycythemia rubra vera
F. Congo Red test is positive. Liver biopsy,
kidney biopsy and rectal biopsy for amyloid B. Hemolytic anemia - Thalassemia
infiltration may also be positive. C. Leukemias
D. Lymphoma
E. Myelofibrosis
67
PRACTICAL MEDICINE
68
( 3 )Abdomen
69
PRACTICAL MEDICINE
5 > Ascites B.
C.
Bile
Chylous
Definition : Ascites is the accumulation of free fluid D. Myxedema
in the peritoneal cavity
Table 3.3 : Transudate and Exudate
Diagnosis
,.
Transudate Exudate
I. Generalized distension of abdomen with more Process Passive Active
fullness in the flanks 2. Serous structures Others Only local
II. Shifting dullness can diagnose 500 ml fluid 3. Appearance Clear Clear/turbid
III. Horse-shoe-shaped can diagnose l litre fluid
4. Specific Gravity < 1.015 > 1.015
IV. Fluid thrill seen in tense ascites
5. Proteins <3gm/dl >3gm/dl
V. Other signs:
6. Cells Few Polymorphs or
A. Transverselystretchedumbilicus ('laughing' mesothelial Lymphocytes
umbilicus) cells
B. Divarication ofrecti 7. Clot formation Nit Present
C. Tense and shiny skin 8. Gradient" ;.:1.1g/dl < ,., g/dl
D. Widened subcostal angle *Serum albumin minusasciticfluidalbumin (SAAG)
E. Lower ribs pushed outwards and upwards Routine exudate /transudate system is no longer used in
VI. Diagnosis of small quantity of fluid (Puddle ascites
sign): The patient is put in knee chest position It is advisable to calculae SAAG to classify ascite as follows:
so that the fluid gravitates down to the anterior
1. High SAAG ascites (SAAG � 1.1 g/dl) - It indicates
abdominal wall. The stethoscope is placed over portal Hypertensive Ascites with sensitivity &
this and the anterior abdominal wall is flicked specificity of 97%. Causes: i) cirrhosis of liver; ii) cardiac
for a puddle sound. This can diagnose even l SO cirrhosis; iii) Budd Chiari syndrome; iv) veno occlusive
disease; v) portal vein thrombosis and vi) Fulminant
ml fluid.
liver failure
Causes 2. Low SAAG ascites (SAAG < 1.1 g/dl). Causes :
i) Tuberculosis; ii) Nephrotic syndrome; iii) pancreatitis;
I. Transudates iv) biliary ascites; v) peritoneal carcinomatosis
A. Cardiac failure F. Portal hyp ertension
B. Hypoproteinemia G. Epidemic dropsy Mechanism of Ascites Production
C. Anemia H. Polyserositis l. Increased hydrostatic pressure intravascularly
D. Beriberi I. Meigs syndrome 2. Decreased osmotic pressure intravascularly due
E. Nephrotic syndrome to hypoproteinemia
II. Exudates 3. Increased osmotic pressure extravascularly
A. Peritoneal disease 4. Increased lymphatic pressure
l. Infections: Tuberculosis, bacterial,
Causes of Hemorrhagic Fluid
fungal and parasitic infections
2. Neoplasms l. Trauma of thoracic duct
B. Collagen disorders 2. Parasite infections e.g. filariasis
C. Eosinophilic gastroenteritis 3. Tuberculosis
D. Gynecological: Endometriosis, struma ovarii 4. Thrombosis of subclavian vein
III. Miscellaneous 5. Malignancy involving thoracic duct
A. Pancreatic
....
70
( 3) Abdomen
71
PRACTICAL MEDICINE
C. Cardiac symptoms may be present 6.Consistency: Soft, firm or hard. Hard
D. Diffuse blotchy erythema of skin and other swellings are usually malignant, soft
cutaneous nodules swelling may be cystic.
E. Glaucoma 7. Mobility: This should be determined
by hand in all directions, i.e. from side
F. Detection of argemone oil in cooking
to side and above downward.
medium
8. Parietal or intra-abdominal: This
Management of Ascites can be found out by making the
I. Treatment of cause abdominal muscles taut by raising
the shoulders or the legs. If the
II. Diet: Low sodium diet
lump becomes less prominent it is
III.Diuretics: Spironolactone or furosemide or intra-abdominal. If it becomes more
combination prominent it is parietal. Ifmobile over
IV. Abdominal paracentesis if cardiorespiratory the contracted muscles it is superficial
embarrassment with or without albumin to the muscles and if it is fixed it is
V. TIPS (Transjugular intrahepatic portosystemic adherent to the muscle
shunt) 9. Hernial sites for expansile impulse on
VI. Porta venous shunts for refractory ascites coughing
10. Pulsations (if present): Expansile
72
j
{ 3 > Abdomen
the body of LI Vertebra near its lower body descent of the inflamed gallbladder,
posteriorly. which touches the examiner's fingers.
Transtubercular plane • It passes through the If a stone is present in the common
tubercles of the iliac crest and the body of LS bile duct there is a triad of intermittent
vertebra. colic, intermittent jaundice and fever
Two vertical lines are the right & left lateral with chills and rigors.
planes corresponding to the midclavicular line 4. Courvoisier's law: In a patient with
or either side. obstructive jaundice, a palpable gall
Right Hypochondriac Region
bladder is seldom due to gall stones.
This is because the gall bladder is
I. Swellings in the Abdominal Wall Cold usually shriveled & non distendable
Abscess in long standing gall stone disease.
1. Fluctuant swelling with no signs of Therefore, in a pt. with obstructive
inflammation jaundice, a palpable gall bladder
2. Swelling becomes prominent when the indicates malignancy of gall bladder
abdominal muscles contract or pancreas.
3. Irregularity in the affected rib or deformity Exceptions to courvoisiers law i.e.
of the spine. Obstructive jaundice with a palpable
II. Intra-Abdominal Swellings gall bladder due to gall stone occurs
A. Hepatic in
I. It moves with respiration but is not i. Double impaction ofthe stone (in
mobile sideways the bile duct & in the cystic duct)
2. The swelling is continuous with ii. Gall stones in the cystic duct
the liver dullness without a band of (Mirizzi's syndrome)
colonic resonance iii. Mucocele of gall bladder
B. Gall Bladder C. Sub-Phrenic Abscess
1. Oval smooth swelling, the size of an 1. Pain in the right hyp ochondria! region
egg referred to the shoulders
2. Moveswith respiration,can be moved
2. Diffuse tender swelling in the right
sideways but cannot be pushed down
hypochondrial region
into the loin (like kidney swelling)
3. Signs of septicemia: High fever
Chronic Cholecystitis and Cholelithiasis
with rigors, sweating and marked
I. Pain over the right rectus muscle tachycardia
radiating to the inferior angle of
4. Screening: Raisedand fixed diaphragm
scapula, aggravated after fatty meals.
with gas under it
Often the patient makes an attempt
to get relief by frequent belching 5. Features ofthecausativecondition e.g.
or vomiting but relief is seldom perforated peptic ulcer, liver abscess
complete. D. Stomach and Duodenum
2. Gall bladder may be palpable. I. Carcinoma of Pylorus:
3. Murphy's sign is positive: i.e. a. There is an irregular firm lump,
Tenderness under the right costal which moves on respiration
margin at the lateral border of the b. Patient is usually elderly and has
rectus muscle when the patient takes anorexia and weight loss
a deep breath. This occurs due to the
73
PRACTICAL MEDICINE
74
( 3 > Abdomen
- 75
PRACTICAL MEDICINE
coughing and reducibility of swelling 4. Barium meal: Filling defect with
.is present spasm of the terminal ileum and
elevated position of the cecum
Desmoid Tumor of the Rectus Sheath
B. Carcinoma of the Cecum: Refer carcinoma
It is a fibroma that arises from a deeper part of the of colon, Refer Pg. 74
rectus abdominis muscle either spontaneously C. Amebic Typhlitis
or after an abdominal operation. The features
I. Irregular, firm, tender lump
are:
2. History of amebic dysentery
l. It is common is females
3. Stools will show E. histolytica
2. Firm rounded swelling which recurs after
operation (Recurrent growths become D. Impaction by Round Worms
more malignant than the original one) Irregular lump
II. Small Intestine and Mesentery IV. lliopsoas Sheath
Tuberculosis with Tabes Mesenterica A. Iliac Abscess
I. Irregular firm lump in sickly children and This results from infection of a hematoma in
young adults the traumatized iliacus muscle. It resembles
2. Subacute intestinal obstruction appendicular lump except:
3. Tuberculous lesions in thelungsand lymph I. The symptoms are all along over the
nodes iliac fossa and not shifted to this area
III. Retroperitoneal Sarcoma 2. A clear space is found between the
abscess and the iliac crest in case of
l. Young patient
an appendicular lump but not in an
2. Huge, firm, nodular mass attached to the iliac abscess
posterior abdominal wall
B. Cold Abscess from Pott's Disease
3. Edema offeet ifthere is pressure on inferior
I. Since it gravitates down deep to the
vena cava
inguinal ligament into the thigh,
IV. Stomach and Duodenum: Refer Pg. 73 fluctuation on either side of the
V. Colon: Refer Pg. 74 inguinal ligament is present.
Right Iliac Fossa 2. Gibbus of the spine clinically and
confirmed radiologically.
I. Parietal Swellings: Refer Pg. 75
V. Gall-Bladder
II. Appendkular Lump
A huge distended gall bladder with enlarged liver
I. Irregular, firm, tender lump initially fixed, may descends as low as the right iliac fossa.
slightly movable later and tympanic
VI. Unascended Kidneys
2. Leucocytosis
l. Swelling characteristically reniform
3. Signs of inflammation over the skin if the
2. IVP: Pelvocalyceal system in connection
abscess approaches the surface
with the swelling
III. lleocecal Region
VII. Undescended Testes
A. Hyperplastic Ileocecal Tuberculosis
When palpable, it is always pathological:
l. Irregular, firm, tender, intermittent
I. Hard, irregular, fixed lump if malignant
lump oflong duration
2. Caecum is pulled upwards 2. Absence of tests in scrotum
3. Tuberculous manifestations in lymph VIII.Uterus and the Appendages
nodes and lungs Swellings in connection with the uterus and
76
< 3) Abdomen
the appendages usually are associated with 2. Copious discharge of mucus per rectum
m enstrual disturbances. Vaginal examination and frequency of micturition.
will confirm the origin of the swelling in the 3. Rectal examination reveals bulging of the
right iliac fossa. anterior wall of the rectum.
Hypogastrium Left Iliac Fossa
I. Parietal Swellings: Refer Pg. 75 I. Parietal Swellings: (As above).
II. Urinary Bladder
II. Sigmoid Colon
l. Globular swelling in the hypogastrium
A. Carcinoma
which may extend from symphysis pubis
to the umbilicus 1. Increasing constipation
2. The lump is tender and dull on percussion 2. Loaded colon proximal to stenosis,
3. Pressure induces a desire for micturition pits on pressure
III. Uterus and its Appendages 3. Barium enema: Constant fillingdefect
Spherical midline swelling above symphysis B. Diverticulitis
pubis harder than urinary bladder (it should 1. Evidence of diverticulosis: Flatulent
be a rule to exclude swelling of the bladder by distension oflower abdomen, usually
passing a catheter before concluding that it is in patients over 40 years age
uterine swelling). 2. Evidence of inflammation: Pain and
IV. Fallopian Tube and Ovary tenderness in the left iliac fossa
A. Chronic Salpingitis 3. Barium enema: Saw tooth appearance
l. Attack ofpelvic peritonitis: Pain, fever of multiplediverticula with narrowing
and bladder disturbances of the colon
2. Mass in the midline or on one or other Ill. Iliopsoas Sheath: (As above)
side of the midline IV. Undescended Testes: (As above)
3. Vaginal examination confirms the V. Unascended Kidneys: (As above)
diagnosis
B. Ovarian Cyst or Tumor
1. Mass arising from one side of the 7 Acute Viral Hepatitis
pelvis but later on may become central
Etiology: Acute viral hepatitis can be caused by any
2. Menstruation normal or scanty one of the following:
3. Vaginal examination conf irms
1. Hepatitis A Virus: This is an RNA virus
attachment to the uterine appendages
4. Swelling has dullness over the front Capsid
of the abdomen with resonance in
the flanks (In ascites resonance in the ---l�- Initiation
center and dullness in the flanks) peptide
transmitted by feco oral route. Incubation with a rise in liver function tests. It usually has
period is 2-6 weeks. Usually it does not lead to a chronic severe clinical course.
chronic disease or carrier state. Acute infection 5. Hepatitis E Virus (formerly called enterically
is anicteric in 50% of patients. Usually seen in transmitted non-A non-B hepatitis) is an
children below 15 years age. RNA virus. It resembles Hepatitis A, is
2. Hepatitis B Virus: This is a DNA virus transmitted by feco-oral route and is found to
transmitted parenterally. The incubation period occur in endemic areas like India, Asia, Africa
is 2-25 weeks. About 10% of patients develop and Central America. It is seen to occur in
chronic disease or a carrier state. individuals who are immune to HAY infection.
Nudeocapsicl pro1cin Usually seen in adults and used to be wrongly
(soluhlo. non-p•tr1icuh1hi I rnnt\gl
labelled as 'A' in the past.
Surfoce<:oall 6. Hepatitis F, G and H viruses have been recently
llll!sAg)
described.
7. Other viruses: Epstein Barr virus, cytomegalo
virus, herpes simplex virus, rubella virus and
virus of yellow fever may all cause hepatitis.
'""_'--_,..:;,;.._,.,._ J11<:01nplc-tt?
t.lo1lhlc,slrandc-d
c:in:ular DNA Oinical Features
1. Influenza-like syndrome is common in hepatitis
A with malaise, anorexia and fatigue
F,g 3 21 Hepat,t,s BV,rus
2. Arthritis and urticaria is common with hepatitis
3. Hepatitis C Virus (formerly called non-A B and is probably due to circulating immune
non-B hepatitis) is a single stranded RNA virus complexes
transmitted parenterally. The incubation period 3. Jaundice with dark urine and light stool occur
varies from 2-25 weeks. About 20-30% develop in 50% of patients
chronic hepatitis, 50% of which is chronic active
4. Tender hepatomegaly is common and
hepatitis which would ultimately lead to cirrhosis
splenomegaly occurs in 20% of cases
of liver.
4. Hepatitis D Virus or Delta agent: This is a small Complications of Acute Viral Hepatitis
incomplete RNA virus which is infectious only 1. Fulminant hepatic failure
in presence of Hepatitis B surface antigen. It is 2. Relapsing hepatitis
thus a "superinfection" to hepatitis B infection 3. Cholestatic hepatitis
ora "co-infection" which occurs simultaneously
4. Post-hepatitis syndrome
Hepatitis B 5. Chronic hepatitis
Surface
antigen 6. Cirrhosis of liver
coat 7. Hepatocellular carcinoma
(HBsAg)
8. Aplastic anemia
Delta 9. Henoch Schonlein purpura
antigen
{protein)
10. Renal failure
11. Connective tissue disease
+--B- Single
stranded 12. Papular acrodermatitis
circular
RNA Diagnosis
I. To diagnose Viral Hepatitis
1 F,g.3 22:Hepat1t1sDV1rus!Deltaagent)
1. Typical clinical features
78
--
( 3) Abdomen
2. Elevated SGOT, SGPT, LDH, bilirubin and patients experience nausea in the evening. If
alkaline phosphatase there is persistent vomiting, intravenous fluids
II. To diagnose the type of hepatitis (Tables and must be given. Usually excessive fatty foods are
Figs. 3.8, 3.9 &3.10) not tolerated well and are hence avoided.
1. In Hepatitis A, anti-HAV IgM antibody is 3. Drugs: There are no specific drugs useful for
elevated early followed by anti-HAV IgG viral hepatitis. All hepatotoxic drugs as well as
in 2-3 months. alcohol must be withdrawn.
2. In Hepatitis B, HBsAg is positive. In acute 4. For post hepatitis syndrome: The patient requires
recent infection anti-HBeAb denotes reassurance.
marked infectivity. HBsAg +ve for >6 Table 3.5 : Diagnostic Approach in Acute
months indicates carrier state (See Table). Hepatitis
3. In Hepatitis C, anti-HCV may be positive, Diagnosis Anti- HBsAg Anti-
especially in chronic carriers. The most HAV lgM HBc/gM
sensitive indication is the presence ofHCV 1. Acute Hepatitis A +
RNA.
2. Acute Hepatitis B ±" +
4. In Hepatitis D, HDAg or rising anti-HD V
3. Chronic Hepatitis B +
antibody titre may be present.
5. In Hepatitis E, anti-HEV antibodies or 4. Acute Hepatitis A & B + ±" +
HEV RNA may be present. 5. Acute Hepatitis A on + +
Chronic Hepatitis B
Treatment
6. Acute Hepatitis C, Dor F"
1. Rest: Prolonged bed rest is not usually needed "HBsAg may be sometimes below detectable levels by the
but patients feel better with restricted activities. conventional tests, hence can be negative
2. Nutrition: A high calorie diet should be given. ..anti-HCV, HDAg, anti-HEV can be tested if all three
serological tests above are negative.
It is usually given in the morning because many
79
PRACTICAL MEDICINE
At.:r
Af:r
..........�..
:
�- 1
-.'-.- -
..\
t--t:=.i-
/
HB•A.,,_•·:-_-_-_-_-_-_-_-_-,:-
.I I HB•A ' HBV DNA
--
r:,H
I C'.".BV,:"'DN::--c,--,A--.
.....
Ii
1 11M anti-HBc I
a :---,
• ____ T�t •o.\1:HBrJ
-'!h-r,
� ,-=B::..:•.:..:
..-,- --
AJi.._' -�
. ____J
[_@eAs-- -- ']
, '
.. •·.
-· '
' ··. '·-- --- .................... ��� ..................................
•,
- Time Fig. 3 25 · Reactivation of Chronic Hepatitis Bv1rus 1nfect1on
Time
.-. .
be given within 2 weeks of contact in the
.
At.:r
''
',
, dose of 0.02 ml/kg_ For travelers a dose
'' ' 0.06 ml/kg should be given every 6 months.
: \. Hepatitis A vaccine is now available-
'/ .. -""'
c '-' -...-n-__' �--�
\>- HC\
b. Hepatitis B: A vaccine for active
'---.-------..,--.HCY
�R/IIA
=�
,/ '........ immunization has been prepared from
/ -----------------. HBsAg carrier serum as well as by genetic
Time engineering from recombinant yeast.
F,g 3 24.Acu!eHepat,t1sCV1rus:nfect1on
j
For pre-exposure prophylaxis, Hepatitis B
vaccine must be given at 0, l and 6-month
Prevention interval. The dose is 20 mcg LM. for
l. The patient should avoid salivary transmission immuno-compromised adults and 10 mcg
to others by avoiding kissing, spitting, sharing I.M. for infants and children under 10 years.
food, cigarettes or utensils and sexual contact. For post-exposure cases, a combination
Infected stools and urine in Hepatitis A and E of HBIG (for rapid achievement of high
infections must be disposed off carefully circulating titre of anti-HBs) and hepatitis
2. Immunization B vaccine (for long lasting immunity) is
a. Hepatitis A: All Immune globulin (JG) given.
80
( 3) Abdomen
For perinatal exposure of infantsofHBsAg arthritis of knee, ankle and wrist may occur
positive.mothers, HBIG 0 .5 ml should be along with vasculitis and glomerulonephritis.
given in thigh at birth followed by Hepatitis Prognosis is excellent as these rarely persist
B vaccine IO mcg started with a week of beyond 2 weeks.
birth and repeated at I and 6 months. 5. Hepatitis with aplastic anemia: This is rarely seen
For percutaneous exposure a single dose with acute viral hepatitis. The mortality rate is
of0 .06 ml/kg ofHBIG is given followed by high and no treatment has been effective.
three doses of hepatitis B vaccine.
Chronic Viral Hepatitis
Usually patients retain protective levels for
5 years after complete vaccination. Overview
c. HepatitisD: Thereis noimmunoprophylaxis
• Chronic hepatitis is a condition characterised
to prevent delta superinfection. Susceptible
persons are vaccinated with Hepatitis B by persistent liver inflammation for more than
vaccine. 6 months after initial exposure or diagnosis of
liver disease.
d. Hepatitis C and E: IG prophylaxis in this
hepatitis is not known to be beneficial and Cause of chronic hepatitis are : a) chronic viral
is not recommended. hepatitis (hep. B, Hep. C); b) Auto immune
hepatitis; c) Drug induced; d) Cryptogenic
Variants of Acute Viral Hepatitis (unknown cause).
Fulminant hepatitis: There is rapid onset of liver • Complications of chronic hepatitis include
I.
failure due to rapid liver cell necrosis which cirrhosis, portal HT, liver failure & HCC
occurs due to modification of host response to (hepatocellular carcinoma).
viral infection, allowing rapid viral replication Chronic Hepatitis B (CHBJ
Hepatitis B and C and superinfection with
• The risk of chronicity depends on the age &
delta agent accounts for majority of the
cases. Mortality in 3 weeks is 30% and 90- immune function when a person is infected.
100% above age 60 die. Clinically there is Infection at birth is associated with a 90%
progressive jaundice, hepatic encephalopathy chance of chronic infection while injection in
and hepatorenal syndrome prothrombin time young adulthood in immunocompetent person
is elevated. is associated with a risk of chronicity of only
approximately 1-5%.
2. Cholestatic hepatitis: There are features of
obstructive jaundice with alkaline phosphatase Symptoms of chronic hepatitis range from none,
elevated more than SGPT, during the course to non specific complaints (fatigue, Right upper
of viral hepatitis. It is to be differentiated from quadrant pain), to complication of cirrhosis.
biliary obstruction. The prognosis is excellent, • Extrahepatic manifestation, occur in up to 20%
recovery occurs over few months. of patients with CHB & include arthralgias,
3. Relapsing hepatitis: This occurs several weeks or PAN, glomerulonephritis mixed essential
months after apparent recovery. Sometimes it cryoglobulinemia, polymyalgia rheumatica
may be a second bout of hepatitis with a different and papular aero dermatitis (Gianotti Crosti
virus. Syndrome in children).
4. Viral hepatitis with autoimmune features: It Diagnosis
occurs in 5% of patients with Hepatitis B due
to circulating immune complexes. Serologic & Virologic tests
Anorexia, malaise, fatigue, urticaria, angioedema I. Diagnosis of HBV infection based largely on
migrating arthralgia and non-deforming detection of HBsAg
- 81
PRACTICAL MEDICINE
Table 3.7 : 4 phases of chronic HBV 5. CHB with elevated ALT levels & HBV DNA
insertion >2000 IU/ml.
: ..' iverbiapsy Treatment Treatment not indicated
l. Immune tolerance phase
1. Immune + N N or minimal No 2. Inactive carrier
tolerant inflammation
3. Acute hepatitis B
2. Immune + t Active Yes
active inflammation Drugs
(HBeAg+ve)
Current 1st line therapies
3. Reactivation + i Active Yes
(HBeAg-ve) inflammation 1. Pegylated interferon u- (exception : pregnancy,
decompensated cirrhosis)
4. Inactive + N Nor minimal No
carrier inflammation 2. Nudeoside analogs� Entecavir, Tenofovir
N• Normal Specific drugs
l. Pegylated interferon u: Consider in young, non
2. When HBsAg is detected, further laboratory cirrhotic pts. with low viral load and high ALT.
testing to assess disease status & need for
Treatment : 180 µg/wk s/c for 48 wks.
treatment is indicated.
2. Nucleoside analogues : High antiviral potency;
i. ALT levels
negligible adverse effects, oral administration,
ii. HBV DNA Quantitative (viral load) safe and effective for all ages, suitable for cirrhotic
iii. HBeAg & Anti HBe: To define the type of and HIV coinfected pts.
CHB & end point of therapy.
i. Lamivudine : 100 mg/day; high rate of
iv. Tests for liver disease activity • platelet resistance. ( specific point mutation YM DD
count, total bilirubin, albumin & PT/ INR motify of the HBV polymerase).
V. Liver biopsy � To determine histologic
ii. Adefovir dipivoxil: 10 mg/ day; potentially
grade & stage of disease.
nephrotoxic.
Treatment iii. Entecavir : 0.5 - 1 mg/day; low rate of
l. Goals of treatment resistance.
i. Prevention of long term complications iv. Tenfovir : 300 mg / day; low rate of
(cirrhosis, HCC) & mortality resistance. Adverse events: J. sed bone
density, Fanconi synd. (rare).
ii. Primary goal : sustained suppression of
HBVDNA. v. Others: a. Emtricitabine; b. Clevudine.
iii. Secondary goal: a)Decreasedornormalised Duration of Therapy
serum ALT; b) improved liver histology, c) l. HBeAg +ve: Treat until HBeAg seroconversion
HBeAg loss or seroconversion; d) HBsAg
and stop after consolidation, period 6-12 months
loss.
after HBeAg seroconversion.
Indications for HBV treatment 2. HBeAg · ve : Treat indefinitely because relapse
is common after stopping of therapy.
Treatment indicated
82
( 3 > Abdomen
varied etiology and characterized by hepatic cell in calories and carbohydrates may cause
necrosis, resulting in collapse, proliferation of connec, relative protein deficiency and contribute
tive tissue (fibrosis), nodular regeneration and altered to liver necrosis by infections and toxins.
intrahepatic circulation. b. Infections: Malaria, kala-azar anddysentery
cause malnutrition and contribute to
Classification cirrhosis. Schistosomiasis produces hepatic
1. Viral Hepatitis: Hepatitis B, C and D may lead fibrosis, which may progress to cirrhosis.
to cirrhosis of liver. c. Toxins: Aflatoxin-contaminated foodstuffs
2. Alcohol: An intake of about 80 gm of alcohol may produce cirrhosis. It is produced when
daily, for 15 years, may lead to cirrhosis. groundnuts, pulses or other nuts stored in
3. Prolonged cholestasis moist conditions get contaminated with a
4, Cardiac failure oflong duration induces fibrosis fungus • Aspergillus flavus.
around the central vein. d. Autoimmunity: Autoimmune antibodies
5. Drugs: INH-Isoniazid, methotrexate and as produced in SLE may lead to cirrhosis.
methyldopa may cause cirrhosis. e. Cryptogenic: The cause of cirrhosis is not
6. Congenital disorders: identified.
a. Hemachromatosis:Excessive ironabsorption Pathology
and deposition in the liver leads to cirrhosis.
0 ther features are diabetes, bronze colored The liver is firm, has a gritty feel on cutting and the
skin and myocarditis. cut surface shows fibrous bands surrounding nodules
of various sizes.
b. Wilson's disease: Excessive deposition of
copper leads to cirrhosis. Other features Microscopic examination would show necrosis, col
are lenticular degeneration (involuntary lapse, fibrosis, regeneration and altered circulation.
movements, rigidity), greenish yellow ring Regenerating nodules, by compressing the blood
at the limbus of cornea (Kayser Fleischer supply of the liver cause ischemic damage of the liver
ring) and deficiency of ceruloplasmin. even after the disappearance of the primary cause of
c. Galactosemia: There is deficiency of the liver injury.
enzyme galactose-1-phosphate-uridyl Clinical Features
transferase. Galactose from milk is not
converted to glucose. Infants on milk diet Cirrhosis of liver may progress for years before any
may have malnutrition, diarrhea, jaundice, clinical suspicion is aroused because even 10% of
cataract and hepatosplenomegaly with healthy liver tissue is adequate for metabolic functions
cirrhosis of liver. and liver tissue has a remarkable capacity to regenerate.
The presenting features of cirrhosis are ascites, edema,
d. Alpha-1-antitrypsin deficiency: The normal
hematemesis or hepatic coma. The clinical features can
levels of this enzyme are 150-350 mg/L.
be classified as those due to liver cell failure and those
Levels less than 80 mg/Lmaycause cirrhosis
due to portal hypertension.
(mechanism unclear), pancreatitis and
recurrent lung infections with emphysema. I. Due to Liver cell failure:
7. Miscellaneous: 1. Palmar erythema, spider nevi
a. Nutrition: A diet low in proteins especially 2. Gynecomastia, testicular atrophy and loss
in methionine and choline may cause of libido
fatty liver and cirrhosis. A diet rich in 3. Jaundice - usually mild, may be severe
unsaturated fats (as in vegetable oils) terminally
may increase the susceptibility of liver 4. Ascites, edema and scrotal swelling
to cirrhosis. Similarly, a diet very rich 5. Flapping tremors
83
PRACTICAL MEDICINE
84
{ 3) Abdomen
85
PRACTICAL MEDICINE
86
{3 > Abdomen
C
3% per year
2_20% Hepatic clecotnpcnsr,t1on
5 5-•l0% over 20 years
Acute HCV infection -·-· -+ chronic HCV infection----� Cirrhosis
Hepatic carcinoma
1-4 'Y., per year
Frg.3 26·HCVJnfect1on
characterized by immune & autoimmune enhance treatment response and minimise the emer
features. gence of viral resistance.
• Characterised by presence of circulating hyper
gammoglobulinemia and auto antibodies with
Wilson's Disease
interface hepatitis on liver biopsy. • Wilson disease is a genetic disorders (autosomal
• Treatment in with anti-inflammatory / recessive) in which copper accumulates in the
immunosuppressive therapy e.g. steroids and liver & brain is excess of normal metabolic needs.
Azathioprine. • Diagnosis: i) Low levels ofserum cerruloplasmin
• Liver transplantation in patients who do not i.e. less than 20 mg/ di (Normal: 20-50 mg/ di);
respond to medical therapy. ii) Hepatic copper concentration above 250 µg
/ g. dry copper wt.; iii) clinical findings include
Chronic Heaptitis C presence of kayser fleischer rings, stigmata of
HCV infection is a leading cause of morbidity chronic liver disease & neurologic findings.
and mortality with a global prevalence of 3%.
Treatment is life long
Natural history
i. Chelating agents eg. D-penicillamine, Trientene
Diagnosis
ii. Zinc salts
I. Detectable anti - HCV indicate exposure but
iii. Liver transplantation for acute liver failure or
does not confirm active infection, because anti·
decompensate liver disease.
HCV persistent indefintely after spontaneous or
therapeutic resolution
2. HCV RNA viral load should be performed in
all patients with positive anti-HCV assay & in
10 > Alcoholic Liver Disease
patients in whom antivrial treament is being (ALO)
considered. Alcohol induced liver injury results from chronic
3. HCV genotype - 6 major genotypes (I to 6) alcoholic ingestion which may be classified as :
Treatment I. Alcoholic fatty liver (AF)
l. Standard therapy consists of combination of 2. Alcoholic hepatitis (AH)
pegylated interferon (PEG IFN) and Ribavarin 3. Alcoholic cirrhosis ofliver (AC)
2. Sustained virolgical response (SVR) i.e. HCV Alcohol dehydrogenase (ADH) Acetaldehyde Dehy
RNA negative 24 weeks after end of treatment drogenese (ALDH) Co2 Alcohol Acetaldehyde + H2o
is achieved in 45-80% of patients depending on Oriental flush syndrome : Results from impaired
the genotype. metabolism of acetaldehyde caused by inheritance of
Future the ALDH22 allele seen mainly in persosn from East
Asia (eg. Japan) causing toxic systemic effects such
Protease inhibitors such as Boceprevir and Telaprevir as nausea, headache, flushing & tachycardia of acet
and Polymerase inhibitors such as safosuvir combined aldehyde accumulation. Therefore, tense patients get
with Ribavarin with or without PEG IFN will further symptom ofexcessive flushing after consuming alcohol.
87
PRACTICAL MEDICINE
r- i\Lr.OHOLHEPATrTrs
AF occurs in most heavy drinker but is reversible on
l l'
..
cessation of alcohol consumption.
Iron / 1
V1r;1I Pathology: The liver is enlarged, greasy, yellow and
Malnulrilion -c:..ni�le
Diel i\lcohol Gender
firm. Hepatocytes are distended with fatty vacuoles
which push the nucleus to the periphery. This occurs
Fig. 3 27 Risk factors/ cofactors required fort he because fatty acid oxidation is impaired and they are
developmentofadvancedALD
taken up by the cells and esterified to form triglycerides.
l
Normal Liver
Clinical features: The clinical features are minimum
or absent. There may be tender hepatomegaly only.
(!l0-100%J
Investigations: Usually all laboratory tests are normal.
Sometimes there may be elevation ofSGOT and alka
.------ Fatly Liver ----
line phosphatase.
Alcoholic: hepalilis -------+ Cirrhosis Prognosis: AF has good prognosis. Complete resolu
tion occurs after cessation of alcohol intake.
Fig 3 28 Percentageofheavydrinkerswhodevelop
d1fferentstagesof ALD Treatment: Alcohol intake must be stopped. Nutri
tious diet with high doses of vitamin B complex must
Risk factors of ALD be given.
1. Quantity : Risk of developing cirrhosis with Alcoholic Hepatitis (AH)
ingestion of>60-80 g / day of alcohol in men & AH is an inflammatory lesion characterized by infil
>20 g/day in women for 10 years or longer. tration of the liver with leucocytes, liver cell necrosis
2. Gender : Increased susceptibility to ALD at and alcoholic hyaline deposition.
amounts> 20 g/day (2 units) [ l unit= 10 gm]. Pathology: Liver cells are ballooned, degenerated
3. Hepatitis C : Concurrent HCV infection and necrosed with infiltration with polymorphs and
associated with younger age for severity, more lymphocytes. Hepatocytes contain Mallory bodies or
advanced histology and decreased survival. alcoholic hyaline which are clumps of perinuclear,
deeplyeosinophilic material that represents intermedi
4. Genetics: Gene polymorphisms include alcohol
ate filaments. Mallory bodies are not diagnostic but do
dehydrogenase (ADH) and the cytochrome P450
usually suggest alcoholic hepatitis. They are also seen
system (CYP4502El).
with morbid obesity, jejuno-ileal shunt, uncontrolled
S. Malnutrition : Nutritional status important risk diabetes mellitus, Wilson's disease, Indian childhood
factor for the development of ALD & diet. cirrhosis, etc.
Pathogenesis Clinical Features: This varies from asymptomatic
patient to mild illness to fatal liver cell failure.
The mechanism whereby alcohol produces different Typically it resembles Viral hepatitis
liver lesions is poorly understood. Fatty change may 1. Anorexia, nausea, vomiting, abdominal pain,
be due to increased production and decreased use of malaise, weight loss and jaundice
fatty acids in the liver cells following the conversion 2. Fever as high as 39 · 40 q C may be seen in SO%
of alcohol to acetaldehyde by alcohol dehydrogenase.
of cases
For the development ofalcoholic hepatitis, fibrosis and
3. Tender hepatomegaly is usually present.
cirrhosis, production of toxic metabolites called ad
Splenomegaly occurs in 33% cases
ducts during the conversion of acetaldehyde to acetate
4. Signs of liver cell failure like spider angioma,
may be responsible. In addition, immune reaction to
jaundice, ascites, edema, GI bleeding and
liver cells altered by alcohol may also be involved.
encephalopathy may be present
Determinants of liver injury are :
5. Cholestatic jaundice may occur in some
88
( 3 > Abdomen
Most of the patient recover after several weeks to Prognosis
months after abstinence, however, histological ab
normalities may persist for 6 months. 3 models shown to predict short term prognostic
in Alcoholic hepatitis.
Investigations l. Discriminantfunction (DF) (Maddrey's score):
1. Anemia may occur from GI bleeding, nutritional [ 4.6 x (patients prothrombin time - control
deficiency (folate and B12 deficiency), hyper value in seconds)]+ S. bilibrubin (mg/di). DF
splenism, direct bone marrow suppressant effect value<'. 32 has a poor prognosis with 1 month
ofalcohol and hemolysis due to acanthocytosis. mortality rates of 35-45%.
2. Leucocytosis is usually present. However, 2. Mode/for End Stage Liver Disease (MELD): It
leucopenia and thrombocytopenia could occur includes S. bilirubin level, INR & S. Creatinine
due to hypersplenism. levels. A score of<'. 21 is highly predictive of
90 day mortality.
3. Alkaline phosphatase may be elevated.
3. Glassgow Alcoholic Hepatitis Scale (GAHS)
4. SGOT is high but rarely more than 300 units.
: It includes S. bilirubin, INR, BUN, Age &
Unlike in viral hepatitis where SGPT is higher
WBC count. A score of <'. 9 at days l & 7 is
compared to SGOT, in alcoholic hepatitis SGOT
suggestive of severe alcoholic hepatitis & a
is much higher than SGPT. This is because of
poor prognosis.
greater inhibition of SG PT synthesis by ethanol
which may be partially reversed by pyridoxal Alcoholic Cirrhosis of Liver (AC)
phosphate.
AC is diffuse fine scaring with loss of liver cells and
5. Serum prothrombin is prolonged due to reduced small regenerating nodules (micronodular)
synthesis of Vitamin K dependent dotting
Pathology: With continued alcohol intake, liver cells
factors.
are destroyed and fibroblasts appear at the site of
6. Serum albumin is usually reduced due to injury and stimulate collagen formation. Septae of
impairment in hepatic protein synthesis. Globulins connective tissue appear in the periportal and peri
are high due to non-specific stimulation of central zones which eventually connects portal triad
reticuloendothelial system. Hyperbilirubinemia and central vein. The remaining liver cells which are
may be present, due to decompensation. surrounded by connective tissue, regenerate and form
7. Hypomagnesemia and hyp ophosphatemia may nodules. Usually, cell loss exceeds regeneration. The
occur due to dietary deficiency. Hypokalemia may liver shrinks and becomes hard and nodular
occur due to hyperaldosteronism (aldosterone Alcoholic hepatitis
8.
is normally destroyed in liver).
Gamma Glutamyl Transpeptidase (GGPT) is
!
Alcohol abstinence
raised due to alcoholic abuse irrespective ofliver Nutritional support
disease due to microsomal enzyme induction.
Discriminant function i!: 32
Prognosis or MELD i!: 21
In milder cases, clinical recovery can occur completely. !
However, repeated bouts ofalcoholic hepatitis may lead GI bleed. acli ve infection, hepatorenal syndrome
to irreversible progressive liver injury, abstinence from No I Yes
alcohol can reduce long term morbidity and mortality. !
Prednisolone
l
Pentoxyfylline
Marked hyperbilirubinemia, elevated creatinine, 40 mg p.o. daily x 4 weeks 400 mg lid x 4 weeks
elevated prothrombin time (more than 1-5 times followed by 20 mg daily x 1 week
normal), ascites and encephalopathy are associated & 10 mg daily x 1 week
with poor short term prognosis. F,g 3 29 T,e,)tment /\l9or1thn1 fo1 /\lcohof1c 11eµ<1l1l1s
89
PRACTICAL MEDICINE
Clinical Features: It is usually silent in 10% of cases. form schizonts but develop into male and female gam
The clinical manifestations are like cirrhosis of liver. etes. During the mosquito bite, these gametocytes are
Dupuytren's contracturedue to fibrosis of palmar fascia ingested. They fertilize in the mosquito's stomach and
with resulting flexion contracture of the digits and develop into sporozoites which localize in the salivary
parotid swelling are associated with alcoholism rather glands of the mosquito. These sporozoites enter the
than cirrhosis. human blood stream on a subsequent mosquito bite
and thus complete the cycle.
Laboratory Tests: Similar to alcoholic hepatitis. El
evated blood ammonia may also occur due to impaired Clinical Features
liver function and shunting of portal venous blood
around the cirrhotic liver. 1. Onset: The onset may be insidious with
abdominal pain, nausea, dry cough and malaise.
Prognosis: Similar to alcoholic hepatitis
Rarely it may be acute and with fever and chills.
Treatment: Similar to cirrhosis of liver 2. Fever with rigors: In the early stage, fever may
be persistent for several days but soon it develops
11 > Malaria
into a synchronous periodicity. A classical attack
offever has a chill, rise in temperature to 40-41 °C,
Malaria is a common tropical disease caused by a headache and myalgia. This is followed by several
protozoa, plasmodium, through the bite of female hours of profuse sweating and fall in temperature.
anopheles mosquito. In vivax and oval malaria these paroxysms occur
every 48 hours (benign tertian) whereas in
Types malaria, it occurs every 72 hours (quartan). In
falciparum malaria, the temperature is usually
There are mainly four types of plasmodium infection
causing malaria as follows: persistently elevated or may progress to 48 hour
cycle (malignant tertian malaria). These cycles
I. Plasmodium falciparum (Malignant tertian may be repeated in case of benign tertian malaria
malaria) due to exo-erythrocytic phase.
2. Plasmodium vivax (Benign tertian malaria) 3. Organomegaly: Liver is moderately enlarged and
3. Plasmodium malariae (Quartan malaria) tender. Spleen is often palpable in acute attack. It
4. Plasmodium ovate is soft to firm and occasionally tender.
4. Miscellaneous: Herpes simplex lesions may be
Life Cycle (Fig. 3.30)
present around the mouth. Rarely jaundice may
When an infected mosquito bites an individual, its occur.
saliva, rich in parasites (sporozoites) is injected. The
sporozoites enter he circulation and then the liver Investigations
(pre-erythrocytic phase). It multiplies in the liver 1. Complete Blood Count and Demonstration of
cells forming merozoites. After 5-9 days, the mero parasites: There is normochromic normocytic
zoites enter the red blood cells (erythrocytic phase) anemia. Both thick and thin smears should be
forming trophozoites which subsequently mature to examined for detection and identification of the
become schizonts. The schizonts are discharged int.o malarial parasites. Blood smears must be repeated
the blood stream when the red cells degenerate. This at intervals of 6 12 hours on multiple occasions.
results in an attack of malarial fever. The red cells are Malarial parasites can also be demonstrated
destroyed by the spleen which enlarges and some of on bone marrow examination and by splenic
the schizonts continue to develop in the liver (exo puncture.
erythrocytic phase) causing a relapse. This phase is Criteria for severefalciparum malaria:
absent in falciparum malaria.
a. More than 5% of RBCs infected
Some of the merozoites for unknown reasons do not
b. Parasites index more than 1,00,000/ul
90
( 3 > Abdomen
c. More than 250 parasites per field on thick b. Leucocytes are usually normal. However,
smear leucocytosis without infection may occur
d. Leucocytosis due to cachectin (tumour necrosis factor)
2. Serology: Henry's melanin flocculation test, and carries grave prognosis.
complement fixation test, passive hemaglutina c. Thrombocytopeniamay bedue to decreased
tion test, gel precipitation test and immuno platelet production, decreased platelet
fluorescent technique to demonstrate antibodies survival, increased splenic uptake and
to malarial parasite are useful. sequestration and consumption by DIC.
3. Otherinvestigations: Serum electrolytes, BUN, d. Bleeding may occur due to DIC.
creatinine, blood sugar, ECG, chest X-ray, arterial 4. Renal failure: (defined as urine output
blood gases, blood culture, lumbar puncture if <400ml/24 hours and failure to improve after
necessary. rehydration). The patient may present with loin
4. Newer Methods: Polymerase Chain Reaction pain, vomiting, diarrhea, polyuria followed by
(PCR) and serological tests based on histidine oliguria with passage of dark or black urine, with
rich protein 2 (HRP-2) (e.g. Parasite F and ICT or without fever, tender hepato-splenomegaly,
Ff) and pLDH (e.g. Optimal). anemia, jaundice, hypotension, renal failure and
Complications coma. Acute glomerulonephritis and nephrotic
syndrome may also occur. lntravascular
1. Cerebral malaria: This is an altered state hemolysis, hypovolemia, hyperviscosity and
of consciousness due to the presence of Pl.
intravascular coagulation may be responsible
falciparum. Patient usually has fever and non
for renal failure.
specific symptoms for a few days before the
development of cerebral malaria. There may be Blackwater fever is a condition where renal
mild neck rigidity and retinal hemorrhages but no failure is associated with severe intravascular
white exudates or papilledema. Deep reflexes are hemolysis and hemoglobinuria. If the patient
brisk and plantarsextensor with absent abdominal survives acute phase, urination commences in
reflexes. Psychiatric manifestations, convulsions 4 days and increased creatinine levels return to
and coma may occur. Rarely brainstem may be normal in 3-4 weeks.
involved, manifested by convergence spasm, 5. Pulmonary edema: This occurs due to
ocular bobbing and nystagmus. Cerebellar Table 3. 1 O : Complications of
ataxia, may occur. Rare manifestations are Plasmodium Infections
cranial nerve palsy, extrapyramidal syndromes,
Plasmodium falciparum
polyneuropathy, mononeuritis multiplex, Guillain
Barre-syndrome and rhabdomyolysis. Cerebral malaria including seizures and coma
91
PRACTICAL MEDICINE
In Mosquito InMan
Seorozoices
inj�bv
mosquito bite
��------Sporozoitcs
92
( 3 > Abdomen
RED CELL
MORPHOLOGY TROPHOZOITE SCHIZONT GAMETOCYTE
AND GENERAL (RING FORM)
FEATURES
Very enlarged red cells
..0..
Pale, fine red stippling
(Schuffner's dots]
�
'>
;.., Low or moderate para
sitemia
Thick compact rings > 1/3
12-24 medium-sized
merozoites per cell: Large and round or oval,
� All stages of life cycle size of RBC with single almost fill the cell almost fills the cell
present Red central or eccentric
large chromatic dot. 1 Schuffner's dots present.
Multiple parasites per Few Schuffners dots. single nucleus
, 1-2 clumps of peripheral
cell may be present yellow-brown Fine scattered pigment
Ameboid ring forms in
mature trophozoites. fine hemozoin pigment.
...
- .o.-:
Enlarged red cells, some
. .. . .
oval shaped, some with
fimbriated edges
Pale, fine to coarse red
stippling (Schuffner's
dots) Oval shaped, fills 3/4 of
Low parasitemia Thick compact rings 8-12 large merozoites the cell. Smaller than
> 1/3 size of RBC . per cell. vivax.
Multiple parasites rare
Single chromatic dot Daisy-head arrangement Coarse brown pigment,
Fewer stages present Schuffner's dots present. scattered mainly near
Numerous Schuffner's
dots. Central brown pigment. periphery.
r
Normal or microcytic,
normochromic red cells
Lowest parasitemia
Multiple parasites per
cell rarely found Small, thick compact
No stippling rings< 1/3 size of RBC.
All stages usually present Single chromatic dot, 6 ·12 large merozoites Round, fills 1/2 to 2/3
double dots rare. per cell. of the cell.
Ameboid rings or band Daisy-head arrangement Prominent brown black
across cells in mature Central coarse dark pigment.
trophozoites. brown pigment. Dark nucleus.
-
93
PRACTICAL MEDICINE
94
( 3 > Abdomen
cerebral malaria. The dose is 7 mg/kg D. Treatment of Persistent Hypnozoites in
over 30 min followed by 10 mg/kg P.vivax or P. ovale Infections
over 4 hours and then 10 mg/kg over 8 1. Primaquine: This should be given
hours or until the patient can complete in the dose of7.5 mg BD for 14 days
7 days of oral treatment. Doxycycline usually after doing a G6PD test. This
should also be simultaneously given has no effect on acute attack.
in the dose of 100-200 mg/day.
2. Bulaquine is given 25 mg OD for 5
3. Mefloquine: I t has a rapid days.
schizonticidal action in the single
III. Treatment of Complications
dose of 15 mg/kg orally maximum
dose 1000-1250 mg. It may cause IV. Prophylaxis
nausea, vertigo, light-headedness, 1. Measures should be taken to prevent
confusion, psychosis and fits. mosquito breeding e.g. proper sewage
4. Halofantrine: This is effective in some drainage, and preventing stagnation of
parts of Africa against P. falciparum. water. Spreading oil over the water helps
It is given in the dose of 500 mg every to kill the larva.
6 hours for 3 doses. [n children the 2. Protective measures should be taken by
dose is 8 mg/kg. persons staying in endemic areas. This
5. Qinghaosu: This is discovered from includes sleeping under mosquito net and
herbs by Chinese and is effective wearing protective clothing.
for P. falciparum. Artemisinin 3. Travelers to endemic areas must take
derivatives are rapidly acting, safe and prophylaxis as given in Table below.
effective against multi-drug resistant
Table 3.12 : Malaria Prophylaxis for
infections. Artemether 3.2 mg/kg IM
Travelers
is given followed by 1.6 mg/kg [M
every 12-24 hours until patient wakes Areas with Chloroquine-susceptible P. falciparum
up. Chloroquine 300 mg of base once weekly for 1 week before
exposure, during exposure and for 4 weeks after exposure..
Artesunate 2 mg/kg I. V. stat followed
Areas with Chloroquine-resistant P. falciparum
by I mg/kg 12 hourly. Mefloquine 250 mg of base once weekly for 1 week before
Orally - 100 mg B.D. Day I followed exposure, during exposure and for 4 weeks after exposure
by 50 mg B.D. Days 2-5. or
Chlorguanide (Proguanil) 300 mg daily for 1-2 days before
6. Pyrimethamine and sul fadoxime: exposure, during exposure and for 4 weeks after exposure
A combination of pyrimethamine 25 To Carry for self-treatment of febrile illness when
mg and sulfadoxime 1500 mg helps medical treatment is not available immediately
to cure an acute attack ofchloroquine Pyrimethamine-sulphadoxime single dose of 3 tablets
resistant malaria. containing 25 mg Pyrimethamine & 500 mg su lphadoxime
95
PRACTICAL MEDICINE
The parasite occurs in two forms - amastigote (leishman shaped bodies with a central nucleus, eosinophilic
ial) stage in man or other vertebrates (dog, hamster, etc.) vacuole, and a flagellum.
and promastigote (leptomonad) stage in sandfly. The
amastigote form is a round or oval body, with thin cell Life Cycle (Fig. 3.35)
membrane, round or oval nucleus with kinetoplast (DNA The sandfly bites the infected man and ingests along
containing body and mitochondria) at right angles to the with blood parasites. The amastigote is transformed
nucleus, a thin axoneme from kinetoplast to the margin to promastigote in the stomach of the vector in 5-7
of the body and a vacuole. days. The promastigote multiples and is transformed
The promastigote form is found in sandfly and on during the next blood meal to another man.
culture medium. It consists of long slender spindle The parasites are taken by the phagocytes and they
Amastigolc fonn
Rciiculq-cndothdial
Sn1cm<R•·s1
Bone marrow
Mid-gut of Sandfly
--
Spleen
Liver
RETICULO SANDFLY
ENDOTHELIAL CYCLE
SYSTEM
''' '
�lulllpU�11lon by binary Mulllpllcallon by
res,lon blo•ryffnloo
Pro1111ntigote fonns
Proma�1i..:01c
rann
Days 6-9
96
-----
( 3 > Abdomen
multiply within them by binary fission. The macro patient may be emaciated and anemic with
phages filled with the parasites rupture releasing the wasting, edema, hemorrhagic manifestations,
parasites in circulation which are taken by the cells of diarrhea (GI involvement) and cough (due to
reticuloendothelial system. This leads to enlargement lung involvement).
of spleen and liver . Gamma globulins particularly
JgG is increased but the antibodies present are not Complications
protective. 1. Respiratory: Pneumonia, pulmonary tuberculosis
2. Gastrointestinal: Amebic and bacillary dysentery
Immunology
3. Cancrum oris: Ulcerative lesion near the angle
Amastigote excites a cellular reaction of histiocyte
of the mouth
proliferation followed by invasion of lymphocytes
and plasma cells by the parasites. The sensitized lym 4. Septic infection
phocytes destroy Leishmania-filled macrophages. The 5. Pancytopenia
increased IgG are responsible for formal gel reaction.
Similarly specific antibodies (complement fixing, Diagnosis
hemagglutinating and fluorescent) can be used for I. Direct Evidence:
diagnostic purposes. Parasites may be demonstrated by microscopic
Clinical Features examination of stained film or by culture
examination.
Incubation period varies from few days to few years
a. Microscopic examination: Blood, bone
average 3-6 months.
marrow or splenic aspirate can be examined
l. Pyrexia: This may be continuous, remittent or
under the microscope. The amastigotes
later intermittent. The fever may be preceded
within the macrophages are referral to as
by rigor or vomiting, but is not associated with
LD bodies (Leishman-Donovan bodies).
headache, prostration or sweating. In 20% cases
there may be two spikes of temperature within
24 hours (camel hump fever).
2. Splenomegaly: TI1ere is progressive enlargement
of the spleen which may extend upto the right
iliac fossa. Spleen increases in size with each ln1racellular
episode of fever. 1 leishmania
3. Hepatomegaly and Lymphadenopathy: Liver (LO bodies]
enlargement follows splenomegaly. Usually
lymph nodes are not enlarged, but in African
and Chinese form they may be enlarged.
Fig. 3.36: Le1shmania-D0novan (LD) bodies 1n monocytes
4. Skin: The skin is dry, rough, harsh and in Kala-azar
hyperpigmented. Hair is brittle and sparse. Post.
kala azar dermal leishmaniasis (PKDL) occurs b. Culture: About 1-2 ml. of blood, marrow
one year or several years after recovery. They may or splenic aspirate is cultured in NMN
develop in three forms - depigmented macular (Navy, MacNeal and Nicolle) medium
lesion like tinea versicolor, erythematous papules which consists of 2 parts of salt agar and
or erythematous nodules on ear and face (like one part of defibrinated rabbit's blood. The
nodules of leprosy) All the three types may be material for culture is inoculated into the
present in the same patient. water of condensation of the medium and
incubated at 22-24°C for 1-4 weeks. At the
5. Systemic features : Unlike in other fevers there
end of each week, a drop of condensation
is no apathy, malaise or anorexia. However the
fluid is examined for promastigote. This is
97
PRACTICAL MEDICINE
a slow method and may take one month to 2. Pentamidine isethionate: It is given in the dose
make .a diagnosis of 3-4 mg/kg. daily or on alternate days for
II. Indirect Evidence: 15 injections. Hypotension due to histamine
release may occur. This is prevented by giving
A. Blood Count: There is pancytopenia,
antihistaminics 20-30 minutes before each
but leucocytes are reduced more than
injection. It may also cause liver and kidney
erythrocytes. Eosinophils are usually
damage as well as precipitate diabetes mellitus.
absent.
3. Amphotericin B: In resistant cases of Kala azar
B. Serological Tests
it is given in the dose of 0.1-0.25 mg/kg in 5%
l. Napiers aldehyde test: One ml of serum dextrose slowly on alternate days 3-8 weeks.
is taken and to it a drop or two of 40%
formalde-hyde is added. Jellification Prevention
of milk white opacity within 2-20
I. Personal: Using mosquito nets (22 meshes/inch)
minutes occurs ifKala-azar is of over
fumigation of sleeping quarters and avoiding
3 months duration due to increased
sleeping on ground floor would help.
gamma globulins. This test is also
positive in myeloma, cirrhosis of 2. Community: Man is the reservoir of infection
liver, S Japonicum and African and treating all cases of Kala azar would help,
trypanosomiasis. However it is Measures against eradication of sandflies would
negative in cutaneous leishmaniasis. also be useful.
2. Chopra's Antimony test: 4% urea
13 Typhoid
stibamine solution is added to I
in 10 dilution of serum in distilled
water. Flocculationsoccur in positive
Definition
cases.
3. Brahmachari's test: To I ml of serum, Typhoid is an infectious disease caused by salmonella
distilled water is added. In positive typhi which is a gram negative, non-spore forming
cases a precipitate forms. bacilli.
4. Complementfixation test: This is done Epidemiology
with Witebsky. Klingenstein and
Kuhn (WKK) antigen and becomes Typhoid germs are contracted from food or drink con.
positive in 3 weeks. However, it is not taminated with excreta from carriers or patients. The
specific, being positive in tuberculosis, spread is facilitated by poor environmental hygiene.
leprosy and trypanosomiasis. Immunity following the infection is not sufficient to
prevent relapse.
5. Other serological tests: Indirect
immuno-fluorescence and enzyme Predisposing Factors
linked immuno-sorbent assay
1. Organism: A large number of organisms have
(ELISA) have also been found to be
to be ingested by healthy person to suffer from
sensitive.
typhoid. Smaller inocula may produce the
Treatment disease if the organisms are very virulent or if
the resistance of the host is poor.
l. Sodium antimony gluconate: One ml contains I 00
mg ofantimony. Daily 6 ml is given IM or IV for 2. Stomach acidity: The acid in stomach destroys
salmonella that is ingested. Hence, patients
10-15 days. In children 3 ml daily is given and
having achlorhydria (no acid in stomach) or who
in infants 2 ml daily is given. The course could
take large amounts of antacids to neutralize the
be repeated after a gap of 15 days.
acid in stomach suffer more often from typhoid.
98
- .........
_
( 3 Abdomen
3. Intestinal flora: The normal intestinal flora They do not penetrate beyond lamina propria and
produces short chain fatty acids which are multiply in the lymphoid tissues (Peyer's patches) of
lethal to salmonella. When these are reduced by the small intestine. Inflammatory changes occur with
antibiotics, the patient is more prone to typhoid. accumulation ofleucocytes. Enterotoxin liberated by
thebacteria may form abscess, which may burst causing
Pathophysiology ovoid ulcers. This may cause hemorrhage and if the
Salmonella that cause enterocolitis after ingestion, ulcer reaches the serosa, perforation occurs.
invade the mucosal cells and multiply within them.
lnjestion
---------,
Via thoracic duct into
blood stream
I
I
I
I
I Carrier
Proliferation in
small bowel ---------11.E Gall bladder-1-.J...:..-r.:�.. /
·---\
L�.•
In Peyer's Patches
DIAGNOSIS:
1st week: Blood culture
2nd week: Antibody (Widal)
3rd week: Stool culture
I
4th week: Urine cultu
:__J
99
b
PRACTICAL MEDICINE
Clinical Features organism in their feces for at least one year. Usu
ally they are typhoid patients or persons with biliary
I. Enterocolitis: In enteroco\itis, the infection
tract disease. 'Ihe gall bladder serves as a reservoir
is usually localized in the small intestines and
of infection and this carrier state is asymptomatic. It
colon. The incubation period is usually 12 - 72
may persist for lifetime without antibiotics or biliary
hours but may be up to 2 weeks.
tract surgery. Rarely, urinary carriers may be present.
l. Nausea, vomiting and an early chill are
common initially followed by colicky Investigations
abdominal pain and diarrhea of watery,
l. Culture: Salmonella organisms can be
green, offensive stools.
grown from blood culture or dot culture on
2. Blood mixed with stool and high fever may MacConkey's agar in the first week in 90% of
occur if there is involvement of colon. patient. In the second week, stool culture is more
Symptoms may subside within a week or reliable. The organism can also be isolated in
two. some cases from urine.
II. Enteric Fever: This is clinical syndrome 2. Serology: Widal test determines the agglutinins
characterized by fever, headache, prostration, against somatic (O) and flagellar (H) antigens.
cough, splenomegaly and leucopenia, caused 1his test is negative in the first week, becomes
by S. typhi or paratyphi. The incubation period positive by second or third week and may remain
is 7 14 days. The onset is insidious with the positive for a prolonged period. Hence, a single
following features: positive test is of no diagnostic value, but a
l. Fever: Usually, there is a continuous fever, demonstration of a rising titer in a patient of
which typically rises in the stepladder fever is suggestive of typhoid fever.
pattern in the first week, but it may be 3. Leucopenia: is usually present except in presence
remittent type. Rigors and sweats are not of complications or in children.
common. It is usually accompanied by dull
headache. Complications
2. Abdomen: Mild abdominal discomfort and I. Abdominal
distension occurs with nausea, vomiting
and constipation, which are followed by l. Hemorrhage may occur at the end of
diarrhea (pea soup stools). Hepatomegaly the second week and is characterized by
and splenomegaly occurs. black stools, tachycardia, hypotension and
diarrhea. There is no abdominal pain or
3. Rose-spots: These are erythematous,
rigidity or obliteration ofliver dullness like
maculopapular lesions 2 4 mm in diameter
in intestinal perforation. Transfusions may
which blanch on pressure usually seen on
be needed if there is massive blood loss.
the upper abdomen, back and chest. They
occur in the first or second week. 2. Perforation may occur at the end of the
4. Miscellaneous: Cough due to 'typhoid second week or in the third week. It is
bronchitis' and relative bradycardia may characterized by acute pain in the lower
occur. abdomen, vomiting, abdominal distension,
hypotension and tachycardia. 'Ihe liver
Ill. Clinical course: ln the pre-antibiotic era,
dullness may be obliterated and the
the patient gradually recovered or developed
abdomen becomes tender, rigid and silent
complications in the third or fourth week.
(absent peristalsis).
Relapse occurs in 5-10% of untreated patients
and 15-20% of patients on treatment. 3. Tympanitis
4. Cholecystitis
Chronic Carrier State
5. Splenic infarction
Chronic carriers are those who excrete salmonella
100
( 3; Abdomen
101
PRACTICAL MEDICINE
b. Oral Vaccine (Ty2la) : Oral Vaccine - l Clinical Features in AML and ALL
tablet on alternate days for 4 doses.
Contraindicated in pregnancy in children I. Due to bone marrow failure
<6 yrs. of age. Repeated every 5 years. 1. Due to anemia: Fatigue, pallor, dysnoea
2. Bleeding manifestations: Easy bruising,
petechiae, purpura, bleeding from various
14 Leukemia sites and in various tissues.
Leukemia is a disease of unknown etiology, character 3. Infections and/or fever: Infective lesions
ized by an uncontrollable and abnormal proliferation in mouth, throat, respiratory tract, skin.
of leucocytes and their precursors, which infiltrate II. Due to Organ infiltration
the body tissues. 1. Bony tenderness especially of the sternum
Acute Leukemias 2. Hepatosplenomegaly & lymphadenopathy
( mediastinal,axillary, inguinal and cervical)
Acute leukemia is a hematological neoplasm character
ized by proliferation of malignant hemopoietic blast 3. CNS: Hemorrhage, meningeal infiltration
cells. There should be more than 20% blasts cells in and multiple cranial nerve palsies
the bone marrow at clinical presentation. Untreated, 4. Skin or orbit: Chloromas
acute leukemias are rapidly fatal, median survival 5. Kidneys: Renal failure
being two months. Death occurs from infection or
6. Heart: Cardiomyopathy and pericarditis
hemorrhage or both.
7. Fundus: Roth spots, papilledema
Acute leukemias are subdivided into acute myeloid
leukemia (AML) and acute lymphoid leukemia (ALL) 8. Testes: Swelling, particularly in ALL
on the basis of the blasts present, whether myeloblasts 9. Gum hypertrophy in AML M4/M5
or lymphoblasts. The morphology, clinical features,
Peripheral Blood Picture in AML and ALL
cytochemistry, immunophenotypingand molecular
genetics are used to subdivide AML and ALL into l. Anemia: Normochromic, normocytic
their subtyp es (Tables 3.14, 3.15, 12.5, 12.6) 2. Thrombocytopenia; DIC may be present in M3
Total WBC count may be increased, normal or
Acute Myeloid Leukemia (AML) 3.
low. Neutropenia is present.
AML occurs at all ages. AML is subdivided into 8 4. Variable number of blast cells may be present.
subtypes (Table l l.2) based on morphology and cy "Smear" cells may be present in some ALLs.
tochemistry according to FAB classification.
Bone Marrow in AML and ALL
Acute lymphoid leukemia (ALL)
1. Cellularity: Usually hypercellular
ALL occurs primarily in children and sometimes after
2. Leukemic blast cells > 30% should be present.
the age of 40. FAB classification subdivides ALL into
3 subtypes (Table 11.3). 3. Erythroid cells and megakaryocytes reduced.
102
( 3) Abdomen
M3 Bundles ofrod-like structures (Su Itan Bleeding tendency due to DIC Myeloperoxidase+++
Promyelocytic bodies/"Faggots• in promyelocytes. and thrombocytopenia. PAS+ (diffuse)
Auer rods+ Bilobed nuclei. Young patients.
Microgranular variant also present 15; 17Translocation
103
PRACTICAL MEDICINE
Ll Small uniform blast cells with 6-ALL or T-ALL c-ALL antigen + T-ALL type shows
Small, monomorphic. large regular nucleus surrounded (Null-ALLC-ALL TdT + thymic enlargement
More common in by a thin rim of cytoplasm. rare) PAS+ blocks in
children cytoplasm.
L2 Heterogenous size of blasts with Mostly T-ALL Acid phosphatase+ T-cell type shows
Large,heterogenous. prominent nucleoli and relatively C-ALL or Null- TdT+ thymic enlargement.
More common in adults abundant cytoplasm. ALL Anti-T +
104
>
( 3 Abdomen
1hioguanine 100 mg/m2 orally twice a day for D. Allopurinol before starting antileukemic
7 days. Bone-marrow aspiration is done after 3 agents to prevent hyperuricemia.
weeks and if evidence ofleukemia persists, the E. Mainte nance of good oral hygiene,
above cycle is repeated. adequate nutrition, electrolyte and acid
B. Consolidation therapy: This includes 2-6 base disorders.
courses of combination therapy used for
induction. Recently use ofhigher dose ofcytosine Ill. lmmunotherapy:
arabinoside with daunorubicin or combination This is used because a patient in complete
of non-cross resistant drugs has been found to remission reacts to his blast cells as though they
be ofsome benefit. were foreign tissue. It may be attempted with
C. Maintenance therapy: BCG or allogenic irradiated leukemic cells.
Cytosine arabinoside 60 mg/m2 once a week and Chronic Leukemia
6- 'Ihioguanine 40 mg/m2 twice a day orally for 4
days/week is given for 1-3 years. This increases Chronic leukemias have a more indolent behavior
the duration ofdisease-free survival. and better prognosis than acute leukemias. Chronic
lymphoid leukemia ( CLL) tends to occur in the elderly.
D. Bone-marrow transplant: This has a high cura
Chronic myeloid leukemia (CML) is more common
tive potential. It is done following complete
remission. However, its limitations are high cost in middle age. Juvenile CML occurs in children below
and non-availability of matched donors. 3 years of age.
Results of treatment: Sixty percent achieve Clinical features in CML and CLL
complete remission but only 20% get cured.
I. Due to anemia: Pallor, fatigue, dysnea, etc.
E. All-trans retinoic acid (ATRA) is used for the
IL Due to Organ infiltration:
treatment of acute promyelocytic leukemia
(APML) 1. Hepatosplenomegaly
2. Lymphadenopathy: Usually cervical,
H. Supportive Treatment mediastinal and axillary. Lymphadeno
A. Blood/Platelet/ Granulocyte transfusions pathy is more common with CLL.
B. Combination of higher antibiotics like 3. Cardiorespiratory: Pulmonary congestion,
aminoglycoside (gentamicin, amikacin, infiltration or collapse. Pleural effusion.
etc.) with cephalosporins (cefotaxime, 4. CNS: Meningeal infiltration, cranial nerve
cefazolin, ceftazidime, etc. palsies and paraplegia
C. Treatment of oral, gastrointestinal and 5. Skin: Pruritus and nodules, gout
systemic fungal infections. III. Duetothrombocytopenia: Bleeding tendencies
AML (epistaxis, hematemesis, etc.) in CLL. Platelets
are normal or increased in CML.
IV. Due to increased metabolism: Fever, weight
Consolidation Mainlenance loss, malaise, perspiration and gout.
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PRACTICAL MEDICINE
myelo-cyte, promyelocyte, band forms). Only 3. Hydroxyurea 1-2 gm orally till WBC
occasional blast cells is seen (<10%). Neutrophil count falls to 10,000/cm. It is used
alkaline phosphatase is markedly reduced. in patients with chronic myeloid
Blast crisis in CML is indicated by an increasing leukemia not responding to busulfan.
basophil count. It may be myeloid or lymphoid B. Radiotherapy: This may be useful as a
in origin. Myeloid blast crisis resembles AML, symptomatic measure to reduce the size of
but Auer rods are not seen. Lymphoid blast massively enlarged spleen, when cytotoxic
crisis is rarer and shows lymphoblasts with drugs have failed.
characteristics such as TdT positivity. C. Splenectomy: This may be required when
InCLL: enlarged spleen is causing symptoms.
50,000-2,00,000/cc. Majority(>90%) are mature D. Bone Marrow Transplantation is the only
small lymphocytes. "Smudge" or "smear" cells curative treatment.
(degenerative forms) may be present. Absolute II. Chronic Lymphatic Leukemia
neutrophil count is normal. Neutropenia occurs
A. Chemotherapy:
in advanced CLL.
1. Chlorambucil 6-10 mg/day for 14
3. Platelets are normal or low.
days with a break of 14 days. When
Bone Marrow in CML and CLL WBC count falls below 25,000/c.c.
the dose is reduced to 2-4 mg/day. It
1. Cellularity: Hypercellular is discontinued when the WBC count
2. Erythropoiesis is normoblastic, sometimes falls below 1,000-10,000/c.c.
megaloblastic. Reduced erythroid precursors.
2. Cyclophosphamide: 2-3 mg/kg. I.V. for
3. Leucopoiesis: 6 days.
In CML bone-marrow is hypercellular with B. Radiotherapy: T his is useful for large
myeloid: erythroid ratio increased. There may granular masses if they cause symptoms.
be myelocytes, promyelocytes, eosinophils and
C. Steroids: Prednisolone 40 mg/day may
basophils. Blast cells or promyelocyte more than
improve hemoglobin or platelet count.
30% suggests blast crisis in CML.
In CLL both small and large lymphocytes D. General supportive measures:
are diffusely infiltrated (25-95%). Myeloid 1. Blood transfusion
precursors are reduced. 2. Antibiotics
4. Megakaryocytes are prominent in CML and 3. Gamma globulins
reduced in CLL.
5. Cytogenetics: Philadelphia chromosome may Hairy Cell Leukemia (HCL)
be present in myeloid and erythroid precursor Hairy cell leukemia is a rare type of chronic leukemia
cells in 70-90% of CML cases. with pancytopenia and marked splenomegalywithout
lymphadenopathy. The typical "hairy" lymphoid cells of
Treatment
B-cell origin are seen in the peripheral blood and in
I. Chronic Myeloid Leukemia bone marrow aspirates and splenic imprints. These
A. Chemotherapy:· cells also show a characteristic strong postive tartaric
1. Imatinib Mesylate 400 - 800 mg daily acid resistant acid phosphatase (TRAP) reaction.
is the drug of choice. Newer drugs if
there is imatinib failure.
2. Busulfan 4 mg/day orally, reduced to 15 Malignant Lymphoma
2 mg/day when WBC count falls to Definition : Malignant Lymphoma refers to a large
30,000/c.c.
106
3 Abdomen
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,. ,.
Grade and lymphoid tissues of cervical and ileocecal
1. Small Follicular Large Cell region.
lymphocytic Large Cell tmmunoblastic
4. Histologically there is characteristic "starry sky"
2. FollicularSmall 2. Diffuse Sma It 2. Lymphoblastic appearance ofB lymphoblastic lymphomas with
Cleaved Cell Cleaved Cell
scattered histiocytic reticular cells.
3. Follicular 3. Diffuse Mixed 3. Small Non-
Mixed Small Small and cleaved Cell Mycosis Fungoides
Cleaved and Large Cell (Burkitt's and
Large Cell Non-Burkitt's) Mycosis fungoides, a chronic lymphoma of the skin,
4. Diffuse Large 4. Miscellaneous has three stages:
Cell (Mycosis fungoides, I. Premycotic stage: Lesions similar to eczema or
Histiocytic)
psoriasis
108
( 3 > Abdomen
2. Infiltrative or Plaque stage: This is with (Family Retroviridae, Subfamily Lentivirus). HIV-1
generalized exfoliative erythroderma and is the most common cause worldwide. HIV-1 has
invasion of the blood by typical convoluted many different strains due to mutations. There are
lymphoid cells {Sezary syndrome) three groups M (major, subtypes A-J), 0 {outlier,
3. Nodular or tumour stage: Deeper invasion by rare) and N (very rare). In India, Group M subtype
the tumour and infiltration of lymph nodes and C predominates.
other organs.
Transmission of HIV
AIDS is caused by an infection with HIV-1 or HIV-2 Fig 3.38 · Schematic illustration of HIV components
109
PRACTICAL MEDICINE
Table 3.19: AIDS Defining Conditions for Table 3.20 : Definition of AIDS in adults
Adults and Adolescents <13 yrs (as per CONFIRMED HIV INFECTION WITH:
CDC) Clinical diagnosis (presumptive or definitive) of any AIDS
1. Candidiasis: esophagus, trachea, bronchi or lungs Defining condition (Table 3.19)
OR
2. Cervical cancer: invasive
CD4 count< 200/ µL or %CD4 <14 in asymptomatic adults
3. Coccidioidomycosis, disseminated or extra or children aged>5 years
pulmonary
4. Cryptococcosis - extra pulmonary following skin puncture from a sharp object that
5. Cryptosporidiosis with diarrhea persisting for> 1 is contaminated with blood from an HIV positive
month patient is 0.3% and after mucous membrane
6. Cytomegalovirus disease (other than liver, spleen, exposure 0.09%. (Similar risk for HBV
lymph nodes) transmission is 6-30% and HCV transmission
7. Cytomegalovirus retinitis (with loss of vision) is 1.8%).
8. Encephalopathy:HIV-related Very low risk:Transmission of HIV from an
9. Herpes simplex: Chronic ulcers lasting> 1 month or infected health care worker to patients through
bronchitis, pneumonitis, or esophagitis invasive procedures.
10. Histoplasmosis: Extra pulmonary or disseminated
No risk: Saliva, tears, sweat, urine cannot cause
11. lsosporiasis with diarrhea persisting > 1 month transmission ofHIV. The virus cannot be passed
12. Kaposi's sarcoma through casual or family contact or by insects
13. Lymphoma: Burkitt's such as mosquitoes.
14. Lymphoma: Lymphoblastic 3. Maternal-fetal/infant transmission
15. Lymphoma: Primary, of brain Mother to child risk of transmission is 20-30%
16. Mycobacterium avium complex or M. kansasii before birth. The risk increases to 50-65% during
17. Mycobacterium tuberculosis, any site (pulmonary, birth and 10-20% via breast milk. A single dose of
disseminated or extrapulmonary) Nevirapine given to the mother at onset of labor
18. Mycobacterial infection: other species or unidentified and a single dose to the infant after birth reduces
species, extrapulmonary or disseminated
the risk of HIV transmission. Breast-feeding
19. Pneumocystisjirovecci (carinii)pneumonia should be avoided. However, in developing
20. Pneumonia: recurrent countries like India, breast-feeding prevents
21. Progressive multifocal leucoencephalopathy infectious diseases and provides immunity to the
22. Salmonella septicemia: Recurrent child, and is therefore advocated after counseling
23. Toxoplasmosis: brain the mother.
24. Wasting syndrome due to HIV
Pathophysiology and
intercourse, vaginal intercourse (male to female lmmunopathogenesis
higher than female to male), associated STDs or The main action of HIV is to cause the quantitative
genital ulceration. Lower risk of transmission is and qualitative deficiency of a subset of lymphocytes
with oral sex and circumcised males. referred to as T4 (CD4+) helper/inducer lymphocytes.
2. Transmission by blood, blood products or other These lymphocytes express the CD4 cellular receptor
body fluids for HIV on their cell surfacealong with the coreceptors
High-risk: IV drug users who share contaminated (e.g. CCR5, CXCR4). The destruction of these lympho
needles, hemophiliacs, thalassemics and other cytes leads in turn to suppression or compromise in
transfusion recipients, organ transplant patients. the function of host cellular defense mechanisms, not
only to HIV but also to opportunistic infectious agents.
Low-risk: Health care workers and laboratory
personnel who work with HIV-infected Although the CD4+ T lymphocyte and CD4+ mono
specimens. The risk of transmission of HIV cyte lineage are the principal cellular targets, HIV can
110
( 3 > Abdomen
6. Integration 1
1· 2 & 3 4. Reverse 1 7 & 8. Vir al
into host I transcription &
Binding.
entry & ;
fusion
,.-::::===:t:=====::::JC::::::::::====!:====:::-
transcription
Viral 5. Tra)tsportation
genome I translation
:
Coreceptors I RNA 1
CCR5, CXCR4 � :
:
f2y �
i = -4
!
Genomic DNA
9 & 10.
Budding &
cleavage
Antigen
(Receptor) 1-------'------- --I-------.J....-----.:: ••
I I
Drugs& Fusion I CCRS 1NRTI and NNRTI I
lntegrase Protease
Inhibitors I Antagonist IZidovudine Nevirapine I Inhibitors
Mechanism I Didanosine De laviridinel Raltegravir
Inhibitors
Enfuviritde l Maraviroc Saquinavir
ofAction I
I
: Zakitabine Efavirenz I Retonavir
I 1 Stavudine : tndinavir
1 Lamivudine I Nelfinavir
.
IAbacavir .I
F,g.3 39· Repl1cat1on Cycle ofHIVand Drugs targeting different stage of the cycle (Also Refer Ch 15)
1. BIN DI NG: HIV binds via the viral envelope protein gp 120 to the CD4 receptor on the target host eel I.
2. CORECEPTORS (CCR5 and CXCR4) facilitate entry of virus into the host cell.
3. FUSION of the virus with the host cell membrane and internalization of pre-integration complex (viral RNA and enzymes
surrounded by capsid protein)
4. REVERSETRANSCRIPTASE ENZYME converts the viral RNA genome to double stranded DNA.
5. TRANSPORTATION of the DNA to the host nucleus.
6. IN TEGRATION into the host genome by viral enzyme integrase. The HIV provirus remains latent at this stage until the
infected cell is activated by a number of cellular and viral factors. This is the reason for the interval between the time of
infection and disease expression.
7. TRANSCRIPTION ofprovirus DNA into viral rnessenger(mRNA) and genomic RNA.
8. TRANSLATION of m RNA into proteins.
9. BUDDING: The viral proteins, enzymes and genomic RNA are assembled at the cell membrane and budding of the progeny
virus occurs at special regions of the host cell membrane.
10. RELEASE: The viral enzyme protease catalyses the release of mature virions from the host cell. The vi rions infect other host
cells that express CD4 receptors.
potentially infect virtually any cell that expresses CD4 Immune Abnormalities in HIV Disease
(e.g. T and B lymphocytes, macrophages, astrocytes,
A broad range of immune abnormalities has been
microglial cells, Langerhans' cells, fibroblasts, Chro
documented in HIV-infected patients. These include
maffin cells, dendritic cells, alveolar macrophages,
both quantitative and qualitative defects in lymphocyte,
thymus cells).
monocyte/macrophage, and natural killer (NK) cell
Immune Response to HIV Infection function, as well as the development of autoimmune
phenomena.
Both humoral and cellular immune responses to HIV
develop soon after primary infection.
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PRACTICAL MEDICINE
Laboratory Tests for Diagnosis of HIV to appear within 2 weeks of infection, and the
Infection period of time between initial infection and the
development of detectable antibodies is rarely
Table 3.21; Laboratory Criteria for HIV longer than 3 months (window period).
Infection for Adults
The CDC criteria for a positive interpretation of
Positive result from an HIV antibody screening test
Western Blot test is the presence of antibodies to
confirmed by a positive result from a supplemental HIV
antibody test any two of three proteins p24, gp41 and gp 160/
gp 120.
And/Or
"Indeterminate" results are repeated after 4-6
Positive result from any of the following HIV virologic
(i.e,, non•antibody)tests: HIV nucleic acid (DNA or RNA)
weeks.
detection test, HIV p24 antigen test or HIV isolation. 3. Antigen Detection: The detection of HIV
1. Antibody Screening Tests: The standard by the p24 antigen capture assay, an ELISA
screening test for HIV infection is the detection type assay, in serum or CSF is the key to early
of anti-HIV antibodies in the patient's serum diagnosis. The p24 antigen is a soluble protein
using enzyme·linked immunosorbent assay from the core of the virus. Plasma p24 antigen
(ELISA or EIA). HIV-1/HIV-2 combined EIA levels rise during the first few weeks following
assays are now being used worldwide. This test infection, prior to the appearance of anti-p24
is highly sensitive (>99.5%) but not optimally antibodies. The antigen may be detected for upto
specific. False positive results can occur in cases six weeks and then disappears with antibody
of: antibodies to class 11 antigens, autoantibodies, sero-conversion. The antigen is not detectable
hepatic disease, recent influenza vaccination, during the asymptomatic clinically silent phase
acute viral infectionsand children < 18 months for a variable period of upto 10 years or more.
whose mothers are HIV-infected The reappearance of p24 antigen precedes onset
of the symptomatic phase of AIDS.
2. HIV Antibody Test for confirmation of
positive ELISA tests is done by Western Blot 4. HIV DNA:Polymerase chain reaction (PCR)
(immunoblotting) assay or immunofluorescence techniquesare used to detect very low levels of
assay. It tests the presence of antibodies in the viral DNA integrated into the host genome.
patients' serum against HIV antigens of specific 5. HIV RNA levelsin plasma or serum (plasma
molecular weights. Antibodies to HIV begin viral load or PVL) are determined by RT-PCR
Level
or
Ag/Ab
Infection lweoks)
Clinical TIME
I ················-····............. -.........Attyfnplomafo:::: phasu (ClinkiLl LJ.lu,nc)·)--------1
PrimDry Acu1e HtV· Symplom.illt:
Stage Cunsl:ilnHorml
Jnfcclicm Syndrome All)S
Symp1nms
I F•g 3. ll) · D1,1grJ111m,,t1c R,c>p1e,ent,1t1011 of Ant,9011 ,rnd Antibody Response and CD� counts and PVL 111 HIV1nfect1on and AIDS
112
( 3 > Abdomen
Table 3.22 : Initial Evaluation
History Symptoms, past and present history (personal, high risk behavior, family history,
gynecological, treatment etc.)
Physical Examination Routine complete examination including dermatological, oral, genital, pelvic,
systemic, fundus, etc.
Hematology& Urinalysis Routine
Blood Chemistries Routine including LFT, BUN, creatinine, etc.
Lipid profile and glucose (fasting) To rule out existing CAD, diabetes prior to ART
HIV Antibody Confirm HIV·1 infection & rule out HIV-2 infection
CD4+ T lymphocyte count Baseline level by flow cytometry
HIV RNA levels (viral load) Baseline plasma vira 1 load (PVL)
HIV Resistance Testing For patients with HIV RNA > 1 ooo copies/mL
Chest X-ray To rule out TB & other infections
VDRL/TPHA To rule out syphilis
Pap Smear& pregnancy test To rule out cervical intraepithetial neoplasia & pregnancy prior to ART
Serology for hepatitis A, 8, C To rule out co-existing viral hepatitis
Mini-mental status examination Baseline study
(reverse transcriptase PCR), bDNA (branched gitis. It lasts 1-2 weeks and resolves spontaneously as
DNA) or nucleic acid sequence-based assays. the immune response to HIV develops. Most patients
These tests are useful for patients with a positive will then enter a phase of clinical latency, although
or indeterminate ELISA and an indeterminate occasional patients will experience progressive immu•
Western blot or in patients in whom serologic nologic and clinical deterioration. It can be identified
testing may be unreliable (such as those with by recent appearance of HIV antibody or by presence
hyp ogammaglobulinemia). of viral products with negative or weekly reactive HIV
6. Viral Isolation: HIV can be cultured from tissue, antibody.
peripheral blood cells or plasma.
Asymptomatic Infection
Monitoring of HIV Infection The length of time between infection and development
Measurement ofthe CD4+ Tlymphocytecount (flow ofdisease varies greatly, but the median is estimated to
cytometry) and level of plasma HIV RNA (plasma be 10 years. HIV disease with active viral replication
viral load or PVL) are important in the routine evalu usually progresses during this asymptomatic period
ation and monitoring of HIV-infected individuals. and CD4+ T-cell counts fall. The rate of disease pro
They are measured at diagnosis and usually every 3-6 gression is directly correlated with plasma HIV RNA
months thereafter. levels. Patients with high levels of HIV RNA progress
to symptomatic disease faster than do those with low
Clinical Manifestationsof HIV Infection levels of HIV RNA.
113
PRACTICAL MEDICINE
114
< 3) Abdomen
Table 3.27 : Primary and Secondary Prophylaxis for prevention of Ols
Opportunistic Agent Indications for starting Drug & Dosage (First choice)
Mycobacteriumtuberculosis (TB) Tuberculin test >Smrn or high risk INH sensitive: INH 5 mg/kg/dayPO qds +
Or prior positive test without treatment pyridoxine 50 mg PO qdsx9 months
Pneumocystis cariniipneumonia CD4 < 200/mm3 or rapid clinical TMP/SMX 1 OS tablet PO qds
{PCP) deterioration or prior PCP Pentamidine aerosol 300 mg/month
Mycobacterium CD4 < 50/mm 3 Azithromycin 1200 mg PO weekly
avium-intracellulare (MAC) Or prior documented disease Or Clarithromycin
Toxop/asmagondii Positive lgG antibody and TMP/SMX 1 OS tablet PO qds
CD4<100/mm3
Herpes simplex Frequent/severe recurrences Acyclovir 200 mg PO tds or Famciclovir
250 mgPObds
Candida albicans, Crytococcosis CD4 < 200/mm3 Fluconazole 1 00-200 mg
Frequent/severe recurrences PO once/week
115
PRACTICAL MEDICINE
116
( 3 > Abdomen
opportunistic infections and neoplasms, or side remain the cornerstone of HIV prevention efforts.
effects of ART(Refer to Table 3.30). While abstinence is an absolute way to prevent sexual
transmission, other strategies include 'safe sex practices
Post Exposure Prophylaxis (PEP) such as use of condoms together with the spermatocide
Antiretroviral drugsfor PEP should be started within nonoxynol-9. Avoidance of shared needle use by ID Us
the first few hours and no later than 72 hours after is critical. If possible, HIV-positive women should
occupational and non-occupational exposureand avoid breast-feeding (in India breast-feeding is benefi
continued for 28 days (See Table). HIV testing should cial and mixed feeding is absolutely contraindicated)
be done initially and following 3 and 6 months. as the virus can be transmitted to infants via this route.
Prevention of exposure is the best strategy and stresses
Prevention the use of universal precautions and proper handling
Education, counseling, and behavior modification of needles and other potentially contaminated objects.
Table 3.30: Complications in HIV infection and AIDS - Features, Diagnosis and
Treatment
System Fear urns Diagnosis Treatment
RESPIRATORY SYSTEM
Upper Respiratory Tract Acute bronchitis, sinusitis, CT/MRI Antimicrobial agents
Infection (URTIJ fever, nasal congestion,
S.pneumoniae, H.influenzae headache
Pneumonia Pneumonia, sinusitis, X-ray Antimicrobial agents
S.pneumoniae, H.influenzae bacteremia
Pneumocystis pneumonia Fever, cough,dyspnea, night X-ray; Demonstration of Trimethoprim/
(PCP) P.jiroveci (carinii) sweats, thrush, unexplained organism in sputum, BAL, sulphamehtoxazole DS 2
weight loss transbronchial or open lung tablets PO for 21 days followed
biopsy by secondary prophylaxis
Tuberculosis: M. tuberculosis Cough, hemoptysis, shortness Positive sputum smear or Anti-tuberculosis treatment:
of breath, chest pain, weight X-ray showing TB Standard 4-drug regimen for
loss, fever, night sweats 6-9 months. For TB involving
CNS: 12 months.
Atypical Mycobacterlal Weight loss, fever, night Organisms in blood,sputum or Clarithromycin 500 mg PO
infections M.avium, sweats; Dissemination to bone involved tissue; X-ray ql 2h + Ethambutol 15 mg/kg
M.intracel/ulare (MAC) marrow, lung, liver, lymph PO q24h;
nodes Can add rifabutin,
ciprofloxacin or amikacin
Fungal infections of the lung Fever, cough, dyspnea, Chest X-ray, sputum Anti-fungal agents
Cryptococcus, Coccidioides hemoptysis examination
immitis, Aspergillus,
Histoplasmosis
Kaposi's Sarcoma (KS) Purplish vascular nodules on Biopsy of suspected lesion; Optimal ART & observation;
skin, mucous membranes, Chest X-ray
viscera
Single or Iimited lesions Radiotherapy, 1ntra1esional
vinblastine. cryotherapy
Extensive disease Interferon- a, liposomal
daunorubicin
Lymphomas: lmmunoblastic, Fever, seizures, mass lesions in MRI, CT scan Combination
Burkitt's, Primary CNS oral mucosa chemotherapy,steroid s.
lymphomas radiotherapy
117
PRACTICAL MEDICINE
CARDIOVASCULAR SYSTEM
HIV-associated Edema, dyspnea, dilated Chest X-ray, ECG. Echo ART, treatment for heart
cardiomyopathy cardiomyopathy with failure, IV lmmunoglobulin
congestive heart failure
Pericardia! Effusion Asymptomatic or chest pain, Echo, pericardia! fluid culture Treat underlying condition,
dyspnea, cardiac tamponade, and cytology start ART if idiopathic, NSAIDS,
pericardia! friction rub steroids.
Pericardiocentesis if
tamponade is present
Non-bacterial thrombotic Fever, weight loss, Heart murmur, Chest X-ray, Antimicrobial therapy
endocardltis unexplained embolic Echo, blood culture according to isolated organism
phenomena
GASTROINTESTINAL SYSTEM
Oropharynx: Dysphagia/odynophagia Pseudomembrane, Candida: Fluconazole 100 mg
Thrush (Candida) examination of scraping POq24h
Hairy leukoplakia (EBV) EBV: Topical podophyllin or
Aphthous ulcers anti-herpes virus agents.
Aphthous ulcers: Topical
anesthetic, thalidomide
Esophagus: Esophagitis Odynophagia, retrosterna I Upper endoscopy Systemic therapy as indicated
(CMV, HSV, Candida); pain
Neoplasm (KS, lymphoma)
Stomach: Ach lorhydria, Ach lorhydria: Gastric Gastric pH at endoscopy Stop ART drug, if cause.
Kaposi's sarcoma, Lymphoma discomfort Treat underlying condition.
Obstructive jaundice
Intestine: Infections due to: Fever, anorexia, fatigue, Stool and blood examination Treat underlying infection as
Bacteria (S.typhimurium, malaise, diarrhea & culture, Endoscopy with per diagnosis
Shigella, Campylobacter. biopsy
S.typhi, S.flexneri)
Fungi (Histoplasmosis,
Coccidioidomycosis,
Penicilliosis)
Parasites (Cryptosporidia,
Microsporidia, lsospora be/11)
Viruses (CMV colitis)
Rectal: Infections (HSV), Peri rectal ulcers. erosions Examination Treat underlying condition as
neoplams (KS) per diagnosis
AIDS Enteropathy Chronic diarrhea, weight loss Histology of small bowel Treat underlying condition as
per diagnosis
HEPATOBILIARY SYSTEM
HepatitisB Asymptomatic or symptoms HBAAb, HBSAg, HBCAb&in Enticavir + pegylated
of hepatitis, elevated I iver chronic cases HBEAg, HBEAb interferon.
enzymes & HBV DNA levels, imaging ART Combination Therapy
Hepatitis A vaccine if non-
immune.
Hepatltis C Asymptomatic, elevated liver HCV Antibody or HCV RNA Pegylated interferon +
enzymes positivem, imaging Ribavirin (C/1 in pregnancy).
Hepatitis A & B vaccine if non·
immune.
us
< 3) Abdomen
system Features Diagnosis Treatment
Granulomatous hepatitis, Asymptomatic or symptoms Liver enzymes elevated, liver If ART-induced, stop offending
hepatic masses, biliary tract of hepatitis,elevated liver biopsy, imaging drug.
disease, Hepatitis G virus enzymes
ENDOCRINE SYSTEM
Avascular necrosis Hip or shoulder pain Osteonecrosis on MRI Stop offending drug, if any
Hyponatremia {SIADH), Symptoms of condition Serum sodium,thyroid Stop offending drug,if any.
hypothyroidism, function tests Treat underlying condition as
hyperthyroidism per diagnosis
HIV-associated nephropathy Asymptomatic to symptoms Proteinuria, ultrasound, ART; ACE inhibitors and/or
{HIVAN) of renal failure biopsy prednisone60 mg/d for 1
month, then taper
Genitourinary tract Skin lesions,dysuria, Clinical and Urine Examination Treat underlying condition as
infections (e.g. HSV, syphilis, hematuria and/or pyuria, per diagnosis
candidiasis) vaginal discharge, etc.
RHEUMATOLOGICAL DISEASES
Arthritis - reactive Pain in joints. Arthrocentesis with culture, NSAIDs, pain relievers
{Psoriatic, septic) Urethritis, skin lesions & gram stain, urethral swab for Methotrexate causes
Conjunctivitis {gastroenteritis) Chlamydia and gonorrhea, increased 01, used only in
HLAB27 severe cases
Polymyositis Musculoskeletal pain for >3 Clinical examination & biopsy Low dose naltrexone
months at multiple sites of muscle, EMG
HEMATOPOIETIC SYSTEM
Anemia, neutropenia, Signs of Mild or severe anemia CBC, red cell indices,retie Anemia: Blood transfusions;
thrombocytopenia (ITP, TTP) or neutropenia, bleeding in count, serum iron, Bl 2, folate iron if IDA, erythropoietin;
severe ITP studies avoid drug, if drug-induced;
Neutropenia: G-CSF if ANC
<750/mm'
/TP:ART
Persistent Generalized Enlarged lymph nodes > 1 cm; Clinica I examination No treatment
lymphadenopathy (PGL) In 2 or more extra-inguinal
sites for>3 months with no
obvious cause
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PRACTICAL MEDICINE
Seborrheic dermatitis Waxy erythematosus plaques Clinical appearance ART, ketoconazole cream,
usually on face and scalp topical steroid
Eosinoph i lie pustular Multiple erythematous, Skin biopsy ART, corticosteroids,
folliculitis papular, severely pruritic isotretinoin, phototherapy
eruptions on upper trunk, face
Psoriasis& lchthyosls May be preexisting condition Clinical examination ART, standard therapy
Reactivation herpes :z:oster Shingles- may be multi· Clinical examination, Acyclovir, Famciclovir
dermatomal immunofluorescence to
distinguish from HSV
Herpessimplexvirus (HSVJ Skin & recurrent oral/ Viral culture ofHSV Acyclovir, Famciclovir
anogenital lesions
Molluscum contagiosum White, u mbilicated, Clinical appearance ART
diffuseskin eruptions in groin
Condyloma acuminatum Extensive vegetating lesions Clinical appearance; ART; Surgery, cryotherapy
in perianal or oral area due to Histopathology
human papilloma virus
NEUROLOGICAL DISEASES
Opportunistic infections Toxoplasma: Fever, Cryptococcus: CSF India ink Toxop/asma: Sulfadiazine
(Toxoplasmosis, headachace, focal examination. & pyrimethamine with
Cryptococcosis, neurological deficits, ocular Detection of antigen in serum, leucovorin for 4-6 wks. And
cytomegalovlrus, TB) disease CSF, tissues; prophylaxis.
Crytococcus: Meningitis. MRI/CT; T. gondilgG antibodies Crytpococcus: IV amphotericin
May also have pulmonary in serum B 0.7 mg/kg daily with
disease. flucytosine 25 mg/kg qid for 2
CMV: Encephalitis, wksfollowed byfluconazole
polyradicu litis, 400 mg/day PO for 1 O wks
and 200 mg/day PO till CD4
+ count > 200 cells/µl for 6
months CMV: Gancydovir
5 mg/kg IV BDS + lifelong
Valganciclovir 900 mg PO OD
Neoplasms {primary CNS Focal neurological deficit or MRI/CT, SPECT, PET scan, EBV ART
lymphoma) seizures, fever, DNA Steroids and radiotherapy
Definitive diagnosis-
stereotactic brain biopsy
Aseptic meningitis Headache, photophobia, CSF examination Usually resolves
meningismus spontaneously
HIV Encephalopathy {AIDS StageO to 4: mild to severe CSF examination; MRI/CT; HIV ART with drugs which
dementia complex) neurological symptoms (HIV- RNA inCSF; penetrate the CSF Ii ke AZT,
associated neurocognitive MMSE (mini-mental status ABC,d4T. NVP. IDV
impairment (HCNI)) examination)
Myelopathy or spinal cord Vacuolar myelopathy or pure CSF examination
disease sensory ataxia; dementia
Peripheral neuropathy (HIV/ Pain, aching, burning, or Clinical, EMG Withdraw offending drug.
Drug-induced) tingling at distal extremities Continue ART. Symptomatic
treatment
120
� 3, Abdomen
Progressive multifocal Multifocal neurologic deficits JC virus DNA levels in CSF; ART
leukoencephalopathy with or without changes in MRI
(PML), mental status
OPHTHALMOLOGIC DISEASES
CMV retinitis Painless, progressive loss of Ophthalmological exam; Ganciclovi r intraocular implant
vision Differentiate from benign + valgancilovir for 21 days
"cotton-wool spots" fol lowed by maintenance dose
GENERALISED WASTl NG Involuntary weight loss> 10% Clinical examination Steroids, given with caution
SYNDROME with fever, chronic diarrhea or due toOI
fatigue lasting > 30 days. Androgenic hormones, growth
hormones, total parenteral
nutrition
NEOPLASTIC DISEASES
Kaposi's sarcoma, Non-Hodgkin's lymphoma, Primary CNSlymphoma, Cervical/anal cancer (see above)
121
1 > Proforma VIII. Mediastinal compression:
A. Dysphagia
History B. Hoarse voice
I. Cardinal symptoms: C. Dyspnea and dry cough
A. Cough D. Swelling over face
B. Expectoration General Examination
C. Hemoptysis
I. Built and nutrition
D. Breathlessness
IL Nails and conjunctiva: Pallor, dubbing, cyanosis,
E. Wheeze icterus
F. Chest pain Ill. lymphadenopathy (especially scalene node
IL History of tuberculosis: and cervical nodes), edema of feet, JVP
A. Evening rise of temperature, night sweats IV. TPR, BP
B. Anorexia and weight loss V. Spine
C. Hemoptysis VI. Stigma of tuberculosis:
D. Pleurisy, meningitis, lymphadenitis in past A. Phlyctenular conjunctivitis
or in family, TB contact B. Scars and sinuses in neck or bones
Ill. Habits: Alcohol, smoking, tobacco or gutka C. Thickened spermatic cord
chewing D. Erythema nodosum
IV. Aspiration: Foreign bodies, vomitus.
E. Skin: Cutis vulgaris, scrofuloderma etc.
V. For Industrial diseases: Occupation, residence
VII. Neck: Thyroid swelling. Tracheal tug
near factories or mills
VIII. Homer's syndrome: Ptosis, miosis, anhydrosis,
VI. Allergy:
enophthalmos and absent ciliospinal reflex
A. Family history of asthma, hay fever, eczema
IX. Upper respiratory tract:
B. Rhinitis and Sinusitis: Nasal discharge, pain
A. Sinus tenderness
and tenderness over sinuses, headache,
recurrent cold B. Throat and tonsils
VII. Past history: C. Posterior pharyngeal wall for posterior
nasal drip
A. Measles, influenza or whooping cough in
childhood (If bronchiectasis) D. Alae nasi
B. Diabetes X. Gums and teeth
C. Exposure to TB, STD, HIV
( 4 ) Respiratory System
123
PRACTICAL MEDICINE
,---- - --
The subcostal angle is acute, about 70° and
the interspaces are broader anteriorly than
posteriorly.
!
. Fig.4.4. Funnel chest (Sternal depression]
124
{ 4 ) Respiratory System
unduly concave forwards and the ribs are A. Increased respiratory rate (tachypnea)
less oblique. This is seen in emphysema, old I. Exertion and excitement.
age and infancy. The Ratio of AP diameter
2. Fevers e.g. pneumonias
to transverse diameter is normally 5:7. In
the barrel-shaped chest it is l: l or more. 3. Anoxemia and acidosis
4. Spinal deformities: Kyphosis or scoliosis 4. Anemia and poisoning
(Ch. I) due to any cause may lead to 5. Pain whilst breathing e.g. pleurisy
asymmetry and may decrease the size of the B. Decreased respiratory rate (bradypnea)
thoracic cage and restrict lung movements
I
1. Narcotic poisoning e.g. opium
and volume.
2. Brain tumour
C. Dyspnea: Breathlessness
Table 4.1 : Dyspnea: American Thoracic
Society (ATS) Scale
Grade Degree Description
5. Bulging: One side may bulge in pleural 2 Moderate Walks slower than persons of same
effusion,pneumothorax, tumors,aneurysm, age
empyema necessitans, cardiomegaly or 3 Severe Stops after walking 100 yds or after
scoliosis. Localized bulging is seen in few minutes on level ground
aortic aneurysm, pericardia! effusion, liver 4 Very Severe Too breathless to leave the house or
abscess, chest wall tumors etc. breathless on dressing or undressing
6. Depression or flattening: One side of the Table 4.2 : Dyspnea: Modified Medical
chest or a part of it may be depressed Research Council (MMRC) Scale
or flattened in fibrosis, collapse, pleural
Grade Description
adhesions, unilateral muscle wasting due
to poliomyelitis or congenital absence of Breathlessness only with strenuous exercise
pectoralis muscles. 2 Breathless when hurrying on level or walking
7. Flat chest (phthinoid chest): The uphill
II. Respiratory Rate The normal respiration has regular rhythm with
inspiration longer than expiration. Irregular
The normal rate in adults is 16 20 respirations respiration may be of the following types:
per minute {in children about 40 per min.) It
A. Cheyne-Stokes Respiration: This consists
bears a definite ratio with the pulse rate of about
of rhythmical alteration of apnea and
1:4.
hyperpnea due to anoxemia. Anoxemia
125
PRACTICAL MEDICINE
126
( 4 Respiratory System
127
PRACTICAL MEDICINE
Significance
I. TVF is increased in
1. Consolidation which may be due to
pyogenic or tuberculous infections
The position of mediastinum in various
respiratory diseases is given in the table. 2. Following pulmonary infarction
The apex beat alone may be shifted in scoliosis, 3. Surrounding a malignant lesion
funnel shaped depression of the sternum and superficial cavity.
with cardiac disease. II. TVF is decreased in
Table 4.4 : Position of Mediastinum in A. Pleural diseases:
Respiratory Diseases 1. Pleural effusion
Central Shifted to Shifted to opposite side 2. Pneumothorax
same side (Push)
(Pull) 3. Hydropneumothorax
1. Bronchitis 1. Collapse 1. Pleural B. Bronchial diseases:
effusion
1. Bronchial obstruction
2. Bronchial 2. Fibrosis 2. Pneumothorax
asthma C. Lung diseases:
3. Bronchiectasis 3. Pleural 3. Hydropneumothorax 1. Emphysema
thicken-
ing 2. Pulmonary fibrosis
4. Emphysema 3. Pulmonary collapse
5. Pneumonia
6. Lung abscess
7. Interstitial
fibrosis
128
( 4 J Respiratory System
in pleurisy due to rubbing ofthe two pleural
surfaces. It is usually felt at the peak of
inspiration or early expiration.
2. Bronchial Fremitus: This occurs in
bronchitis, bronchial asthma and chronic
obstructive lung disease.
3. Palpable Rale s: Thi s o ccurs i n
bronchiectasis, pulmonary fibrosis and
pulmonary congestion.
IX. Tenderness
Tenderness over the chest wall may be present
in local injury, myositis, amebic abscess ofliver,
F,g. 4.16:Clav,cular Percussion
pyogenic abscess ofliver and empyema.
of resonance or displaying extreme dullness is a stony
B : Percussion dull note. It is classically encountered over a pleural
The normal percussion note of the chest is due to the effusion, because fluid dampens the vibration of both
underlying lung tissue, containing normal amount of the chest wall and the underlying relaxed lung. It may
air in the air vesicles, air sacs and air passages. It has also occur in lung fibrosis with pleural thickening or
a distinctive and clear character with low pitch. The with solid intrathoracic tumour.
front of the chest yields a more resonant note than Tympany: This is a drum like resonance, which is
the back, because of the lesser bulk ofmusculature in normally encountered over the stomach, intestines,
front than at the back. larynx and trachea. When it occurs over the chest
Impaired note: When the amount of air in the alveoli wall it may be due to:
decreases, as in consolidation, infiltration, fibrosis and l. Pneumothorax
collapse ofthe lung, the lung fails to vibrate sufficiently 2. Superficial empty cavity
to the percussion stroke. This causes loss ofresonance
resulting in an impaired note. 3. Emphysema
Dull-note: An impaired note ofgreater degree is a dull Sub tympany {Skodaic resonance): A hyperreso-nant
note. In addition to consolidation, infiltration, fibrosis note with a boxy quality, which occurs due to the
and collapse oflung, it is found in pleural thickening. relaxed lung just above the level of pleural effusion.
Stony dull note: A percussion note completely devoid Hyper-resonance: A note in between in pitch between
normal resonance and tympany can be elicited over
the normal lung tissue by keeping the chest wall in full
inspiration, during percussion. It occurs in:
l. Pneumothorax
2. Emphysema
3. Large cavity with a thin wall
4. Congenital lung cyst
5. Emphysematous bullae
6. Eventration of diaphragm
Bell tympany: "Inis is a high pitched tympanic or
metallic sound, heard over the chest in case of massive
pneumothorax. When a silver coin is placed on the
F,g 4 15 Percusso1n of Chest affected side and percussed with a second silver coin,
129
PRACTICAL MEDICINE
the ear or stethoscope applied over the opposite side of dullness on the right side anteriorly, on
the chest may detect a clear bell like sound resembling inspiration and expiration serves to determine
the sound of"hammer on an anvil''. the range of lung expansion and movement of
diaphram. It is restricted in :
I. Kronig's Isthmus
1. Pulmonary diseases at lung base e.g.
Definition: Kronig's isthmus is a band of pulmonary fibrosis
resonance 5-7 ems in width, connecting lung 2. Empyema
resonance over the anterior and posterior aspects
3. Hepatic amebiasis
of each side of the chest. It is bounded medially
by dullness of the neck muscles and laterally by 4. Sub-diaphragmatic abscess.
dullness of the shoulder muscles. 5. Diaphram palsy
Abnormalities:
V. Traube's Area OR Space
l. Absence on either side suggests pulmonary
fibrosis due to tuberculosis. It is bounded above by the lung resonance, below
by the costal margins, on the right by the left
2. Increased width of resonance suggests
border of liver and on the left by spleen.
emphysema.
It is normally occupied by the stomach, hence on
II. Liver Dullness and Span percussion the note is tympanic due to stomach
gas. IfTraube's area is dull it suggests:
Normal liver dullness is in the right intercostal
space, in the fifth space in the mid-davicular I. Pleural effusion on the left side.
line, in the seventh space in the anterior axillary 2. Splenomegaly
line and in the ninth space in the scapular line. 3. Fundic tumor
Liver dullness may be present in the fourth space 4. Full stomach
in the mid-davicular line in amebic or pyogenic
abscess of the liver, diaphragmatic paralysis or VI. Shifting Dullness
collapse of the lower lobe of the lung. In case ofhydropneumothorax in sitting position
It may be pushed down to the sixth space in the there is a hyp erresonant note above followed
mid-clavicular line in emphysema, right-sided by dullness below. On changing the posture to
pneumothorax, air in the peritoneal cavity and supine, this area ofdullness of the fluid changes
terminal cirrhosis. as air and fluid will shift. This is shifting dullness
and always signifies presence of both air and
Ill. Cardiac Dullness
fluid.
On the left side of the chest wall, the lung
resonance is encroached by an area of cardiac VII. Coin-test
dullness due to the presence of the heart. The A coin is placed flat on the chest and struck
cardiac dullness is normally in the third and with another coin. On auscultation of the back
fourth left parasternal line and the fifth left mid of the chest on the same side, a metallic or bell
davicular line. like sound is heard.
This area of dullness may be decreased in Cause: Pneumothorax
emphysema, and left sided pneumothorax. It
may be increased with cardiomegaly and push VII. Percussion Myokymia
of the heart to the left side. In a chronically wasted individual as in
IV. Tidal Percussion pulmonary tuberculosis, a percussion stroke over
the front of the chest, dose to the sternum, may
Percussion of the upper border of the liver cause a transient twitchingofthemusdes, which
130
( 4 ) Respiratory System
type of breathing, presence of any foreign sounds and
vocal resonance.
The stethoscope should be firm!y placed over the chest
to prevent sounds resulting from the movement of the
chest. Hair on the chest wall may produce a crackling
sound and may be mistaken as rates. A similar sound
may occur in nervous patient due to shivering.
I. Breath Sounds
1. Vesicular: This is characterized by active
inspiration due to the passage of air into
the bronchi and alveoli followed without
a pause by passive expiration due to the
elastic recoil of the alveoli which occurs
maximally in the early phases giving an
apparent impression of short expiration.
is more marked on the side of the pulmonary
The character of the sound is rustling due
affection. This is called percussion myokymia.
to the passage through the alveoli which
Limitations ofpercussion selectively transmits lower frequency
sounds and dampens the high frequency
1. It is not possible to percuss deeper than 5 cm. sounds. It is normally heard over the chest.
Hence it is not possible to detect a lung lesion
The normal breath sounds are vesicularand
covered by a layer of air more than 5 cm thick
not bronchial because the lungs and chest
or fluid 1 cm thick.
wall act as an acoustic filter narrowing the
2. A lesion less than 2 cm in diameter does not range of audible frequencies to 100-400 Hz.
cause any change in the percussion note.
2. Bronchial: This is characterized by active
3. Free fluid less than 200 ml in the pleural cavity inspiration due to the passage of air into
may not be detected on percussion. the bronchi. The alveolar phase is absent
131
PRACTICAL MEDICINE
132
(4 Respiratory System
133
PRACTICAL MEDICINE
134
( 4 ) Respiratory System
Causes Causes
a. Cavitycommunicatingwithbronchus. I. Transudative Pleural Effusion
b. Diffuse consolidation oflung adjacent
1. Congestive Heart Failure
to bronchus.
2. Cirrhosis
4. Succussion Splash
This is the splashing sound heard over the 3. Nephrotic Syndrome
chest either with the stethoscope or with 4. Pulmonary Embolization
the unaided ear applied to the chest wall, 5. Myxoedema
when the patient is shaken suddenly by the 6. Superior Vena Cava Obstruction
examiner.
II. Exudative Pleural Effusion
Causes
l. Infectious Diseases
a. Hydropneumothorax
a. Bacterial Infections
b. Large cavity containing fluid and air.
c. Herniation of stomach or colon into b. Tuberculosis
the thorax. c. Fungal Infections
5. Post-tussive Suction d. Viral Infections
A sucking sound heard over the chest wall e. Parasitic Infections
during the long inspiration that follows a 2. Neoplastic Diseases
bout of coughing. It indicate thin-walled
a. Metastatic disease
compressible lung cavity, communicating
with the bronchus. b. Mesothelioma
6. Post-tussive Rates 3. Pulmonary Embolization / Infarction
Rates which are not audible during normal 4. Collagen Vascular Diseases
respiration but are heard after making the a. Rheumatoid Arthritis
patient cough are post-tussive rales. They b. Systemic Lupus Erythematosus
signify cavity filled with thick material
c. Drug-Induced Lupus
which is dislodged during coughing
allowing air to bubble through the e. Sjogrens syndrome
remaining fluid, producing the rates. f. Wegners Granulomatosis
g. Churg - Strauss Syndrome
h. Sarcoidosis
3 Pleural Effusion 5. Gastointestinal disease
Definition: Pleural effusion is collection of excess a. Esophageal perforation
quantity of fluid in the pleural space.
b. Pancreatitis
Pathophysiology: Pleural fluid is secreted by the
c. Intraabdominal abcess
parietal and visceral layers of pleura. Majority of the
fluid is absorbed by the lymphatics and the remainder d. Amoebic Liver Abcess
is absorbed by the lung or chest wall across the meso e. Diaphgramatic hernia
thelium. Excessive fluid collects (according to Frank f. After abdominal surgery
Starlings law of hydrostatic pressure) due to excessive g. Post-liver transplant
back pressure from the visceral surface (e.g. CCF),
6. Drugs and Toxins
decrease in serum proteins (e.g. nephrotic syndrome),
pulmonary inflammation or lymphatic obstruction a. Drug induced pleural diseases
( e.g. pneumonia, infiltrating tumor) or increase nega Nitrofurontoin, Methylsergide,
tive pressure in pleural space (e.g. Atelectasis). Bromocriptine
b. Toxins : Asbestos
135
PRACTICAL MEDICINE
136
{ 4 > Respiratory System
M
fluid is not due to fat but due to lecithin, MIid Pleural Effusion
Rluo1;nUCJ11
on Plmn,-ray<lic>I
r
�:�;£;�, '::::1
200cc
I. Tuberculosis of
flu,J
collecls P,'i\4fili'
2. Nephrosis
3. Heart disease
4. Malignancy
llypoccbolc
•lomogt.'flOW
D. Cholesterol Effusion: Peculiar glistening, Mo<lcra1c Lo Scwrc
__'\,
cholesterol crystals. ,.,_,.
mfcnor
i,;,p11r.,�il.
Causes: ----Ab..0« of
A11 bronchogram
- -� ..
Long-standing effusion, e.g. tuberculosis, :mJ broncbo�' asculor
markings(cfr,ncumonl31
carcinoma, nephroticsyndrome, myxedema
and post myocardial infarction.
VI. Iatrogenic Pleural Effusion (including Drug
•llc•rt
induced)
Lung
U)·podcnS<" lluid �n in
Causes: 1hc dcpend.an1 J')()Akl'II ...
id
4. Drugs e.g. Practolol, methysergide
5. Drug induced eosinophilia e.g. aspirin,
PAS, sulphonamides, nitrofurantoin
6. Drug-induced lupus e.g. hydralazine, F,,..,.� Loculatod EfTu,ion
procainamide, alpha methyl dopa l:ITUSl<)fl•
'Van1shtng.
Appc:irs ,\p�'31'$
Tumour'
C011nJ. Cigar-shaped
VII. Recurrent Pleural Effusion liC'C'1I in
CCF
Causes: �fajor
fissure
I. Tumors ::. APV)C,.,· Later.al View
137
PRACTICAL MEDICINE
138
( 4 ) Respiratory System
D. Auscultation: B. Hemorrhagic
1. Diminished or absent breath sounds C. Milky
below the level of the effusion.
D. Greenish: Pseudomonas, Streptococcus,
2. Bronchial breathing at the level of
Pneumococcus
pleural effusion due to relaxed lung.
3. Egophony at the level of the pleural E. Gold paint: myxedema
effusion. F. Anchovy sauce - ruptured amebic liver
4. Diminished or absent vocal fremitus abscess
below the level of the fluid. II. Microscopic
III. Investigations: A. Lymphocytic predominance - chronic
A. CBC,ESR conditions like tuberculosis, resolving
B. Sputum Examination: Gram and Ziehl pneumonia, fungal infections, carcinoma
Neelsen's stain and culture. and myxedema
C. X-ray chest B. Polymorphic predominance - Acute
L Homogenous opacity conditions like acute bacterial infections
2. 0 bliteration of costophrenic angle on and rheumatic fever
the affected side ( 150 ml of fluid) C. Eosinophilic predominance
3. Concave upper border (Eilis's curve)
4. Shift of the mediastinum to the Table 4.5 : Pleural Fluid with and without
Systemic Eosinophilia
opposite side
With Systemic Without Systemic
Radiologically, pleural effusion can be
Eosinophilia Eosinophi/ia
classified as free or loculated as given
1. Tropical eosinophilia. 1. P/europulmonary am-
below:
ebiasis
1. Free classical: Mild (blunting
2. Pulmonary eosinophi lia 2. Fungal infection
of costophrenic angle on lateral
decubitus view) or moderate to 3. Vasculitis e.g. Polyarteritis 3. Foreign protein in pleural
severe (homogenous opacity with nodosa space
classical lateral-medial, superior 4. Hydatid disease 4. Blood in pleural space
inferior curve with mediastinal shift 5. Hodgkin's disease 5. Collagen disease. SLE
to opposite side.
6. Drug induced 6. Pulmonary infarction
2. Free subpulmonic: additional elevation
of diaphragm 7. Frequent aspiration
139
PRACTICAL MEDICINE
G. Light's criteria using serum and pleural fluid 1. Septicemia /Toxic look Present Absent
albumin and LDH are used to differentiate 2. lntercostal spaces Red, shiny, edema- Normal/
transudate from exudate. tous, tender Bulging
Exudative Pleural Effusion meets atleast 3. Clubbing Present Absent
one criteria, Transudative meets none:
4. Opacity on X-ray Obliterates the rib Not so
i. Pleural fluid protein / serum protein shadows
> 0.5.
Ill, Table 4.8: Differences Between
ii. Pleural fluid LDH / serum LDH > 0.6.
Pericardia! and Pleural Effusion
iii. Pleural fluid LDH more than two
Pericardia/ Pleural effusion
thirds normal upper limit for serum. effusion
These cr iteria misid entify 25% of
1. Mediastinal Absent Present
transudates as exudates. shift
H. Serum-to-pleural fluid albumin gradient
2. Dullness poste- Absent Present
(ser um albumin minus pleural fluid riorly
albumin) of < 1.2 g/dL indicates the
3. Traube's area Not obliter- Obliterated in left
presence of exudate. Difference >3.1 gm/ ated sided effusion
di indicate it is Transudative.
4. Heart sounds Muffled Diminished atthe
Sequelae of Pleural Effusion apex, but heard better
elsewhere
l. Permanent collapse of the lung (compression
collapse) IV. Table 4.9 : Differences between Liver
2. Pleural thickening. adhesions and bronchiectasis Abscess and Right Pleural Effusion
3. Empyema Liver Abscess Right Pleural
Effusion
Differential Diagnosis
1. Dullness highest In the mid- In theaxilla
I. Table 4.6: Differences between point clavicularline
Thickened Pleura and Pleural 2. T idal percussion No movements of Movements
Effusion diaphragm may be present
ThickenedPleura Pleural Effusion 3. lntercostal tender- Present Present only in
1. History Long standing Acute ness empyema
2. Intercostal Depressed Bulging V. Effusion due to Heart Failure
spaces
l. Most common cause of pleural Effusion.
3. Mediastinum No shift or shift to the Shift to the op-
same side posite side 2. It is Transudative and usually bilateral.
4. Percussion Dull Stony dull with 3. Diagnostic thoracentesis is usually not
note increased resis required. Heart failure should be treated.
tance
4. A pleural fluid NT - ProBNP > 1500 pg/ml
S. Breath sounds Diminished Absent is diagnostic of pleural effusion secondary
6. X-ray No dense opacity, Dense opacity, to congestive heart failure.
upper level not well- concave upper
defined, cosophrenic border, cos to· VI. Synpneumonic or Parapneumonic Effusion :
angle not obliterated, phrenic angle This is said to occur when there is simultaneous
calcification may be obliterated pneumonia in the lung covered by pleural
seen
effusion.
140
( 4 > Respiratory System
l. It is associated with bacterial pneumonia, pleural effusion, collapse, consolidation,
Lung abscess, or bronchiectasis which are congestion or a local area of dullness.
the most common causes of exudative 4. Pleural fluid is exudative, glucose level is
pleural effusion. It is also associated with reduced.
malignancy and pulmonary infarction.
5. For definitive diagnosis : Pleural fluid
2. Patient usually present with Acute cytology (diagnostic), other modalities like
(Bacterial) orsubacute (Anaerobic) onset of Thorocoscopy, CT or USG guided biopsy
fever, chest pain, cough with expectoration; of pleural thickening / nodules.
weight loss and mild anaemia if subacute.
VIII. Mesothelioma
3. The physical findings of pleural effusion
1. Primary tumours of mesothelial cells lining
which are altered are:
the pleural cavities; most related to Asbestos
a. Bronchial breath sounds are very well exposure.
heard
2. Patients have chest pain and shortness of
b. Rales may be present breath.
c. Vocal resonance is increased because 3. Most signs are similar to pleural effusion
the relaxed lung is filled with exudate due to other causes, but mediastinal shift
in consolidation, which is a good will be to the same side.
conductor of sound.
4. X-ray chest-Generalised pleural thickening
4. Following features may indicate empyema: with shrunken hemithorax.
a. Patient not responding to current 5. Thoracoscopy or open pleural biopsy
antibiotics. establishes the diagnosis.
b. Grossly purulent fluid. 6. Treatment
c. Pleural fluid WBC > 50,000 / µI or a. Opiates for chest pain
PMN > 1000 / µl.
b. Oxygen for shortness of breath.
d. Pleural fluid pH < 7.20. (other causes
- oesophageal rupture, Rheumatoid IX. Effusion secondary to pulmonary embolization
pleural, TB pleuritis, Lupus Pleuritis) 1. Patient usually presents with Dyspnea.
e. Pleural fluid glucose < 60 mg/di. 2. Pleural Effusion is exudativeortransudative.
f. LDH > 1000 IU/L. 3. Treat underlying emboli i.e. Anticoagula
g. Positive Microscopy or culture of tion. If pleural effusion increases in size
pleural fluid. after anticoagulation, patient has either
h. TNFa levels higher than 80 pg/ml recurrent emboli or a complication like
also suggest Empyema. Hemothorax or Pleural infection.
VII. Effusion Secondary to Malignancy X. Tuberculous Pleural Effusion
l. Second most common type of Exudative l. Usually associated with primary TB and
Pleural Effusion. Lung carcinoma, Breast occurs due to hypersenstivity reaction to
carcinomaand Lymphoma accountfor75% tuberculous protein in pleural space.
of cases. 2. Clinical features : Fever, weight loss,
2. Dyspnea is out of propectin to the size of dyspnea, pleuritic chest pain, dry cough
pleural effusion. Other systemic features to along with classical signs of pleural effusion.
note are - weight loss, cachexia, clubbing, 3. Pleural fluid examination:
non-metastatic manifestations of the a. Exudate with small lymphocytes
tumor. predominant
3. Patient may present with signs of
141
PRACTICAL MEDICINE
142
(4 > Respiratory System
3. Treated with Tube Thoracostomy. It also 3. Chest physiotherapy to encourage expansion
allows quantification of bleeding. oflower chest
4. Lacerated pleura treated by apposition of 4. For recurrent pleural effusion e.g.
pleural surfaces. malignancy.
5. If pleural hemorrhage exceeds 200 ml/h, 1. Pleurodesis - Pleural abrasion, Talc,
thoracoscopy or thoracotomy should be Doxycydine.
done. 2. Placement of Sma ll Indwelling
XV. Miscellaneous causes Catheter
1. Serum Amylases level elevated in II. ForEmpyema
oesophageal rupture or pancreatitis I. Antibiotics: The correct antibiotic could be
2. Intra abdominal abcess - Patient is febrile, best selected by culturing the pleural fluid
high PMN in pleural fluid; no pulmonary followed by antibiotic sensitivity tests. The
pathology. antibiotics have to be given for 3-6 weeks or
even more till the patient becomes afebrile,
3. Ascites with pleural effusion - Benign
WBC count returns to normal, drainage
ovarian tumor (Meig's syndrome), Ovarian
reduces to less than 100 ml/day and there
hyperstimulation syndrome.
is radiological clearance. The antibiotics
4. Post CABG: (a) Effusion within first few used are a combination of Beta-lactam
weeks are typically left sided, bloody, large aminoglycoside and metronidazole.
numbers of eosinophils, responding to one 2. Intercostal drainage: Continuous intercostal
or two thoracentesis; ( b) Effusions after first drainage with a tube may be required till the
few weeks are typically left sided, dear, with patient is afebrile, lung expansion is full and
small lymphocyte predominance and tend WBC count returns to normal.
to recur.
3. Intrapleural thrombolytic agents like streptokinase
Treatment diluted in l O ml saline breaks down the loculation
and improves drainage.
I For Pleural Effusion
4. Thoracostomy with decortication.
1. General: Rest, adequate nutrition, vitam ins
5. Video Assisted Thoracic Surgery.
2. Management offluid: Thoracocentesis or
6. Open drainage and rib resection.
pleural tapping if large effusion, cardio-
respiratory embarrassment or empyema
4 > Collapse / Atelectasis of
Lung������
Definition
It is defined as airlessness with shrinkage of the lung
which may be secondary to obstruction, compression,
contraction or surfactant loss. Failure of the lung to
expand at birth is called atelectasis neonatorum.
Classification
l. Acute or chronic - depending on rapidity of
development of collapse.
2. Partial or total - depending on the degree of
collapse.
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144
{ 4 > Respiratory System
c. Useful in evaluating mediastinum, ILD usually have an acute I chronic phase.
pleura, hilum, chest wall, rest of lung and They can occassionally be recurrent with intervals of
concomitant pathologies. sub•dinical disease.
3. Other Imaging Techniques : MRI, Virtual Histopathologic patterns in ILD :
Bronchoscopy.
l. Desquamative Interstitial Pneumonia (DIP)
4. Pulmonary Function Test : Shows a restrictive
pattern of abnormality. 2. Respiratory Bronchiolitis
Arterial Blood Gas Analysis: Shows Hyp oxemia 3. Diffuse Alveolar Damage (Acute or Organizing)
5.
particularly if acute. 4. Bronchiolitis Obliterans with Organizing
Pneumonia (BOOP)
Complications
5. Non-specific Interstitial Pneumonia (NIP).
]. Infection 6. Usuaul Interstial Pneumonia (UIP).
l. Spontaneous pneumothorax from ruptured 7. Lymphocytic Interstitial Pneumonia.
bullae of compensatory emphysema
Diagnosis
Treatment
l. Duration of Illness:
Aims at treating underlying cause.
i. Acute Presentation (days to weeks) :
1. Pleural Aspiration / ICD in pleural effusion / (a) Allergy (drugs, fungi, helminths),
pneumothorax, hydropneumothorax. (b) Acute Interstitial Pneumonia
2. Removal of foreign body, impacted mucus. (AIP), (c) Eosinophilic Pneumonia, (d)
Hypersensitivity Pneumonitis {unusual)
3. Treatment of endobronchial tumor - surgery,
radiation, chemotherapy, laser, airway stenting. ii. Subacute Presentation (weeks to months)
may occur in all ILD : (a) Sarcoidosis,
4. In case of mucus plugg ing. Mucolytis,
(b) Drug Induced ILD, (c) Alveolar
nebulization, physiotherapy, measures like
Hemorrhagic Syndrome, (d) Cryptogenic
postural drainage, chest wall percussion and
Organizing Pneumonia (COP), (e) Acute
vibration, forced expiration technique.
Immunologic Pneumonia - complicating
5. Oxygen, Analgesics, Antibiotics for secondary SLE or Polymyositis.
infection.
iii. C hronic Pre sentation (months to
years) (Most ILD) : (a) Sarcoidosis, (b)
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--�---------------------------�
Classification of lnterstial Lung Diseases (ILD)
!
Predominant Inflammation
Based on Histopathology
l
Predominant Granulomatous
and Fibrosis reaction
I
IAlveolitis, Interstitial Inflammation IGranulomasl
I
and fibrosis)
!
Etiology
l
Etiology
! l
Etiology Etiology
Known Unknown Known Unknown
1. Asbestosis 1. Idiopathic Interstitial Pneu 1. Hypersensitivity 1. Sarcoidosis
2. Fumes, Gases monia, IPF, DIP. All'. COP. Pneumonitis 2. Granulomalous
3. Radiation NIP. (organic dusts] vasculitides
4. Aspiration pnl'u· 2. Connective Tissue Diseases - 2. Inorganic Dusts : :1. Wegners Granulo
monia SLE, RA AS, SS, Sjogrcn's Silica. Beryllium matosis, Polyangi
5. Residual of ARDS Syndrome tis, Churg Strauss.
6. Drug (Antibiotics, 3. Pulm. Hemorrhage syn 4. Langerhans cell
Amiodarone, Gold dromes e.g. good pastures. granulomatosis.
& Chemotherapy 4. Pulm. Alveolar Proteinosis 5. Bronchocentric
drugs. 5. Lymphocytic infiltration granulomatosis
7. Smoking, Related disorders 6. Lymphomatoid
DIP, Respiratory 6. Eosinophilic pneumonia gra nu I omatosis
Broncholitis, 7. Lymphangioleiomyomatosis
Primary Langer- 8. Amylodosis
hans Cell Histiocy- 9. GVHD (Graft versus Host
tosis (PLCH) Disease)
10.GI / Liver Disease Inflamma
lory Bowel Disease. Primary
Biliary Cirhosis
11.Inheriled disease : Tuberous
sclerosis, Neurofibromatosis.
ARDS: Adult Respiratory Distress Syndrome; ILD: Interstitial Lung Disease; DIP: Desquamative Interstitial Pneumonia:
IPF : Idiopathic Pulmonary Fibrosis; AIP : Acte Interstitial Pneumonia: COP : Cryptogenic Organising Pneumonia;
NIP : Non-Specific Interstitial Pneumonia; SLE : Systemic Lupus Erythematosus; RA : Rheumatoid Arthritis;
AS: Anklyosing Spondylitis; SS : Systemic Sclerosis; GI : Gastro Intestinal
146
( 4 > Respiratory System
j
Dust, Fumes,
Drugs, Infection,
Cigarette Smoke,
Radiation, other diseases
Autoimmune disorders
j -
Wound
Intact ------ --
-, Healing >------ Abberant
Genetic predisposition
- Autoimmune condition
- Superimposed diseases
I Lung Homeostasis I - Excess inury to lung may overwhelm
reparative mechanisms
Predominant Predominant
Granulomatous R�ponse
!Interstitial Fibrosis !
All these lead to irreversible scarring of alveolar Airway & Vasculature
e.g. Hypersensitivity pneumonitis - symptoms pneumonia grouped under interstitial lung disease
temporally related to hobby (pigeon breeders) with predominant inflammatory type and unknown
or workplace (Farmer's lung). etiology. It has poor response to treatment and Bad
7. Other important past history Prognosis
a. History of Travel - for parasitic infection Clinical Manifestations
(causing pulmonary eosinophilia).
1. It has a chronic presentation : Age Group > 50
b. History of risk factors for HIV infection
yrs, Men more commonly affected; 60% to 75%
from all patients : Several processes occur
are smokers.
at time of initial presentation or during
clinical course. e.g. HIV Infection, BOOP, 2. Symptoms
AIP, Lymphocytic Interstitial Pneumonitis a. Exertional Dyspnea
or Diffuse Alveolar Hemorrhage. b. Non productive cough
Idiopathic pulmonary fibrosis: (diffuse c. Fatigue
fibrosing alveolitis) (Hamman Rich d. Weight loss
syndrome) 3. Signs
It is the most common type of idiopathic interstitial a. Tachypnea
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148
( 4 > Respiratory System
4. Lung Transplantation
6
1. Pathologic and Radiologic evidence ofUIP
AND Pneumothorax
2. Any of the following criteria Definition: Pneumothorax refers to air within the
a. DLC02 < 39%. · pleural space.
b. Decrement in FVC :a 10% during 6 Causes
months of follow up.
A. Primary Spontaneous Pneumothorax (PSP)
c. Decrease in Sp02 below 88% during
It is a pneumothorax that occurs without a
6 min - walk test.
precipitating event in a person who does not have
d. Honey combing on HRCT known lung disease. Usually most individuals
Patients with IPF andco-existantemphysema (COPD) with PSP have unrecognized lung disease, with
develop pulmonary hypertension early and have a the pneumothorax resulting from rupture of a
worse outcome. subpleural bleb.
Acute deterioration ofIPF & Acute Exacebration Risk Factors
1. Acute deterioration secondary to 1. Smoking: Cigarette smoking is a significant
a. Infection risk factor. Respiratory bronchiolitis, a form
of airway inflammation associated with
b. Pulmonary Embolism
cigarette smoking, may contribute to the
c. Pneumothorax development and recurrence of PSP.
d. Accelerated clinical course 2. Family history : Autosomal dominant,
Exacerabation ofIPF -Criteria for diagnosis autosomal recessive, polygenic, and
i. Worsening dyspnea within few days X-linked recessive inheritance mechanisms
to 4 weeks have all been proposed. The autosomal
dominant Birt-Hogg-Dube syndrome,
11. New developing diffuse ground glass
which predisposes patients to benign skin
opacity and / or
tumors and renal cancer, is associated with
Consolidation superimposed on an increased incidence of PSP.
background reticular or honey comb
3. Other: Marfansyndrome, Homocystinuria.
pattern consistent with UIP pattern.
B. Secondary Spontaneous Pneumothorax (SSP)
iii. Worsening hyp onemia.
It is defined as a pneumothorax that occurs as
iv. Absence of infections, pneumonia, a complication of underlying lung disease.
sepsis and heart failure.
Etiologies
Treatment
1. Chronic Obstructive Pulmonary Disease:
i. No effective treatment 50 to 70 percent of SSP is attributed to
ii. Mechanical ventilation often required COPD. Rupture of apical blebs is the usual
iii. If patient survives - recurrence common and cause.
usually results in death. 2. Cystic Fibrosis : Usually due to rupture of
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PRACTICAL MEDICINE
apical subpleural cysts. Factors associated C. Iatrogenic: Central line insertion, surgery,
with an increased risk of pneumothorax lung biopsy, faulty tracheostomy.
include infection with Pseudomonas IV. Artificial: It was induced in the past for severe
aeruginosa or Aspergillus species or a prior tuberculosis (At present this is obsolete because
episode of massive hemoptysis. of antituberculosis drugs).
3. Lung Malignancy : Both primary and
Types
metastatic lung malignancy have been
associated with SSP. The mechanism 1. Simple or closed Pneumothorax: The opening in
is endobronchial obstruction with air the lung is very small and heals rapidly. Therefore,
trapping. there is no continuous communication between
4. Necrot izing Pneumonia : SSP can the lung and the pleural cavity. The pleural
complicate the course of necrotizing pressure on the affected side remains sub
pneumonia due to bacterial infection, atmospheric. A simple pneumothorax usually
Pneumocystis jirovecii, tuberculosis, and has only modest repercussions unless the
less often fungi. patient has limited respiratory reserve or is
being mechanically ventilated. Radiographically,
a. Bacterial Pneumonia : SSP has been
simple pneumothoraces tend to be small and
associated with bacterial pneumonias
without mediastinal shift to the contralateral
caused byStaphylococcus, Klebsiella,
side.
Pseudomonas, Streptococcus
pneumoni ae, a n d anaerobic 2. Open Pneumothorax : The opening between
organisms. Extension of bacterial the lung and the pleural cavity remains patent.
infection into the pleura can lead to Pressure in the pleural cavity is equal to that
development of empyema. of the atmosphere. It occurs when a traumatic
chest wall defect persists, through which air
b. Pneumocystis jirovecii : The enters the pleural space during inspiration {ie, a
pathogenesis of SSP in PCP is likely
"sucking wound"). As a result, the mediastinum
alveolar and pleural tissue invasion
shifts toward the normal side during inspiration
and rupture oflarge subpleural cysts
and the lung on the injured side remains
that are caused by tissue necrosis.
collapsed. During expiration, air exits the pleural
c. Tuberculosis : The pneumothorax is space through the chest wall defect and the
usually due to rupture of a tuberculous mediastinum swings back. Expiratory air from
cavity into the pleural space. the normal lung (ie, "pendulum air") fills the
5. Catamenial Pneumothorax : Refers to a collapsed lung. The "mediastinal flutter" may
pneumothorax occurring in association cause respiratory failure. Radiographically, an
with menses due to thoracic endometriosis open pneumothorax is characterized by a visible
6. L ess Common Causes : Ankylosing chest wall defect and by expiratory mediastinal
spondylitis, asthma, histiocytosis shift towards the injured side.
X, interstitial lung disease (eg, 3. Tension Pneumothorax : The opening between
i d i o p a t h i c p u l m o n a r y f ib r o s is), the lung and the pleural caity is "valvular" - air
lymphangioleiomyomatosis, Marfan can enter the pleural cavity during inspiration
syndrome, metastatic sarcoma, rheumatoid but cannot escape during expiration. Therefore,
arthritis, and sarcoidosis. a positive pressure (exceeding atmospheric
III. Traumatic and Iatrogenic pressure) occurs on the affected side. This
A. Penetrating wounds: Stab wounds, fractured rapidly leads to respiratory failure and a is a
ribs, crush injury. medical emergency. Radiographically, tension
B. Non-penetrating wounds: Steering wheel pneumothorax shows a distinct shift of the
impact against the drivers' chest. mediastinum to the contralateral side.
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{ 4 Respiratory System
4. Others:
a. Pneumothorax ex vacuo : This rare type
of pneumothorax forms adjacent to an
atelectatic lobe. It is seen preferentially with
atelectasis of the right upper lobe and is
the result of rapid atelectasis producing an
abrupt decrease in the intrapleural pressure
with subsequent release of nitrogen from
pleural capillaries. Treatment consists
of bronchoscopy rather than chest tube
drainage. Radiographically, pneumothorax
ex vacuo is suggested when an atelectatic
lobe or lung, particularly right upper Fig 4 29: Bilateral pneumothorax
lobe atelectasis, is surrounded by a focal
pneumothorax. 2. Symptoms due to SSP are generally more severe
than those associated with PSP, presumably
b. Bilateral Postoperative Pneumothorax:
because patients with SSP have less pulmonary
Bilateral pneumothoraces are seen
after cardiac surgery, particularly in reserve due to underlying lung disease.
recipients of heart-lung transplants. 3. Sudden onset of dyspnea and pleuritic chest
They are a consequence of extensive pain. The severity of the symptoms is primarily
mediastinal dissection allowing a related to the volume of air in the pleural space.
unilateral pneumothorax to propagate 4. Evidence of labored breathing and hemodynamic
to the contralateral hemithorax. A compromise (eg, tachycardia, hypotension)
single thoracostomy tube is able to suggestsa possible tension pneumothorax, which
evacuate both pleural cavities. This type of necessitates emergency decompression.
pneumothorax has been dubbed "buffalo
Signs
chest;· since these animals have pleural
spaces that communicate anteriorly and, A. Closed pt1eumothorax
as a result, they are susceptible to bilateral 1. Reduced chest movement
pneumothorax . 2. Hyper-resonant note on percussion
Conditions Mimicking Pneumothorax 3. Absent air entry
l. Bullae : Large subpleural bullae can mimic 4. Mediastinal shift to opposite side
a loculated pneumothorax . Both bullae and 5. Coin Test
pneumothoraces usually have a straight or 6.-1.TVF, VR
convex pleural contour laterally, but only bullae
B. Open pneumothorax
typically have a medial border that is concave to
the chest wall. All the signs of dosed pneumothorax, plus -
2. Trauma : Herniated Stomach following trauma 1. Crackpot sound on percussion
2. Amphoric breath sounds
Diagnosis
3. Voice and cough sounds may be heard with
Symptoms metallic echo.
1. Primary spontaneous pneumothorax (PSP) C. Tension pneumothorax
usually occurs when the patient is at rest. Patients All the signs of closed pneumothorax, plus -
are typically in their early 20s, with PSP being 1. Displacement of the mediastinum with
rare after age 40. respiration
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PRACTICAL MEDICINE
152
NE , 4 Respiratory System
can produce a veil-like opacity, more With the patient in sitting position, a
opaque than a pure pneumothorax and Needle ( 14 guage) is inserted into the
less opaque than a pure hydrothorax . pleural cavity in the second space in
Lateral decubitus the mid-davicular line or in the fifth
nd space in the axillary line. The other
i. A pneumothorax can be most easily
detected with a lateral decubitus view. In end of the needle is connected to the
ng this position, most pleural airaccumulates underwater seal.
in the non-dependent lateral location. 2. If there is no cardiorespiratory embarrasment
le. ii. The visceral pleural line appears either a. If pneumothorax is small (:::;: 3 cm between
lt, straight or convex towards the chest wall. lung and chest wall): Supplemental oxygen
h. iii. As little as 5 mL ofpleural air may be visible and observation.
st on a lateral decubitus chest radiograph. b. If pneumothorax is large(> 3 cm between
,t 2. Computed Tomography lung and chest wall):
This is the most accurate imaging modality for i. Needle Aspiration.
the detection of pneumothorax. Even small ii. Tube Thoracostomy (Chest Tube
11 amounts ofintrapleural gas, atypical collections Insertion) : if needle aspiration fails.
ofpleural gas, and loculated pneumothoraces can iii. Thoracoscopy (VATS): See below.
be identified by CT. In addition, complex pleural
pathology (eg, pleural effusion, pneumothorax) iv. Chemical Pleurodesis : If air leak
can be optimally displayed by CT scanning. persists.
Pleural interventional procedures are also c. Re c urren t Pne umot ho rax
facilitated by CT guidance. Hydropneumothorax : Chest Tube
insertion and Thoracoscopy. Chemical
3. Ultrasound : Ultrasound of the chest is
Pleurodosis may be performed.
sometimes used to evaluate situations in which
the diagnosis must be made emergently at the Supplemental oxygen : administered to facilitate
bedside, such as an ICU patient or a trauma resorption of the pleural air.
patient in the emergency department, so-called Aspiration : Aspiration is most easily accomplished
point-of-care ultrasound. with a commercially available thoracentesis kit. Once
In the presence of a pneumothorax, smooth, no more air can be aspirated, the catheter can be
horizontal echogenic lines are seen above and removed or left in place attached to a one-way valve
below the pleural line and there is absence of (Heimlich Valve).
lung sliding and B lines. Tube thoracostomy : Chest tube (:0:22 Fr) or chest
Treatment catheter (:514 Fr) is connected to a water seal device,
with or without suction and left in position until the
Initial management is directed at removing air from the pneumothorax resolves. The chest tube can be removed
pleural space, with subsequent management directed if the pneumothorax has not reaccumulated.
at preventing recurrence.
Thoracoscopy: Video-assisted thoracoscopy (VATS)
Initial management: The choice ofprocedure depends
-With this procedure, pleurodesis is created by pleural
on patient characteristics and clinical circumstances:
abrasion or a partial parietal pleurectomy; when neces
l. If cardio-respiratory embarressment: sary, an endoscopic stapler can be used to resect bullae.
a. Supplemental oxygen Persistent air leak : A more aggressive approach is
b. Treatment of shock needed if an air leak persists after three days. For
c. Aspiration of pneumothorax: patients whose lung has expanded >90%.
Chest Tube Inser tion (Tube A Heimlich valve can be attached to the chest
Thoractostomy) or tube.
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PRACTICAL MEDICINE
Autologous blood or tube can be infused into 2. Hydatid Cysts
the pleural space for chemical pleuradesis 3. Fungal infection
• Performing video-assisted thoracoscopy to 4. Abscess
oversew the area of leak and perform mechanical B. Neoplasms
pleurodesis.
l. Bronchogenic carcinoma
Failure of lung reexpansion : For patients who have
2. Metastasis
a persistent air leak and whose lung is less than 90
percent expanded, the preferred procedure is VATS. 3. Lymphoma
Recurrence prevention C. Traumatic: Resolving hematoma
a. Pleurodesis via VATS orchemical pleurodesis via D. Congenital
tube thoracostomy (talc, bleomycin, tetracyclin l. Infected bronchogenic cyst
derivatives like doxycycline or autologus blood 2. Sequestration
can be used). E. Immunological
b. Thoracotomy : T he indications for open 1. Rheumatoid
thoracotomy are the same as those for VATS.
Thoracotomy is presently recommended only if 2. Wegener's granulomatosis
thoracoscopy is unavailable or has failed. During F. Vascular: Pulmonary infarction
thoracotomy, apical pleural blebs are oversewn On CXR 3/4'h of circumference should be well
and the pleura is scarified. defined in order to call it a cavity.
C. Smoking cessation: may help prevent recurrent Table 4.13 : Types of Pulmonary Cavities
pneumothoraces. Thin shaggy walled Thin smooth waited Thick walled
154
( 4 ) Respiratory System
8 Bronchogenic
Carcinoma
Bronchogenic carcinoma must be considered in all
cases, esp. > 40 years, or smokers presenting with
respiratory involvement particularly with signs of:
I. Collapse
II. Consolidation
III. Cavitation
IV. Mediastinal obstruction
V. Pleural effusion
VI. Apical dullness, wasting of upper limb and
Horner's syndrome
Table 4.1 S : Differences between various
types of Bronchogenic Carcinomas
Epider- Adeno- Anaplas- Alveolar
moid carcino- tic cell
mo Fig 4 32 X ray chest 1n a case ofllronchogen1l carcinoma
showing collapse L upperlobe,v,th d1>sen11nated
1. Situation Central Periph- Either Both
metastasis I
eral -- --- - -�- ---
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156
( 4 > Respiratory System
157
PRACTICAL MEDICINE
l
C::.Olcifi<:.01ion
calcified. :/ / \ '-
Sequclae to
Pulmonary TB
8
A number of such tubercles may merge to form an l'ocu0.J'
and �
)-.,
1
,J
(
158
{ 4 ) Respiratory System
3. It may actively progress merging into post· density involving complete lobe yet the
primary pulmonary tuberculosis. general condition of the patient is good.
4. It may lead to hematogenous spread of tubercle Prognosis is excellent. It may be due to
bacilli leading to miliary tuberculosis or inflammatory exudate, collapse or caseous
tuberculous meningitis. pneumonia.
Clinical Features 2. Bronchiectasis
A. Symptoms 3. Obstructive emphysema
1. There may be no symptoms 4. Pleural effusion
2. Fever for a brief period, which is often B. Allergic
passed off as influenza. Evening rise of I. Erythema nodosum
temperature. 2. Phlyctenular conjunctivitis
3. Anorexia and weight loss
C. Due to hematogenous spread
4. Cough and wheeze due to pressure oflymph
I. Miliary tuberculosis
nodes on bronchi
B. Signs 2. TB meningitis
1. There may be no detectable physical sign. 3. Tuberculosis of bone, joints, kidneys and
2. General debility: A thin, pale, fretful child skin, any organ.
with loss of skin elasticity and less glossy Post-primary Pulmonary Tuberculosis
hair. Pathogenesis
3. Local areas of rales or rhonchi.
C. Radiology Post-primary pulmonary tuberculosis may
In adults the pulmonary component is more rise in any one of the four ways:
obvious, whereas in children the glandular 1. Direct progression of primary lesion
component is more obvious.
2. Reactivation of the primary lesion when the
Radiological findings are: individual's defenses have waned
1. Soft confluent shadow (suggesting
3. Hematogenous spread of the disease from the
exudative process)
primary focus
2. Linear shadow (suggesting fibrosis)
4. Exogenous superinfection with drug resistant
3. Cavity: Initially irregular, later smooth
bacilli.
walled
4. Thin walled bullae The lesions of reinfection have the same basic tubercu
-
lar pathology. Hyperallergy and immunity acquired as
5. Blocked cavity
a result of first infection exert two opposing influences.
6. Calcification
As a result of hyper allergy there is a considerable tis
7. Bronchiectasis especially in the upper zones sue destruction and as a result of immunity there is a
8. Bronchial cold abscess: Elongated solid constant attempt at healing by localization and fibrosis.
dense shadow There is no tendency ofinvolvement of draining glands.
9. Enlarged hilar nodes When the immunity is high, exudative lesions are re
10. Miliary mottling placed by fibrotic lesions giving a nodular appearance.
11. Tuberculoma The lesions spread along the peribronchial lymphatics
12. Primary complex giving a typical X-ray appearance of infiltration - patchy
opacities interspersed with normal parenchyma. In
Complications
healing, the peribronchial granulation tissue is replaced
A. Pulmonary: by fibrosis, which leads to dilatation of bronchi by
I. Epituberculosis: Dense homogenous traction (post-tuberculous bronchiectasis).
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PRACTICAL MEDICINE
When immunity is low and the tempo of activity high, chest or there may be signs of pleural effusion.
tuberculous material may be aspirated through the pneumothorax, hydropneumothorax, consoli
bronchi into other parts of the same or the opposite dation, collapse, fibrosis or cavitation. Some
lung producing fresh lesions. The caseous material times the only sign present may be localized
liquefies and discharges into a bronchus so that a cavity rhonchi or post tussive rates especially at the
forms. Cavity is a favorable breeding ground for the apices.
tubercle bacilli. (Caseous material has l x 10·1 bacilli Table 4.16 : Differences between
/ gm, Cavity has 1 x 10�). Progressive Primary Complex and Post
The common sites of tuberculous lesion are the poste primary TB
rior segment of the upper lobe or the apical segment of Progressive Primary Com- Post Primary TB
the lower lobe. This is mostly due to decreased blood plex
flow and relatively good ventilation of the upper lobe 1. Increased Hilarlymph node 1. Absence of lymph node
in the upright position. (usually)
2. Primary complex in any part 2. Usually apical fibrosis
Clinical Features
of the lung
160
( 4 ) Respiratory System
5. Specimen Microscopy
a. Traditional method - Ziehl-Neelson
6. Culture Techniques
Stain.
a. Conventional methods
b. Can detect upto 70% ofculturepositive
samples with lower limit of detection i. Agar based media takes 10 12
of 5 x 103 organisms / ml. days.
c. Modifications include ii. Egg based Lowenstein Jensen
i. Use of Bleach Medium takes 18-24 days.
ii. Us e o f G u a n i d i n i u m More sensitive than smear examination
Hydrochloride and allows for biochemical identification
of species enhancing specificity.
iii. Fl uorescent M i c r oscope -
Auramine and rhodamine stains. b. Automated Liquid Culture Method:
d. WHO 2010 guideline : Only two i. Mycobacterial Grower Indication
sputum sspecimens required. One Tube (MGIT) 960 TB
sample should be an early morning Employs fluorescent technology
sample. that enables result in 7-10 days.
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PRACTICAL MEDICINE
162
( 4 l Respiratory System
4. Direct Rapid Methods for screening Complications
MDR-TB:
l. Dry pleurisy, pleural effusion or empyema
a. Nitrate Reduction Assay (NRA):
Based onabilityofM. tuberculosis 2. Chronic bronchitis and laryngitis
to reduce Nitrate to Nitrite. 3. Cor-pulmonale
b. Microscopic observation broth, 4. Aspergillosis
drug susceptibility assay: Based 5. Amyloidosis
on observation of characteristic 6. Anemia
cord formation ofM. tuberculosis
7. Tuberculosis of other organs
is complex that is visualized by
inverted microscope. Treatment
c. Thin Layer Agar (TLA) : I. Bed rest in a Sanitorium/ Hospital: In the past,
ShortTurn around timeofl l days. pleasant rural or mountainous surroundings,
Microscopic Examination of fresh air, good food and graded exercises were
growth on solid media using the only modes of therapy. With chemotherapy,
TH 11 Middle Brook agar in the results are as good without bed-rest as with
quadrant petri plates containing it. However bed rest is advised for the following:
isoniazid, rifampicin, PNB and 1. Very ill patient with extensive disease
one without additive. 2. Infectious cases with sputum positive for
Indications of DST: AFB or very extensive disease radiologically.
1. Ideally should be done in all cases ll. Chemotherapy:
prior to start of Anti TB Rx. Classification of Antitubercular drugs
2. For definite diagnosis Bacteriocidal : Isoniazide, Rifampicin,
a. All previously treated cases. Streptomycin, Pyranzinamide
b. All cases of HIV with active TB Bacteriostatic : Ethambutol, Thiacetazone,
c. Developing activeTB after contact Par a-amin o s alic ylic acid (PAS),
with MDR TB cases. Ethionamide.
Case definitions (WHO Guidelines 2010)
d. All new cases in an area where
level of MDR cases is >73% (In l. Tuberculosis suspect:
India it is< 3%). Any person who presents with symptoms
e. Treatment failure cases or signs suggestive of TB.
10. Bronchoscopy- trans thoracic aspiration 2. Case of Tuberculosis
BAL. A definite caseofTB orone in which a health
11. Scalene Lymph Node Biopsy worker has diagnosed TB and has decided
to treat the patient with a full course ofTB
12. Lung Biopsy treatment.
II. Imaging 3. Definite Case of Tuberculosis
1. X-ray chest: AP, PA, Lateral, Lordotic- to A patient with Mycobacterium Tuberculosis
see apical area of lung complex identified from a clinical specimen,
2. Fluoroscopy- outdated either by culture or by a newer method such
3. Bronchography as molecular line probe assay.
4. CT Scan a. New Patients : New patients have never
had treatment for TB, or have taken anti
5. MRI
TB drugs for less than one month.
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164
< 4 ) Respiratory System
isoniazid (H), Rifampicin (R), Pyranzinamide (Z) b. P/H of Acute Viral Hepatitis
and Etahmbutol (E) are given for 2 months (Intensive c. Currentexcessivealcoholconsumption
Phase). This is followed by HR for4 months (Continu [Hepatotoxic reactions are more
ation Phase). Daily regimen during both phases is common].
optimal. However alternative regimen with dosing 3
B. Unstable or Advanced Liver disease I ALT
times per week is acceptable if administered via DOTS
� 3 times ULN following regimens used
(Directly Observed Therapy - Short Term).
a. Two Hepatotoxic drugs
In settings where the level of lsoniazoid resistance
among new TB cases is high and isoniazid susceptibil • 9 months HRE
ity testing is not done before the continuation phase 2 mths HRSE followed by 6 mths
begins, following regimen is given: Intensive Phase - 2 of HR.
HRZE and Continuation Phase 4 HRE. 6 • 9 mths of RZE.
Treatment of Extrapulmonary TB (EPTB) b. One Hepatotoxic drug
A. HIV Testing is important in patients with or 2 mths of HES followed by 10
suspected of having EPTB. months of HE.
8. EPTB is treated with same Regimen as for c. No Hepatotoxic drugs
Pulmonary TB except 18 - 24 mths of STM, ETB and
9· 12 monthsoffreatment for TB meningitis Fluoroquinolone.
(because of risk of severe disability and
3. Renal Failure and severe renal insufficiency:
mortality}.
Regimen - 2 mths of HRZE followed by 4
9 months of treatment for TB ofBones and
mths of HR [No dose adjustment of H&R
joints (because of difficulties in assessing required as they have biliary excretion.
treatment response). There is significant renal excretion of ETB
C. In TB meningitis Ethambutol should be replaced and metabolities ofPZA so dose adjustment
by streptomycin. is required].
Tretment Regimens in special population [STM avoided as there is increased risk of
l. Pregnancy and Breast Feeding ototoxicity).
A. With the exception of streptomycin, first Note : All patients receiving Isoniazide, should receive
line Anti TB drugs are safe [STM is ototoxic pyridoxine supplementation to prevent peripheral
to thefetusI neuropathy.
B. No contraindication for Breast feeding. Management of Previously Treated Patients
Should continue with full course of AKT. Previous TB treatment is a strong determinant of drug
C. After active TB in the baby is ruled out, resistance and previously treated patients comprise
baby should be given 6 months oflsoniazid 13% of the Global TB.
preventive therapy, followed by BCG Drug Resistant Tuberculosis is defined as a case of
vaccination. tuberculosis who are excreting bacilli resistant to one
D. P yr i d o x i n e s u p p l e m ent a t i o n i s or more anti-tubercular drugs.
recommended fo r all pregnant or breast Multidrug Resistant - TB (MDR - TB) is defined
feeding women taking isoniazid. as disease due to M. tuberculosis that is resistant to
2. Liver disorders Isoniazid and Rifampicin with or without resistance
A. Usual regimen can be given to following to other drugs.
patients provided that there is no clinical XDR -TB: MDR strains that are resistant to all fluo
evidence of chronic liver disease roquinolones and to atleast one of three second line
a. Hepatitis virus carriers injectable agents.
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PRACTICAL MEDICINE
Table 4.19 : Standard Regimens for 2. Ifsmear positive at month 3, obtain culture
Previously Treated Patients and DST.
Drug Sensitivity Likelihood of MDR 3. Smear or Culture positivity at the fifth
Testing month or later ( or detection ofMDR T B
Likelihood of MOR High (Failure) Medium or low at any point) is defined as treatment failure
(Relapse. Default) and necessitates re-registration and change
Conventional While awaiting DST Results: of treatment.
method C. New Pulmonary TB patients whose sputum smear
DSTAvailable EmpiricalMDR" 2HRZES/1 HRZE microscopy was negative at start of treatment.
Regimen. (Regimen /5 HRE (Regimen
modified once DST modified once 1. Recheck sputum smear at end of2 months
resu Its are avail- DST results are and if negative, no further sputum
able) available) monitoring is required.
DSTNotAvailable EmpiricalMDR. 2HRZES/1 HRZE 2. Clinical monitoring is more importnat -
Regimen / 5 H RE for full
course ofRx Body Weight is the most useful indicator.
(Regimen should be modified once D. Extra Pulmonary TB
DST results or DRS data are available) Clinical monitoring is more importnat - Body
*Emperital MOR Regimen :Refer Pg. 167 Weight is the most useful indicators.
Drug SensitivityTesting (DST): Rapid Molecular based Management of drug - induced hepatitis
methods with results available in 1-2 days to confirm /
H, R, Zcan all cause liver damage. Rifampicin can cause
exclude M DR-TB and guide choice ofre g imen
asymptomatic jaundice without evidence ofhepatitis.
Management depends on
Mono Resistance TB is defined as resistance to one
Anti-tuberculosis drug. a. Whether patient is in intensive or continuation
Poly Resistance TB is defined as resistance to more phase.
than one Anti tuberculous drug. b. Severity ofliver disease
Monitoring during treatment c. Severity ofTB
To Ensure cure, compliance. To monitor side effects d. Capacity of Health Care Unit to manage side
A. Sputum smear microscopy in New Sputum Positive effects.
Pulmonary TB patients: Treatment
1. For smear positive pulmonary TB patients l. All drugs should be stopped. Ifpatient is severly
treated with first line drugs, sputum ill, non-hepatotixc regimen of streptomycin,
smear microscopy may be performed at ethambutol and fluoroquinolone should be
completion ofintensi ve phase oftreatment. started.
2. Ifsmear -positive at month 2, {i.e. intensive 2. It is necessary to wait for LFT to revert to
phase) obtain sputum smear again at month normal and clinical symptoms to resolve before
3. If smear remains positive at month 3, re-introducing anti-TB drugs. Ifnot possible to
obtain culture and DST. perform LFT, advisable to wait for extra 2 weeks
3. Smear or Culture positivity at the fifth after resolution ofjaundice and upper abdominal
month or later ( or detection ofMDR - TB pain/ tenderness before restarting TB treatment.
at any point) is defined as treatment failure
3. If hepatotoxicity does not resolve, non
and necessitates re-registration and change
hepatotoxic regimen consisting of STM, ETB,
of treatment.
FQ given for 18-24 months.
B. Sputum smear microscopy in previously treated
patients. 4. 0 need rug induced hepatitis has resolved, drugs
1. Smear is obtained at end oflntensive Phase are reintroduced one at a time. If symptoms
i.e. at month 3. recur or liver function tests become abnormal as
166
( 4 > Respiratory System
the drugs are reintroduced, the last drug added Table 4.20 : Groups of Drugs to treat
should be stopped. It is advised to start with MOR-TB
Rifampicin because it is less likely than H or Z
Group Drug
to cause hepatotoxicity and is the most effective
agent. After 3-7 days H may be reintroduced. Group 1 Pyrazinamide (Z)
First Line Oral Agents Ethambutol (E)
5. Alternative regimen depending on drug Rifabutin (Rfb)
implicated:
Group2 Kanamycin (KM)
a. If 'R' is implicated : 2 months of SHE Injectable Agents Amikacin (AM)
followed by 10 months of HE. Capreomycin (CM)
b. Jf'H' is implicated: 6-9 months of RZE. Streptomycin (S)
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PRACTICAL MEDICINE
2. After conversion, bacteriological monitoring is treatment and develop new drugs that
recommended monthly for smears and quarterly target these specific genes.
for cultures. Factors influencing response to treatment
3. Monitoring by clinician should be at least 1. Adequate Chemotherapy
monthly until sputum conversion, then every 2. Regular Intake of Drugs (Compliance)
2-3 months.
3. Optimal Duration
4. Weight should be monitored monthly.
4. Severity Of Disease
5. Such large number of smear and culture for 5. Rest
follow up is not possible at least 5 smears and
6. Diet
cultures must be done at follow up (4, 6, 12, 18
and 24 months). 7. Nursing
6. X-ray should be done every 6 months. 8. Climate
Adjuvant Therapies for MDR - TB 9. Psychological Factors
III. Corticosteroids: Corticosteroids are useful
l. Surgery: Resection Surgery -indicated in patients
in tuberculosis because· they exert anti
who remain sputum positive, with resistance to
inflammatory, anti-allergic and anti-collagenous
large numberof drugs, and localised pulmonary
effects. Indications:
disease. Chemotherapy to be given 2 months
prior and continued 18-24 months post surgery. I. Tuberculous meningitis
2. Collapse therapy : Reversible surgical therapy 2. Miliary tuberculosis
which involves collapse of lung by artificial 3. Tuberculosis of adrenal glands with
pneumoperitoneum or pneumothorax used Addison's disease
for cavity containing diseased lung. 4. Tuberculosis ofserous sacs, ureter, fallopian
3. Laser therapy tubes.
a. Tried in some countries. 5. Drug hypersensitivity
b. Effective in multicavitatory disease with Corticosteroids are given in the dose of 40-60
heavy bacterial load. mg/day of prednisolone for 6-8 weeks, and
tapered over the next 2-3 weeks. They are to be
c. Thought to have a role in rapid killing given only under the cover of anti-tuberculous
of bacteria; increases and improves therapy, otherwise there may be flaring up of
penetration of Anti TB drugs in walled tuberculosis.
off lesions and helps in early closure of
cavities. It is of proven benefit in tracheal
4.
and endobronchial growth.
Immunotherapy and Immunomodulation.
10 > Chronic Obstructive
a. Use of Mycobacterium Vaccine.
Pulmonary Disease
b. Enchancing pro-inflammatory cytokines (COPD) (Emphysema
• IL2, IL 12, IFN-y, TNF-a., Inhibiting and Chronic Bronchitis)
anti-inflammatory cytokines IL-4, 5, I 0.
c. Use of Thalidomide, Transfer factor, Definition
Indomethacin, Levamisole. Emphysema is characterized by enlargement of the
d. Mycobacteriumw (lmmuvac) - has been airspaces distal to the terminal bronchioles, either
used in Leprosy. from dilatation or destruction of their walls.
5. Gene Therapy Chronic bronchi tis is dinically defined aschronic cough
with expectoration for three months for two consecu
To detect drug resistance before start of
tive years, with other known causes being ruled out.
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{ 4 ) Respiratory System
COPD is a common preventable and treatable disease, cigar, water pipe) and maijuana are
characterized by progressive airflow limitation associ also risk factor.
ated with an enhanced chronic inflammatory response c. Passive exposure to smoke - also
to noxious particles or gases. known as environmental tobacco
Exacerbations and comorbidities contribute to overall smoke.
severity on individual patients. d. Smoking during pregnancy affects
Mechanisms of Airflow Limitation in COPD: fetus by affecting lung growth and
Srnal I Airway disc,um l'arunchymal <lcslrucl ion development of immune system.
Airway innunmmlion Loss of alveolar auachmonts
Ainvay fibrosis. Lmnitml plugs Dt.."Crc.:1scd Elastic Recoil
e. Occupational exposures, including
I
Incrcasccl airway resistance organic and inorganic dust and
� Airflow Limilution __J chemical agents and fumes are
appreciated risk factors.
Prevalence f. Wood, Animal during, crop residues
and coal, typically burned in open
I. Higher in smokers than non smokers
fires or poorly functioning stoves or
2. Higher in those over age 40 heating in poorly ventilated dwelling
3. Higher in men than women. - important risk factor.
Risk factors influencing disease g. Outdoor air pollution - in urban areas.
development and prognosis Role is unclear, but is small compared
to smoking. Air pollution from fossil
A. Genetic predisposition : fuel combustion is associated with
l. a-1 Antitrypsin gene decrement in lung function.
2. MMP 12 gene 5. Socio economic status: Poverty is clearly a
3. a-nicotine ACh receptor risk factor but the components of poverty
that contribute to this are unclear. Risk is
4. Hedge Hog interactivity protein gene
inversely related to socioeconomic state.
B. Environmental factors 6. Asthma I Bronchial hyper reactivity :
1. Age: Ageing itselfis a risk factor for COPD. a. Asthma may be a risk factor but
2. Gender: In past prevalence was more in evidence is not conclusive.
men than women. But due to increase in b. Bronchial hyp er reactivity can
smoking in women prevalence rates are exist without clinical diagnosis of
now approaching equality. asthma and has been shown to be an
3. Lung growth and development important predictor of COPD as well
a. Any factor that affects lung growth as an indicator of increased risk of
during Gestation and childhood has decline in lung function in patients
potential for increasing individual with mild COPD.
risk for COPD. 7. Infection
b. Factorsin early life termed "Childhood a. Severe childhood respiratory infection
Disadvantage Factors" were as has been associated with reduced lung
important as heavy smoking is in function and increased respiratory
predicting in early adult life. symptoms in adulthood.
4. Exposure to Particles b. Susceptibility to infection plays an
a. Cigarette smoke important role in exacerbation of
COPD but effect on development of
b. Other types of tobacco (e.g. pipe, disease in less clear.
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{ 4 > Respiratory System
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PRACTICAL MEDICINE
However patient must stay indoors in foggy has concurrent OSA then there is a definite
weather and sleep with dosed windows. benefit.
G. Expectorants and mucolytic agents: A hot VII. LVRS (Lung Volume Reduction Surgery) is a
drink acts as a simple expectorant in surgical procedure in which parts of lungs
clearing the airways. Bromhexine has been are resected to reduce hyperinflation, making
found useful in liquefying sputum and respiratory muscles more effective by improving
aiding airway clearance. their mechanical efficiency (lengh / tension
H. Chest physiotherapy: Postural drainage relationship).
and proper breathing exercises, especially Increase elastic recoil pressure � improves
expiration, must be taught to the patient. expiratory flow rates and reduces exacerbation.
II. Long term management: It is more beneficial in predominant upper lobe
I. Quit smoking emphysema.
II. A. Bronchodilators VIII. Broncltoscopic LVR shows modest improvement:
Increase chances of pneumonia, hemoptysis,
1. � 2 agonists • Shortacting - Fenoterol,
COPD exacerbation
Salbutamol, levosalbutamol. Longacting :
Formoterol. Indacaterol, Salmeterol. IX. Lung Transplant
2. Anticholingergics - short acting Criteria-: any l
Ipratropium bromide oxitropium bromide. a. History of exacerbation - associated
Long acting : Tiotropium. with hypercapnia.
3. Methylxanthines (minimal role now) b. Pulmonary Hypertension or Cor
Aminophylline, Theophylline pulmonale, despite 02 Treatment.
B. Steroids c. FEV 1 < 20% predicted with DLCO <
20% with homogenous distribution
of emphysema.
Inhaled Systemic X. Bullectomy: in Bullous emphysema.
- Beclomethasone • Prednisolone
- Budesomide - Methylpruclnisole
- Fluticasone
11 Pneumonia
C. PDE - 4 inhibitors - Roflumilast
Definition: Pneumonia is inflammation of the pa
III. Pulmonary rehabilitation - exercise training renchyma of the lung.
IV. Vaccines - H influenza and pneumococcal
vaccine yearly. Etiology
V. Home 02 : > I 5 hr/ day, in patients with chronic l. Bacterial: Pneumococcus, Staphylococcus,
respiratory failure has shown to increase survival. Streptococcus, H. influenza, E. coli, Klebsiella,
Pseudomonas, etc.
Indication
2. Atypical: Viral, Rickettsial, Mycoplasmal.
L Pa0 2 < 55 mmHg or Sa02 < 88%.
3. Protozoa!: E. histolytica.
2. Pa0 2 <60 or Sa0 2 < 88% with evidence
of pulmonary HT, Peripheral edema
4. Fungal: Actinomycosis, As pergillosis,
Histoplasmosis, Nocardiosis.
suggestive ofcongestive cardiac failure and
polycythemia 5. Allergic: Loeffler's syndrome.
VI. Non-Invasive Ventillation (BiPAP): is useful in 6. Radiation
those with pronounced daytime hypercapnia. 7. Collagenosis: SLE, Rheumatoid arthritis,
Improves survival but not quality oflife. If patient Polyarteritis nodosa.
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( 4 > Respiratory System
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PRACTICAL MEDICINE
8. Signs of consolidation in the chest 2. It is more common in males.
9. Radiologically, hazy, relatively uniform 3. Febrile flu like illness with URTI for about
density 5 days is followed by cough, mucopurulent
B. Staphylococcal sputum and sometimes hemoptysis.
1. It commonly occurs during epidemics of 4. X-ray: Bilateral patchy involvement with
influenza. pleural effusion.
2. Pneumonia can be very severe. lt may be G. Mycoplasma
fatal within a few hours.
l. It affects children of 5 15 years age.
3. Abscesses, looking like a thin walled cyst
2. There is mild fever with coryza.
on X-ray are common. ln children these
may rupture to form pyopneumothorax. 3. X-ray shows patchy infiltration.
C. Klebsiella 4. IgM c old agglutinin by ELISA or
1. This is common in middle aged or elderly complement fixation test may be detected
alcoholics. during first week of infection and up to 2-4
2. lt commonly involves the upper lobes or weeks.
more than one lobe. Treatment
3. There is a strong tendency to abscess
formation. A. General Measures
4. Sputum is viscid, jelly-like, blood stained, l. Position should be most comfortable.
rusty or purulent. 2. Diet: Initially light diet. With improvement
5. It may clear up with or without residual the patient may gradually return to full diet.
fibrosis or may end fatally. 3. Fluids: Copious fluid intake is advised
D. Gram-negative bacilli (H influenza, E. coli, as patient loses fluid from sweating and
Coliform bacilli, Proteus and Pseudomonas overbreathing.
aeruginosa). 8. Chemotherapy
It arises mainly in hospitals in patients receiving l. Pneumococci: Procaine penicillin 8 lakh
corticosteroids or immunosuppressive drugs, l.M. daily or Ampicillin or Tetracycline
those with tracheostomy, urinary tract infections 0.5 gm 8 hourly orally.
or debilitating disease. 2. Staphylococci: Crystallinepenicillin 10 lakh
E. Viral IM 6 hourly or Cloxacillin 0.5 gm 6 hourly
1. The presenting symptoms are headache, orally.
general aches, prostration and fever. 3. Klebsie/la: Chloramphenicol 0.5 gm 6 hourly
2. There may be no respiratory symptom orally or Ciprofloxacin 500 mg 8 hourly
or sign and it is often discovered when a orally or Cefotaxime 1 gm IV 6 hourly.
routine X-ray of the chest is taken. 4. E.coli, Proteus, Pseudomonas: Carbenicillin
3. Paroxysmal cough and mucoid sputum 100-300 mg/kg/day in an IV drip or
may be present. Gentamicin 80 mg IM 8 hourly or IV
4. Localized diminished breath sounds and Ciprofloxacin 200 mg 12 hourly or IV
scattered rates may be present. Ceftazidime 1 gm 6 hrly.
F. Legionella 5. H. influenza: Crystalline penicillin 10 lakh
1. Legionella isa small aerobic, gram-negative units I.M. 6 hourly with Streptomycin 0.5
coccobacillus. Infection is acquired gm IM twice a day.
through water shower and air-conditioning 6. Legionella
system. I. Erythromycin 1 gm 8 hourly IV for
174
( 4 ) Respiratory System
13 wks followed by 500 mg qds for 2 B. Reduced resistance or local predisposing cause:
wks. Chronic bronchitis, hypogammaglobulinemia,
2. Doxycycline IOOmg twicea day orally myelomatosis, lupus
for 3 weeks. C. Recurrent aspiration: Achalasia cardia, pharyngeal
3. Rifampici n 600 mg twice a day orally pouch, bronchial tumour or bronchiectasis
for 3 weeks.
Other drugs are Ciprofloxacin and Co Unresolved Pneumonia
trimoxazole. In Legionella endocarditis, I. Staphylococci, Klebsiella or Tuberculosis
the treatment with antibiotics has to be
2. Neoplasm
continued for 3-12 months.
Symptomatic: For pain, cough etc. 3. Elderly
C.
D. Convalescence 4. Uncontrolled diabetics
1. Once the fever subsides, the patient may
12 > Bronchiectasis
sit up in the chair.
2. Breathing exercises must begin as soon as
possible to clear the lungs of inflammatory
DEFINITION: Bronchiectasis is an abnormal and
products .
permanent dilatation of one or more bronchi that
Complications involves lung in either a Focal or Diffuse Manner. It
1. Herpes labialis has classically has been characterized as Cylindrical,
Tubular (most common), Varicose or Cystic.
2. Pleural effusion and empyema
3. Lung abscess Epidemiology
4. Pneumothorax l. Varies according to etiology: e.g.
5. Pericarditis, endocarditis a. Cystic fibrosis (CF) patients� clinically
6. Peritonitis significant bronchiectasis present in late
7. Meningitis adolescence or early adulthood.
8. Septic arthritis b. Bronchiectasis� Classically affects Non
9. Peripheral thrombophlebitis smoking patients, women older than 50
years of age.
10. Jaundice
2. In General
11. Uremia
a. Incidence increases with age
12. Circulatory failure
b. More common in women than men.
Prognosis
Pathogenesis
The following factors make the prognosis poor:
A. Visious Cycle
I. Staphylococcal, Klebsiellaortype3pneumococcal Susceptibility to
pneumonia
Poor Mucodliary
I'
e.g. Im:1��:�:�cfon1y
dcaram:o
2. Very young or very old people
Single severt!
3. Very high or very low WBC count Inreclion .g. cystic fibrosis
c g B J'crtusis
4.
1
Positive blood culture
5. Jaundice Damaged Airways. Mir.robial coloni1
..1tion]
Poor Secretion ----+ of Bronchial Trt..>c
Recurrent Pneumonia Clearance
!
Conlinucll Chronic;
Inllammalion
(Two or more attacks within a few weeks)
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PRACTICAL MEDICINE
I.Focal 1. Obstruction (e.g. Aspirated foreign body; a. Chest Imaging (CXR &/or HRCT)
Tumors· Endobronchial, Carcinoids, Lymph b. Bronchoscopy
nodes; Impacted Secretion) c. Induced sputum for AFB.
176
( 4 ) Respiratory System
accumulation ofsecretions, secondary infection Investigations
and further weakening of the bronchial wall
which is pulled apart due to negative pressure (Also see Table 4.23)
and this results in permanent dilatation of the 1. Hemogram will show neutrophilic leucocytosis
bronchi. during the acute infective phase.
2. ESR is raised.
Types
3. Sputum will be thick and purulent with plenty of
I. Saccular or cystic: affects major or proximal pus cells. The infective organism may be grown
bronchi that end in large sacs by the fourth on culture.
generation of branching
4. CXR
II. Cylindrical or fusiform: affects sixth to eighth
generation of bronchi, probably less severe, a. May be normal with mild disease.
clinically "dry" b. Saccular type- prominent cystic spaces with
III. Varicose: intermediate between saccular and or without air fluid levels corresponding to
cylindrical dilated airways.
Clinical Features c. Tram Tract appearance in longitudianl
section & ring shadows in cross section
Symptoms due to thickened and dilated airways.
1. Persistent productive cough with ongoing thick, d. Opaque tubular or Branched Tubular
tenacious sputum production/ purulent sputum. Structure - due to dilated airways filled
2. Hemoptysis (40-70%) - due to bleeding from with secretion.
friable, inflammed airway mucosa; massive 5. HRCT : Modality of choice
hemoptysis often due to bleeding from 1. Tram Track sign • due to airway dilatation
hypertrophied bronchial artery. and thickening.
3. Bronchiectasis sicca - Patients are either
2. Signet Ring Sign - a cross sectional area
asymptomatic or have a non productive cough
associated with Dry Bronchiectsis ofupper lobe. of the airway with a diameter of 1.5 times
that of adjacent vessel.
4. Dyspnoea & wheezing - Reflects widespread
parenchymal destruction or COPD. 3. Lack of Bronchial Tapering � including
5. Systemic symptoms - fatigue, wieght loss, presence of tubular structures within 1 cm
myalgias. from pleural surface.
6. Acute Exacerbation - (a) amount of sputum 4. Tree in Bud appearance� dilated airways
increases; (b) sputum becomes more purulent + thickened walls & inspirated secretions.
and often more bloody; (c) systemic symptoms 5. Cysts emanting from Bronchial wall
like fever may be more prominent. � especially pronounced in cystic
bronchiectasis.
Signs
Treatment : Major goals : Treat infection, decrease
1. Combination of crackles, Ronchi, wheeze· reflect inflammation, clear airway, Treat cause.
damaged airways contaning secretion.
I. Antibiotics : based on culture and gram stain.
2. Clubbing and cyanosis is the classical diagnostic
Empirical • Amoxicillin, Trimethoprim •
finding is the presence of coarse leathery rales
Sulphamethoxazole, levoflox. Pseudomonas
especially at the base of the lungs posteriorly.
: oral quinolone or iv - aminoglycoside,
3. Wheezing may be present due to associated carbapenem, 3rd generation cephalosporin.
asthma or bronchospasm.
Treatment for 10-14 days. Long term treatment
4. Advanced Disease with Chronic Hyp oxemia -
is for recurrent / persistent infections
patients may develop cor pulmonale and right
heart failure.
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PRACTICAL MEDICINE
E
A D
D
B
C
Bronchicc1asis-Plain x-ray Bronchiccta.is-U RCT
A-Air-fluid level
B-Cyslic.
C-Tubular.
D-Saccular
Bronchicctasis
D E-Bronchial cu1-off
due lo mucoid
B impaction
C
Bronchicctasis-Bronchogmphy
178
( 4 ) Respiratory System
C. Fungi: Histoplasma capsulatum, Coccidiodes 3. Dulln ess on percussion & few coarse
immitis, Aspergillus crepitations during early phase
D. Parasites: Amebas, lung flukes 4. Signs of cavity or local consolidation may occur
when pus is expectorated out
II. Pulmonary Infarction
5. Signs of pleural effusion may mask other signs
A. Pulmonary thromboembolism
B. Septic embolism (Staphylococcus aureus, Investigations
anaerobes, Candida) l. CBC: Polymorphonuclear leucocytes
C. Wegener's granulomatosis 2. Sputum: Pus cells, causative organisms on
III. Neoplasm staining and culture.
A. Metastatic malignancies (very common) 3. Chest X-ray: Large homogenous opacity or
B. Bronchogenic carcinoma a cavity showing a fluid level may be seen.
Associated involvement of pleura may be noted
C. Lymphomas by obliteration of CP angle.
III. Others 4. Fiberopt i c bronchoscopy: to rule out
A. Infected cysts and bullae bronchogenic cause of lung abscess
B. Silicosis 5. CT Scan if necessary
C. Coal miner's pneumoconiosis Complications
Pathophysiology 1. Dry pleurisy
Lung abscess is more common in the right lung. It is a 2. Empyema
solid yellow mass of inflammatory tissue surrounded by 3. Pneumothorax
necrotic wall. As the disease progresses, the solid mass 4. Brain abscess
may be transformed to liquid pus. Microscopic-ally it 5. Hemoptysis
consists of dense infiltration of polymorpho-nuclear
leucocytes. Alveolar walls are destroyed. Treatment
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PRACTICAL MEDICINE
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PRACTICAL MEDICINE
size after 36 months of observation, the need of the needle is more reliable. Percutaneou s
for further CT monitoring is determined on a needle aspiration obtains material for cytology,
case-by-case basis. For patients who are suitable but does not biopsy a core of tissue. As a result,
candidates for surgical resection and have a single it is more helpful for confirming malignancy
GG nodule that is> 10 to 15 mm in diameter and than establishing a specific benign diagnosis
persists for >3 months, we typically offer the Percutaneous needle aspiration may be
option of surgical resection, as some patients complicated by pneumothorax, which can be
prefer resection to the anxiety associated with clinically significant in patients with coexisting
ongoing monitoring. emphysema. Bleeding is a less frequent
3. A part-solid nodule with a solid component <5 complication.
mm is followed by serial CT scans at 12, 24, and 3. Percutaneous needle biopsy -. In this
36 months. If the solid component is �5 mm, procedure, a core of tissue is obtained using a
then the nodule is biopsied or resected. cutting needle. Up to 97 percent of patients with
FDG-PET - 18-fluorodeoxyglucose positron a malignant or benign lung nodule will obtain a
emission tomography (FOG PET) can help distinguish definitive diagnosis using this procedure .
malignant and benign lesions because cancers are 4. Surgical resection -Excision can be performed
metabolically active and take up FOG avidly. It is by thoracotomy or thoracoscopy (also called
indicated for patients with a solid or part-solid SPN that video assisted thoracic surgery 'or VATS) if the
is8 to 10 mm or greater in size and has an intermediate lesion is located close enough to pleural surface
probability of malignancy, especially if the patient has to allow VATS resection.
increased surgical risk.
182
( 4 ) Respiratory System
184
< 4 > Respiratory System
> Hepatopulmonary
mixed venous oxygen content difference.
16 Pulmonary findings
Syndrome l. Dyspnea may be accompanied by pulmonary
Hepatopulmonary syndrome is considered present findings that are more specific for HPS:
when the following triad exists:
a. Platypnea - Platypnea is an increase
Liver disease in dyspnea that is induced by moving
• Impaired oxygenation-Orthodeoxia into an upright position and relieved by
• Intrapulmonaryvascular abnormalities, referred recumbency.
to as intrapulmonary vascular dilatations b. Orthodeoxia - Orthodeoxia refers to a
(IPVDs) decrease in the arterial oxygen tension (by
The unique pathological feature 5>fhepatopulmonary more than 4 mmHg [0.5 kPal) or arterial
syndrome is gross dilatation of the pulmonaryprecapil oxyhemoglobin desaturation (by more than
lary and capillary vessels, as well as an absolute increase 5 percent) when the patient moves from
in the number of dilated vessels. A few pleural and a supine to an upright position, which is
pulmonary arteriovenous shunts and portopulmonary improved by returning to the recumbent
anastomoses may also be seen. position. The presence of orthodeoxia
in a patient with liver disease is strongly
Causes
suggestive(present in 88% patients) of H PS,
Hepatopulmonary syndrome (HPS) is a complication although it can be seen in other situations
of liver disease. (eg, post-pneumonectomy, recurrent
1. It is most commonly associated with portal pulmonary emboli, atrial septa! defects,
hypertension (with or without cirrhosis), and chronic lung diseaset
although chronic liver disease of virtually any It is hypothesized that platypnea and orthodeoxia
etiology can be associated with HPS. in HPS are caused by preferential perfusion of
2. Also some acute liver diseases are associated eg. IPVDs in the lung bases when the patient is
ischemic hepatitis. upright.
No specific type of liver disease, severity of liver disease, l.. Hypoxemia - Severe hypoxemia (PaO ?
or laboratory abnormality predicts HPS. <60 mmHg) in the absence of coexisting
185
PRACTICAL MEDICINE
186
( 4 > Respiratory System
187
1 > Proforma G. Hemoptysis
H. Hematuria
History I. Hemiplegia
I. Cardinal Symptoms J. Phlebothrombosis
A. Dyspnea on exertion or Breathlessness - V. Symptoms Suggesting Congenital Heart Disease
including paroxysmal nocturnal dyspnea, A. Cyanotic spells
orthopnea, platypnea and trepopnea B. Squatting episodes
B. Chest Pain VI. Pressure Symptoms (Due to Enlarged Left Atrium
C. Cough or Aneurysm of Aorta)
D. Expectoration A. Hoarseness of voice (pressure on the
E. Hemoptysis recurrent lar yngeal nerve), Ortner's
syndrome
F. Palpitation
B. Dysphagia (pressure on esophagus)
G. Syncopal attacks
IL VII. Miscellaneous
Symptoms of Congestive Cardiac Failure (CCF)
A. Family History: Hypertension, diabetes,
A. Exertional breathlessness
coronary artery disease, hyperlipidemia,
B. Edema of feet, puffiness of face, anasarca
congenital heart disease, cardiomyopathies
C. Distension of abdomen and pain in B. Past History of hypertension, diabetes.
right hypochondrium, anorexia, nausea, coronary artery disease, hyperlipidemia,
vomiting
obesity, recurrent lower respiratory
III. Symptoms of Rheumatic Heart Disease (RHD) infection, tuberculosis, syphilis, STD, HIV
A. Fever with sore throat infection,
B. Fleeting joint pains and swelling C. History of hospitalization
C. Involuntary movements (chorea) 1. Number of admissions
D. Nodules under the skin (rheumatic 2. Duration of each admission
nodules) 3. Investig ations done e.g. ECG,
IV. Symptoms ofInfective Endocarditis (SBE) X-ray, Echocardiography, cardiac
A. Pyrexia catheterization
B. Petechial hemorrhages 4. Diagnosis reached, if known
C. Pads of finger are tender (Osler nodes) 5. Drugs given e.g. diuretics, digitalis.
D. Palpable spleen 6. Relief obtained or not
E. Phalangeal dubbing 7. Advised surgery/intervention or not
F. Prolonged treatment with high doses of D. History of cardiac surgery, angioplasty or
penicillin valvuloplasty
( 5 ) Cardiovascular System
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PRACTICAL MEDICINE
190
< 5 ) Cardiovascular System
JV. Dilated Veins Over the Chest Wall systole. It is seen in LV volume overload or
Dilated veins over the chest wall may be present diastolic overload eg.
in the following conditions: (a) aortic regurgitation; (b) mitral
1. Intrathoracic obstruction regurgitation; (c) high output states; (d)
2. Superior and inferior venacava obstruction patent ductus arterosis, VSD; (e) A.V.
fistulas; (f) Thin chest wall.
3. Right sided heart failure
3. Heaving Apex: Is exaggerated in aplitude
V. Scars and Sinuses: Scars of previous cardiac
and lasts for more than 2/3rd of systole. It
surgery may be present (e.g. horizontal
is well sustained. It is seen in LV pressure
lateral thoracotomy scar for closed mitral
overload or systolic overload e.g. (a) aortic
commissurotomy. repair of coarctation of aorta,
stenosis, (b) HOCM, (c) Coarctation of
B.T. Shunt Surgery, or ligation of PDA; vertical
Aorta, (d) Systemic hypertension.
midline sternotomy scar of coronar y artery
bypass, open mitral commissurotomy or valve 4. Double Apical Impulse : Felt in (a) LV
replacement). Sinuses were commonly seen in Aneurysm; (b) Hypertrophic obstructive
the past due to tuberculosis of spine. cardiomyopathy; (c) LBBB
5. Diffuse Apex : is > 3 cm in diameter
B : Palpation or occupies more than one intercostal
J. Apex Beat space. (a) LV Aneurysm; (b) Severe LV
Dysfunction; (c) LV Dilatation, e.g. Aortic
Apexbeat is the lower most and outer most point
Regurgitation.
where maximum cardiac impulse is felt. It gives
a gentle thrust to the palpating finger. 6. Triple or Quadruple Impulse felt in HOCM.
Normally, it is located in the fifth left intercostal 7. Retractile Impulse: is systolic retraction or
space within the mid-clavicular line. It is indrawing of the apical impulse. It is called
normally confined to one intercostal space or Broadbents Sign. It is seen in Constrictive
less than 2.5 cm in diameter. It lasts for less than Pericarditis.
50% of systole. 8. Absent Apex Beat on the Left Side:
Abnormalities of Apex Beat Non cardiac causes (a) obesity, thick chest
1. Tapping Apex : is the palpable first heart wall; (b) Emphysema; (c) Left pleural
sound felt in mitral stenosis due to loud effusion with shift of heart to the right.
S 1 and right ventricular enlargement. It is Cardiac causes : (a) Dextrocardiac;
a short and sharp systolic tap. (b) Pericardia! Effusion; (c) Dilated
2. Hyperdynamic Apex : Is exaggerated in cardiomyopathy; (d) LV Dysfunction e.g.
amplitude and lasts for less than 2/3rd of : Coronary Artery Disease.
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PRACTICAL MEDICINE
C: Percussion
Percussion is mainly done to determine the boundaries
of the heart. Percussion of the cardiac dullness has its
limitations because fallacious results may be obtained
Ill. Diastolic Shock due to greater part of the heart being surrounded by
This is the palpable second heart sound. Either the resonant lung. The roots of the great vessels at the
the pulmonary or the aortic component may base of the heart produce a dull note that cannot be
be palpable. A loud P 2 suggests pulmonary distinguished from cardiac dullness.
hypertension, whereas a loud A 1 suggests However, percussion is useful to detect pericardia!
systemic hypertension or aortitis. effusion, aortic aneurysm, etc. rather than the size of
IV. Thrills the heart. Normally the right, left and upper borders
are percussed. The lower border of the heart cannot
Thrills are palpable vibrations (like the purring
be percussed because it cannot be distinguished from
of a cat that is felt by the hand) associated with
liver dullness.
heart murmurs. They are best felt with the palm
of the hand. It is intensified if the chest wall is I. Left Border: The patient must be percussed in the
thin, site of production is near the surface of the fourth and fifth space in the mid-axillary region
chest wall and the blood flow is rapid. and then medially towards the left border of the
heart. The resonant note of the lung becomes
Presence of a thrill is a definite evidence of the
dull. Normally the left border is along the apex
presence of an organic disease of the heart. They
beat. If it is outside the apex beat, it suggests
may be systolic (AS, PS, MR, TR, ASD, VSD,
pericardia! effusion.
PDA), diastolic (MS, TS, AR) or continuous
( PDA, rupture of sinus ofValsalva aneurysm, AV 11. Upper border: The patient must be percussed
192
( 5 ) Cardiovascular System
in the second and third left intercostal spaces in Ill. Other Sounds (opening snap, clicks, pericardia!
the parasternal line, which is the line between rub, pericardia! knock, tumour plop).
the mid-clavicular and the lateral sternal line.
Normally there is resonant note in the second I. Heart Sounds
space and dull note in the third space. If there Normally there are four heart sounds recorded pho
is a dull note in the second space it suggests: nocardiographically but clinically in majority of the
1. Pericardia! effusion cases only two heart sounds are usually audible. The
2. Aneurysm of aorta heart sounds are auscultated in all the four areas of
the chest, namely the mitral, tricuspid, pulmonary
3. Pulmonary hypertension
and aortic areas (see Table). The first heart sound is
4. Left atrial enlargement best appreciated in the mitral area whilst the second
5. Mediastinal mass heart sound is best appreciated in the aortic and
III. Right border: lhe patient must be percussed pulmonary areas.
anteriorly in the mid-clavicular line on the right Normally the first heart sound is single because the
side until the liver dullness is percussed. Then tricuspid and mitral components occur simultaneously.
the percussion is done one space higher from The second heart sound is normally split, because the
the mid-clavicular line medially to the sternal
border. Normally the right border of the heart S S S2 S3
•l'----1---...•-
4 1
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PRACTICAL MEDICINE
aortic valve doses earlier than the pulmonary valve. output, e.g. thyrotoxicosis, anemia,
This split of the second heart sound is best appreciated beriberi, A· V fistula.
in the pulmonary area. E. Increased A-V flow from left to right shunt,
e.g. PDA, ASD, VSD.
First Heart Sound (S 1 )
F. Short P-R interval
It is produced by the closure of the mitral and tricuspid
II. Soft First Heart Sound:
valves (M 1 & T 1 respectively). Normally the mitral
valve closes before the tricuspid valve by 20-30 msec. A. Poor conduction of sound through chest
Hence S 1 is appreciated as a single sound. wall
It is a high frequency sound heard best with the dia l. Pericardia! effusion
phragm of the stethoscope. 2. Emphysema
It is timed with simultaneous palpation of the carotid 3. Thick chest wall
pulse. S 1 indicates the onset of systole 4. Obesity
Abnormal First Heart Sound B. Rigidity and calcification of A-V valve e.g.
I. Loud mitral stenosis with calcified valves
II. Soft C. Mitra! and tricuspid regurgitation
III. Variable D. Prolonged P-R interval
IV. Widely Split E. Acute Ml, LV aneurysm, cardiomyopathy
V. Reverse Split III. Variable First Heart Sound
I. Loud First Sound: A. Atrial Fibrillation
Due to increased excursion of the AV valves B. Complete Heart Block
leaflets away from each other during their C. A.V. Dissociation
opening, there is a loud sound when they close
IV. Widely split first heart sound:
(similar to a door which when open to a wider
angle, closes with a louder sound). Splitting of the first heart sound occurs when
the Tricuspid valve closes late as compared to
A. Normal in children
Mitra! Valve.
B. Sinus tachycardia
In RBBB or VPC originating from LV, the LV
C. Prolonged A-V filling due to A-V stenosis systole starts first resulting in MV closing earlier.
e.g. mitral stenosis, tricuspid stenosis This is followed by RV systole which results in a
D. Increased A-V flow from high cardiac late TV closure, thus causing a split S 1 (M,-T).
194
( 5 ) Cardiovascular System
A. Electrical 2. VPC, originating from RV
1. RBBB 3. RV Pacing
2. VPCs originating from LV 4. Idioventricular Rhythms originating
3. LV Pacing from RV
4. Idioventricular rhythms from LV B. Mechanical :
B. Mechanical 1. Severe MS
1. TS 2. Left Atrial Myxoma
2. Right Atrial Myxoma Splitting is best heard in the Lower Left Sternal
Border. If it is heard well at the apex, it should
3. Ebsteins Anomaly (Sail Sound)
be differentiated from a S4 preceeding S 1 or a
V. Reverse Splitting of First Heart Sound: ejection click following S1 •
It means when M1 occurs later than T 1 •
Second Heart Sound (52 )
A. Electrical :
l. LBBB It is normally has two components, produced by clo
L
sure of the aortic valve (A) and pulmonary valve (P /
I
Normally, it is a high frequency sound, heard better
II
in the aortic and pulmonary area.
NonM.1
It is normally split because the aortic valve closes before
the pulmonary valve. The A1 is normally louder than
,.,r,
11
s, s,
P2• During inspiration, the splitting of A2 P2 becomes
11
wider. During expiration the splitting of A2P2 is nar
Split
s, rower and S1 may be heard as a single sound.
M, T 1 A, P, MT, The opposite occurs during expiration leading to Nar
row Expiratory Split of S 2•
11
s.-s,
--
II
Abnormal Splitting of S 2
s, s, 11,I', I. Widely Split Second Heart Sound
S 1 -Ejection
A. Electrical
Click
s, Click
II
A,1\ S, Click
1. RBBB
2. Left VPB
F1g.S 7 First Heart Sound 3. LV Pacing
- -----
- ----- ----------- -�
Inspiration
l
Fall in Intrathoracic Pressure Increased Capacitance of Pulmonary Vascular Bed
-I- ,I.
Increase in Venous Return to the Right Ventricle Pooling of Blood in Pulmonary Vasculature
+
Increase RV Stroke Volume & RV Ejection Time Reduced Venous Return to the Left Atrium &
(time to ejects the volume of blood in RV) Left Ventricle
+ +
Decreased LV Stroke Volume & LV Ejection Time
Delayed Closure of Pulmonary Valve
,I.
Delayed P2 Early closure of Aortic Valve
!
rn--------------Early A,
195
PRACTICAL MEDICINE
return to Right atrium but the left to right II. Reverse Splitting of Second Heart Sound
shunt across the ASD leads to increased RV A single S2 during inspiration and split S2 during
filling, RV stroke volume and RV ejection time. expiration is called Reverse Split ofS2 • It occurs
This minimises respiratory variation of the RV sinee pulmonary valve closes earlier than Aortic
volumes and leads to a wide and fixed split S2• Valve. It occurs due to early closure ofPulmonary
Another mechanism of wide and fixed split S 2 Valve (early P.) or delayed closure ofaortic valve
is related to pulmonary hangout interval. In (late A/
ASD, there is increased pulmonary blood flow A. Electrical
due to increased volume of blood in RV due
I. LBBB
to left to right shunt. This leads to increased
capacitance of pulmonary vascular bed, during 2. Right VPB
both phases ofrespiration (normally, an increase 3. RV Pacing
in capacitance ofpulmonary vascular bed occurs 4. WPW syndrome
during inspiration). B. Mechanical
The pulmonary valve is expected to close when I. Aortic Stenosis
the pressure in the RV falls below the pressure 2. HOCM
in the pulmonary artery. However, in reality the
3. Hypertension
pulmonary valve closes later ( the PV closes at
the level of the incisura of the pulmonary artery 4. Coarctation of Aorta
tracing). The hangout interval is measured from 5. LargePDA
the incisura on the pulmonary artery tracing 6. LV Failure
(PV closes) to the same level of the RV pressure III. Single Second Heart Sound
tracing (Figure 5.9).
A. Diminished Intensity of A 1 or P1:
This hangout interval is determined by
1. AS
pulmonary capacitance and RV ejection time.
2. PS
196
< 5 ) Cardiovascular System
.. ii. Pulmonary Artery Dilatation
Ai
Normal
I
A, P, iii. A.S.D.
s,
II
Si s,
r
s:
2. Soft P2 : May be perceived as a single S:
Inspiration Expiration i. Pulmonary stenosis
Wido
Split A2 P, A PJ
ii. Tetrology of Fallot
I, s I
s, iii. Thick Chest Wall, COPD, Obesity
s, 3. Loud A1
s, z s!
Inspiration Expiration i. Systemic Hypertension
Wide
J
Fixed ii. Aortic Aneurysm
Split A, P, A, p t
s,
I s.I I
iii. Aortitis (Syphillitic aortitis produces
"Tambour quality of A2)
s, s, S2
Inspiration Expiration
iv. Hyperkinetic circulatory states
Reverse 4. Soft A1 : May be perceived as a single S1
I I
Split
s, i. Aortic stenosis
p� A� P, A,
II
ii. Aortic Regurgitation
s,
I]s s, s, Third Heart Sound (S3)
�
Inspiration Expiralion
1 Single Normally only two heart sounds are audible. The third
I s1
I
heart sound is heard in the following conditions:
s, s, s,
II
s1
l. Normal up to 30 years and in children, atheletes
and pregnancy
(Diminished Intensity (A, Syncronous 2. MR
0£ A, or Pi) withP) 3. TR
Fig 5 l D Second Heart Sound
4. CCF
5. Myocardial infarction
Normally Ai -P, Interval
6. ASD, VSD, PDA
During Inspiration: 40-50 msec
During Expiration : <30 msec 7. High output state
3. Pulmonary Atresia 8. Dilated cardiomyopathy
4. Tetrology of Fallot Mechanism:
B. P1 synchronous with A! Normally the third heart sound is a low frequency
1. VSD sound, heard because of the first rapid filling phase
3. Single ventricle of the ventricular diastole when blood flows from the
C. Concealed bysystolic murmur I Continuous atria into the ventricles.
Murmur In MR and TR during systole some blood goes
back into the atria and hence there is increased
D. Others : Trunous Arteriosis
flow into the ventricles during the first rapid
IV. Narrowly Split S 1: Pulmonary hypertension filling phase resulting in the third heart sound.
Abnormality of Intensity of S2 • In heart failure there is increased atrial pressure
1. Loud P2: P2 is called loud if it is louder than the and hence increased first rapid filling results in
A2• It is loud in the third heart sound.
i. Pulmonary Hypertension
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PRACTICAL MEDICINE
It is important to note that in significant mitral stenosis Quadruple Rhythm: 4 audible heart sounds S1 + S 1
the third heart sound is never heard because rapid + S3 + S4
filling of the ventricles is not possible because of a Summation Gallop : S3 & S4 are merged due to tachy
stenosed A-V valve. cardia S 1 + S2 + (S 3 & S 4)
Factors that prevent detection of third heart sound
are environmental noise, emphysema, obesity, failure Palpable HeartSounds
to apply the bell properly and examining the patient in I. Palpable S2(P2) (Diastolic shock): denotes
sitting position. It disappears on standing up. A latent pulmonary hypertension
third heart sound can be made audible by rolling the II. Palpable SI: Tapping' apex beat ofmitral stenosis
patient onto the bed from sitting position to lying
position or by passive straight leg raising. III. Palpable S4: 'Double' apex beat (HOCM), severe
aortic stenosis
If the heart rate is over 100 beats/min, discrimination
of third or fourth heart sound is not possible and the II. Murmurs
triple rhythm (gallop) is called summation gallop.
Murmurs are abnormal heart sounds caused by vi
Right ventricular third heart sound is located at the bration of the valves or the wall of the heart or great
left lower sternal border rather than the apex and often vessels. Murmurs may be systolic (ifit is between first
increases on inspiration. It may radiate to right supra and second heart sound) or diastolic (if between the
clavicular fossa. It is commonly seen in cor pulmonale. second and first heart ·sound) or continuous. Levine
Table 5.3 : Third Heart Sound grades systolic murmurs as follows:
Right Left Ventricular 53 Table 5.4 : Grading of Systolic Murmurs
Ventricular S,
Grade I : Very faint murmur only audible with effort
Site Tricusped Area Mitral Area (Apex)
Grade II : Faint murmur but clearly and definitely audible
Best heard in Supine Left lateral
position Grade Ill : Moderately loud murmur but no thrill
Increase with Inspiration Expiration Grade IV : Loud murmur with thrill
respiration
Grade V : Louder with thrill and can be heard with stetho
Change with iso- No change Increases scope halflifted off chest wall
metric hand grip
Grade VI : Murmur with thrill heard even if stethoscope is
Fourth Heart Sound {54) just lifted up from the chest wal I.
It is a low frequency sound. It occurs due to rapid emp Diastolic murmurs have only Grades I to IV.
tying of atrium into a non-compliant ventricle in late Factors for production of murmurs.
rapid filling phase due to atrial contraction; heard best 1. Flow of blood through an abnormal orifice. e.g.
with the bell ofa stethoscope. Normally it is inaudible.
in mitral stenosis or regurgitation.
It is heard in the following conditions:
2. High velocity flow through a normal orifice. e.g.
1. Elderly> 60 years.
in anemia, hyperkinetic states.
2. Myocardial infarction,LV failure (summation
gallop, quadruple rhythm S 1 - S2 - S3 - S4) Innocent Murmurs
3. AS,HOCM Soft systolic murmurs heard in patients without any
4. PS cardiac abnormality are called Innocent murmurs.
5. Pulmonary or systemic hypertension
Characteristics
6. MR,AR, TR
7. Hyp erkinetic states 1. More commonly heard in children (Still's
murmur)
Gallops
2. Usually heard in the pulmonary area
Triple Rhythm: 3 audible heart sounds - S 1 + S2 + S3 / $4
198
{ 5 > Cardiovascular System
I I
7. Soft, short and blowing in nature 6. P.S.
8. Heart sounds are normal ESM
IAm�I I
9. Usually localized
Differential Diagnosis
I. Pulmonary ejection murmur s, Click A, pt s,
2. Vibratory murmur Fig 5.12 Latesystol1cmurmurofMVP
I
2. Tricuspid Regurgitation (TR)
Organic Murmurs 3. VSD
I
5. AR (Functional) 5. High output state
pulmonary hyp ertension
6. Aneurysm 6. P.R.(Functional)
ESM
s,
II
A, P, s,
199
PRACTICAL MEDICINE
200
( 5 > Cardiovascular System
The interval between the onset of the due to excessive ejection of blood from the
second heart sound and the opening snap ventricles into the blood vessels
(A2-0S interval) is a good guide to judge J. Pulmonary Ejection Click
the severity of mitral stenosis. The shorter
This is best heard during expiration.
the A2-OS interval, the more severe the
It is the only right-sided event, which
mitral stenosis.
is increased on expiration.
Table 5.6: Differences between Opening
Snap and Split Second Sound Causes
Opening Snap Split Second a. Dilatation of pulmonary artery
(A2-0S) Sound (A2-P2) b. Pulmonary stenosis
1. Interval between Longer-0.04- Shorter- 0.04 • c. Pulmonary hypertension
the two sounds 0.12sec 0.05sec
2. Aortic Ejection Click
2. Area Heard just inside Second and third
the apex lntercostal space This is transmitted to the apical area.
3. Character louder and Softer Causes
sharper
a. Aortic aneurysm
4. Relation to respi- None The split increase b. Aortic regurgitation
ration on respiration.
c. Aortic stenosis
5. Occurrence lnMSorTS Normally present
d. Coarctation of aorta
Table 5.7: Differences between Opening
e. Hypertension
Snap and Third Heart Sound
Opening Snap
3. Midsystolic Click/Non-ejection
Third Heart
(A2-0S) Sound(A2 S3) Click
1. Sequence of 0.04-0.12 sec 0.12-0.l?sec Produced by prolapse of AV
sounds afterA2 after52 valve leading to tensing of chordae
2. Area Heard just inside Heard at the apex tendineae.
theapex Causes:
3. Relation to Increase on Disappears on sit- a. Mitra! valve prolapse
posture standing ting/standing
b. Tricuspid valve prolapse
4. Physiological Never Upto 30 years
C. Pericardia) Rub
5. Occurrence lnMSorTS lnMR orLVF
This is caused by slashing movements
6. Pitch High Pitch Low Pitch
imparted by the heartbeat to the exudate
A2 -0S interval can be 0.04 - 0.12 sec. within the pericardia! sac. It gives rise to
a to-and-fro type of sound due to forward
Opening snap is absent when there is: and backward shifts of the exudate during
1. Mild mitral stenosis systole and diastole.
2. Calcified mitral valve Characteristics
3. Mitra! stenosis with associated mitral l. Creaking, rasping,leatheryorscratchy
regurgitation 2. Synchronous with the heart beat, both
B. Systolic Ejection Clicks during systole and diastole, but louder
They are produced due to opening of during systole
semilunarvalves. They are high pitched, 3. Best heard anywhere over the
click-like sounds that come immediately precordium
after the first heart sound and are best heard 4. Not transmitted
in the aortic or pulmonary areas. They are
201
PRACTICAL MEDICINE
202
( 5 ) Cardiovascular System
Table 5.9 : Phases of Valsalva Manouver Table 5.1 O : Dynamic Auscultation
Plw,e Heart Blood Mechanism Manouver RightSided Le�Sided HOCM MVP
Rate Pressure Murmur (eg. Murmur
TR) (eg.MS)
Phase I No Increases Increased lntrathoracic
(onset of change pressure & transient 1. Inspiration t ,I. t t
strain) rise of LV output&arte
rial pressure
2. Expiration .f. 1 .f. J.
203
PRACTICAL MEDICINE
surrounded by cardiac histiocytes called Aschoff cells primary infection, self-limiting lasting 6 weeks
or Anitschoff cells. Mccullaris patch in chronic RF. to 6 months.
Symptoms are initially irritability followed by
Clinical Features
uncoordinated spasmodic movements of hands,
Table 5.11 : Modified Jones Criteria for face and feet with facial grimacing.
Diagnosis of Rheumatic Fever Signs:
Major Criteria Minor Criteria a. Tongue appears like a "bag of worms" due
Carditis Clinical: to continuous movements
Migratory polyarthritis Fever b. "Spoon-dish" hands due to hyperextension
Sydenham's chorea Arth ra lgias
of MCP joints and flexion at wrist
Subcutaneous nodules Laboratory:
Erythema nodosum Elevated ESR or CRP c. "Milkmaid" grip causing irregular repetitive
marginatum Prolonged PR interval (ECG) squeezing on shaking hands.
Essential Criteria: 4. Erythema marginatum is a non-pruritic, flat,
Evidence of recent Gp A circular or serpiginous rash on the trunk and
Streptococcal infection
,.
thighs.
Positive throatculture 2MAJOROR 5. Subcutaneous nodules are firm, colorless, painless
or
nodules 1-2 cm, in size, near the tendons or bony
2. Elevated streptococca I - 1 MAJORAND2 prominences of joints, especially elbows. They
antibody (anti MINOR are a late manifestation.
streptolysin O (ASO),
anti-DNAase) or Atypical Arthropathy in Rheumatic Fever
PLUS
3. Rapid antigen l. Grisel's Syndrome: Occasional involvement of
ANYONEOFTHE
detection test or ESSENTIAL CRITERIA Atlanto-occipital joint.
4. Recent scarletfever 2. /accoud's Arthropathy: Chronic deformity of the
l. Carditis hands after polyarthritis
a. Pericarditis: Chest pain, pericardia! friction Diagnosis
rub 1. Antibodies to Streptococcus Gp A
b. Myocarditis, tachycardia, soft S 1 , Carey a. ASO positive > 200 Todd units. A rising
Coombs murmur titer is more significant.
c. Endocarditis: Murmurs of MS, MR, AS
b. Others: Anti-deoxyribonuclease B, anti
or AI. In adults, aortic valve is most
hyaluronidase, Anti streptokinase.
commonly affected. In children, mitral
valve involvement with MR is most 2. Rapid Antigen DetectionTest: Latex agglutination
common. or enzyme immunoassay on throat swab
d. Cardiac failure due to acute MR 3. ESR and CRP raised, Anemia, Leucocytosis
e. Cardiac enlargement 4. ECG: Prolonged PR (first degree heart block),
f. Infective endocarditis (IE) Second degree or complet heart block
2. Migratory polyarthritis involving knees, ankles, 5. 2-D Echo
elbows, wrists. No residual deformity. Management
Course: Inflamed joint (red, warm, tender)->
completely resolves in 2 weeks-> another joint
l. Hospitalise or bed-rest if carditis
involved. 2. Treatment ofStreptococcal infection (duration I 0
3.
days):Penicillin V 250 mg BD or erythromycin
Sydenham's chorea/St. Vitus Dance: Late
250 mg qds orally or inj. Benzathine penicillin
manifestation, mainly in females, 6 months after
IM 1.2 million units single dose. Alternatives
204
( 5 ) Cardiovascular System
for patients with penicillin allergy: Macrolides, Staphylococcus aureus, Pneumococcus, group A Strep
: roxithromycin, azithromycin or sulfadiazine. tococcus, Gonococcus, Brucella and Rickettsia. They
3. Treatment of manifestations: commonly follow tonsillectomy, dental extraction or
a. Arthritis: Anti-inflammatory agents: suppurative cellulitis.
Salicylates: Aspirin 100 mg/kg/day in 4-5 In narcotic addicts the endocarditis may affect the
doses or NSAIDs: Ibuprofen: 200-400 mg right side of the heart and the common organisms are
tds Proteus, Pseudomonas and Klebsiella.
b. Carditis and cardiac failure: Following open-heart surgery fungal endocarditis is
i. Steroids: Prednisolone l-2 mg/kg/ common with Histoplasma, Candida or Aspergillus.
day or inj. Methyl prednisolone, if Listeria endocarditis is common in patients on im·
life-threatening for 2·3 weeks, then munosuppressive therapy.
taper Pathogenesis
ii. Aspirin during tapering of steroids
for 4-6 weeks The characteristic lesions in endocarditis are veg
etations over the valve leaflet. Sterile thrombotic
111. Rest, steroids, diuretics, digoxin, ACE
vegetations form due to trauma to the endocardial
inhibitors for cardiac failure
cells. Thrombi may form over a sub-endocardial in
c. Chorea: Self-limiting, no specific treatment. flammatory reaction such as in acute rheumatic fever
Drugs like diazepam, haloperidol can be or myocardial infarction. When bacteremia occurs,
used. the surface of the vegetation can become secondarily
Prophylaxis (Secondary) infected and converted to the typical vegetations of
infective endocarditis. This results from deposition of
Drugs:
platelets and fibrin over the bacteria. The vegetations
1. Benzathine penicillin 1.2-2.4 mega units IM then become a protective site through which phagocyte
every 3-4 weeks cells penetrate poorly.
2. Penicillin V 250 mg BD orally Endocarditis occurs at a site where blood flows through
3. Erythromycin 250 mg qds orally a narrow orifice and at a high velocity, from a high
Duration: to a low-pressure chamber. Lateral pressure is lowest
l. Patient with rheumatic fever without carditis -5 and the velocity of blood greatest a short distance
yrs after attack or upto 18 yrs of age, whichever downstream from the opening between the chambers.
is later A decrease in lateral pressure lowers perfusion of the
intima, resulting in an area more susceptible to infec
2. Patient with rheumatic fever with carditisbut
tion. This is the location where infective endocarditis
without valvular disease - 10 yrs after attack or
initially develops. Hence it occurs on the right side in
up to the age of 25 yrs of age, whichever is later
VSD and on the pulmonary artery in PDA. Endocar
3. Patient with rheumatic fever with carditis and ditis does not usually occur when there is only a small
valvular disease - upto 40 yrs of age; some pressure gradient as in ASD or when the congenital
advocate lifelong prophylaxis defect is large enough to abolish the pressure gradient.
A high velocity stream of blood can produce satellite
4 Infective Endocarditis infected lesions at distant points of impact. Hence,
endocarditis occurs more frequently with incompetent
It is a microbial infection of the heart valves or the than pure stenotic lesions and is characteristically seen
endothelium in proximity to congenital or acquired on the atrial side in mitral valve and on the ventricular
cardiac defects. side in aortic valve lesions.
Organisms l. Vegetations may become extensive (as in fungal
endocarditis) and completely occlude the valve
The common organisms are Streptococcus viridans, orifice.
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PRACTICAL MEDICINE
2. The valve tissues may be rapidly destroyed III. Signs of Embolic Episodes
resulting in incompetence of the valve e.g. l. Petechiae: This occurs due to embolic
Staphylococcus aureus endocarditis. episodes, anemia or toxic damage to the
3. Areas of healing may cause scar formation and vessel. It is found in the conjunctiva, palate,
consequent stenosis or insufficiency of the valve. buccal mucosa and extremities. It is called
4. The infection may spread leading to conduction splinter hemorrhage if it occurs under the
abnormalities, rupture of chorda tendineae, nail.
papillary muscles or the ventricular septum. 2. Osler nodes: They occur singly or in crops,
This carries grave prognosis. due to vasculitis. They are transient, tender,
red nodules, the size of pinhead to pea, on
Clinical Manifestations the finger pads, the sides of the fingers and
I. Signs of Infection toes and thenar and hypothenar eminences.
They disappear in few days. They may
l. Fever with chills and rigors coming down
also be seen in SLE, typhoid, gonococcal
with sweating. If there is associated cardiac
infection.
failure, fever may be absent for as long as
4 months. 3. Janeway's lesions: They are subepithelial
microabcesses and are large non-tender
2. Progressivenormochromicand normocytic
macules over palms and soles. These are
anemia.
commonly seen in acute endocarditis.
N.B Microcytic, hyp ochromic anemia by 4. Peripheral vascular embolization: This may
itself can cause low-grade fever, petechiae, involve larger vessels like carotids or radials,
systolic murmur and splenomegaly. resulting in hemiplegia and painful fingers.
3. Tachycardia If an embolus sits at the bifurcation of an
4. Clubbing: It takes 3-6 weeks to develop. It aorta it will cause Leriche's syndrome that is
disappears once the patient is cured characterized by acute onset of paraplegia,
5. Splenomegaly: Spleen enlargement is not impotence and absent pulsations of lower
gross. If spleen suddenly enlarges, is tender Jim bs that become cold, cyanosed and later
and a rub is present over the spleen, it gangrenous.
suggests splenic infarction. 5. Pulmonary embolism: This resembles
6. Febrile proteinuria hemor r hagic bronchopn eumonia.
Pulmonar y embolism occurs if the
7. Leucocytosis
vegetations are on the tric uspid or
8. Blood culture: Usually organisms are grown pulmonary valves or if there is a left to
on blood culture right shunt.
II. Cardiac Signs 6. Optic fundi:
1. Signs of a pre-existing cardiac lesion is a. Roth's spots: These are flame-shaped
usually present except in patients with or canoe-shaped hemorrhages with
congestive cardiac failure, atrial fibrillation, central pallor. They are seen in severe
renal failure or severe debility anemia, leukemias and collagen
2. Changing intensity of the cardiac murmur. vascular diseases in addition to
3. Appearance of new murmurs infective endocarditis.
4. ECG: Prolonged PR interval. AV block may b. Embolization of the retinal artery:
be present if the septum is involved. This leads to blindness.
There may be no cardiac signs especially if c. Papilledema due to embolic cerebral
the right side of the heart is involved. infarction or renal involvement.
206
( 5 ) Cardiovascular System
207
PRACTICAL MEDICINE
is stopped it may be necessary to repeat the 2. Development of heart failure
entire "desensitization". 3. Aortic valve involvement
If the patient still develops severe
4. Prosthetic valve involvement
reaction, Vancomycin may be used as for
streptococcal endocarditis. 5. Old age
D. Other organisms Prophylaxis
1. E. coli and Proteus mirabilis: Penicillin,
Indications:
Ampicillin or cephalosporin
2. Salm onell a: Ciprof l oxacin o r I. Prosthetic heart valves
Chloramphenicol 2. Prior endocarditis
3. Klebsiella: Cefotaxime 3. Unrepaired cyanotic congenital heart disease
4. Enterobacter, Pseudomonas and 4. Repaired congenital heart defects (for 6 months)
Proteus other than P mirabilis: 4. Valvulopathy developing after cardiac
Piperacillin, Ceftazidine, Amikacin transplantation
or Ciprofloxacin.
Treatment:
5. Fungal: Amphotericin B 1 mg/kg/day
I. Oral hygiene must be optimum.
IV and Flucytosine PO 150 mg/kg/
day in 4 divided doses. 2. For dentalmanipulations and other procedures in
the oropharynx, prophylaxis is directed against
E. Emperic Therapy till culture report
Streptococcus viridans.
available:
Ampicillin IV 2 g 4 hourly + Nafcillin IV Oral regimens: Amoxycillin 2 gm PO one hour
2 g 4 hourly+ Gentamicin IV lmg/kg 8 prior to procedure.
hourly or Vancomycin IV I mg/kg/day 12 For penicillin allergic patients: Erythromycin or
hourly (for penicillin-allergic patients) + Clarithromycin 500 mg PO 1 hr before procedure
Gentamicin I mg/kg 8 hourly. or Clindamycin or Cephalexin.
Parenteral regimens: Ampicillin 2 g IV within
Response to Therapy
I hr before procedure or Clindamycin 600 mg
I. The blood culture becomes negative within IV I hr before procedure.
several days after the onset of therapy. 3. For genitourinary or gastrointes tinal tract
2. Regression offever, weight gain and a fall in ESR procedures or surgery, prophylaxis is directed
occur soon, but may take several weeks. against enterococci with Ampicillin 2 gm IV +
3. Hematuria and proteinuria disappear along with Gentamicin 1.5 mg/kg IV or IM half an hour
the therapy. before the procedure followed by one dose of
Amoxycillin PO 1.5 g 8 hours later.
4. Regression of dubbing takes several weeks.
4. Cardiac surgery: Prophylaxis is directed against
5. Splenomegaly may persist for many months. staphylococci and consists of 2 gm Methicillin,
6. Although anemia may respond in several weeks, Oxacillin, Nafcillin or Cephalothin IV every 4
the rise in hemoglobin may be very slow. hourly starting I hour before the procedure and
continuing for several days.
Prognosis
208
( 5 ) Cardiovascular System
Causes: The commonest cause ofIHD isatherosclerotic interventricular septum (IVS) - and the circumflex
coronary artery disease. Other causes are: (CX) - which supplies the posterior and variable
J. Atherosclerotic coronary artery disease amounts of the inferior LV, sinoatrial (40%) and
atrioventricular nodes and sometimes LV apex and
JI. Other coronary artery diseases
posterior wall. RCA supplies the RV, sinoatrial node
l. Coronary artery spasm (60%) and posterior part of IVS.
2. Coronary arteritis The dominant circulation refers to the artery which
3. Embolism gives rise to the "posterior descending artery" which
4. Coronary A-V malformation supplies posterior part ofIVS. Hence it may be either
right dominant or left dominant circulation. Right
III. Valvular diseases
dominant is more common.
l. Aortic stenosis and regurgitation
2. Mitra! valve prolapse Coronary Physiology
IY. Other cardiac disease During stress, the coronary blood can be increased
l. Hypertrophic cardiomyopathy 5-6 times the basal values. This is regulated by coro
nary autoregulation mechanism. In the resting state,
2. Collagen disease
coronary blood flow is adequate until there is 75% or
3. Syphilis more narrowing of epicardial artery.
V. Increased demands During stress, the perfusion pressure does not increase,
l. Thyrotoxicosis but the increased flow is maintained by coronary vaso
2. Anemia dilatation, which is controlled by various metabolites
3. Beriberi like adenosine, prostaglandins, carbon dioxide and
hydrogen ions. The coronary vascular resistance would
The exact cause for initiation and progress of fall to 20-25% of basal state in response to maximal
atherosclerosis are unknown. However, certain factors demand on exercise. The ability to lower the resistance
may be responsible. These are called Coronary risk to flow at rest, even when there is an 80% reduction
factors. in the diameter of a large coronary artery, allows a
Table 5.12 : Coronary Risk Factors patient to be asymptomatic in spite oflarge reductions
Reversible Irreversible in internal diameter of the artery.
1. Tobacc o smoking 1. Sex: Male Clinical Presentations
2. Hyperlipidemi a 2. Familyhistory oflHD
I. Angina • typical and atypical
3. Diabetes 3. Type A personality
2. Acute myocardial infarction
4. Hypertension Doubtful
3. Ischemic cardiomyopathy
5. Obesity 1. Hypercal cemia, homocystenemia,
fibri nogen, lipoprotei n 'a'
4. Cardiac arrest
6. Physical inactivity 2. Cardiac transpl ant at ion
5. Sudden cardiac death
7. Stress 3. Traceelement s
6. Asymptomatic coronary artery disease detected
on the routine medicalcheckup (Silent ischemia)
Coronary Anatomy
Angina Pectoris
There are 2 coronary arteries - left (LCA) and right
Heberden in 1769 gave the first description of typical
(RCA) that arises from the aorta at the sinus ofValsalva.
angina pectoris. It is substernal pain or heaviness.
The left main (LM) stem is short and divides into left radiating to both arms or ulnar border ofthe left arm,
anterior descending (LAD) - which supplies major jaw, teeth, occipital region or epigastrium.
part of the left ventricle (LV ) and the anterior part of
Variation to the above may be 'gas' in the substernal
209
PRACTICAL MEDICINE
- - -
cg S 17 :A:Co•onilryAr(j c:g-dµhyofl e!iCo·o·,a•yA•tery ·1?ACn,i1alVew.:B:Co•onc1ryAng cg·aphyof,eftCoronary
Arlery ,n RAOCaudalv,ew. (CJ Coron,11yAng,ographyof Right Coro11ilryArtery rn LAOCra111alV1ew
region or pain in the areas of radiation without sub Spasm may be caused by increased alpha
sternal pain. adrenergic activity during early hours ofmorning
Sometimes there may be breathlessness or fatigue due or due to platelet aggregation. Though coronary
to low cardiac output. arteries can be normal on angiography, in 50% of
patients there may be associated coronary artery
Types obstructive disease. Beta-blockers may aggravate
I. Stable: It occurs with known physical effort and the spasm and hence are contraindicated.
is relieved with rest and nitrates. Cold weather, 5. Post infarction angina: Some patients with
smoking, emotional upset, high altitude, sexual myocardial infarction develop angina 2 days
intercourse and straining at stools can also to 8 weeks following the infarction. Most of
aggravate it. them have multivessel disease and residual
2. Nocturnal: Angina appears in the middle of the myocardial ischemic. They require early coronary
night due to left ventricular failure which may angiography and appropriate treatment.
be precipitated by dreams causing release of Table 5.13 : Assessment of Chest Pain
catecholamines a full urinary bladder or transient Modified Canadian Cardiovascular Society Criteria
hypoglycemia. Grade
3. Unstable: This is also called Preinfarction angina I. Angina only on strenuous or prolonged exertion
as 20% of these patient develop myocardial
II. Angina climbing two flights of stairs
infarction within 4 months.
Ill. Angina walking one block on the level
The following types of angina! pains are called
unstable angina: IV. Angina at rest
210
(5 > Cardiovascular System
of mitral regurgitation or papillary muscle It is contraindicated in unstable angina,
dysfunction or basal rales may be present. acute myocardial infarction, heart failure,
arrhythmias, A-V blocks, severe aortic
Table 5.14 : Functional Classification of
fatigue, Palpitation, Dyspnea or Anginal stenosis and debilitating conditions.
Pain{New York Heart Association (NYHA)] 4. Thallium Stress Test: This test is done by
injecting Thallium whilst the patient
In a patient with established cardiac disease: exercises and then the regional myocardial
1. No/imitations to physical activity. Ordinary physical ac perfusion is assessed by using a gamma
tivity does not cause undue fatigue, palpitation, dys camera. Thallium is picked up only by
pnea or anginal pain. normal myocardium; ischemic areas would
II. Slight limitation of physical activity: Comfortable ai appear as perfusion defects. However, scans
rest. Ordinary physical activity results in fatigue, palpi taken 2-4 hours after exercise may show
tation dyspnea, or angina I pain.
reperfusion of Thallium in the ischemic
Ill. Marked limitation of physical activity: Comfortable a1 zone signifying reversible ischemia. The
rest. Less than ordinary physical activity causes fa
tigue, palpitation, dyspnea or angina I pain.
necrosed area continues to remain cold.
This has 85% specificity and sensitivity.
IV. Symptoms at rest: Inability to carry on any physical ac
tivity without discomfort.Symptoms offatigue, palpi 5. Holter Monitoring: Ambulatory ECG
tation, dyspnea or anginal pain may be present even monitor may detect episodes ofST segment
at rest. It any physical activity is undertaken, discom changes during normal activities. Some of
fort is increased.
the episodes ofST segment changes during
II. Diagnostic Tests: normal activities. Some of the episodes of
1. ECG: In 50% of patients with angina, ST T changes may not be accompanied by
resting ECG may be normal at rest. During symptoms (Silent ischemia).
angina! episode, ST depression (stable/ 6. Echocardiography and Doppler study: This
unstable angina) or elevation (Prinzmetal is helpful to judge the regional wall motion
type) may be present. These may disappear abnormality, left ventricular thrombus,
with rest or following sublingual nitrates ejection fraction and mitral and mitral
or nifedipine. regurgitation. Stress echocardiogram can
2. Cardiac Enzymes (CK-MB, Trop T/Trop I): identify regional wall motion abnormality
In angina, cardiac enzymes are normal. In immediately after exercise.
a patient with typical chest pain and ECG 7. Coronary angiogram: This is a specific
changes of ST depression, if enzymes are test to diagnose blockage of coronary
normal, then it is UNSTABLE ANGINA. arteries and its location and severity. It
If enzymes are raised, then it is a non-ST is usually indicated in severe angina not
segment elevation Ml (NSTEMI). responding to medical treatment in whom
3. Stress testing: This is done with treadmill or revascularization through angioplasty or
bicycle ergometer using standard protocols by pass surgery is planned.
like Bruce's. The workload is gradually
increased by increasing the speed and Differential Diagnosis
elevation of the treadmill. The patient is I. Non-coronary cardiac causes
exercised up to predicted target heart rate
1. Cardiomyopathy: There is usually a gallop
(220 - Age in years) or till there is ECG
rhythm with systolic murmur of papillary
changes of ischemia, hyp otension gallop,
muscle dysfunction. However, chest
pain, fatigue, dyspnea or hypotension.
pain is more prolonged and not typically
This test though very popular can give both constricting. Echocardiogram identifies
false positive and false negative results. cardiomyopathy.
211
PRACTICAL MEDICINE
2. Mitra/ valve prolapse: The chest pain is in the substernal area radiating to the jaw
rarely typical angina!, is usually prolonged, or arm and precipitated by food. There may
associated with anxiety and is more as associated dysphagia for liquids more
common in females. A mid-systolic click than solids. ECG is normal and barium
with a murmur may be present. studies would show the spasm.
II. Neuropsychiatric (anxiety state): The pain is 3. Cholecystitis and Gallstones: The pain
usually stabbing or jabbing without any relation is usually in the epigastrium or right
to exertion. It also lasts longer and may be hypochondrium with nausea and vomiting.
associated with palpitations, perspiration and Gallstones can be seen on sonographic
cold limbs ECG is usually normal. examination of upper abdomen.
III. Musculoskeletal 4. Peptic Ulcer: The pain has burning characte r
1. Costochondritis (Tietze's syndrome): There and has no relation to effort. It also lasts
is local pain and tenderness with swelling longer.
over costochondral junction, which may be 5. Splenic flexure syndrome: Distension of
mistaken as angina. ECG usually normal. splenic flexure of colon can cause precordial
2. Cervical Spondylitis: There is usually pain referred to the shoulder. The pain has
radiating pain from the neck going to the no relation to efforts and is often relieved
arms and sometimes chest. It is associated on passing flatus or stools.
with paresthesia ECG is normal and X-ray
Management
spine may show cervical spondylitis.
3. Herpes Zoster: In the pre-eruptive phase, I. Treatment of acute attack
herpes zoster of the left side of chest may I. Di-Nitrates: Glycerine trinitrate 0.5 mg.
mimic angina. However, it is usually in or isosorbide dinitrate 5 mg sublingually
the distribution of the nerve root. Once relieves the attack in 2 5 minutes
eruptions appear as typical herpetic (Mononitrates are contraindicated). Rarely
vesicles, the diagnosis is clear. relief may nor occur or may be followed
IV. Pulmonary rapidly by a relapse. It may cause slight
heaviness in the head and hypotension. It
I. Pneumothorax(Left-sided): Maycausechest
is also available as ointment to be applied
pain, which may suggest IHD. However,
on the skin.
there is shift of the mediastinum to the
right and decreased breath sounds. 2. Beta-blockers or Calcium channel blockers:
May be used to decrease pain.
2. Pneumonia: Left sided pneumonia can cause
chest pain, which can mimic angina. There II. Prevention of anginal attacks
is usually no relation to exertion but the 1. Modification of life style: Life style should
pain is aggravated on inspiration. Fever and be changed to avoid precipitating factors.
constitutional symptoms may be present. Exertion, especially following meals,
V. Gastrointestinal walking uphill against the wind must be
avoided. Emotional disturbances like anger
I. Hiatus hernia: The chest pain is usually a
and anxiety must be avoided if possible.
feeling of heartburn or indigestion, which
occurs after meals on postural changes 2. Rest and Exercise: Bed rest is usually not
without any relation to effort. It can mimic required unless there are frequent attacks
nocturnal of postprandial angina. Stress or there is angina decubitus. Exercise that
test is usually normal and barium studies does not cause pain or breathlessness may
of esophagus may demonstrate the lesion. be allowed.
2. Achalasia Cardia: There is squeezing pain 3. Controlofrisk factors: The risk factors must
212
{5 > Cardiovascular System
be controlled if present. Hypertension,
Transducer diabetes and hyperlipidemia ( with statins)
� � 4("-vt--- -----Ly
I II III R L F
Fig.5 21 ECG showing acuteanteroseptal myocardial infarction There are 1nvertedTwaves 1n leads f and aVLand QS pattern ,n
leadsVl,V2andV3.
213
PRACTICAL MEDICINE
214
( 5 ) Cardiovascular System
in severe cases and is often associated with In the leads opposite to the site ofinfarction there
cardiogenic shock. is ST depression even earlier than ST segment
4. Collapse: The patient maybe pale, ashen grey elevation (Reciprocal Changes).
or cyanosed with intense perspiration. The Depending upon the area involved these changes
patient may be restless, excited and rarely are seen in respective leads:
unconscious. I. Anterior: I, aVL. V 1 - V6
B. Signs: 2. Lateral: V5V6
l. Pulse: Fast and feeble pulse is usually 3. Antero-septal: V.,-V�
present.
4. Medial: V 1 -V2
2. BP: Initially there isa rise in BP, which may
5. Inferior: II, III, aVF
be followed by a fall especially if cardiogen ic
shock occurs. 6. Right Ventricular: ST deviation in V_1R
3. Heart sound: The heart sounds are usually 7. Posterior: ST depression with tall T and R
muffled. A third heart sound gallop may in v. and v2
be heard with a typical tic-tac rhythm. New onset LBBB: May be sign of AMI requiring
4. Lung signs: The lungs may be normal or a thrombolysis
few basal rales may be auscultated if there III. Serum Enzymes: Myocardial necrosis leads
is left ventricular failure. to liberation of certain enzymes which may
5. Late signs: On the second or third day mild be elevated in blood, SGOT, LDH, Troponin
fever of38-39 C may occur. Pericardia! rub and CPK levels rise. The isoenzymes Troponin
may transiently appear around the same and CPK (MB fraction) are more specific for
time. myocardial infarction. The importance of these
is as follows:
Table 5.15 : Differences between Angina
Pectoris and Myocardial infarction Table 5.16 : Serum Enzymes in
Angina pectoris Myocardial
Myocardial Infarction
infarction Enzyme Normal Earliest Peak by Normal by
Value Rise in
Chest pain Short duration Longer dura -
often relieved by tion usually not SGOT 0-35 U/L 8-12 hr 36-48hr 7·10days
nitrates relieved so rapidly
by nitrat es LDH 45-90U/ml 12·24hr 24hr 8-14days
Precipitating Exertion or follow- May be absent CPK 25·90U/I 8hr 24-30 hr 3-4days
factors ing meals or cold CPK·MB 4·6%ofCPK 4-8 hr lB-24 3-4days
Breathlessness, Absent Present <60ng/h 4-12 hr 24-48 hr 7-14days
Troponin
vomiting, collapse T/1
and sweating
215
PRACTICAL MEDICINE
2. Activity: Bed rest must be given at least a. Sublingual nitroglycerine 0.3 - 0.4
for the first 24-48 hours. The traditional mg should be repeated every 5-10
approach is to prescribe prolonged bed rest min until chest pain is relieved or
because early ambulation may precipitate tachycardia and hypotension occurs.
arrhythmias and heart failure, cause b. Beta-blockers: Metoprolol 5 mg IV
extension of the infarction and later lead to over 2 minutes. Repeated after 5 min
the development of ventricular aneurysm for 3 doses.
and r upture. With uncomplicated c. Morphine hydrochloride 15 mg SC
myocardial infarction, mobilization can or 2-4 mg IV slowly should be given
be started by the second day and patient if the chest pain is not relieved by
216
( 5 ) Cardiovascular System
nitrates in 30 min. Morphine has 3. Tissue-type plasminogen activator
vagotonic effects. Hence, in inferior (tPA) and other fibrin specific
wall infarction with conduction antithrombolytics have greater clot
disturbances, pethidine 50100 mg selectivity than streptokinase or
IM is preferred. Pentazocin with urokinase and tPA at therapeutic doses
diphenylhdramine is the alternative does not cause systemic fibrinolysis.
if morphine is not available. Recently large quantities of tPA have
6. Prevention of ventricular fibrillation: All been obtained by successful cloning
patients were earlier treated with lidocaine and expression of human tPA gene in
to prevent ventricular fibrillationespecially Escherichia coli.
if there is no cardiac failure or shock. Indications /or thrombolysis:
However, this is no longer indicated. Thrombolytic agents are indicated in the
first 3 hours after onset of symptoms and
Reperfusion Therapy
are alternative to primary PTCA due to
J. During the first 12 hours (Hyperacute phase) logistic difficulties with PTCA.
A . Intravenous thrombolysis: Thrombolysis Contraindicated in patients with active
should be given within 3 hours ofi nfarction bleeding, BP> 180 mmHg SBP, or>110
but can be given upto 12 hours. The agents mmHg DBP, H/0 hemorrhagic CVA at any
used are: time in the past, non-hemorrhagic CVA in
i. Streptokinase: 7,50,000to 15,00,000 last l year and aortic dissection. Relative
units over 30-60minutes. contraindications are pregnancy. peptic
ulcer, breathing diathesis, major surgery
ii. Urokinase: 15,00,000units over 30-60
in last 2weeks, use of streptokinase in last
minutes.
2years.
iii. Fibrin Specific Agents:
Side Effects : Allergic reaction to
l. Tissue Plasminogen Activator (tPA) streptokinase ,hypotension, bleeding
(15 mg bolus IV followed by 50 mg
B. Percutaneous transluminal coronary
IV over 30min followed by 35mg IV
angioplasty (PTCA):
over60mins).
It is the best therapy for patients with
2. Tenecteplase (TNX} 0.53mg/kg over
STEMI. It implies balloon dilatation of the
10sec
stenosed infarct-related artery. It is usually
3. Reteplase{rPA) lOmillion units bolus accompanied by non-balloon techniques:
over 2·3 min, which is repeated after
l. Stents: Bare-metal stents or Drug-
30min.
B. Mechanism of Action Table 5. 17 : Types of PTCA
1. Streptokinase binds to plasminogen Typeof PTCA Indications
to form an activator complex that Primary PTCA or AMI presenting > 3 hr after onset of
converts it to plasmin , which lyses PrimaryAngioplasty pain or < 3hr, if PTCA facilities are
in Ml (PAM/) readily available in hospital
the thrombus.
RescuePTCA Thrombolysed patients who have
2. Urokinase, a product of human renal persistent or recurrent chest pain/
tubular cells actsas a direct activator of ST elevation after> 90 min (Failure of
the fibrinolytic system. It is more clot Thrombolysis}
specific than streptokinase and causes Elective PTCA After thr ombolysis, prior to discharge
less bleeding complication, reduction or on follow-up
of fibrinogen and antigenicity. Facilitated PTCA Accompanied by use of Gpllb/llla
inhibitors
217
PRACTICAL MEDICINE
218
( 5 > Cardiovascular System
reflex tachycardia. However, in cases with and increasing supply, (inflation of the
recurrent or persistent ischemia after balloon in diastole increase coronary
myocardial infarction, especially where perfusion pressure). However, because of
the pathogenetic mechanism is likely to the significant rate of complications and
be coronary vasospasm, it is useful. It is logistic difficulties associated with IABP,
also used if beta-blockers or nitrates are it is reserved only for very severe cases of
not tolerated or are contraindicated. angina not responding to other measures.
E. ACE inhibitors or ARB decrease ventricular
Prognosis
remodeling and therefore decrease
mortality and are used in all AMI patients Bad Prognostic indicators in AMI
specially if associated with decreased KV 1. Old age, stress, history of diabetes
function (e.g. Ramipril or Losartan (See 2. Previous myocardial infarction
Ch. 15 for details)).
3. CPK > 2000 IU/ml
F. Nitroglycerine and Nitrates: Nitrates reduce
infarct size by reducing preload increasing 4. ECG:
collateral blood flow to the ischemic a. Development of new intraventricular
zone and relieving coronary vasospasm. conduction defects
Nitroglycerine (NTG) can be given b. Poor LV function
sublingually or as ointment. For severe c. Persistent heart block
and recurrent angina I.V. NTG is given
at 10 mcg/min., increased every 5 min. 5. Angiogram: Absent collaterals to jeopardized
by 10 mcg/min. until angina is controlled myocardium (non-patency of MI-related
coronary artery)
or systolic BP is less than 100 mmHg or
the dose has reached 200 mcg/min. If the 6. Cardiogenic shock
patient's condition is stabilized for 48 hours
Common Mechanisms of Death
and no re-infarction occurs. I.V. NTG is
Following Myocardial Infarction
discontinued and the patient put on oral
nitroglycerine or isosorbide dinitrate. 1. First few hours - Ventricular Fibrillation
I.V. NTG is given to patients who are 2. First few days - Pump failure
normotensive with left ventricular failure 3. First few months - Reinfarction
(Pulmonary wedge pressure> 16 mmHg
and cardiacindex less than 2.5 L/min/M2). Treatment of Complications
G. Ni troprusside (NP): NP is useful for
Left Ventricular Failure
hypertensive patients, in the dose of I 0
mcg/min and increased every 5 minutes A. Diuretics: Furosemide 20-40 mg IV every 6
by 5 mcg/min until angina is controlled hourly is given if there is dyspnea or hypoxia,
or systolic BP is 120 mmHg. If there is no especially if pulmonary wedge pressure is over
cardiac failure it can be combined with 18 mmHg. It favorable alters the myocardial
beta-blockers, which will prevent reflex oxygen supply by reducing left ventricular end
tachycardia. diastolic volume and tension, which not only
H. Intra-aortic balloon counterpulsation decreases myocardial oxygen demand but also
(IABP): This helps to maintain circulatory increases coronary perfusion. However, it must
support for patients with cardiogenic shock. be used carefully in mild failure brisk diuresis
It favorably affects myocardial oxygen may reduce left ventricular filling pressure,
balance by decreasing demand (deflation activate renin-angiotensin system and arginine
of the balloon decreases the afterload) vasoconstriction, deteriorating the patient.
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220
( 5 ) Cardiovascular System
E. Vascular lesion: be breathless even in propped up
I. Hypertension position (orthopnea).
2. Aneurysm of aorta Paroxysmal nocturnal dyspnea and
cough commonly occurs because
[I. High output failure
of reduced vital capacity in supine
A. Thyrotoxicosis
position, reabsorption of tissue
B. Anemia and hyp oproteinemia fluids from the lower limbs into the
C. Beriberi circulation and depressed respiratory
D. AV Fistula center during sleep. The attacks are
E. Cirrhosis ofliver classically precipitated at night and
may be characterized by sudden
F. Cor pulmonale
awakening with extreme suffocation,
G. Paget's disease of bone cyanosis, perspiration and air hunger.
II. Left Sided or Right Sided Cardiac Failure (given The patient may cough up frothy
below) sputum, which may be pinkish (due
III. Systolic or Diastolic Cardiac Failure to pulmonary edema). The episode
I. Systolic Cardiac Failure : It results from may last from 5-20 minutes or more.
impaired systolic function and reduced 2. Due to reduction inforwardflow: due
cardiac output. Usually seen in Ischemic to inadequate output ofleft ventricle.
Heart Disease. It is managed mainly Blood flow to the vital organ suffers
by ionotropic agents e.g. Dopamine, resulting in mental confusion,
Dobutamine and Digoxin. insomnia weakness and fatigue.
2. Diastolic Cardiac Failure (Heart Failure B. Signs
with a normal ejection fraction (HFNEF) 1. Gallop rhythm: Gallop rhythmor triple
: It results from impaired diastole or rhythm occurs due to the audibility
reduced relaxation and ventricular filling. of thi rd or fourth heart sounds which
It is usually seen in systemic hypertension, resembles the sounds produced by
constrictive pericarditis, restrictive galloping of horses. Normally in
cardiomyopathy and IHD. It is managed an adult only two heart sounds are
with vasodilators (ACE Inhibitors or heard. In cardiac failure, there is
Calcium Channel Blockers). increased resistance to filling of left
ventricle, hence blood flow through
Clinical Features
the atrio-ventricle valve is prolonged
I. Left Ventricular failure and results in the third or fourth heart
A. Symptoms sound. Associated with tachycardia it
1. Due to back pressure effect: Inability produces the classical tic-tac rhythm.
of the left ventricle to eject adequate 2. Pulsus alternans: Left ventricular
blood leads to congestion in the failure alters the contractile forces of
pulmonary blood vessels. This the heart, which may cause alternate
causes exertional breathlessness. As large and small pulses without any
the disease progress breathlessness change in rhythm.
increases and occurs even at rest. The 3. Basal rales: Due to back pressure and
patient maybe comfortable only in the congestion of the Ju ngs, rales may be
propped up position and increased heard at both the lung bases initially
vital capacity due to lowering of the and later throughout the lung fields.
diaphragm. Later the patient may Fluid collection in the interstitial
221
PRACTICAL MEDICINE
spaces may cause rhonchi even in the ventricular enlargement and evidence
absence of rales. of the primary disease causing right.
4. Cheyne Stokes respiration: This is sided heart failure may be present.
alternate periods of apnea and B-Type Natriuretic Peptide (BNP): It is released
hyperpnea, which occurs due to left by the ventricle in response to stretch or elevated
ventricular failure. Signs of cardiac filling pressures. It can be measured in the blood
enlargement and of the causative and is very useful in diagnosis, monitoring and
disease may be present. prognosis of heart failure. BNP levels are very
II. Right Ventricular Failure sensitive and specific for heart failure. BNP less
than 100 pg/ml rules out cardiac failure.
A. Symptoms
1. Due to back pressure: Management
a. Pulmonary: Cough, dyspnea and The treatment of cardiac failure aims at restoring the
hemoptysis balance between the metabolic demands of the body
b. Por t a l: An orexia, nausea, and he heart's ability to meet these demands.
vomiting, abdominal fullness
1. Rest: Complete bed-rest is the keystone of
after meals and pain in the right
treatment. When the patient is dyspneic, bed
hyp ochondriac region
rest is given with the head end of the bed raised
c. Renal: Nocturia and oliguria to 45". The legs should be kept below the pelvis
d. Peripheral: Edema of feet. to prevent the fluid present in the legs to return
2. Due to diminished cardiac output: to vascular system and precipitate pulmonary
Weakness and fatigue edema. Once weight loss and adequate diuresis
B. Signs occur, the patient may be allowed to sit on the
bedside chair or use a bedside commode and
I. Raised jugular venous pressure:
he can be gradually mobilized. Prolonged bed
Normally at 45� position of the
rest may predispose to venous thrombosis and
patient, the jugular veins are not
pulmonary embolism, which can be prevented
visible. In cardiac failure, it is visible
by leg exercise and elastic bandage wrapped
in the neck and at times may reach
around the legs.
up to the angle of the sternum.
2. Hepatomegaly: Liver is enlarged and 2. Diet: The basic aim is to restrict sodium in diet.
tender due to congestion; systolic The amount of salt to be restricted depends
pulsations may be present if there is upon the severity of cardiac failure. Normal diet
tricuspid regurgitation. contains l O· l 5 gm of sodium chloride or 46 gm
of sodium. On avoiding salt in food and table
3. Edema: Edemaclassically occurs over
salt this can be reduced to 2-4 gm of sodium/day
the legs and is pitting in character. If
and on completely avoiding salt in preparation,
the patient has been continuously
this can be further reduced to l gm sodium/day.
supine, edema may not be present
Salt substitutes may be used to make the diet
over the legs but may be present over
more palatable.
the sacrum because in that position,
it is the most dependent part. Due to edematous gastrointestinal tract,
4. Signs of TR and RV Enlargement: digestion and absorption are poor. In addition,
Pansystolicmurmur overthetricuspid larger meal may cause pooling of blood to the
area, increased in inspiration due to gastrointestinal tract, thereby interfering with
tricuspid regurgitation may occur. diuresis. Hence, instead of the traditional three
In late stages, cyanosis and cardiac meals, it is advisable to give frequent, small,
cachexia may occur. Signs of right liquid feeds.
222
( 5 > Cardiovascular System
If the patient is obese, loss of weight must be tablets). The usual digitalizing dose is 1.5 mg.
achieved by strict caloric restriction. For maintenance 0.25 mg daily is adequate.
Usually fluid restriction is not required in cardiac 5. Sympathomimetic amines: Catecholamines
failure. However, if edema is present with low stimulate the cardiac beta-adrenergic receptors
serum sodium, fluids should be restricted. and can be used to treat cardiac failure, but their
Diuretics: In cardiac failure, there is always effect increases the oxygen consumption and
3.
sodium and water retention. Hence diuretics are increases the work of the heart. Newer agents
given to increase sodium extract ion. Furosemide are free of these side effects and have been used
40 mg orally or parenterally is a very potent in the treatment of acute and chronic cardiac
and the most commonly used diuretic. Since failure.
the diuretic response is dose related, it can be a. Dopamine: At low doses of 3-5 mcg/kg/
increased if required. Since furosemide results min. dopamine increases the contractility
in loss of sodium, chloride and potassium of the heart by direct stimulation of
ions, the latter should be supplemented orally the beta-adrenergic receptors cause
either as potassium chloride or as orange juice vasoconstriction in all the vascular
and coconut water, both of which are rich in beds which increases arterial pressure,
potassium. Alternately, potassium sparing peripheral resistance and myocardial
diuretics like spironolactone 25 mg four times oxygen consumption. In severe cardiac
a day, triamterene or amiloride hydrochloride failure dopamine can be combined with
can be used along with it. nitroprusside, which reducesafterload and
Other diuretics used are Torsemide, thus increases cardiac output and decrease
Hydrochlorthiaz ide, Ch lor thalido n e, filling pressure.
lndapamide, Metolazone. b. Dobutamine: It has a predominant effect on
Some patients with mild cardiac failure can be the cardiac beta- l receptors with very slight
satisfactorily treated with a diuretic alone. Most activity on the vascular alpha and beta-2
patients will however require additional therapy. receptors. At infusion rates of2.5-15 mcg/
Failure of diuretic therapy may be due to high kg min. it increases cardiaccontractilityand
salt intake, electrolyte disturbances, inadequate cardiac output, decreases filling pressure
renal perfusion or severe reduction in cardiac and causes minimal change in peripheral
output. resistance. In acute myocardial infarction
dobutamine increases cardiac output by
With the use of all diuretics it must be 20% withoutaltering the heart rate or blood
remembered that the compromised left ventricle pressure. Dobutamine increases collateral
is dependent on its preload to maintain the flow to the ischemic myocardium, thereby
cardiac output.
reducing the infarct size. The inotropic
4. Digitalis: Digitalis and the related cardiac effects ofdopamine do not persist beyond24
glycosides have a direct cardiotonic action. They hours whereas those ofdobutamine persist.
increase the force ofmyocardial contraction and Both these drugs are complimentary and
decrease the work of the heart. Digitalis can be can be used together, dopamine is useful in
administered intravenously, intramuscularly or hypotension, dobutamine is useful in low
orally, rapidly or slowly. In rapid digitalization cardiac output because it causes reduction
full digitalization is achieved within 24 hours in filling pressures.
and is usually given parenterally. Ifthe patient is 6. Bipyridines: These are non-glycoside positive
already on digitalis or has only recently stopped inotropic agents that are affective both orally
it, rapid digitalization parenterally may cause and intravenously. They reduce right and
toxicity and hence it should be given orally. left ventricular filling pressures and systemic
The commonly used drug is digoxin (0.25 mg
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PRACTICAL MEDICINE
vascular resistance with increase in cardiac is needed with elevated filling pressures,
output. This effect persists beyond 24 hours an acceptable cardiac output and normal
unlike dopamine. The two drugs useful in this blood pressure. It is started at 5-10 mcg/
group are Amrinone and milrinone. min. and increased by 10 mcg every 10-15
Amrinone is given intravenously as a bolus min. to a total dose of 100-200 mcg/min.
of 0.75 mg/kg over 2-3 minutes followed c. Hydralazine: It is an arterial dilator which
by a maintenance infusion of 5-10 mg/kg/ produces slight decrease in BP, large
min. The side effects that can occur are fever, decrease in systemic arterial resistance and
thrombocytopenia, nephrogenic diabetes 2 5-70% increase in cardiac output. Usually
insipidus, hepatitis and gastrointestinal it is given in the dose of 25 mg 6 hourly
disturbances. and increased gradually up to 100 mg 6
Milrinonederived from amrinone, ismore potent hourly. In this dose lupus erythematosus
and with lesser side effects. may occur in 15% of patients. It is usually
combined with nitrates or nitroprusside.
7. Vasodilators: In cardiac failure with loss of
cardiac reverse, an increase in compensatory d. Prazosin: This reduces the peripheral
afterload results in increase in end-diastolic resistance by blocking the vascular alpha-I
volume and pressure accompanied by a reduction ad renergic receptors. Decreases in arterial
in stroke volume. Vasodilators are useful by and left ventricular filling pressures, as
reducing afterload. They can be subdivided into well as systemic vascular resistance and
those with a predominant action on the venous increases in cardiac output result from
system (venodilators), those with a predominant both arterial and venous dilation.
action on the arterial system (arterial dilators) With acute use, heart size decreases and
and those that have relatively equal effects on treadmill exercise performance improves.
both the systems (balanced dilators). However, tolerance develops on continuous
a. Nitroprusside: Sodium nitroprusside acts use, which does not improve by increasing
directlyon the vascular smooth muscle and the dose but by adding a diuretic. The
has a balanced dilator effect which reduces initial dose is I mg increased gradually to
pulmonary congestion and increases a maximum of 10 mg/day.
cardiac output. It has a rapid onset of action e. Angiotensin-Converting Enzyme inhibitors:
and short half-life. It is given in the dose Captopril is a balanced vasodilator that
of5-l0 mcg/min and increased every 10· dilates both venous and arterial systems
15 min by5-10 mcg until the pulmonary and thus reduces both the preload and
wedge pressure has reduced to 18 mmHg afterload and increases cardiac output. Peak
or side effects occur. effects are observed within 90min following
oral administration. Renal perfusion is
b. Nitrates: They act as predominant veno
selectively increased out of proportion to
dilators with mild effects on the arterial
the increase in cardiac output. Caution
system and increase the cardiac output by
must be exerted if it is used with venous
about 18-25%.
dilators like nitrates. The usual dose initially
Sustained reduction in left ventricular is 6.25 mg three to four times gradually
filling pressure occurs for 4-5hours with increased to50-100 mg four times. Other
20 mg oforal isosorbide, for 1-5 hours with ACE Inhibitors include Enalapril, Ranipril,
sublingual administration and for 3-6 hours Lisinopril and Quinapril. They can lead
with cutaneous administration. to adverse reactions like dry cough,
IV nitroglycerine can be used in cardiac angioedema, hyperkalemia and raised
failure where predominant vasodilatation creatinine.
224
( 5 ) Cardiovascular System
In case patients are intolerant to ACE Management of Acute Left Ventricular
Inhibitors, Angiotensin Receptor Blockers Failure (LVF)
(ARBs) can be used. They include drugs
1. Rest in bed is given in a position that is most
like Losartan, Valsartan, Telmisartan, comfortable to the patient.
Olmisartan and Candisartan. They are
2. Morphine: lSmg morphineor lOOmg pethidine
less likely to produce cough as compared
I.M is given to relieve pain and allay anxiety.
to ACE-Inhibitors.
They also caused dilation of veins reducing the
f. Nesiritide : Recombinant BNP. It is a venous return to he heart.
vasodilator used in refractory cardiac
3. Oxygen: 6-8 liters/min (through Wolfe's bottle)
failure. It is given intravenously in a bolus
is given.
of 2 µg/kg followed by an IV infusion of
0.01 µg/kg/min. 4. Aminophylline: 250-500 mg. I.V. improves
cardiaccontractibilityandrelievesbronchospasm.
8. Inodilator Levosimendan : It is a calcium
5. Digitalis: Rapid digitalizat ion is done
channel sensitizer. It has a positive ionotropic
intravenously unless contraindicated.
and vasodilatory effect. It is used in acute
decompensated cardiac failure. It is given 6. Diuretics: Furosemide 40 mg. I.V. is given. It
intravenously in a loading dose of6-12 µg/kg/ may be given up to l 00 mg. if required.
minute over 10 minutes followed by 0.05 - 2 µg/ 7. BP Control: Vasopressors are given if BP is low
kg/min infusion. and hypotensives are given if BP is high.
9. Oxygen: Oxygen (through Woulfe's bottle) at the 8. Diet: Salt free diet is given till LVF improves.
rate of5-8 liters/min should be given especially Later, restricted salt diet is given.
in patients with lung disease, lung congestion 9. Phlebotomy: Removal of500 ml of blood was
or coronary heart disease. done in the past. It reduces the load in the heart
10. Miscellaneous by reducing the venous return from the limbs to
the right atrium.
a. Tranquilizers: Diazepam 2-5 mg three times
a day or phenobarbitone 30-60 mg twice or
thrice a day is useful to aHay anxiety and
achieve adequate sleep. 7 > Mitral Stenosis (MS)
__ ___ _.__
b. Mechanical measures: In cases of ascites Causes
or hydrothorax causing respirator y
A. Rheumatic heart disease: Mitra! stenosis occurs
discomfort, aspiration of fluid is helpful.
usually after 5 years age and is the commonest
Massage of lower limbs to maintain
cause of MS
peripheral circulation helps to prevent
phlebothrombosis. B. Congenital: Mitral stenosis occurs early in life
and may be associated with other congenital
11. Cardiac Re-synchronization Therapy : Or
anomalies
Biventricular Pacing : It is used in patients with
symptomatic refractory cardiac failure with C. Lutembacher's syndrome: Acquired MS + ASD.
conduction abnormality or Left Bundle Branch D. Atherosclerosis in the elderly due to calcification
Block (LBBB). This therapy involves pacing the and fibrosis of the valve, valve ring and chordae
right atrium, right ventricle and left ventricle to tendineae
improve synchrony of the cardiac chambers. E. Endomyocardialfibrosis
12. Left Ventricular Assist Device (LVADs): Like F. Hurler's syndrome: Due to deficiency of alpha-
Intra-aortic balloon pump. lmpella device, 1-iduronidase. There is corneal clouding,
Heart-Mate, Thoratic are considered when growth and mental retardation, coarse features,
medical management fails. They are usually used multivalvular, coronary, great vessel disease and
as a bridge to cardiac transplant or CABG. cardiomyopathy.
225
PRACTICAL MEDICINE
227
PRACTICAL MEDICINE
229
PRACTICAL MEDICINE
230
-����A��:
( 5 ) Cardiovascular System
Upper lobe va�culature �nrley·� !incs seen- 'Bats-Wingappearnnce- Enlarged RVH Hacmo-
more promtnent intorst1hal ndcma •i<lnmric.
Interstitial & Pulmonary pulmonar y con us &
oedema poriphoral ·pruning' of nodules
vessel
I
Fig. 5 26: X-ray chest· Mitra I valve disease (MS and MR)
�-·· . ... . -.
�LAE
LA thrombus
Fig 5 29 Lateral chest X-ray and 2-D Echo 1n parasternal long
axis view showing reduced M1tralvalvearea
231
PRACTICAL MEDICINE
6. Prophylaxis for infective endocarditis: Refer the MV is dilated using special dilators
IE Pg. 208. or fingers. Done on a beating heart.
B. If symptomatic Mitral stenosis: Indications/Contra-indications: Same
l. Medical Line of Treatment as for BMV
a. Bed Rest Complications: Scar on LA may lead
b. Salt free diet to atrial fibrillation, embolic events,
c. Diuretics like furosemide 40 mg/day MR
d. Digitalis if there is congestive cardiac Advantages: Cheaper than BMV
failure. Digoxin 0.25 - 0.5 mg is b. Open Mitral Commissurotomy
given daily. It also protects against (OMC)/Valvuloplasty
fast ventricular rate, should atrial Procedure:Cardiopulmon�ry bypassis
fibrillation occur. Beta-blockers, necessary. The MV commissures can
calcium channel blockers (verapamil be opened, LV clots removed, sub
or diltiazem) also used for decreasing valvular apparatus can be loosened.
ventricular rate. Indications: Clots in LA, MS with MR,
e. Anticoagulants (warfarin) if there is MS with Wilkins score > 8
an embolic episode or recent atrial
c. Mitral Valve Replacement (MV R)
fibrillation (avoided if infective
Indications: Sarne as OMC + Calcified
endocarditis is suspected).
MV or IE with MS
2. Treatment of Complications
Prosthetic valves:
3. BALLOON MITRAL VALVULOPLASTY
(BMV) • Bioprosthetic valves (porcine aortic
Procedure: Catheter is inserted through valves, bovine pericardium, cadaveric
femoral vein and passed into IVC, right valves) or
atrium and trans-septally to left atrium. • mechanical valves: Tilting disc valve
The balloon is inflated at the valve orifice (St Judes valve), Ball in Cage valve
to dilate the MV opening. (Starr Edwards valve)
Indications Disadvantages: Bioprosthetic valves have a
a. Uncomplicated MS with thin leaflets shorter life, whereas metallic valves need
and no calcification (Wilkins score long-term anticoagulants
<6) Normally Patient of MS never has LVH; if
b. Pregnancy with MS LVH Occurs, Suspect:
c. Elderly with operative risks A. Associated Ml, AS or Al
Contra-indications
B. Hypertension due to renal embolism
a. Calcified valve, thickened cusps, sub
C. Ischemicheart disease due to coronary embolism
valvular apparatus widening (Wilkins
score >8) D. Cardiomyopathy
b. Clots in LA
232
< 5 > Cardiovascular System
2. Hypertension B. Dyspnea, orthopnea, PND
3. Ischemic heart disease C. SIS of pulmonary hypertension, RVF or atrial
4. Cardiomyopathy fibrillation (Refer MS Pg. 225)
5. Myocarditis Diagnosis
6. Acute rheumatic fever A. Low, collapsing pulse (Water-hammer pulse)
B. Organic B. Hyperdynamic apex
1. Rheumatic C. Systolic thrill in the mitral area
2. Mitral valve prolapse D. Muffled first heart sound
3. Infective endocarditis E. Loud third heart sound (0.12-0.17 sec after S)
4. Papillary muscle dysfunction F. Widely split second heart sound, even in the
5. Endomyocardial fibrosis absence of pulmonary hypertension, because
of early closure of aortic valve.
6. Collagen disorder: SLE, Marfan'ssyndrome,
Ankylosing spondylitis, Pseudoxanthoma G. Pansystolic murmur best heard in the mitral
elasticum,Hurler's, Ehlerk Danlossyndrome area with the diaphragm and conducted to the
axilla and back. It is increased on exercise and
7. Ruptured chordae tendineae. Trauma,
has no relation to respiration. Conducted to base
following myocardial infarction, primary
of heart if posterior mitral leaflet involved.
chordal dysplasia
8. Congenital (endocardial cushion defect,
parachute mitral valve with Ostium
primum defect)
9. Following methysergide therapy
10. Iatrogenic: Post BMV, CMC
Pathophysiology
In mitral regurgitation, during systole, a portion of
the left ventricular stroke volume is being ejected back H. Flow murmur· Soft mid-diastolic murmur heard
into the left atrium rather than forward into the aorta. only in severe MR.
However, left ventricular function does not deteriorate I. If pulmonary hypertension is present, features
till late. Since there is no obstruction to the flow across of pulmonary hypertension as mentioned with
the mitral valve in diastole, left atrial pressure, is also mitral stenosis are present.
not elevated in early stages and pulmonary venous J. 'Cooing' or 'musical' or 'seagull' quality of
and arterial hypertension too does not occur early. murmur in papillary muscle dysfunction or
In late stages, left ventricle dilates to accommodate rupture of chordae tendinae
the increased volume. The increased wall tension
and the increased myocardial mass from ventricular Investigations
hypertrophy increase myocardial oxygen demand I. ECG: The ECG may be normal in early stage.
and ultimately leads to left ventricular failure. As the
l. Left atrial enlargement or overload pattern
left ventricular filling pressure rises, there is increase
appears if the patient is in sinus rhythm.
in left atrial and pulmonary venous pressure leading
to pulmonary venous and later pulmonary arterial 2. Left ventricular hypertrophy occurs as
hypertension. regurgitation increases.
3. If pulmonary hypertension occurs
Symptoms biventricular hypertrophy pattern occurs.
A. Fatigue, weakness
233
PRACTICAL MEDICINE
� � .,JL_ "!'---_,J_
I II III R L F
iY� JL�
v, V2 VJ V4 V., v6
F,g 5 32 ECG from a pat1entw,thm1tral regurg1tat1on showing leftventr1cularhypertrophy(sum ofSwave,nV, and R wave 1nV�
more than 35 cm I. and left atrial hypertrophy(b1fid pwave 1n lead 11-p-m,traleand b1phas1c p·wave,n leadV" with prominent,
negative wave.) {
...- - - - --�--- ----- - - -- .
4. Atrial fibrillation present due to LA
enlargement.
II. X-ray chest: It is usually normal in mild mitral
regurgitation.
l. Initially there is left atrium enlargement,
leading to straightening of the left heart
border, and double density between both
the main bronchi.
2 Later, left ventricular dilatation leads to
cardiomegaly.
III. Echocardiogram: It gives valuable information,
which aids in diagnosing and assessing the Differential Diagnosis
severity of mitral regurgitation (MR).
A. Table s.20 : Differences between MR
l. Increased left ventricular end-diastolic andVSD
dimensions along with large atrium, hyper
MR VSD
dynamic motion of the septum suggests
1. History History offever History of pal pi tat-
mitral regurgitation. with fleeting joint ions and dizzi nesj
2. The anterior mitral leaflet may be thickened pains from early chi Id hood
or calcified. 2. Systolic thrill At the apex, At left sternal edge
3. Pulsed Doppler and Color Doppler would 3. First sound Muffled. Normal
reveal mitral regurgitation flow and help 4. Third sound Present Absent
to assess the severity. 5. Pansystolic Best heard at Best heard at
murmur apex and con- left sternal edge
Echocardiography helps to rule out others causes of ducted to the left and conducted to
mitral regurgitation like mitral valveprolapse, infective axilla and back the right side
endocarditis, ruptured chordae tendineae. 6. Enlarged left Present Absent
atrium
234
( 5 ) Cardiovascular System
235
PRACTICAL MEDICINE
B. Surgical: Pathophysiology
MitraJ regurgitation is well-tolerated lesion The mitral valve leaflets may be large Alternatively
with slow progression. Surgical mitral valve there may be enlarged mitral annulus, abnormally long
repair (valvuloplasty or annuloplasty) or chordae or disordered papillary muscle contraction.
valve replacement is done in the following Myxomatous degeneration of the mitral valve may be
situation: present on histology.
I. Severe mitral regurgitation (NYHA During ventricular systole, a mitral valve leaflet pro
Class III or IV) lapses into the left atrium that may cause abnormal
2. Severe pulmonary hypertension ventricular contraction, and mitral regurgitation.
3. Progressive increase in LV size Clinical Features
demonstrated radiologically or by
Echocardiogram and hemodynamic I. Usually the patients are asymptomatic. There may
decompensation. be atypical chest pain, angina or palpitations.
4. Ruptured chordae tendineae and 2. Mid-systolic (non ejection) click is heard due to
resistant infective endocarditis. prolapse of the valve and tensing of the chordae
tendineae that occurs during systole 0.14 sec
after S 1
9 Mitral Valve Prolapse 3. Late systolic murmur due to mitral regurgitation
(MVP) may occur.
(Synonyms: Barlow syn., floppy mitral 4. Click and murmur occur earlier with standing or
valve, systolic click murmur syndrome, Valsalva maneuver (decreased LV volume) and
billowing mitral leaflet syn.) occur later with squatting or isometric handgrip
or exercise (increased LV volume).
Mitral valve prolapse is commonly seen in young
women with familial incidence. Usually posterior cusp Complications
prolapses. In Read's syndrome, both the anterior and
I. Severe MR
posterior cusps prolapse and hence valve replacement
is invariably required. 2. Endocarditis in patients with MR
3. Sudden death
Causes
4. Arrhythmias - ventricular and supraventricular
Its cause is unknown, but in some cases it may be a 5. Chest pain
genetically determined collagen tissue disorder as
6. Embolic phenomenon
sociated with:
I. Normal variant: Mild MVP is so common that 7. Transient ischemic attack (TIA)
it is regarded as a normal variant. It is often seen Investigations
in patients with anxiety neurosis.
I. Chest X-ray: This is usually normal unless there
2. Rheumatic heart disease
is significant mitral regurgitation.
3. Ischemic heart disease
II. ECG: This may be normal or may show T wave
4. Congenital heart disease, ASD (Secondum type),
inversion in inferior (II, Ill and aVF) and lateral
Ebstein's anomaly
(V • - V 6) leads.
5. Hypertrophied cardiomyopathy
Ill. Echocardiogram: This confirms the diagnosis
6. Connective tissue disorders: Marfan's, Ehlers by demonstrating both on M mode and 2-D.
Danlos,SLE posterior movement of one or both mitral valve
7. Thyrotoxicosis cusps into the left atrium during systole.
236
< 5 ) Cardiovascular System
B. Syphilis
C. Infective endocarditis
D. Congenital disorders:
1. Bicuspid aortic valve
2. Marfan's syn., Ehler-Dantos syn.
3. High VSD
4. Coarctation of aorta
5. Supravalvular aortic stenosis
6. Aneurysm of sinus ofValsalva
E. Connective tissue disorders:
l. Rheumatoid arthritis
2. Ankylosing spondylitis
3. Reiter's syndrome
4. Systemic lupus erythematosus
5. Pseudoxanthoma elasticum
6. Takayasu's arteritis
F. Severe systemic hypertension
G. Traumatic rupture of the cusp
F,g 5 35and5 36 2DEcho1nleftparasternallongax1sv1ew H. Dissecting aneurysm of the ascending aorta
(upperone)&ap1cal 4chamber view (lower one) showing I
m1tral valve prolapse
I. Large ventricular aneurysm
J. Following methysergide therapy
IV. Color Doppler studies
Pathophysiology
Treatment In aortic regurgitation, blood flows back from the aorta
l. Reassurance to asymptomatic patient into the left ventricle during diastole. To maintain ad
2. Beta blockers: Propranolol l 0-20 mg twice a day equate cardiac output, total amount of blood pumped
or atenolol 50 mg daily is useful for atypical chest into aorta must increase and hence left ventricular
pain and palpitations. size increases. Angina occurs not only because ofleft
ventricle enlargement leading to increased requirement
3. Mitral valve plication or replacement may be
of blood, but also because the coronaries are filled in
required for severe mitral regurgitation.
diastole and in AR, blood leaks back into the ventricles
4. Treatment of atrial fibrillation if present. in diastole. In addition, in syphilitic patients, there is
5. Antiarrhythmic agents if VPC or significant coronary osteitis, which reduces the coronary filling.
arrhythmias.
Complications: Same as for MS
6. Prophylaxis against infective endocarditis,
especially those with murmurs. Diagnosis
7. Low dose aspirin or anticoagulants for TIA
A. Blood Pressure: High systolic BP, low diastolic
BP (wide pulse pressure). Very often Korotkoff
237
PRACTICAL MEDICINE
C. Diastolic thrill in the aortic area and third and *If Water-hammer pulse is absent in a case of aortic regur
fourth left intercostal spaces in parasternal region gitation it suggests one of the following associated lesions:
D. Second sound narrowly split with loud A2. 1. Mitral stenosis 2. Aortic stenosis
E. Early diastolic murmur, de crescendo, soft and
3. Hypertension 4. Marked myocardial degeneration
blowing, in the aortic area, over the midsternum
and to the left, transmitted to the apex, best heard 2. Corrigan's sign (dancing carotids) · rapid
with the diaphragm and the patient leaning upstroke collapse of carotid artery pulse
forward and holding his-breath in expiration. If bilaterally
the diastolic murmur is best heard to the right 3. De Musset's sign: To and fro motion of the
of the sternum (aortic area) it suggests A.R. due head synchronous with the cardiac pulse
to dilatation of ascending aorta as in syphilis, 4. Quincke's sign: Increased c apillar y
Marfan's syndrome, ankylosing spondylitis pulsations felt by applying gentle pressure
and dissecting aneurism of ascending aorta. If on the nails or gently grasping the fingers
the diastolic murmur is better heard in left 3rd
5. Traube's sign: Pistol shot sound over tht
intercostal space, it suggestA.R. due to pathology
femoral arteries
of aortic valve as in rheumatic heart disease,
infective endocarditis etc. 6. Duroziez' murmur: Diastolic murmur
heard over the femoral artery when tht
diaphragm of the stethoscope is pressed
distally
7. Hill's sign: There is increase in femoral artery
pressure over the brachial artery pressure
by more than the normal difference of 10
mm Hg. The larger this difference, the more
severe is the aortic incompetence
Fig.5.37 Earlyd1astol1cmurmurof AR Table 5.23 : Differences between Acute
! - -- -- - -
238
( 5 ) Cardiovascular System
(Mild AR: 20-40 mm Hg; Moderate AR: III. Echocardiogram
40-60 mm Hg; Severe AR: >60 mm Hg) I. Vigorous cardiac contraction and dilated
left ventricular cavity
Rare Signs
1. Lighthouse Sign: Blanching & Flushing of
forehead.
2. Landolfis Sign: Alternate dilation & constriction
of pupils
3. Becker's Sign: Pulsation of Retinal Vessels
4. Muller's Sign: Pulsation of Uvula
5. Rosenbach Sign: Pulsatile Liver
6. Gerhard's Sign: Pulsatile Spleen
7. Mayer's Sign: Diastolic Drop in BP> 15 mm Hg
when arm is raised
F,g. S 39. Echoca,d,oga phy ,n P..r.isternal Long Ax,s � 1ew
B. Lincoln Sign: Pulsating Popliteal
w, th Aortic Reg u rg,1a11on
9. Locomotor brachia/is: Sign of atherosclerosis
JO. Dennisons sign: Pulsative Cervix
Investigations
I. Chest X-ray
1. LVH and dilatation
2. Dilatation of the ascending aorta
3. Ascending aorta wall calcification in
syphilis
II. ECG: Left ventricular hyp ertrophy (volume
overload) - Tall R waves and deeply inverted T
waves in the left sided chest leads and deep S
waves in the right-sided leads (LV strain)
F,g 5.40· 2D [cho1n p.;ra;;ternal long axis v1ewshow1ng
Pn'arqed LV and LA from a patient with AR
239
PRACTICAL MEDICINE
240
( 5 ) Cardiovascular System
b. LV end-systolic volume> 55 ml/m2 Symptoms
c. LV end-systolic diameter>55 mm Angina, syncope, exertional dyspnea, fatigue, pulmo
d. Cardiomegaly on X-ray nary edema, sudden death
e. LV Strain on ECG
Diagnosis
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PRACTICAL MEDICINE
242
< 5 ) Cardiovascular System
c. Table 5.29 : Differences between AS 4. Rheumatic fever prophylaxis
and Hypertrophic Obstructive 5. Treatment of cardiac failure
cardiomyopathy (HOCM)
AS HOCM
Surgical
1. Double apex Uncommon Common l. Balloon dilatation ofaortic valve gives temporary
Common
relief from obstruction.
2. Presys tolic gallop Uncommon
2. Aortic valve replacement with a prosthetic or
3. Second sound Paradoxical split- Single
ting tissue valve should be done for everyone with
aortic stenosis.
4. Systolic Second right Along left sternal
murmur space, conducted border and
to the carotids conducted to the
Mechanism of syncope in Aortic Stenosis
apex 1. Due to reduced cardiac output there is
5. Relation of sys- Murmur softer Murmur louder reduced circulation to the brain. On exercise,
tolic murmur to vasodilatation occurs in the muscles due to
Valsalva maneu-
ver or standing
utilization of metabolites, which further reduces
the effective blood flow to the brain.
6. Associated AR Common Uncommon
2. If calcification occurs in the aortic valve, it may
D. Supravalvular AS also affect the Bundle of His, which is very near.
1. There are equal pulses. Right radial better This may lead to heart block and Stokes Adams
than left. syndrome.
2. No ejection click is heard. 3. If the patient is working at the peak of the
3. Systolic thrill and murmur is transmitted to Starling's curve, exercise would not increase the
the carotids, suprasternal notch and along required increased cardiac output.
right sternal border. Prognosis
4. Facies: Prominent forehead, depressed
Life expectancy in patients developing angina is 4 yrs,
bridge of the nose, overhanging lips and
deformed teeth. syncope 3 yrs, dyspnea (LVF) 2 yrs.
5. Mental retardation, "elfin" facies, hoarse
6.
voice {Williams syn.)
Hypercalcemia
12 > Cyanotic Congenital
Heart Disease
Complications
Cyanotic congenital heart diseases are caused by ob
Same as mitral stenosis struction to the right heart outflow associated with
either an intracardiac or a great artery communication
Treatment
proximal to the obstruction. The level of obstruction
Medical and associated shunt is given in the Table:
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PRACTICAL MEDICINE
recurrent respiratory infection and severe heart b. Pulmonary artery may be dilated and
failure. aneurysmal and in long-standing calcified
2. In adolescence, exertional fatigue, dyspnea with pulmonary oligemia peripherally.
and cyanosis develop. Hemoptysis is late and c. A prominent aortic knob suggests that the
preterminal. shunt is at great vessels level.
3. Infectiveendocarditis, cerebral abscess, clubbing 11. Echocardiography: This helps to diagnose the
and erythrocytosis causing dizziness, headache underlying cardiac defect, direction of shunt
fatigue and blurred vision may occur. and presence of pulmonary hypertension.
4. Differential cyanosis and clubbing occur in PDA Table 5.30 : Differential Diagnosis of
with right to left shunt. Reversed differential Eisenmenger's Complex
clubbing and cyanosis ( clubbing and cyanosis of Patent Ventricu- Atrial Septa/
fingers with pink toes) occurs in PDA with right Ductus far Septa/ Defect
to left shunt and transposition of great vessels. Arteriosus Defect
244
( 5 > Cardiovascular System
erythrocytosis and must be treated with Variants
allopurinol.
I. In 5% of cases the left anterior descending
4. Acute hemorrhagic episodes may require platelet coronary artery has an anomalous origin from
transfusion in patients with thrombocytopenia. the right coronary artery or from the right sinus
5. Pregnancy and oral contraceptives should be ofValsalva
avoided as they lead to pulmonary thrombosis 2. ASDor patent foramen ovate occur in 25% of
and embolism. Tubal ligation carries risk from cases (pentalogy ofFa/lot'sJ.
associated vasovagal effects. Intrauterine devices
3. Aortic regurgitation, secondary to bicuspid aortic
may cause bleeding in these patients who have
valve, infective endocarditis or aortic leaflet
abnormal hemostasis and also may predispose
prolapse may occur.
to infective endocarditis.
4. Acyanotic Fallot's: In some cases of Fallot's
6. For those with advance pregnancy and heart
tetrad, pulmonary stenosis is mild and hence
failure, bed-rest is necessary in last trimester.
Oxygen may help. Spinal and general anesthesia right ventricular pressure is lower than left
should be avoided. Induced vaginal delivery and sided pressure. There is left to right shunt across
the VSD and the patient is not cyanosed but
chemoprophylaxis for infective endocarditis
must be given. pink.
5. ASD, PS with RVH (Trilogy ofFallot)
7. Heart-Lung transplant may help and offers some
hope at least for the future. Diagnosis
Tetralogy of Fa/lot (TOF) A. Central cyanosis, clubbing and polycythemia.
Tetralogy of Fallot is the most common cyanotic Cyanosis occurs because of overriding of the
congenital heart disease presenting after 1 year of age. aorta and polycythemia because of hypoxia.
Cyanosis may appear at birth or after
Fallot's· tetrad consists of:
B. Squatting episodes relieve breathlessness or
1. VSD (infracristal type)
cyanotic spells because there is:
2. Infundibular pulmonary stenosis
1. C ompression of femoral artery which
3. Overriding of aorta increases the resistanceto the left ventricular
4. Right ventricular hypertrophy. outflow and left ventricle, thus reducing the
Of these 4 features only the first two are of primary right to left shunt and hence more blood
physiological importance. goes to the lungs to be oxygenated.
2. Compression of femoral veins reduces
Fallot's Physiology (Hemodynamics in
the venous return thus reducing the right
TOF)
ventricular pressure and right to left shunt.
Pulmonary stenosis is the most physiologically impor 3. Diminished right to left shunt by the
tant defect (It results in RV hypertrophy). PS causes above two mechanisms reduces the
right heart pressure to be higher than left heart pres acid metabolites reaching the brain and
sure, which result in a "right-to-left" shunt across the depressing the respiration.
VSD. The blood is also directly shunted into the aorta
C. Hypoxic/Cyanotic attacks and syncope: Onset
(which overrides the septum).
usually during crying or after exertion. These
TheVSD is large and hence produces no murmur. The are characterized by crying, cyanosis, tachypnea,
blood flow through the PS results in ejection systolic syncope, convulsions and sometimes death.
murmur. More severe the PS, more the shunting of It occurs due to systolic contraction of a
deoxygenated blood through the VSD and into the hypertrophied pulmonary infundibulum, which
aorta, thus leading to more cyanosis. causes cessation of pulmonary blood flow.
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PRACTICAL MEDICINE
Investigations
I. ECG
1. Right axis deviation. Right Ventricular Enlargement
2. Clock wise rotation. Concave
3. Moderate right ventricular hypertrophy pulmonaiy
with upright 'T' waves in chest leads. bay
4. RVH with or without RBBB Elevation
II. X-rays ofapex
1. Coeur en Sabot (boot-shaped) heart because: Dutch-Shoe
a. Right ventricular hypertrophy lifts shaped heart
the apex clear off the diaphragm. Fig. 5.45 :Chest XrayTetrologyofFallotw1th Coren Sabot or:
b. Cap of the left ventricle above the apex Boot Shaped Heart J
of the right ventricle. 3. Paradoxical embolism is possible because
c. Pulmonary bay is deep due to of right to left shunting.
hypoplastic pulmonary artery. C. Cerebral thrombosis
2. Unilateral rib notching. D. Iron deficiency anemia
3. Oligemic lungfields. E. Epilepsy
III. Echocardiogram F. Congestive cardiac failure usually is uncommon,
but may occur if:
Two-dimensional echocardiography and Color
Doppler helps not only to delineate VSD but 1. High VSD with AR
also to diagnose associated ASD and/or PDA. 2. Infections - Pulmonary TB or IE
Overriding of aorta can also be demonstrated. 3. Associated cardiomyopathy
4. Associated severe anemia
Complications
5. Coronary thrombosis
A. Syncope from infundibular hypertonus and 6. Myocarditis
death.
Treatment
B. Cerebral abscess occurs because:
1. Polycythemia leads to sludging. A. Medical line of treatment
2. Lung, which normally filters off bacteria, 1. Of Cya notic Spells:
does not do so because of shunting. a. Knee chest position
246
( 5 ) Cardiovascular System
247
PRACTICAL MEDICINE
Tricuspid Atresia
DEFINITION: Tricuspid atresia is absence of orifice
between the right atrium and right ventricle.
Both the atria are enlarged and thickened. In 40%
there is patent foramen ovale and in the rest there is
associated ASD. Mitral valve annulus is dilated with
thickened valve leaflets. Left ventricle is enlarged and
hypertrophied. Right ventricle is small or atretic.
Associated Lesions
F19.S.46:Ebste1nsAnomaly
j
1. Transposition of great vessels
Clinical Features
2. Co-arctation of aorta
l. Dyspnea, fatigue and cyanosis
3. VSD
2. Right ventricular impulse is absent
3. First and second sounds may be split Clinical Features
4. A scratchy rub like mid-systolic ejection murmur l. First and second heart sounds are single. Second
may be heard in mid and lower sternum. heart sound (aortic) may be loud.
5. Murmurs of tricuspid insufficiency and relative 2. Loud systolic murmur of VSD or Pulmonary
tricuspid stenosis may be present. stenosis may be present. Decrease intensity of
this murmur with increasing cyanosis suggests
Investigations VSD closure.
ECG 3. Mid-diastolic mitral flow murmur may occur
4. Continuous thoracic bruits due to systemic-
l. Right atrial enlargement pulmonary collaterals may be present.
2. Right axis deviation
Investigations
3. Wide bizarre and splintered QRS complex
4. First degree A-V block, right bundle branch ECG
block supra-ventricular tachycardia and type B
WPW syndrome. I. Left axis deviation
2. Biatrial and left ventricular hypertrophy
X-ray Chest
l. Enlarged globular cardiac silhouette X-ray chest
2. Right atrial enlargement Blunt elevated apex similar to Fallot's tetrad
3. Straightening of upper left cardiac border due Echocardiography
to leftward displacement of right ventricular
This confirms absence of tricuspid valve, small right
infundibulum
ventricle, normal mitral valve and dilated annulus
Echocardiography
Treatment
Demonstrates the anatomy of the cardiac defect.
l. Medical: Similar to Fallot's tetrad
Treatment 2. Surgical: To increase pulmonary blood flow, a
l. Medical: Similar to Fallot's tetrad Rashkind balloon septostomyor a shunt (e.g. Glenn
248
{ 5 > Cardiovascular System
or Blalock) is performed. If pulmonary flow is artery and directing the left ventricle to the
too great, PA banding is done in the first year of truncus.
life. Correction of the defect is done after 2 years
age using 'Fontan' atriopulmonary connection. Total Anomalous Pulmonary Venous
Connections (TAPVC)
PersistentTruncus Arteriosus (TA) In TAPVC, the 4 pulmonary veins converge in a
Persistent truncus arteriosus consists of a single or common collecting sinus, from where the blood is
common outflow trunk that arises from the base ofthe drained into the right atrium through an anomalous
heart giving rise to systemic, pulmonary and coronary venous drainage.
circulation. It is invariably associated with VSD. TYPES: Supra cardiac, cardiac and infracardiac
Pathophysiology Pathophysiology
If the pulmonary stenosis is not significant and VSD Almost all patients with TAPVC have associated inter
large, truncal pressure equals that of the ventricles and atrial communication. Volume overload leads to right
large pulmonary blood flow may lead to L. V. overload atrial, right ventricular and pulmonary hypertension.
and cardiac failure. Ifhowever, there is significant pul The clinical course depends upon whether pulmonary
monary stenosis, pulmonary blood flow is decreased venous obstruction exists, the magnitude ofright ven
and there is hypoxia but normal heart size. The patients tricular outflow resistance and size of the interatrial
in between these two extremes may survive for many communication.
years with near normal function. If there is obstruction to the pulmonary venous drain
age, severe pulmonary edema or marked pulmonary
Clinical Features hypertension occurs. If there is inadequate interatrial
communication, right heart failure and pulmonary
1. Patient presents with cardiac failure and cyanosis
hypertension and pulmonary arteriolar disease ensues.
2. Wide bounding pulse may be present. Pulmonary stenosis may protect the individual from
3. Second sound is usually single; split may be excessive pulmonary flow and heart failure.
present due to extra-truncal vibrations. murmur
with a thrill may be present. Clinical Features
5. High pitched diastolic decrescendo murmur of The clinical features resemble those of ASD associated
truncal regurgitation may be present. with moderate cyanosis.
Investigations
I. X-ray chest
1. Marked rightward convexity with right
aortic arch
2. Cardiac pedicle is narrow due to absence
of prominent pulmonary artery
II. Echocardiography
Absence of pulmonary valve and demonstration
of the origin of the pulmonary artery from the
truncus establishes the diagnosis.
Treatment
1. Medical: Treatment of cardiac failure
2. Surgical: VSD patch closure with placement of I F g. 5 47 X-ray ofSupracarci1acTAPVCw1th Snownnn-
conduit from the right ventricle to the pulmonary I__. __ --��earanceorF1g�e�8appeara11ce ..
249
PRACTICAL MEDICINE
250
( 5 ) Cardiovascular System
Associated Lesions Investigations
A. VSD I. ECG
B. ASD 1. Normal in infancy
C. Aortic stenosis 2. Left ventricular and left at rial hypertrophy
D. Coarctation of aorta 3. Ifassociated pulmonary hyp ertension there
will be right ventricular hypertrophy
E. Endocardial fibroelastosis
4. Prolonged PR interval
F. Pulmonary stenosis
5. Atrial fibrillation sometimes
Associated Syndromes
II. X-rays
A. Downs Syndrome Trisomy 21 l. Left atrial and left ventricular hypertrophy
B. Congenital Rubella Syndrome (Deafness, 2. Marked pulmonary plethora
Cataract and PDA or Pulmonary Stenosis)
3. Aortic knuckle prominent
C. Fetal Hydantoin Syndrome due to phenytoin.
4. Notch between the aortic knuckle and the
Diagnosis pulmonary artery is obliterated
Symptoms: Recurrent respiratory infection in child 5. Calcified ductus
hood, dyspnea and angina. C. Echocardiogram would demonstrate the patent
ductus and color Doppler would suggest the
Signs direction of flow.
A. Signs of wide pulse pressure
Complications
B. Pulsations ofpulmonary artery and pulsations in
suprasternal notch A. Pulmonary hypertension
C. Heaving apex beat B. Infective endocarditis
D. Gibson's murmur: It is a continuous murmur C. Congestive cardiac failure
increased at the end of systole and early diastole
and accentuated by exercise and expiration. It is Differential Diagnosis
best heard in the pulmonary area or higher up This includes all causes of continuous murmur as
(below the clavicle in 2"d intercostal space). It is given above.
'machinery' or 'train in tunnel' in character. It is
absent: Treatment
l. Below the age of 3 years A. Medical Treatment:Indomethacin - O.lmg/kg/
2. In heart failure dose 12 hourly for 3 doses (if diagnosed within
3. If there is right to left shunt 2 weeks of birth)
E. Mid-diastolic mitralflow murmur may be heard. B. Surgical Treatment: Ligation and excision of
the ductus. All these cases require surgery unless
F. If there is pulmonary hypertension there will be
contraindicated.
signs of pulmonary hypertension as described
in mitral stenosis. In addition, there will be: Contraindications of surg ery
l. Differential cyanosis i.e. cyanosis more in Absolute contraindications:
the lower limbs than upper limbs, more l. Eisenmenger's complex
apparent after a hot bath 2. Where ductus is compensatoryalongwith:-
2. Disappearance of Gibson's and mitral mid a. Preductal coarctation
diastolic murmurs b. Transposition of great vessels
c. Tricuspid or pulmonary atresia
251
PRACTICAL MEDICINE
Relative contraindications: Diagnosis
l. Infective endocarditis (for 3 months). A. Recurrent respiratory infection of childhood
2. Congestive cardiac failure. and failure to thrive
C. Trans-catheter closure - using coils, plugs or B. Moderately collapsing pulse
umbrellas
C. Biventricular hypertrophy
D. Systolic thrill over 3«1, 4•h left parasternal regions
14 > Ventricular Septal E. Pansystolic murmur in the 3 rd and 4'hleft
Defect (VSD) --''------
F.
parasternal region, conducted to the right side
Mid-diastolic mitral flow murmur at apex
Congenital VSD, the most common congenital heart
G. S3 may be audible at apex
disease, occurs as a result of incomplete septation of
the ventricles. H. Signs ofpulmonary hypertension, if present
Sites Investigations
1. Perimembranous (most common) I. ECG
2. Muscular (apical, central, marginal, multiple- l. Normal
Swiss cheese pattern) 2. Biventricular hypertrophy
3. Inlet 3. Right bundle branch block
4. Outlet(infundibular)
II. X-rays
Associated syndromes 1. Normal
I. Trisomy 21, 18, 13 2. Biventricular hypertrophy with equiphasic
2. Cri du Chat syndrome R & S waves in V3 & V 4 (Kate-Watchel
phenomenon)
3. Fetal alcohol syndrome
3. Pulmonary plethora
Causes Ill. Echocardiogram with Doppler would define
A. Isolated the ventricular septa! defect and associated
B. VSD is invariably present in: anomalies
1. Eisenmenger's disease Complications
2. Fallot's tetrad
A CCF at 30-40 yrs
3. Pulmonary atresia
B. Pulmonary hypertension (Eisenmengers)
4. Common A-V canal
C. Infective endocarditis
5. Double outlet right ventricle
D. Arrhythmias (ventricular, supraventricular,
C. VSD is commonly present in:
complete heart block)
l. Tricuspid atresia
E. Recurrent respiratory infections or lung abscess
2. Transposition of great vessels
F. AR (if high VSD)
D. VSD is coincidental in:
1. Pulmonary and infundibular stenosis Differential Diagnosis
2. PDA Mitra! Regurgitation: Refer Pg. 232.
3. ASD
Management
4. Coarctation of aorta
5. Mitral valve deformities as in MS and MR. 1. 30 50% dose spontaneously by 3 yrs (especially
muscular or membranous types)
252
( 5 ) Cardiovascular System
253
PRACTICAL MEDICINE
G. X-rays
1. Marked dilatation of pulmonary trunk
2. Right ventricul ar and right atrial
hypertrophy
3. Hilar dance on screening
H. Echocardiogram (Transesophageal) will
demonstrate the defect in the septum.
Complications
I. Recurrent chest infections
2. IE
3. Pulmonary HT {Eisenmenger's complex)
4. Atrial fibrillation/SVT
Associated Lesions
A. Acquired Mitra! stenosis (Lutembacher's
F,g.5 48 X r�y •1ASDw th 'efttor gl't shv,t
syndrome)
254·
( 5 ) Cardiovascular System
255
PRACTICAL MEDICINE
Associated Anomalies
A. PDA
B. VSD
C. Bicuspid aortic valve
D. Congenital cerebral berry aneurysms
E. Secondary congenital endocardial fibroelastosis
__ ..
Rib F. Anomalous origin of right or left subdavian
Notching G. Turner's syndrome
..;....
H. Male sex
F,g 5 51 Rib 11otch1ng
I. Congenital AS
C. X-rays
I. Dock's sign - Rib notching due to dilated Complications
collaterals. Rib notching does not involve A. Infective endocarditis
the first and second ribs because first and B. Congestive cardiac failure
second intercostal arteries are not involved
C. Hypertension and its complications
in the collateralization process.
D. Ruptured berry aneurysm and subarachnoid
2. Shallowfigureof3silhouette-uppernotch is
hemorrhage
because ofpre- and post-stenotic dilatation
E. Aortic rupture
D. ECG : In infants the ECG is usually normal.
Left ventricular hypertrophy and left atrial F. Premature coronary artery d_isease
enlargement may occur in adults. If it occurs
Treatment
in infants it suggests associated left ventricular
outflow tract obstruction or endomyocardial A. Medical
disease. Right ventricular hypertrophy suggests I. Sedation
associated VSD. RBBB is common. 2. Anti-hypertensives
E. Other tests
3. Prophylaxis for infective endocarditis
I. Echocardiography and Color Doppler in
4. Treatment ofLVF
256
( 5 ) Cardiovascular System
B. Surgical 2. Saccular: A portion of the circumference is
Preferably between 5 and 20 years of age involved and consists of outpouching with a
mouth. Thoracic aortic aneurysm is usually
1. Balloon angioplasty (dilatation) of the saccular.
coarctation
2. Dacron or Teflon graft and end-to-end Etiology
anastomosis 1. Atherosclerosis
3. Aortic valve repair 2. Syphilis
4. Restrict energetic activities for six months 3. Connective tissue disorders: Marfan's syndrome,
post -operatively Ehlers-Danlos syndrome, lupus erythematosus.
5. Post-surgical hypertension is common. 4. Congenital diseases: Bicuspid aortic valve,
6. Follow-up for Premature coronary artery Turner's syndrome, Noonan's syndrome
disease 5. Iatrogenic: Post cardiac surgery or post cardiac
catheterization
257
PRACTICAL MEDICINE
258
( 5 > Cardiovascular System
lnnommalc ....E--'HI�.
1. Tuberculous
Superior 2. Rheumatic
vcna cuva
3. Pyogenic
4. Viral
5. Uremia
6. Post-myocardial infarction
7. Malignancy of bronchi, breast or lymphatics
8. Amebic abscess rupturing into the pericardium
Uncommon
Fig 5 54 D1agramaticsect1onofmed1ast1numshow1ng 1. Traumatic
relations of aorta with various important structures which 2. Collagen disease
are compressed
3. Blood dyscrasias: Leukemia, purpura
II. Abdominal
4. Scurvy
A. X-ray abdomen: A curvilinear or linear
5. Myxedema
rim of calcification corresponding to
the aneurysmal wall may be present. In 6. Radiation therapy
an unruptured aneurysm, psoas muscle 7. Post-pericardiotomy syndrome
shadow is intact and there is gas in the 8. Ruptured aneurysm of aorta in pericardium
bowel over the aneurysm. 9. Fungal: Actinomycosis, histoplasmosis
B. Sonography and CT scan: This helps to Secondary to inflammation in surrounding tissue
10.
evaluate the size of the aneurysmal sac as e.g. pleurisy
well as the thickness of its wall.
C. Aortography: This is helpful when the
diagnosis is in doubt as also to evaluate
the patency of the renal and iliac arteries.
However, it is potentially hazardous and
expensive.
Management
I. Medical
a. Treatment of hypertension and to avoid
smoking and tobacco.
b. Role of anticoagulants with large dots
II. Surgery: Aneurysmectomy with replacement
with synthetic prosthesis. This is particularly
reqmred if the size is more than 5 ems.
F 19 5.55 :X-,ay cl-.est show,ng Pencardi�leftu,,an
-. � -
259
PRACTICAL MEDICINE
Diagnosis Treatment
A. Precordial pain may be of 3types: I. Treatment of cause
l. Typical precordial pain which is stabbing II. Supportive
and increases on inspiration, coughing and A. Bed-rest
body movements and radiating to the neck,
B. Analgesics
arms and back
2. Dull aching pain C. Adequate diet
3. Pain in the right lower chest because of III. Steroids: 60-80 mg. prednisolone tapered after
hepatic distension 3weeks if:
B. Constitutional symptoms like fever, sweating, A. Post-pericardiotomy
weight loss, dyspnea B. Post-myocardial infarction
C. Pulse: Pulsus paradoxus C. Idiopathic.
D. /VP: markedly elevated and increases on IV. Pericardial Aspiration: This must be done
inspiration (Kussmaul's sign) if there is rapid accumulation of fluid or
E. Apex beat is not felt or very feebly felt cardiorespiratory embarrassment.
F. Increased cardiac dullness - upper border in V. Pericardiectomy:
the second space, right border parasternal and A. For chronic, recurrent effusions
left border outside the apex
B. For thick pyogenic effusions
G. Heart sounds faint and muffled
H. Pericardial friction rub
I. Hepatomegaly 19 > Cardiom�path ___
J. Ascites out of proportion to edema
K. ECG shows low voltage of the QRS complex Definition
L. X-ray: Water bottle configuration in upright Cardiomyopathies are diseases that involve primar
position ily the myocardium and not the result of congenital,
In any patient with hepatic enlargement and ascites one valvular, hypertension coronary, pericardial or arte
must always look for full jugular veins, especially on rial diseases.
inspiration. Ifpresent, a clinical diagnosis ofper icardia/
Clinical Types
effusion must be made and the other signs of it must
be looked for. l. Dilated (D) (Congestive): Left & right ventricular
260
( 5 ) Cardiovascular System
enlargement, impaired systolic function, cardiac 2. Toxic: Alcoholic
failure, arrhythmias and embolization. 3. Pregnancy
2. Restrictive (R): Endomyocardial scarring or 4. Metabolic: Hypocalcemia, Hypophosphatemia
myocardial infiltration result in right or left 5. Selenium deficiency
ventricular filling. 6. Chronic uncontrolled tachycardia
3. Hypertrophic (H): Disproportionate left 7. Right ventricular dysplasia.
ventricular hypertrophy involving the septum
move than the free wall. Clinical Features
261
PRACTICAL MEDICINE
262
{ 5 ) Cardiovascular System
X-ray chest: There may be mild to moderate left ven
tricular enlargement. 20 > Fitness for Surgery
Echocardiogram: This may demonstrate septa! hy (Pre-operative
pertrophy and systolic anterior motion of the mitral Evaluation)_
valve. The left ventricular cavity is small.
Table 5.38 : Cardiovascular Risk Factors
Treatment in General Surgery
A. Drugs 1.Major
l. Beta-blockers: Beta- blockers relieve angina a) Age > 70 years
and syncope in 33% patients. b) Myocardial infarction in past 6 months
2. Calcium antagonists : Verapamil and c) Clinical-Third heart sound, Elevated JVP
Diltiazem reduce the stiffness of the
d) Catheterization data - Ejection fraction
ventricles and reduce the elevated diastolic
< 30%, Triple vessel or Left main disease
pressures.
2,Minor
3. Disopyramide has been used in some
patients to reduce LV contractility and a) Duration of anesthesia > 3 hours
outflow gradient. b) Thoracic or upper a?dom inal surgery
B. Dual chamber pacemakerreduces outflow c) Aortic stenosis
gradient by altering the pattern of ventricular d) Hypertension
contraction
C. Surgery
Myotomyormyectomyofthehypertrophicsegment
may improve the patient symptomatically.
D. Gene Therapy in the future.
263
1 > Proforma ballismus, flexor spasms, fasciculations.,
titubation.
History III. Sensory symptoms
A. Tingling, numbness, root pains
I. Name, Age, Sex, Occupation, Right or Left
B. Feeling hot and cold water during a bath
handed, Consanguinity
C. Feeling the ground well or ground feels like
II. Motor symptoms cotton wool.
A. Power: IV. Sphincter disturbances
1. Upperlimbs: A. Bladder:
a) Proximal: Lifting the arm above 1. Feeling the sensation of bladder
the head, eating. fullness
b) Distal: Sewing, writing, buttoning, 2. Initiation ofmicturition immediately
turning a key in a lock, etc. when desired
2. Lower limbs: 3. Controlofmicturition, once the desire
to micturate has occurred
a) Proximal: Climbing stair up and
down, squatting and getting up 4. Complete evacuation of the bladder
or a feeling of residual urine
from squatting position.
5. Inability to pass urine at all
b) Distal: Slippers falling from foot
6. History of catheterization
c) Running, walking with or without
B. Bowel: Constipation / Loose Stools
suppo r t , standing witho ut
support, moving limbs in the C. Impotency: In males
bed or complete paralysis. V. Cranial nerves
Truncal : turning in bed. A. Sensation of smell - 1st CN
B. Nutrition: Wasting of muscles (proximal
B. Vision - acuity and color - 2nd CN
or distal), atrophy, hypertrophy. C. Diplopia, squint - 3rd, 4th, 6th CN
D. Sensations (Tingling, numbness over the
C. Coordination:
face, and difficulty in chewing) - 5th CN
1. Unsteadiness (For cerebellar ataxia).
E. Facial asymmetry, dribbling of saliva from
2. Difficulty in feeling the ground and the angle of the mouth, stasis offood in the
unsteadiness increasing in the dark. mouth- 7th CN
(For sensory ataxia). F. Vertigo, tinnitus, deafness - 8th CN
3. Difficulty in reaching the target. G. Hoarse voice, nasal twang, nasalregurgitatiotl
D. Involuntary movements: dysphagia - 10th + 9th CN
Chorea, athetosis, tremors, dystonia, hemi- H. Dysarthria - 12th CN
< 6 ) Central Nervous System
VI. Higher functions F. Hallucinations, delusions
A. Mental symptoms G. Speech
B. Speech disturbances II. Cranial nerves
C. Sym ptoms of raised intracranial tension: A. ICN: Sense of smell in each nostril
headache, projectile vomiting, blurred B. lICN: Acuity ofvision, field ofvision, color
vision, altered sensorium, photophobia, vision and fundus examination
diplopia
C.Ill, IV, VI CNs:
D. Unconsciousness
l. External ocular movements on follow
E. Convulsions: Inquire for aura, tonic and and command
clonic convulsions deviation of eyes,
2. Pupils: position, shape, size, equality,
incontinence of urine and stools, tongue reaction to light and accommodation
bite, fall and injuries. Post convulsion and ciliospinal reflex
drowsiness or unconscious�ness. Sleep
3. Nystagmus
attacks.
4. Ptosis (IIIrd)
VII. For Etiology
D. VCN:
A. Hypertension, diabetes, heart disease
l. Sensations over the face
B. Tuberculosis, syphilis, HIV infection
2. Masseters, pterygoids and temporalis
B. Trauma and fever muscles
C. Vaccinations, drugs or sera administered 3. Corneal and conjunctiva( reflexes and
D. Alcohol, smoking, tobacco chewing, gutka, jaw jerk
recreational drugs E. VIICN:
E. Similar episode in the past, in the family l. Eye closure, frowning, raising the
or in the surrounding eyebrows
2. Blowing, whistling and showing the
General Examination
teeth
I. Build, nutrition 3. Nasolabial fold, Platysma
II. Nails and conjunctiva: Pallor, clubbing, cyanosis, F. VIJICN:
icterus l. Hearing tick of the watch.
III. Lymphadenopathy, edema of feet, JVP 2. Rinne's test
IV: TPR, BP - look for postural drop 3. Weber's test
V: Spine: For kyphoscoliosis G. JX,XCNS:
VI. Skin: For hypopigmentedareas, hyperpigmented 1. Uvula on saying 'ah' - central or
areas, cafe-au•lait spots, nodules, etc. deviated to one side
VIL Thickened nerves 2. Gag reflex
H. XIICN:
Central Nervous System Examination
I. Tongue movements
I. Higher functions
2. W a s ting, fasc iculations a n d
A. Consciousness fibrillations
B. Behavior III. Motor system
C. Intelligence A. Nutrition: Wasting or hypertrophy
D. Memory - past and present B. Tone: Normal, hypertonia or hypotonia
E. Orientation in time, place and person C. Power: Graded from O to V
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PRACTICAL MEDICINE
D. Coordination: By finger-nose test, knee heel Ill. RS
test, rapid alternate movements at the wrist. A. Chest expansion
E. Involuntary movements. B. Dullness or hyperresonant note
IV. Sensory system C. Breath sounds
A. Superficialsensations: Touch, temperature, D. Foreign sounds
pain
E. Vocal resonance
B. Deep sensations: Position, joint and
vibration
C. Cortical sensations: Tactile localization,
tactile discrimination, tactile extinction
2 > Examination
and astereognosis A: Higher Functions
D. Calf tenderness or anesthesia of the calves
I. Consciousness
V. Reflexes Consciousness is a state of awareness of one's
self and one's environment.
A: Superficial, B: Deep, C: Primitive.
Sleep: Sleep is a state of physical and mental
Graded:Absent(-·),depressed(+), normal(++),
inactivity from which the patient can be aroused
brisk (+++) and brisk with clonus (++++).e.g.
to normal consciousness.
BJ TJ SJ Kl N Catatonia: Catatonia is a state during which
Right +++ +++ + ++++ rigid plastic postures of limbs for long hour s
are assumed. The person is unresponsive, mute
Left ++ +++ +++ ++
and immobile. It may occur in psychosis or with
BJ: Biceps Jerk; TJ: Triceps Jerk; SJ: Supinator Jerk; KJ: Knee frontal lobe and hypothalamic lesions.
Jerk; AJ : Ankle Jerk
Akinetic mutism: Akinetic mutism is a state
VI. Miscellaneous during which the patient remains immobile,
A. Signs of meningeal irritation: making no sound, follows movements slowly
Neck stiffness, Kernig's sign, Brudzinski's with his eyes and allows himself to be fed and
sign. nursed. This is seen with lesions ofdiencephalon
and brainstem.
B. S.L.R. and Lasegue's sign
Drowsiness: This is a pathological state that
C. Skull and spine resembles normal sleep. Patient can be aroused
D. Gait including Romberg's sign with an external stimulus, but reverts back to
his drowsy state on withdrawal of the stimulus.
Relevant Examination of other Systems
Semicoma: Semicoma is a pathological state,
I. CVS which requires stronger stimulation to arouse
A. Valvular heart disease: Heart sounds, the patient, though his reflexes are normal.
murmur Stupor: Stupor is often considered synonymous
B. Blood pressure in supine and standing to semicoma, whereas some doctors regard it as
a state between drowsiness and semicoma.
position : For hypertension, postural
hypotension. Coma: Thisisthedeepestlevelofunconsciousness.
Patient is immobile, all the reflexes are absent
C. Peripheral pulsations including carotid and plantar response is extensor (See Ch. 7 &
pulsations pg. 290).
D. Bruits: Over carotids or eyeballs
II. AS II. Delirium
A. Hepatosplenomegaly Delirium is the acute state of confusion with
excitement and hyperactivity.
B. Ascites
266
( 6 > Central Nervous System
Causes an epileptic attack points to temporal lobe
1. Infective: Septicemia, typhoid, cerebral origin.
malaria 2. Teichopsia preceding an attack of migraine
°
2. Withdrawal state: Alcohol represents 0ccipital visual hallucinations.
3. Toxic: Overdose of aspirin, amphetamine, 3. Grandiose delusions are the hallmark of
atropine, etc GPI (Neurosyphilis).
4. Deficiency of thiamine and nicotinic acid
VI. Insight
5. Metabolic: Renal failure, porphyria
Lack of insight is seen in:
Ill. Delusions I. Lesions of frontal lobe
Delusions are false beliefs, which cannot be 2. With deteriorating intelligence
corrected in spite of evidence to the contrary.
Delusions have to be distinguished from VII. Emotional State
superstitions, which are a part of the cultural
Hostile, depressed or euphoric. Whether the
traditions in certain societies. emotions are appropriate or not.
Causes
Causes oflncontinence of emotions/ Emotional
I. Holistic: Delusions of disordered or lability
diseased body, e.g. the body is riddled with
1. Pseudobulbar palsy
cancer or his sex is changing. This is seen
in schizophrenia or depressive illnesses. 2. Cerebral arteriosclerosis, multi-infarct state
2. Delusions of guilt: Patient may blame 3. Organic dementia· vascular
himself excessively for some trivial lapse 4. Multiple sclerosis
and expect to be imprisoned or hanged for
the same. This is seen in depressive states. VIII. Memory
3. Delusions of grandeur: e.g. A patient who A. Defect in registration: This is largely due
is a beggar may say that he is the richest to inattention. It is seen in:
man in the world, and is about to marry I. Toxic delirium
the Premier's daughter. This is seen in GP! 2. Manic states
mania and paranoid schizophrenia.
3. Senile dementia
Significance: False beliefs on a background of a
8. Defects in retention: This is seen in organic
clear consciousness are of more grave significance
cerebral disturbances like:
than those occurring when consciousness is
clouded. 1. GP!
2. Frontal lobe lesion
IV. Hallucinations 3. Senile dementia
This is false perception of sensations in the C. Defects in recall: This is seen in:
absence of any sensory stimulus e.g. humming 1. Post traumatic states
in the ears when there is no sound or seeing
2. Epilepsy
somebody who does not exist. This has to be
distinguished from illusion, which is altered 3. Korsakoff's psychosis
perception to sensory stimulus, e.g. mirage in 4. Ganser's syndrome
the desert. 5. Hysteria
Dementia is an acquired deterioration of cognitive
V. Thought Content
abilities. It comes in the way of performing activities
I. Sudden onset of fear or depression before of daily living. Memory is most commonly affected.
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PRACTICAL MEDICINE
268
{ 6 ) Central Nervous System
defect in learning to read. Hence here Wernicke's Area (Posterior temporal lobe and adjoin
mirror writing is secondary to mirror ing parietal region) (Area 22): This is concerned with
reading. comprehension of language and selection of words to
4. Reading is the ability to communicate convey meaning. In lesions of this area, spontaneous
through the written word. speech is normal, fluent and articulation is normal.
However the speech may contain incorrect words ( ver
5. Sign language is ability to communicate
bal paraphasias), incorrect letters (literal paraphasias)
by gestures.
and nonsense words (neologisms).
6. Touch language is communication by the
Occipitotemporal (lingual) gyrus is the visuopsychicarea.
written word employed by the blind in
The posterior part of the superior temporal gyrus is
reading.
the auditory (auditopsychic) cortex. The final sensory
Disorders of Language & Speech pathway leads to the inferior part of the post central
gyrus for coordination of the meaning of the informa-
The disorders of language and speech occur with le tion and the organization of any response that may be
sions of the dominant hemisphere. About 90% of the required. If any motor response is expected, then a relay
population have left cerebral dominance i.e. they are of information goes to the precentral gyrus (the motor
right handed and 10% have right cerebral dominance coordinating centre and from there, to the motor speech
i.e. they are left-handed. But among left handed people area if verbal response is expected.
60% have left cerebral dominance.
Types of Dysphasia/ Aphasia:
Dysphasia/ Aphasia Sensory (Wernicke's) dysphasia:
Definition: Dysphasia is difficulty with language func Auditory: The patient is unable to carry out simple
tion. It occurs due to lesions in the language areas of verbal commands in absence of loss of hearing. The
the dominant cerebral hemisphere. lesion is in the posterior part of the superior temporal
Pathways: The main language areas are shown below: gyrus (word deafness).
Broca's Area (Inferior frontal region) (Area 44): This Visual: Inability to read in absence of loss of vision
is concerned with generation of motor programs for (word blindness). The lesion is in the medial occipi
the production of words or parts of word. Damage totemporal gyrus. It is associated with inability to
to this area causes reduced number of words, poorly write (dysgraphia).
articulated, non-fluent speech and grammatical errors. Nominal: Inability to name objects. The lesion is in
The speech has a tele grammatic quality. the left temporoparietal region.
BROCA's (Non Fluent Apha· Lost"Telegraphic" Present Lost Lost Lost Lost
sia)
WERNICKE's (Fluent Aphasia) Present verbal paraphasias Lost Lost Lost Lost Lost
Neologism
CONDUCTION Present Present Lost Lost
ANOMIA Word finding pauses Present Present Lost Present Present
TRANSCORTICAL MOTOR Lost Present Present Present Present Present
TRANSCORTICAL SENSORY Present Lost Present Present Present Present
GLOBAL APHASIA Lost Lost Lost Lost Lost Lost
ISOLATION OF SPEECH Echolalia ++ Impaired (No purposeful speech)
AREA
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270
( 6 ) Central Nervous System
271
PRACTICAL MEDICINE
,. Nutrition
For Lower limbs: Measure the circum.
ference 16 ems above patella and 10 ems
A. Hypertrophy of Muscles: Some patients below the tibial tuberosity (knees). A
of muscular dystrophy may develop large difference in the circumferences gives
muscles especially calves, buttocks and objective evidence of wasting.
infraspinati. These muscles are weak in Causes
spite of their size. Hence they are called I. Parietal Lobe Lesions
pseudohyp ertrophy.
II. Vertebral Lesions
B. Wasting of Muscles: Wasting of muscles
A. Craniovertebral anomalies
may occur in several diseases as mentioned
below. The wasted muscles are flabby, B. Vertebral metastasis
smaller and softer than normal. When there
is associated fibrosis, the muscles feel hard,
inelastic and shortened (contracture).
To muscles
or masllCation
272
{ 6 > Central Nervous System
273
PRACTICAL MEDICINE
274
(6 > Central Nervous System
and oflong duration precipitated by alarm, relaxation begins. It can be elicited by
excitement or fatigue with resistance tapping on the tongue, deltoid or other
usually increasing with increased force or muscular masses, which produces a
passive movement of the limb. "dimple" that disappears slowly.
6. Reflex rigidity: [tis characterized by muscle
Ill. Power
spasm in response to pain e.g. board-like
rigidity ofthe abdomen in peritonitis; neck The power of all the muscles should be tested at
rigidity in meningitis. each joint in both the upper and lower limbs both
7. Gegenhalten phenomenon: Here there is against gravity and against resistance. Power in
stiffening of a limb in response to contact individual muscles is graded as follows:
and a resistance to passive changes in Table 6.7: MRC Grading of Power
position and posture. The strength of the Grade O : No power
antagonists increase as one increase s force Grade I : Flicker of contraction only
to change the position of the limb. rt can Grade II : Movement with gravity eliminated
be mistaken for Hysterical rigidity. Grade Ill : Movement against gravity
Causes: Encephalopathy, frontal lobe Grade IV : Movement against gravity & some resistance
disorders toxic (manganese, carbon Grade V : Normal power
monoxide), drugs (reserpine, pheno
thiazines) and extrapyramidal (dystonia,
athetosis and spasmodic torticollis)
8. Myotonia: There is increased muscle
tone and contraction. There is tonic
perseveration of muscular contraction
and relaxation occurs slowly. Sudden
movement may be followed by marked
spasm and inability to relax. Repetition
Fig 69·T('Sting PowerofB,ceps
of movement often brings about ease ,·- -------
of relaxation and gradual decrease in
hypertonicity.
Percussion myotonia can be elicited by
mechanical stimulation: Abrupt tapping
of the thenar eminence with hammer
is followed by opposition of the thumb,
which persists for several seconds before
275
PRACTICAL MEDICINE
276
( 6 > Central Nervous System
No. Muscle Cord Segment Nerve Action
radial extension of hand
45. Ext Policis brevis and longus C7-C8 Radial Ext of thumb Radial ext. of hand
46. Ext indices C7 (8 Radial Ext of index finger andhand.
47. lliopsous L1 ·L3 Femoral Fl and Ex of Hip.
48. Sartorius L2·L4 Femoral Fl and Ex of Hip.
49. Quadriceps Femoris L3· L4 Femoral Ext ofleg
50. Pectineus L2-L3 Obturator Add of hip
51. Adductor longus L2·L3 Obturator Add of hip
52. Adductor brevis L2·L4 Obturator Add ofhip
53. Adductor magnus L2 -L4 Obturator Add ofhip
54. Gracilis L2· L4 Obturator Add of hip
55. Obturator externus L3-L4 Obturator Add and Lat rot ofhip
56. Gluteus moximus LS ·S2 Inferior gluteal Abd ofhip
57. Gluteas meduis and minimus l4·S1 Superior Gluteal Abd and Med rot ofhip
58. Tensor fasciae latae L4-51 Superior Gluteal Abd and Med rot ofhip
59. Piriformis Sl ·52 Superior Gluteal Fl of hip
60. Piriformis LS·Sl Superior Gluteal Lat rot ofhip
61. Obturatorintemus LS-52 Br from Sacral plexus Lat rot ofhip
62. Gemelli L5·S2 Br from sacral plexus Lat rot of hip
63. Quadractus L4-S1 Br from sacral plexus Lat of rot ofhip
64. Priceps Femoris L5-S1 Sciatic El of leg, Ext ofhip
65. Semitendinasus Semi menibra- LS· 51 Sciatic Fl of leg Ext ofhip
nosus
66. Tiabialis anterior L4 Deep peroneal Df & Inv of foot
67. Extensor DigitorumLongus LS-51 Deep peronea I DF of foot Ext of 11-V toes
68. Extensor hallucdlongus LS Deep peroneal DF of foot and Ext of great toe
69. Extensor digitorum brevis 51 -S2 Deep peroneal Ext of great toe and 3 medial toes
70. Peronei L5-51 Superficial peroneal PL F avoid EV of foot
71. Gastrocnemius & plantaris Sl ·S2 Tibial Plantar Fl of Foot & Fl of knee
72. Soleus 51-$2 Tibial Plantar Fl of Foot & Anti-gravity mus
73. Flexor Digitorum Longus Sl -52 Tibial Plantar Fl of 4 lateraltoes
74. Flexor Hallusis Longus $1 ·52 Tibial Fl of Great toes
75. Tibialis Posterior L4 Tibial Add of foot
Fl= Flexor/Flexon Ext= Extensor/Extension Abd =Abductor/Abduction
Add= Adductor/Adduction Med - Medical Lat = Lateral Rot= Rotation
The various muscles of the upper and lower limbs, with their root value, nerve supplying and function are given in Table
6.2. The various movements of upper and lower limb muscles are shown In Fig. 6.6 to Fig. 6.27.
Fig 6 1 2 Testing 1nvers1on of foot ·T1b1al1s anterior and Fig 6 13 Testing Evers1on of foot Perone1 long us and
posterior (T1b1al and peroneal nerve) (L4) brev1s, Extensord1g1torum brev1s (Peron ea I nerve) (51)
- ---� - - . - ---- -- - -- � - - - ------------- ..
277
PRACTICAL MEDICINE
r
F1g.6 18:Testing elbowflex1on (half supinated)
Brach1orad1alis (Radial nerve)(CS-6)
. � . - -- ··-· -- -
Triceps
l
----.- - -L
_,_
_ _
//
·
Fig 6 24 TestingThumbAbduct1on-Ab ductorpol1c,s
brev1s (Median nerve) (Dl I
Fig.6.21 Testing (1) Ebowpronat,on PronatorTeres and
----- - ----·-· --· -- -- ._. .... -- .. -
Pronator quadratus (Mediannerve) (C6), (2) W r,st extens Ion
Allextensor muscle (Radial nerve){C6 7)
-· . -�- - -
Fig.6.22 Testing fingerflex1on - Flexord,g1 torum Fig 6 25 · P1nch1ng movement Flexor pol1c1s longusand
'
profundus (Me dian and Ulnar nerve) ((8) Flexord 91torum (Median nerve) (C8)
. - ··---- -� . -- - -- � ,-.,.- ., - -
279
PRACTICAL MEDICINE
/'
280
(6) Central Nervous System
Pronator Drift : This is a test used to detect mild arm maintaining a steady position with the eyes
weakness. It is a subtle sign of an upper motor neuron either open or closed. Ifhefalls it is generally
lesion. The patient is asked to hold both arms fully ex backwards or forwards.
tended in front of him with the palms facing upwards In a unilateral cerebellar hemispheric lesion
and hold the position. When positive, the affected or in a unilateral vestibular lesion the patient
side arm tends to drift down and pronation occurs. will sway or fall towards the involved side.
IV. Ataxia The head may be tilted towards the involved
side with the chin rotated towards the sound
Causes side.
A. Cerebellar In hysteria there may be a false Romberg's
l. Cerebellar tumor or abscess sign, often with marked unsteadiness, but
2. Vascular lesion
3. Cerebellar degeneration
4. Encephalitis
5. Hereditary ataxias
6.Drugs: Alcohol, eptoin, piperazine
citrate, streptomycin
7. Labyrinthitis
B. Sensory
1. Peripheral neuritis
2. Tabes dorsalis
3. Posterior column lesions: Subacute
combined degeneration of spinal cord
4. Parietal lobe disorders
C. Labyrinthine
1. Acute labyrinthitis
2. Meniere's disease
3. Drugs: Streptomycin
D. Central: Vascular lesion in medulla affecting
vestibular nucleus
Tests
l. Romberg's Test: The patient is asked to stand
with his feet closely approximated, first
with his eyes open and then with his eyes
dosed.
In sensory ataxia the patient is able to
maintain the upright position while the eyes
are open, but when the eyes are closed he
sways. This is a positive Romberg sign (Fig.
6.29).
In the vermis or mid-line cerebellar lesion,
there is difficulty in standing erect and
281
PRACTICAL MEDICINE
slowly at first, and then rapidly, with eyes
open and then again with eyes dosed.
In sensory ataxia the patient may carry out
the act without much difficulty while the
eyes are open, but may be unable to find
the nose when the eyes are closed.
In cerebellar ataxia there may be intention
tremors, dysmetria and dyssynergia.
Intention tremors are characterized by
hyperkinesis which becomes more marked,
more coarser and more irregular as the
finger approaches the nose.
Fig 6.36·Tandem walking In dysmetria the patient may stop before he
reaches his nose. In dyssynergia the act is
with swaying at the hips rather than the not carried out smoothly and harmoniously
ankles. but is decomposed into its constituent parts.
2. Tandem Walking: The patient is asked 4. Finger to Finger Test: The patient is asked to
to walk in a straight line by placing one abduct the arms to the horizontal and then
heel directly in front of the opposite toes, bring in the tips of the index fingers in a
both with eyes open and with eyes closed. wide circle to approximate them exactly in
(Fig. 6.30) the mid-line. In unilateral cerebellar lesion
In sensory ataxia the patient may walk fairly the arm on the involved side will sag and
well with eyes open, but on closing his eyes undershoot so that the finger on that side
he sways and staggers. will be below the one on the normal side.
r.;;;;;;;;;;;:-::-...:- -
In vermis lesions the patient sways with
eyes open and tends to fall in any direction
especially forwards or backwards. In
unilateral cerebellar hemisphere lesion the
patient deviates towards the side oflesion.
3. Finger Nose Test: The patient is asked to
abduct and extend the arm completely and
then to touch the tip of his index finger to
the tip of his nose. The test is performed
282
( 6 ) Central Nervous System
and then push it along the shin in a straight
line to the great toe. Dysmetria, dyssynergia
and intention tremors as in finger nose test
are looked for.
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PRACTICAL MEDICINE
284
( 6 ) Central Nervous System
b) Cerebral hypoxia 4. Tumor
c) Trauma 5. Demyelinating: Disseminated sclero�
d) Vascular sis
e) Tumor G. Fasciculations: They are visible twitches of
f) Infection: Encephalitis hyperirritable muscle fibers due to chronic
degenerative disease of their anterior horn
g) Toxic: Iron, copper, phenothiazine
cells. Once the anterior horn cells are
h) Drugs: Phenothiazine completely destroyed, the fasciculations
3. Segmental (symptoms localized to one cease.
part)
Fasciculations are irregular and inconstant.
a) Spasmodic torticollis (Due to They may be absent at rest, but they can be
s p a s m o f t r a p e z ius , brought out by mechanical stimulation,
sternocleidomastoid and other fatigue and cold.
neck muscles)
Causes
4. Focal
I. Motor neurone disease
a) Blepharospasm
2. Spinomuscular atrophy
b) Writer's cramp
3. Poliomyelitis
c) Hemifacial spasm
4. Intramedullary tumors
d) Oromandibular dystonia
e) Metabolic disorder: Amino acid 5. Syringomyelia
disorders (h omocystinuria), 6. Syphilitic amyotrophy
lipid disorders, Leigh's disease, 7. Diabetic amyotrophy
Wilson's disease 8. Hypoglycemia
Types 9. Hypoxia
1. Dopa Responsive Dystonia
10. Organophosphorus poisoning
2. Myoclonic dystonia
H. Fibrillations: Fibrillations are contractions
F. Myoclonus: It is a brief shock-like muscular limited to a single muscle fiber or a small
contraction, which may involve the whole group of muscle fibers. Hence they are
muscle or a small number of muscle demonstrated only on E.M.G. and clinically
fibers. The contraction may be too slight they may be seen only if present on the
to cause movements or may cause violent tongue.
movements. It is decreased by voluntary I. Flexor Spasms: In a patient with slow
relaxation. It usually disappears during compression of the spinal cord due to an
sleep. intact rubro-spinal tract which maintains
Lesion the extensor tone of the lower limbs, the
1. Olivo dentate system attitude of the patient is extension and
the flexor withdrawal reflex is inhibited.
2. Cerebral cortex
This is paraplegia in extension. When the
Causes rubrospinal tracts are also affected, the
1. Infections: Encephalitis lethargica, extensor tone can no longer be maintained
inclusion encephalitis and the flexor withdrawal reflex cannot
be inhibited. This gives rise to a sudden
2. Degenerative: Cerebral lipidosis,
involuntary contraction of the flexors of
subacute spongiform encephalopathy
the lower limbs in paraplegia. This is called
3. Vascular flexor spasm. Once the rubro-spinal tracts
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PRACTICAL MEDICINE
are totally damaged the patient assumes a weakness and wasting. Theyare also called
flexion attitude of the lower limbs due to false fibrillations.
flexor withdrawal reflex and is said to be Causes
in paraplegia in flexion.
1. Physiological: Unaccustomed
J. Tics and Habit Spasms: These are
exercise, cold or when going to sleep
involuntary stereotype movements which,
to start with, are voluntary as they serve 2. Anemia and debilitating conditions
some purpose ( e.g. contraction ofplatysma L. Titubation : Involuntary nodding of head
with a tight collar) but later persist even seen in lesions of vermis of cerebellum and
though the stimulus that initiated the old age.
movement has ceased. They relieve tension.
Theycan be inhibited by an effort of will, but D: Sensory System
re-appear when the attention is diverted.
Sensation can be divided into :
The severe form of the condition is Gilles
de la Tourette's disease which is multiple A. Superficial : Pain / temperature / superficia l
convulsive tics. touch, carried by spinothalamic pathway.
Types B. Deep : Crude touch, joint position, vibration
l. Motor tics: Simple (Clonk and carried by dorsal, coloumn pathway.
Dystonic) and complex C. Cortical : Can be tested only when other
2. Vocal tics: Simple and complex sensations are intact.
K. Myokymia: Theyare transient or persistent, 1. Touch: This is tested with cotton wool or the
quivering or flickering movements which head of the pin on all the parts of the body (Fig.
affect a few muscle bundles within a single 6.42A).
muscle but usuallyare not extensive enough 2. Pain: Superficial pain is tested with a pin prick
to cause movement at a joint. They are not on all the parts of the body and any area where
limited to the muscle fibers and undulating it is not felt adequately is noted. Deep pain is
and more widespread than fasciculations. tested by pressing the calves, tendo Achillis or
They occur due to irregular discharge
testes. It is lost in tabes dorsalis, whereas calves
spreading to and through various muscle
are tender in peripheral neuritis (Fig. 6.42B).
bundles. There is no associated muscle
3. Temperature: Two test tubes, one containing
286
{6 > Central Nervous System
terminal interphalangealjoint, either up or down
by holding the sides of digits. Pulp of finger is
not touched. Patient is asked to tell the direction
i.e. either up or down (Figs_ 6.42 D and E).
6. Vibrations: A tuning fork of 128 vibrations per
second is vibrated and placed on some bony
prominence of the patient. The patient is asked
to indicate if he feels the vibrations (see figure
6.42C)_
7. Cortical sense: Tactile localization, tactile
Mid discrim ination, tactile extinction and
Brain
stereognosis 2 point discrimination and
graphasthesia (see figure 6.42 F and G).
Sensory changes in various diseases are as below:
1. Polyneuropathy: Symmetrical glove and
Pons stocking anesthesia (affecting distal parts more)
involving all the modalities of sensations. There
is calf tenderness (Fig. 6.44)_
2. Cauda Equina and Conus Lesion: Loss of all
modalities of sensations involving especially
lower sacral segments leading to perianal
Nucleus of
V nerve anesthesia (also Refer Pg. 336) (Fig. 6.45).
3_ Multiple Roots Involvement: T here are
varying degrees of impairment of cutaneous
sensations in the distribution of the nerve
roots. Pain sensation is more affected than
touch.
4. Complete Section of Spinal Cord: All forms of
sensations are abolished below a particular level,
with a narrow zone of hyperesthesia at the upper
margin of the anesthetic zone. In some patients
Spinal cord with high cord compression sacral fibers may be
spared resulting in sacral sparing (Figs- 6.46 and
6.47).
F,g 6.43 .Sensory Pathway 5. Hemi-section of Spinal Cord: Pain and
----�- ·------- -
- -
temperature is lost a few segments below a
hot water and the other crushed ice is taken and particular level on the opposite side whilst
placed on all the parts of the body. T he patient vibration, position and joint senses are affected
is asked to denote if he feels the temperature. on the same side (Fig_ 6.48).
4. Position: The patient is explained the procedure. 6. Syringomyelia: Loss of pain temperature
With his eyes closed, a part of his limb / arm is sensation (fibers of which cross the cord in the
placed in a definite position and then he is asked anterior commissure). Touch, vibration, joint
to denote the position or place the other limb in and position senses are normaL This is also called
a similar position. dissociate anesthesia (Fig. 6.49).
5. Joint Sense : Patients eyes remain closed. After
7. Anterior Spinal Syndrome: Loss of pain,
fixing the joint, the finger / toe is moved at
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PRACTICAL MEDICINE
l
F1g.6 46 Complete section of spina
Fig 6 44 Glove and stocking cord (1) Zone of hyperesthes1a, (2) Loss
anesthesia F,g 6 45 · Perianal anesthesia of all modal1t1es of sensations
I
Fig 6 50 Loss of pos1t1on and v1brat,on Fig 6 51 :Contralateral loss of F,g 6 52 lpsilaterallossofsensat,ons
sense(Posterior spinal syndrome) sensations(Brain-stem syndrome) (Thalam1c syndrome)
I
288
< 6 ) Central Nervous System
temperature and touch below a level on both Finger pulp, lips : 3 - 5 mm
sides with preserved position,joint and vibration Palm: 2 -3 mm
sense, e.g. Anterior spinal artery thrombosis. Sole :4 cm
8. Posterior Spinal Syndrome: Loss of position, Dorsum of foot : 5 cm
joint and vibration sense below a level with
normal touch, temperature and pain senses, e.g. Back: 5 ems.
Tabes dorsalis (Fig. 6.50). 12. Hysterical:
9. Brain Stem Syndrome: Loss of touch, pain A. Complete hemianesthesia with reduced
and temperature on same side of the face and hearing, vision, taste and smell as well as
opposite side of the body due to involvement reduced vibration only over one half of the
of trigeminal tract or nucleus and lateral skull.
spinothalamic tracts (Fig. 6.51 ). B. Sharply defined sensory loss not confined
to the distribution of the root or cutaneous
10. Thalamic Syndrome: Loss of all modalities of
sensations on the opposite side of the body. nerve.
Position sense is more affected than any other C. Postural sense is rarely affected.
sensation. There may be spontaneous pain and E: Reflexes
discomfort (thalam ic pain) ofthe most torturing
and disabling type (Fig. 6.52). I. Superficial Reflexes
11. Parietal Lobe Syndrome: There is loss of The superficial reflexes have, in addition to
discriminative sensory function: a spinal reflex arc, a superimposed cortical
A. Loss oftactile localization: Patient is unable pathway, a "cerebral arc ». Impulses ascend
to localize the site touched. through the spinal cord and brain stem to the
B. Loss of tactile discrimination: When two parietal areas of the brain and have connections
stimuli are applied together, one near the with the motor centres in the pyramidal or the
other, the patient appreciates both as one premotor areas. Efferent impulses then descend
stimulus. in the pyramidal tracts. Hence a lesion of the
reflex arc or a lesion at a high level anywhere
C. Tactile extinction: When two stimuli are
along the pyramidal pathway abolishes the
applied simultaneously to two symmetrical
superficial reflexes.
portions of the body, the patient neglects
the one on the opposite side of the lesion,
though individually he appreciates the
stimulus on both sides.
D. Astereognosis: Patient is unable to appreciate
objects (like coins, keys etc.) by touch alone.
E. Primary modalities of sensations may be
affected in deep-seated parietal lobe lesions.
F. Two Point discrimination (Figs. 6.42 F and
G): This is performed with a divider. The
patient is asked to distinguish the contact
of 2 separate points of the divider when
applied simultaneously. The distance at
which the patient is unable to distinguish
the two points as separate is measured. The 3
minimum distance is different in different ,,g 6 54 Methods of elic,t,ng pla11tar ,eflex (l) Gondil
(press dow11), (2) Bab1nsk1 (stroke). (3) Schaefer (squeeze);
parts of the body which is normally:
(4)Gorclon (squeeze), (5) Oppenheim (stroke)
- -- --
. -�-· --
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PRACTICAL MEDICINE
290
( 6 ) Central Nervous System
E. Anal Reflex (S4-SS)
Elicited by stroking or pricking the skin on
mucous membrane in the perianal region.
Response: Contraction of the external anal
sphincter.
Absent:
I. Lesion of the local reflex arch of S4-SS.
2. Pyramidal lesions.
F. Hoffmann's Sign
Method: The patient's hand is pronated and
the observer grasps the terminal phalanx of the
middle finger between his forearm and thumb.
With a sharp flick, the phalanx is passively flexed
Note: and suddenly released. A positive response
consists of a sharp twitch with adduction and
l. Abdominal reflex may be presented inspite flexion of the thumb and flexion of the fingers.
of pyramidal lesions till late in motor
neuron disease and cerebral palsy. Significance: It is an index of muscular
hypertonia rather than of pyramidal lesion as
2. Beevor's sign in lesions at Tl O level. There is such. It is not always positive in presence of a
lossoflower abdominal muscle contraction pyramidallesion. It may beelicitable in a nervous
but retained upper abdominal muscle individual with no organic disease. Ifit is present
contraction. So on eliciting the abdominal on one side only, it is likely to be significant.
reflex, the umbilicus gets pulled upwards.
C. Cremasteric Reflex (Ll)
Elicited by stroking the skin on the upper, inner
aspect ofthe thigh, from above downwards with
a blunt point.
Response: Contraction ofthe cremasteric muscle
with homolateral elevation of the testicle.
Absent:
I. Lesions oflocal reflex arch of L2
2. Pyramidal lesions
3. Hydrocele
H. Wartenburg's sign :
4. Hernia
D. Bulbocavernous Reflex (S2-S4)
Elicited by pressing the glans penis.
Response: Contraction of the bulbocavernous
muscle felt at the junction of the penis and the
scrotum.
Absent:
I. Lesion of the local reflex arch of S2-S4
2. Pyramidal lesions
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PRACTICAL MEDICINE
The patient's hand is supinated. Examiner Table 6.9 : Deep Tendon Reflexes
pronates his hand and interlocks his fingers with Reflex Nerve Mode of e/ic,ta- Response
the patients. The patient pulls his fingers away tion
against the examiners resistance. Normally, the Biceps Musculo Blow upon the Flexion of the
thumb extends. In pyramidal tract lesions the C-5-6 cutaneous biceps tendon elbow
thumb adducts and flexes. This indicates early
Supinator Radial Blowupon Flexion of the
stage ofpyramidal tract disease (this is equivalent C-5-6 the tendon of forearm with
to Babinski reflex in the lower limb}. brachioradialis at supination
the distal end of
II. Deep Tendon Reflexes the radius
Physiology: The tendon reflex is the reflex Triceps Radial Blow upon the Extension of the
C-7-8 tricep tendon arm
contraction of muscle or part of a muscle in
response to stretch. Hence the sudden stretch, Finger Median Blow upon the Flexion of the fin·
brought about by tapping the tendon evokes a Flexion and ulnar palmar surface gers and thumb
C6-Tl of the semiflexed
sharp muscular contraction. fingers
Reinforcement of the tendon jerks may be Knee Femoral Blow upon the Extension of the
achieved by clenching the fists or by pulling the L3,4 quadriceps knee
flexed fingers ofthe two hands against each other tendon
(Jendrassiks maneuver), as these movements Ankle Sciatic Blow upon the Plantar flexion of
increase the activity of the gamma efferent S-1-2 tendocalcaneous the ankle
system.
292
6 Central Nervous System
(Al , (8)
(C)
F,g.6.62: Deep Tendon Reflexes (A) Biceps Jerk, (B)Tricep5Jerk, (Cl Knee Jerk and (D) Ankle Jerk
293
PRACTICAL MEDICINE
F. Urinary Bladder
Anatomy
The bladder consists of both smooth muscles
(the detrusor and the internal sphincter) and
by sharply dorsiflexing the ankle. It is striated muscles (the external sphincter). The
present in pyramidal lesions above S-1. detrusor and the internal sphincter receive
nerve supply from sympathetic (L 2,3 and 4)
Ill. Primitive Reflexes and parasympathetic (S, 2, 3 and 4) nerves. Both
nerves have afferent and efferent fibers.
A. Sucking/rooting Reflex: Gentle stroking of
the center oflips or corner oflips will result The parasympathetic afferent fibers which sub
in sucking or rooting response, respectively, serve pain and stretch sensation from the bladder
in direction of stimulus. pass up the spinal cord in the spinothalamic tract,
lying on its outer aspects. The parasympathetic
B. Grasp Reflex: Stroking in between thumb
efferent fibers contract the detrusor and relax the
and index finger will cause grasping of
internal sphincter, thus stimulateemptying ofthe
finger. Stroking the back of the hand may
bladder. The sympathetic efferent fibers on the
release the grasp.
other hand relax the detrusor and contract the
C. Pa/momenta/ Reflex: Stroking the palm will sphincter, thus inhibit emptying of the bladder.
cause ipsilateral contraction of the chin
The external sphincter is supplied by the
(mentalis).
pudenda! nerve (S2-3). Its afferent fibers
D. Glabel/ar Tap: Repeated tapping of patient's carry touch and pressure sensations from
glabella with the index finger produces the urethra to the posterior column of the
2-3 blinks maximally in a normal person. spinal cord, whilst its efferent fibers (which
It is said to be positive (abnormal) when are from the anterior horn cells) are under
the voluntary control so that it is possible to
inhibit spontaneous emptying of the bladder.
The supranudear fibers of the efferent nerves
lie close to the pyramidal tract. The paracentral
lobule is the cortical centre for the control of
voluntary activity of the bladder.
Physiology
The rise of intravesical pressure to about
25 ems of water sets off afferent impulses
from the bladder wall stretch receptors. At
the cortex they are recorded as "desire to
micturate." If the circumstances are favorable,
para-sympathetic efferents and pudenda!
Fig.6.65 GlabellarTap
294
· 6 . Central Nervous System
nerves are stimulated. Voluntary relaxation tract, voluntary control of micturition
of the external sphincter and the perinea! is lost. Hence, when the circumstances
muscles initiate the act of micturition whereas are favorable and the patient wants to
contraction of the detrusor muscle and initiate micturition, he is not able to
relaxation of the internal sphincter empty the do so immediately. After sometime the
bladder. If the circumstances are not favorable micturition reflex arc is stimulated and the
the sympathetic fibers are stimulated and patient voids urine. This is called hesitancy.
parasympathetic inhibited which contracts Again when the circumstances are not
the internal sphincter and relaxes the detrusor favorable, and the urge to mic turate occurs,
muscle. This increases the volume of the patient is unable to hold back the urine
bladder and thus intravesical pressure falls (because the voluntary cortical inhibitory
and the urge to micturate disappears. control is lost) and patient may soil his
clothes. This is precipitancy.
When more urine accumulates again, the
intravesical pressure rises and the same sequence The treatment for precipitancy is to use a
of events recur until the bladder can no longer condom catheter and attach a bag to it.
expand to reduce the intravesical pressure and Diagnosis: A positive diagnosis is made
the urge remains till the patient passes urine. by cystometry only. It shows voiding
contractions. To differentiate uninhibited
Neurogenic Bladder vs Non bladder from chronically inflamed bladder
Neurological Bladder I 00 mg Banthine is given I. V. and
In elderly patients commonly due to Benign cystometry repeated . In uninhibited
Prostatic hyperplasia (BPH), they face urinary bladder, the voiding contractions disappear
symptoms. When predominant symptoms are as they are mediated via cholinergic fibers.
urgency, hesitancy, poor stream / interrupted In chronically inflamed bladder they persist
stream, post void dribbing, they arise from BPH as non-cholinergic fibers mediate it.
(non-neurogenic bladder). B. Reflex Bladder
When Predominant symptoms are urgency, Etiology
frequency, precipitancy, and episodes of l. Transverse myelitis
involuntary passage of urine with a normal
2. Trauma
stream they indicate underlying neurolgical
3. Neoplasms
cause (neurogene bladder).
4. Meningitis
Neurogenic Bladder 5. Disseminated sclerosis
Table 6.10 : Five types of neurogenic Pathogenesis
bladders Acute transection of the cord causes
Type Lesion retention of urine during the stage of
spinal shock. If the urethral sphincter is
1. Uninhibited bladder .. Cortico regulatory tract
unable to maintain the pressure of the
2. Reflex bladder .. Spinal cord above S2
urine in the bladder, it gives way and urine
3. Autonomous bladder .. At S2, S3 and S4 level dribbles out causing retention of urine
4. Motor atonic bladder .. Motor efferents with overflow. Once a certain amount of
5. Sensory atonic bladder .. Sensory afferents
urine has been passed, pressure within the
bladder falls and the urethral sphincter
A. Uninhibited Bladder tone prevents further evacuation of
This occurs in cerebrovascular accidents, bladder. This leads to retention of residual
head injuries, brain tumors, etc. Here, urine. When more urine accumulates and
since the lesion is in the cortico-regulatory
295
PRACTICAL MEDICINE
pressure builds up in the bladder, the 4. Bladder washes: In any patient with an
urethral sphincter gives way and once indwelling catheter, bladder washes
again urine dribbles out. with antiseptic solutions like Candy's
When the stage of spinal shock passes, as lotion must be given twice a day.
a result of unopposed descending spinal 5. Bladder exercise: Once the stage of
impulses, reflex bladder activity begins spinal shock has passed, the bladder
since the local reflex arc is intact. The muscles must be stretched, else they
bladder can be stimulated by cutaneous will atrophy and lead to a small
stimuli or pressure over the hypogastrium capacity bladder. This is prevented
and a complete evacuation of bladder by bladder exercises. The catheter is
occurs. This is called automatic bladder. clamped for a few hours every day
This facilitated activity may involve the which is gradually increased so that
rectum causing mass evacuation ofbladder urine accumutates in the bladder and
and rectum. stretches it. It can be evacuated by
Slowly developing and partial lesions of releasing the clamp once the sensation
the cord do not cause spinal shock so that of fullness occurs or after a few hours.
the initial retention with overflow does Once automatic bladder develops and
not occur. These lesions cause automatic the patient is well trained, catheter
bladder activity with precipitancy of may be removed.
micturition. C. Autonomous Bladder
Diagnosis: Clinical examination will reveal Etiology
spinal cord lesion and cystometry will show l. C o ng e n i t a l: S p i n a b i fi d a,
sudden and uncontrollable voiding. meningomyelocele
Treatment: 2. Trauma: Gunshot, auto accidents
l. Catheterization of the bladder must 3. Infective: Arachnoiditis, radiculitis
be done when there is retention of
4. Neoplasms of the cord
urine to prevent the bladder muscles
from being over stretched. Again S. Surgery: Combined perinea! and
compression of the bladder wall by abdominal resection
urine leads to ischemic necrosis of Clinical Features
the bladder as the blood supply of the l. Loss of bladder sensation
bladder lies within the bladder wall. 2. Inability to initiate micturition
2. Urinaryantibiotics: Urine examination normally. Patient learns to void urine
for pus cells and RBCs and urine by applying external force to the
culture must be done. Usually urinary bladder.
infection is a rule oncecatheterization 3. Stress incontinence may occur if
is done and suitable antibiotics must there is paralysis of periurethral
be given. striated muscles, which can no longer
3. Aluminium hydroxide: T his is compress and elongate the urinary
given once a catheter is put in the sphincter when the intravesical
bladder to prevent the formation pressure is markedly elevated.
of phosphatic stones. Aluminium 4. This is usually associated with
hydroxide prevents the intestinal saddle shaped anesthesia and absent
phosphate absorption by combining bulbocavernous reflex.
with it and forming aluminium
Diagnosis: Cystometry- Absent sensation
phosphate.
296
< 6 > Central Nervous System
and positive Urecholine supersensitivity 2. Decrease in size and force of stream
test. and interrupted stream.
Treatment 3. Rec urrent episodes of u rinary
1. Cutaneous vesicostomy infections.
2. If there is continuous incontinence Diagnosis: Cystometry - Normal
of urine sensations. No involuntary contractions
a) Ureteroileostomy of detrusor. Urecholine sensitivity test is
b) Diamond-shaped wedge to be positive.
constructed at the urethrovesical Treatment
junction to narrow urinary 1. Urethral drainage
sphincter
2. Parasympathomimetic agents
D. Sensory Paralytic Bladder
Etiology Meningeal Signs
1. Tabes dorsalis I. Neck Stiffness: It is characterized by stiffness of
2. Pernicious anemia the neck and resistance to passive movements,
3. Diabetes with pain and spasm on attempted motion. The
4. Disseminated sclerosis chin cannot be pla<;ed upon the chest.
5. Syringomyelia Causes
Pathogenesis: There is loss of bladder A. Meningitis
sensation, which leads to overdistension of B. Subarachnoid hemorrhage
bladder. Initially there is normal capacity
C. Tetanus
and complete emptying. Gradually the
bladder capacity increases and residual D. Strychnine poisoning
urine appears. E. Hysteria
Clinical Features: Initially these patients F. Cervical spondylosis
are asymptomatic. Gradually there is G. Meningism
terminal dribbling, and later, overflow In meningitis neck stiffness is absent in severe
incontinence. and terminal cases or in very young infants.
Treatment: The patient must be advised
to void frequently even ifhe does not get
bladder sensation. J
E. Motor Paralytic Bladder
Etiology
1. Poliomyelitis
2. Polyradiculopathy
3. Congenital anomalies
4. Tumor
5. Trauma
II. Kernig's Sign: With the hip flexed, the knee is
Pathogenesis: Since the sensory nerves are
extended. Normally it can be done up to 135°.
intact, bladder if left alone, distends and
In meningitis it is restricted due to spasm of the
decompensates.
hamstrings. (Fig. 6.48)
Clinical features
III. Brudzinski's Sign:
1. Painful distension of the bladder and
inability to initiate micturition. A. Neck sign: On flexing the neck, there is
flexion of the hips and knees.
297
PRACTICAL MEDICINE
-::;P
' -<'=<r'
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.../y
v... ' •
(>1I
1I
I I
I I
I I
' '
I I
I I
I I
- -
B. Leg sign: On flexing one leg, the other leg First (Olfactory) Nerve
also flexes. It is present in meningitis.
Anatomy: The olfactory receptors in the nasal septum
C. Symphysissign: Pressureon symphysispubis and lateral wall ofthe nasal cavitygive central processes
is followed by flexion of both lower limbs. that form bundles, the filaments of the olfactory nerve
D. Cheek Sign: Pressure against the cheeks which penetrates the cribriform plate of the ethmoid
below the zygoma causes reflex flexion at bone and enters the olfactory bulb and then to the
the elbows, with an upward jerking of the olfactory tract in the sulcus on the orbital surface of
arm. the frontal lobe. Some of the fibers of the olfactory
IV. Bikele's Sign: The patient is seated with arms tract decussate with those from the opposite side and
elevated extended and externally rotated and then they enter the piriform lobe of the temporal lobe
forearm flexed. The examiner attempts passive (primary olfactory cortex) and then terminate in the
extension of forearm at the elbow. Resistance amygdaloid nucleus, septal nuclei and hypothalamus.
to extension occurs in brachia! neuralgia and Testing: The sense of smell is tested by asking the
meningitis. patient to sniff various non-irritating substances (like
Straight Leg Raising Test (SLR) tea, coffee, dove oil, peppermint oil etc.) separately in
With the patient supine and both legs extended, one leg each nostril and identify the odor. Irritating substances
is passively flexed at the hip keeping the knee extended. like ammonia are avoided because they stimulate, in
Normally it can be lifted up to 90". It is restricted in addition, the trigeminal nerve. Each nostril is to be
meningitis and sciatica. tested separately.
Lasegue's Sign: Anosmia
Once the leg is raised at a particular level for theS.L.R. Causes
test and the patient gets pain at that level, the foot is
A. Local disease of the cribriform plate of ethmoid
dorsiflexed. If the pain worsens, it is due to Sciatica.
bone
B. Subarachnoid hemorrhage
3 Cranial Nerves C. Neoplastic:
l. Tumors in the olfactory groove
Can be divided into:
2. Frontal lobe tumors
A. Pure Motor : III, IV, VI, XI, XII
D. Infection:
B. Pure Sensory: I, II, VIII
1. Tabes dorsalis
C. Mixed : V, VII, IX, X
2. Meningitis
298
6 Central Nervous System
E. Metabolic: Visual acuity for near vision is tested by Jaeger's
I. Refsum's disease chart. The test types are of varying sizes. The
near vision is recorded as the smallest type that
2. Paget's disease
the patient can read comfortably.
3. Hypoparathyroidism
Significance: Visual acuity is most often impaired
F. Deficiency: Zinc by changes in the shape of the globe and in the
G. Hysteria refractory characteristics of the transparent
H. Idiopathic media of the eye. Once refractory errors are
excluded, changes in visual acuity are secondary
Parosmia and Cacosmia to lesions in the macular region or its projection.
Parosmia is perversion of smell and cacosmia is All compressive and most of the non-compressive
unplesant odors. These are rare phenomena and seen lesions of the optic nerve reduce visual acuity
following head-injury or with psychiatric illness like even before a field defect can be detected.
depression. Cacosmia is seen in atrophic rhinitis. Visual acuity is unimpaired in unilateral lesion
dorsal to the optic chiasma.
Second (Optic) Nerve 2. Visual Field
Anatomy: The fibers of the optic nerve, from the To test the field of vision by confrontation method,
retina, pass backwards to the optic chiasma, where the examiner must sit opposite the patient at a
the inner half decussate, whereas the outer halfremain distance of2 feet. To test the right eye, the left eye
on the same side, forming on optic tract. Each optic ofthe patient is closed. He is asked to look fixedly
tract passes backwards to the superior colliculus, from at the left eye of the examiner, which should be at
where part of the fibers goes to the lateral geniculate the same level as that of the patient. The examiner
body, optic radiation and finally the occipital cortex holds a pencil between the patient's face and his
around the calcarine sukus (visual centre). own and keeps it moving from outside towards
Test: The optic nerve can be tested by testing the visual the patient's eye in all the four directions. The
acuity, visual fields and color vision. patient is asked to indicate as soon as the pencil
1. Visual Acuity: The visual acuity is examined at is visible in a particular direction. It is presumed
bedside with finger counting at a distance of l that the examiner's field of vision is normal.
meter. Detailed testing requires equipment not Hence if the patient sees the pencil at the same
available at the bedside and cooperation of the time as the examiner, his field of vision in that
patient, which is often lacking in patients with direction in that eye is normal. If the examiner
brain disorders. sees the pencil before the patient, the patient is
likely to have restriction of field of vision in that
Visual acuity for distant vision can be measured
by Snellen's test types which are a series of letters direction. When any abnormality is suspected
of varying sizes so constructed that the top letter in the field of vision, accurate charts should be
is visible to the normal eye at 60 meters and prepared by perimetry.
the subsequent lines at 36, 24, 18, 12, 9, 6 and 5
meters respectively. Visual acuity is expressed
as d/D. (d. distance at which the letters are
read - 6 metres and D. - distance at which the
letters should be read). Each eye should be tested
separately. The patient reads down the chart as
far as he can. If only the top letter of the chart
is visible, the visual acuity is 6/60. A normal eye
should be able to read up to seventh line i.e. the
visual acuity is 6/6.
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PRACTICAL MEDICINE
L. R
' Visual l'iclds :
,CJ)
_ ___ ( ",i.
_.,,,.;) (
0
Q
/
1-'1
-
: i
l .........__;
i
Rc1ina >
D
D 0
Optic
111.!rYC
4
Optic
chiasma
�
j) ,tj
Optic
lract
Lateral
gcniculutc
body
"' _7 ,._}
'1
l
7
Fig 6 69: Field defects associated with lesions of the optic pathways
300
( 6 ) Central Nervous System
,.
Papil/itis Papil/edema
,.
Primary Secondary
1. Guillain Barre syndrome
Optic disc Chalky white Normal
2. Leukemias and reticulosis
2. Disc margins Clear cut Hazy
3. Pseudo tumor cerebri
3. Veins Normal Dilated and tortuous
4. Anemia
4. Arteries Mild attenuation Markedly attenuated
5. Emphysema
5. Hemorrhages Absent Present
6. SLE
6. Exudates Absent Present
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PRACTICAL MEDICINE
C. Deficiency: Vitamin B 1 and B 12 When both medial rectus muscles are activated
D. Toxic: to converge the eyes, Edinger-Westphal nuclei are
activated and constrict the pupils (basis of accom
1. Tobacco, alcohol
modation reflex).
2. Drugs: INH, chloroquine, ethambutol
The final relay of the pathway is in the ciliary ganglion
enteroquinol
in the posterior orbit from where it reaches the con
3. Metals: Lead, mercury, arsenic strictor muscle of the pupil. This completes the light
E. Metabolic: Diabetes reflex pathway.
F. Vascular
Types of Pupillary Changes
Optic Atrophy A. Pin-point pupils
Causes Causes:
A. Familial 1. Poisonings
1. Cerebro-macular degeneration a) Organophosphorous
2. Hereditary ataxias b) Morphine
3. Leber's hereditary optic atrophy c) Barbiturates
4. Congenital optic atrophy
d) Alcoholic (Macewen's pupils)
5. Retinitis pigmentosa
e) Carbolic acid
B. Secondary to papilledema
2. Iatrogenic: Overdosage of neostigmine in
C. Secondary to optic neuritis treating myasthenia gravis
D. Optic conditions: 3. Pontine hemorrhage
1. Trauma
4. Hyperpyrexia: Sunstroke
2. Retinitis
5. Iritis
3. Obstruction to central vein
6. Miscellaneous:
4. Glaucoma
a) Syringomyelia
5. Tumour from optic nerve or its sheath
b) Cavernous sinus thrombosis
6. Arachnoiditis affecting optic nerve
c) Transient after Gasserian ganglionec
Pupils tomy
The pupillary size is controlled by: d) Apneic phase of Cheyne Stokes
1. Constrictor fibers innervated by parasympathetic phenomenon
nervous system B. Dilated pupils
2. Dilator fibers controlled by sympathetic nervous Causes
system
1. Parasympathetic paralysis
Since pupillary changes do not affect vision, majority
a) Vascular accidents in mid-brain
of pupillary abnormalities are asymptomatic.
b) Tentorial herniation
Parasympathetic Pathways
c) Aneurysm of carotid artery
Light falling on the retina is conveyed via optic nerve,
optic chiasma and then through both optic tracks to 2. Sympathetic stimulation
both lateral geniculate bodies. Fibers subserving light a) Cervical rib
reflex are relayed via peri aqueduct to both Edinger b) Irritative lesions in neck
Westphal nuclei. Hence, light falling on either eye,
c) Aneurysm of aorta
constricts both pupils (basis ofconsensual light reflex)
d) Mediastinal tumor
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6 Central Nervous System
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PRACTICAL MEDICINE
Accommodation
�;(<Ii]> ', //
ganglion.
� It
Fig. 6.71 : Argyll Robertson Pupils: (a)Mios1s and no
I
response to light, (b)Pupils constricts on accommodation
1
g) Syringomyelia
h) Herpes zoster ophthalmicus Light
�/\�
j) Trauma behind the eyes
Site of lesion: This is not known.
Accommodation , /
Various theories are as follows: � It
a) j Fig 6 72:Holmes-Ad1ePupils:(a)At restw1dedilated
L--------------- - - --
Damage of fibers from pre-tectal region to
rncular pupils;(b)Slow reaction to light not seen in this
the Edinger Westphal nucleus. figure, (c) More definite response to accommodation.
b) Damage at ciliary ganglion through which
passes fibers for light reflex, whereas fibers Light Reflex
for accommodation reflex pass below it. Afferent: Optic nerve
c) Damage of ciliary fibers in iris. Efferent: Oculomotor nerve
d) Peripheral degeneration of the optic nerve Method: The patient should be asked to look at a distant
and tract where pupillomotor fibers run. object in order to eliminate contraction of the pupils
6. Holmes-Adie Pupils on accommodation. The eye not being tested must be
covered in order to eliminate consensual reaction. A
Features
direct source of bright light is focussed directly into
This is a widely dilated, circular pupil that
reacts very slowly to bright light but reacts
more definitely to accommodation because of
a greater constrictive effect of accommodation.
Both reactions are minimum and due to slow
Table 6.13 : Differences between Argyll
Robertson and Holmes-Adie Pupils
Argyll Robertson Holmes-Adie
304
( 6 > Central Nervous System
, muscle
Afferent: Cervical nerves
Efferent: Cervical portion of spinal cord Horner's Syndrome
Method: A painful stimulus is applied on the neck Sympathetic Pathways
and in a dim light pupils are noted. Normally there is There are 3 neurons on the sympathetic pathways:
mild dilatation of pupils.
1. From hypothalamus to lateral grey mater in the
Significance: This reflex is lost in lesions of the cervical thoracic spinal cord.
sympathetic fibers.
2. From spinal cord to the superior cervical ganglia.
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PRACTICAL MEDICINE
3. From superior cervical ganglia to the pupils and B. Surgery on thyroid and larynx
blood vessels of the eye. Malignant disease in the jugular fossa at the skull
a) Fibers carried in the third nerve innervate base causes various combinations of Horner's
the levator muscle of the eyelid. syndrome and lesions ofIX, X, XI and XII cranial
b) Fibers in the nasociliary nerve traverse the nerves
ciliary ganglion without synapse to supply VI. Miscellaneous:
the blood vessels. Causes
c) Other fibers branch from the nasociliary A. Congenital
nerve as the long ciliary nerves to innervate B. Migraine
the pupils by passing around the eyes.
C. Lesions in the orbit or cavernous
Definition: Homer's syndrome occurs due to paralysis sinus damage both sympathetic and
of the sympathetic fibers which results in ptosis, mio parasympathetic fibers causing semi
sis, anhydrosis, enophthalmos and absent ciliospinal dilated fixed pupils
reflexes.
Variants
Causes
1. Central lesion affects sweating over the entire
I. Hemisphere lesion. head, neck, arm and upper trunk on the same
II. Brain-stem lesion: Since the sympathetic side.
pathways in the brain stem lie adjacent to the 2. Lesions in the lower neck affect sweating over
spinothalamic tract. Homer's syndrome will be the entire face.
associated with loss of pain and temperature on
3. Lesions above superior cervical ganglion may
the opposite side of the body.
not affect sweating at all as the main outflow to
Causes the facial blood vessels and sweat glands is below
A. Vasculitis the superior cervical ganglion.
B. Encephalitis 4. The presence of three neurons in the pathway
C. Multiple sclerosis leads to some useful pharmacological tests
D. Pontine glioma based on denervation hypersensitivity. Decrease
in amine-oxidase due to lesion at or beyond
III. Cervical cord lesion: Since the sympathetic
superior cervical ganglion sensitizes the pupils
fibers are centrally situated there will be usually
to adrenaline 1: 1000, which has no effect on the
bilateral Homer's syndrome with dissociate
normal pupils. Conversely the effect of cocaine
anesthesia and loss of deep reflexes in the arms.
on the pupil depends on its blocking effects on
Causes
the amine oxidase. Therefore cocaine has no
A. Syringomyelia effect on distally denervated pupil. It will only
B. Intramedullary gliomas or ependymomas dilate the pupil in the Homer's syndrome if the
IV. Dl Root lesion: lesion is below the superior cervical ganglion
Causes and there is amine oxidase at the nerve endings
for it to block.
A. Pancoast tumor
B. Cervical rib Nystagmus
C. Avulsion of lower brachia! plexus Definition: Nystagmus is rhythmic oscillation of
Features: Pain in the axilla with wasting of small the eyes
muscle of the arm. Types
V. Sympathetic chain: A. Vertical
Causes B. Horizontal - jerky or pendular
A. Neoplastic infiltration C. Rotatory
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6 Central Nervous System
Causes Table 6.14 : Differences between
A. Retinal: Vestibular and Cerebellar Nystagmus
1. Amblyopia in childhood: Cataract, high Vestibular Nystagmus Cerebellar Nystagmus
myopia, ocular palsy or chorioretinitis
1. Nystagmus is maximum Nystagmus is maximum
2. Optokinetic when visual fixation is when visual fixation is
3. Miner's prevented. attempted.
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PRACTICAL MEDICINE
308
...
{ 6 ) Central Nervous System
III Nerve: In infranuclear paralysis, there is paralysis 5. A very slight slant of the image would make the
of the medial, superior and inferior recti, inferior patient tilt his head slightly away from the side
oblique, levator palpebrae superioris and ciliary of the affected eye to line up the image from
muscles resulting in: the normal eye. Hence the head is tilted to the
I. Diplopia, squint and ptosis opposite shoulder (Bielschowsky's sign) which
causes compensatory intorsion of the normal
2. Eyeballs deviated laterally (Lateral rectus action)
eye and ameliorates diplopia.
and downwards (Superior oblique action).
The normal downward movement of Superior In nuclear paralysis, IV nerve is affected on the op
oblique cannot be tested because the paralyzed posite side as the IV nerve decussates dorsally before
Medial rectus does not allow the eye to adduct. leaving the brainstem.
Secondary action of the muscle is seen. The VI Nerve: In infranuclear paralysis there is paralysis
eyeball is depressed. If the patient makes a of the lateral rectus resulting in:
further attempt to look downwards, the eye will 1. Diplopia and squint
rotate inwards (Intorsion) because the Superior
2. Eyeballs deviated medially
oblique pull sideways across the eye when it is
in this position. In nuclear paralysis, in addition there is facial palsy
and associated brainstem signs.
3. Inability to rotate the eye upwards or inwards
Supranuclear Lesion:
4. Dilated and fixed pupils.
1. There is paresis of conjugate gaze rather than
In nuclear paralysis there is paralysis of individual
individual muscle paralysis.
extraocular muscles but without ptosis or internal
ophthalmoplegia. 2. There is no squint, diplopia or ptosis, as the visual
axes remain parallel.
IV Nerve: In infranuclear paralysis there is paralysis
of the superior oblique muscle resulting in:
l. Diplopia and squint.
2. Eyeballs deviated upwards and inwards on the
same side.
3. Difficulty in reading or going downstairs due to
inability to move eyes downwards and inwards.
4. As the patient tries to move the paretic eye
downwards, there is absence of intorsion. The Conjugate Gaze Palsies
weakness of the muscle in primary position A. Lesion of the Frontal Cortex: This leads to
(looking straight ahead) allows the eye to rotate paralysis of contralateral gaze. Hence the eyes
slightly outwards (Extortion). are deviated to the side of the cerebral lesion and
opposite to the side of hemiplegia.
B. Lesion of the Occipital Cortex: Voluntary
movements are not affected but there is loss of
follow and reflex movements.
C. Lesions of the Basal Ganglia:
1. Irritative: Causes oculogyric crisis.
2. Destructive: Attempted upward gaze causes
jerky, vertical nystagmus, Parkinsonism
and Huntington's chorea.
Light
D. Lesions of the Collicular Area:
F,g. 6 79: Right sided third nerve paralysis
I. Superior colliculi: Paralysis of the conjugate
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6 Central Nervous System
upward gaze with loss of accommodation B. Progressive damage by the prolapsing temporal
reflex. lobe as in tentorial herniation. Here the patient
2. Inferior colliculi: Paralysis of the conjugate becomes drowsy, with dilated pupils, ptosis and
downward gaze with loss of convergence finally full third nerve palsy.
reflex. In third nerve lesion due to compression, pupils
E. Lesions of Pons: are dilated early because the pupilloconstrictor
fibers are located peripherally.
This leads to paralysis of ipsilateral gaze, hence
the eyes are deviated to the opposite side i.e. The sixth nerve is usually involved in raised
same side as hemiplegia. intracranial tension, which leads to tentorial
herniation and pressure of sixth nerve against
Oculogyric Crisis the petrous tip. Hence sixth nerve palsy does
not have localizing value.
Definition: Attacks of involuntary conjugate upward
deviation of the eyeballs. Sometimes the eyes are III. At the petrous tip:
deviated to one side. A. Mastoiditis: T his causes Gradenigo's
syndrome - lesion of V, VI, VII and VIII
Causes
nerves.
1. Post-encephalitis
B. Carcinoma of nasopharynx and paranasal
2. Parkinsonism sinuses: It may infiltrate through the fissures
3. Petit ma! epilepsy of the skull and present as sudden painless
4. Phenothiazine sixth nerve palsy.
5. Neurosyphilis IV. Around the cavernous sinus:
A. Cavernous sinus thrombosis:
6. Head injury
1. Pain and edema over the eyelids
Association
2. Ophthalmoplegia with exophthal
1. Weakness of upward gaze in between the attacks
mos
2. Weakness of convergence B. Aneurysm of the intracranial portion of
Impairment of Convergence the carotid artery:
1. Pain and edema over the eyelids
Lesion: Nucleus of Perlia
2. Blindness
Causes
3. Exophthalmos
1. Disseminated sclerosis 4. Third nerve palsy
2. Encephalitis 5. Ifat the posterior end of the cavernous
3. Trauma sinus, there is associated VI nerve
4. Vascular palsy and irritation of the ophthalmic
division of the V nerve causes pain
Localizing of Lesion: over the face.
I. Within the brainstem: There will be other V. At the superior orbital fissure:
features of brainstem lesions e.g. contralateral A. Ophthalmoplegia without exophthalmos
hemiplegia. B. Pain over the face and loss of corneal reflex
II. In the basilar area: There will be multiple or (V nerve)
bilateral cranial nerve palsy: VI. In orbit:
The third nerve lesion occurs due to: A. Ophthalmoplegia with exophthalmos
A. Compression by a posterior communicating B. Pain and redness of the eyes of Tolosa Hunt
artery aneurysm: Here the onset is acute with syndrome
pain and dilated, fixed pupils.
---
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PRACTICAL MEDICINE
/';.----,-
VII. General:
A. Diabetes: P a i n fu l o r p a i n l e s s
ophthalmoplegia where pupils are
(a)�
always spared because diabetes causes
infarction involving only the central
portion ofthe nerve sparing the peripheral
Attempted Gaze to Left
•
pupilloconstrictor fibers.
with Normal Response
B. Syphilis and Atherosclerosis will produce
'
painless ophthalmoplegia.
Fifth Nerve
Anatomy
The motor nucleus of the trigeminal nerve is situated
in the pons medial to the sensory nucleus. The motor
root emerges from the anterolateral aspect ofthe pons
and passes in the posterior fossa. It overlies the apex of
the petrous bone and leaves the skull via foramen ovale
to join the mandibular division (mandibular nerve).
This supplies temporalis, masseter, pterygoids, tensor
Attempted tympani, tensor veli palati, mylohyoid and anterior
Gaze to belly of the digastric muscles. The sensory root takes
Left origin from the nerve cells in the Gasserian ganglion
Fig. 6.81 . Pathway for conJugate eye movements and enters the lateral surface of the pons. Fibers for
312
( 6 ) Central Nervous System
light touch and proprioception terminate in pons The patient is asked to open the mouth. Normally
while those for pain and temperature terminate in the jaw is central. If there is paralysis on one side,
the bulbospinal root that extends as low as the sec the jaw will deviate to that side being pushed by
ond cervical segment of the spinal cord. Distal to the the healthy lateral pterygoid muscle.
Gasserian ganglion the nerve divides into 3 divisions.
The Ophthalmic (first) division supplies the conjunc
tiva (except that oflower lid), lacrimal glands, medial
part of the skin of the nose, upper eyelids, forehead
and scalp as far as the vertex. The maxillary (second)
division supplies the cheek, front of temple, lower
eyelid and its conjunctiva, side of the nose, upper lip,
upper teeth, mucous membrane of the nose, upper
pharynx, roof of the mouth, soft palate and tonsils.
The mandibular (third) division supplies sensations
to the lower part of the face, the lower lip, ear, tongue
and lower teeth. Fig.6.84 Mas seters
..· ··
spares the angle of the jaw is organic, whereas
one that includes this area may be hysterical.
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PRACTICAL MEDICINE
Method
The patient should turn his eyes to opposite direction.
The examiner should touch the cornea or conjunctiva
from the side with a wisp of cotton. In response to
this stimulus, normally there is blinking or closing of
the same eye (direct response) and the opposite eye
(consensual response).
Significance:
1. In unilateral trigeminal nerve lesion resulting in
corneal or conjunctiva! anesthesia, stimulation
of these structures fails to produce either the
direct or consensual response, but stimulation
of the opposite side elicits both responses.
Main sensory
nucleus of Cornea Fig 6.87: Corneal Reflex
trigeminal nerve O-!Pt1.13 1 m�c
· branc h
onngemmal nerve
Trigeminal response is present, whilst on stimulating the
sensory ganglion
cornea on the unaffected side direct response
is present but consensual response is absent.
3. The conjunctiva! response is less important
clinically than corneal response as it may be
!
absent in a few normal individuals and also in
Medial hysteria.
longirudinal
fasc1culus Lesions
Facial Orbicularis
nerve oculi
Main motor
nucleus of facial l. Supranuclear lesion: Lesions interrupting the
nerve
corticobulbar pathway on one side may cause
Fig. 6.85. Corneal Reflex Arc
contralateral trigeminal paresis. Bilateral lesion
2. In unilateral facial palsy with weakness (pseudobulbar palsy) causes profound weakness
of orbicularis oculi, when either cornea is of muscles of mastication and exaggerated jaw
stimulated, response occurs only on the normal jerk. Thalamic lesion may cause contralateral
side but does not occur on the affected side. anesthesia of the face.
Hence, on stimulating the cornea on the affected 2. Nuclear lesion: This is characterized byipsilateral
side, direct response is absent but consensual atrophy, paresis and fasciculation of muscles
of mastication, ipsilateral hemianesthesia of
the face, ipsilateral tremor and contralateral
hemiplegia. Internuclear ophthalmoplegia and
ipsilateral Homer's syndrome may also occur.
3. Gasserian ganglion lesion: There is severe pain,
paresthesia and numbness on the face from the
upper lip and chin to the anterior part of the ear
with hemianesthesia of the face and weakness
of muscles of mastication.
4. Cerebello-pontine lesion: Usually the ophthalmic
division is commonly affected resulting in early
loss of corneal reflex. There would be, in addition,
Fig 6.86 ConJunct1val Reflex
lesion of the seventh, eighth and sixth cranial
nerves.
314
6 ) Central Nervous System
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PRACTICAL MEDICINE
F1g.6 89: 7th Nerve (A) ShowingTeeth; (B) Blowing Cheeks; (C) Platysma; (D) Frontails;(E) Ob1cularis Ocuil
low tones (because it no longer adequately tightens C. Frontal head of occipitofrontalis: Wrinkling of
the ossicular chain that protects the inner ear from the forehead is lost
loud noise). D. Orbicularis oris: Whistling is not possible
The sensory function to be tested is the taste sensation E. Buccinator: Cheek puffs out with expiration
on the anterior two-thirds of the tongue. Each half of
F. Muscles of facial expression:
the tongue should be tested with the four fundamental
tastes (sweet, sour, bitter and salty) and any asymmetry 1. Flattening of nasolabial fold
should be noted. 2. Drooping of the angle of the mouth on the
The reflexes to be tested are corneal, conjunctiva! and affected side
jaw jerk (Refer fifth nerve). 3. Crooked smile and laugh
316
6 Central Nervous System
PONS
oculi
Orbicularis
Emerging from
oris ----111::I
Stylomastoid Foramen
317
PRACTICAL MEDICINE
4. Impaired salivary secretions and loss of C. Between geniculate ganglion and nerve to
taste over the anterior two thirds of the stapedius
tongue. Features:
5. Eighth nerve lesion - deafness, vertigo. 1. Lower motor neurone type of facial palsy
Causes: 2. Hyperacusis
1. Herpes zoster of the geniculate ganglia 3. Impaired salivary secretions and loss of taste
(Ramsay Hunt syndrome). In addition to over the anterior two thirds of the tongue
the above features, vesicles may be present Causes:
in the external ear and over the palate.
1. Spread of infection from the middle ear
2. Spread of the infection from the middle
2. Trauma
ear.
D. Betweennerve to stapedius andchorda tympani
3. Trauma
Features:
1. Lower motor neurone type of facial palsy
2. Impairedsalivarysecretionsandlossof taste
over the anterior two thirds of the tongue
Causes:
1. Spread of infection from the middle ear
2. Trauma
E. Between chorda tympani and stylomastoid
foramen
Features: Lower motor neurone facial palsy.
Causes:
1. Bell's palsy
2. Tetanus
3. Infective polyneuritis
Fig.6.91: Right sided LMN faSC1al palsy
4. Otitis media
5. Following mastoidectomy
F. Extracranial (e.g. in parotid gland)
Features: Partiallower motor neurone facial palsy
i.e. only a few muscles affected.
Causes: Trauma, inflammation or tumor of
parotid gland
Bilateral lnfranuclear Facial Palsy
Fig.6.92: Loss of wrinkling of right forehead in LMN palsy Features:
1. Flattening of all the normal folds giving a fixed
expressionless mask-like face
2. Paucity of movements of the facial muscles
3. Sagging of the angle of the mouth
4. Dysarthria
5. Bilateral Bell's phenomenon on attempted closure
of the eyelids
318
6 Central Nervous System
Causes: A) Rinne's test: A vibrating tuning fork is
1. Acute infective polyneuritis placed in front of the ear (air conduction)
and then on the mastoid bone (bone
2. Leprosy
conduction). Normally air conduction is
3. Sarcoidosis better than the bone conduction. In middle
4. Myasthenia gravis ear disease, bone conduction is better
5. Myotonia dystrophica than air conduction. In nerve deafness air
conduction is better than bone conduction
Ramsay Hunt Syndrome but both are depressed.
Due to Herpes zoster infection of geniculate ganglion.
Patient presents with vesicular lesion over external
auditory meatus and pharynx. LMN VII nerve palsy,
loss of taste, salivation, lacrimation and hyperacusis
are present. VIII nerve may also be involved.
Mobius Syndrome
Congenital absence of VII nerve. Nucleus presents
with LMN Facial Palsy.
Eighth Nerve
Anatomy: The eighth nerve consists of two parts-the
cochlear (hearing) and the vestibular (equilibrium).
The auditory fibers from the cochlear ganglion are
distributed to the dorsal and ventral cochlear nuclei
in the pons. The vestibular fibers from vestibular gan
glion terminate in a group of nuclei in the pons and
medulla. The secondary auditory tract after partial
rt�,
decussation terminates in the inferior colliculi and
medial geniculate bodies and then proceeds to the Fig.6.95 :RinnesTest-Bone Conduction
I l
internal capsule and cortical centre for hearing. The
(A)�
rr-� (B) �
vestibular nerve is connected with the cerebellum and
I
then cerebrum.
Tests: The eighth nerve should be tested for both the
auditory as well as the vestibular functions.
.. -= /J ..,.
1. Auditory Function: Before testing the auditory
I
function, wax, if present, must be removed from
the ears. Hearing of slight sound in each ear must
be tested either with the watch (tickof the watch)
Fig.6.96: Rinne's test (A} Air conduction (Bl Bone
or rubbing fingers. If there is impairment of
conduction
hearing the following tests are done to determine
whether the disease is of the cochleovestibular B) Weber's test: A vibrating tuning forkisplaced
system or of the middle ear. over the forehead in the centre. Normally,
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PRACTICAL MEDICINE
320
( 6 ) Central Nervous System
4 Bulbar Palsy
Definition: Bulbar palsy refers to weakness of the
lower cranial nerves with or without the affection of
pyramidal, spinothalamic, proprioceptive and sym
pathetic fibers due to lesion in the medulla oblongata.
Fig. 6.99: 11th Nerve-Testing for Sternocle1domastoid ;
. - - When the supranuclear fibers of these lower cranial
Gag Reflex nerves are affected due to a lesion in the pons, mid
brain, internal capsule, corona radiata, basal ganglia or
Reflex centre: Medulla cerebral peduncles, the resultant weakness is referred
Efferent: Vagus to as pseudobulbar palsy.
Method:
Causes
Stimulation of the posterior pharyngeal wall by a
tongue blade or a cotton applicator results in eleva I. Trauma: Basal skull fractures
tion and constriction of the pharyngeal musculature II. Infections: Meningitis, encephalitis, bulbar,
accompanied by retraction of the tongue polio, diphtheria, syphilis, tuberculosis
Significance III. Vascular: Thrombosis, embolism, aneurysm and
1. The reflex may be absent or brisk in hysteria hemorrhage
2. The reflex is lost in lesions of the IX and X nerves. IV. Raised intracranial tension leading to
herniation of the medulla and cerebellar
Twelfth Nerve tonsils:
Anatomy: The twelfth (hypoglossal) nerve arises Tumors, gumma, tuberculoma
from the hypoglossal nucleus in the floor of the V. Degenerative: Syringobulbia, Motor neurone
fourth ventricle in medulla oblongata. The fibers disease
of hyp oglossal nerve emerge medial to the fibers of VI. Demyelinating: Multiple sclerosis
glossopharyngeal nerve and unite into two bundles VII. Congenital: Craniovertebral anomaly
that pass separately through the dura mater and the
VIII.Conditions mimicking bulbar palsy:
hyp oglossal canal of the skull. After leaving the skull
the two bundles unite and pass in the neck and then 1. Myasthenia gravis
to the tongue to which it supplies the motor branches. 2. Tetanus
The supranuclear control is through the corticobulbar 3. Rabies
fibers. The genioglossus is controlled by contralateral
corticobulbar tracts whereas the other muscles have a Clinical Features
bilateral supranuclear control. I. Due to lesions of cranial nerve nuclei:
Tests: The tongue should be observed at rest and on A. IX, X cranial nerves: Nasal twang, nasal
protrusion and various movements are noted. Uni regurgitation, hoarse voice, dysphagia, loss
lateral lesion may cause paresis, atrophy, furrowing, of sensations over the posterior one-third
fibrillations and fasciculations on the affected half of the tongue, weak cough and absent gag
of the tongue. On protrusion, the tongue deviates to reflex, weak cough reflex. In unilateral
the paralyzed side due to unopposed action of the lesion, there is never a complete paralysis
contralateral genioglossus. Bilateral weakness in ad- of deglutition or of articulation, but in
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PRACTICAL MEDICINE
extensive or bilateral lesions there may be lesions usually do not cause any neurological
profound impairment of these functions. deficit because ofbilateral corticobulbar input.
B. XI cranial nerve: Weakness oftrapezius and However, bilateral lesions (pseudobulbar
sternomastoid muscles. palsy) may cause severe dysphagia, explosive
C. XII cranial nerve: Dysarthria, wasting and dysarthria, pathological laughter and crying,
weakness oftongue muscles and sometimes spastic tongue, severe retching and vomiting
fibrillations over the tongue. and exaggerated jaw jerk. The cough reflex is
II. Due to damage to fiber tracts: intact.
A. Pyramidal tracts: Since pyramidal tracts 2. Nuclear or Intramedullary lesions: This may
cross at the lower level ofmedulla, unilateral lead to involvement ofninth, tenth, eleventh and
lesion causes crossed hemiplegia. Due to sometimes twelfth nerve damage with pyramidal
proximity ofthe two pyramidal tracts there signs and other brain-stem signs as mentioned
may be paraplegia or decerebrate type of above. The common causes are syringobulbia,
rigidity. motor neurone disease, demyelinating disease,
B. Spinothalamictracts:Sincethespinothalamic vascular lesion, malignancy and bulbar polio.
tracts are crossed tracts, unilateral lesion In bulbar polio, often the long tract signs are
of these tracts lead to loss of touch, absent.
temperature 3. Jugular foramen syndrome: This consists of
C. Descending tract and nucleus of the affection ofthe ninth, tenth and eleventh nerves.
trigeminal nerve: This causes loss of touch, The common causes are glomus tumors and basal
temperature and pain on the same side of skull fracture.
the face. 4. Retropharyngeal and retroparotid space
D. Spinovestibular and vestibulospinal tracts: lesions: The lesions in this area may affect
Ipsilateral nystagmus and other cerebellar the ninth, tenth, eleventh and twelfth nerves
signs. with or without affection of the sympathetic
E. Spinovestibular and vestibulospinal tracts: chain and seventh nerve. The common causes
Vertigo. are retropharyngeal carcinoma, abscess,
F. Sympathetic tract: Ipsilateral Homer's lymphadenopathy, aneurysm, trauma or surgical
syndrome. procedures.
G. Medial lemniscus: Ipsilateral loss of
proprioceptive sensations.
H. Medial longitudinal fasciculus: Ipsilateral
5 > Hemi�leg_ia__
abducting nystagmus with weakness of Definition: Hemiplegia is paralysis of one half of the
adduction in the opposite eye. body i.e. upper and lower limbs of the same side. It
III. Vital functions: may be associated with weakness of facial muscles
Involvement ofthe dorsal efferent nuclei ofboth on the same side (ipsilateral hemiplegia) or opposite
vagus nerves or pressure on the medullary centres side (contralateral hemiplegia). Hemiparesis signifies
may lead to: weakness.
1. Bradycardia and hyp otension. Causes
2. Respiratory failure.
3. Disturbance in gastrointestinal function. Sudden Onset Hemiplegia
4. Hyperglycemia
I. VASCULAR:
Differential Diagnosis A. Thrombosis:
1. Supranuclear lesions : Unilateral supranuclear 1. Ar terial: Atherosclerosis, arteritis,
syphilis, collagen diseases
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2. Venous: Cortical thrombophlebitis, IV. Todd's Paralysis (Post ictal)
post partum or postoperatively V. Hysteria
B. Embolism usuallyfrom: VI. Metabolic : hypoglycemia, hypokalemia.
1. Heart: Auricular f ibrillation,
Gradual Onset Hemiplegia
myocardial infarction, infective
endocarditis I. Cerebral tumor
2. A r t e r i e s : De tachment of a n II. Chronic subdural hematoma
atheromatous plaque usually from III. Infections: Cerebral abscess, meningitis and
the aorta or the carotid artery encephalitis
3. Veins: Thrombophlebitis especially IV. General paralysis of insane
from the veins of the lower limbs and V. Congenital defects e.g. cerebral agenesis
pelvis
4. Miscellaneous: Post cardiac surgery, Transient or Recurrent Hemiplegia
Caisson's disease I. Transient ischemic attacks
C. Hemorrhage: Rupture of - II. Hypertensive encephalopathy
1. Berry's aneurysm III. Post epileptic
2. Atherosclerotic vessel IV. Congestive attacks of GPI
3. Angiomatous malformation V. Hysterical
D. Hypertensive encephalopathy VI. Multiple sclerosis
E. Arteritis/ Vasculitis VII. Hemiplegic migraine
II. Intracranial Infections:
Hypertensive Encephalopathy
A. Encephalitis
B. Meningitis A. Due to cerebral disturbances:
C. Congestive attacks of GPI 1. Sudden onset of headache, vomiting,
unconsciousness and convulsions
III. Trauma - Depressed Fracture of Skull
Differential Diagnosis
Table 6.16 : Differences between Thrombosis, Embolism and Hemorrhage
Thrombosis Embolism Hemorrhage
1. Age Middle or old Young or old Middle or old
2. Onset Sudden or progressive (stuttering) Instantaneous Catastrophic and progresses rapidly
3. Time Early morning After exertion Post stress/ anxiety
4. Premonitory symptoms May be present Absent Absent
5. Signs of increased intracra- Absent Absent Usually present - headache, vomiting,
nial tension. unconsciousness
6. Convulsions Rare Common Usually absent
7. Neck stiffness Absent Absent Frequent
8. Conjugate deviation of the Absent Absent Present
eyes
9. B.P. High Normal Usually high
10. Leucocytosis Absent Absent Common
11. CSF Usually Normal Normal Blood stained Increased pressure
12. Recovery Usual Usual Not so
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2. Infection Table 6.17 : Differences between
i. Epidural abcess Functional and Organic Paraplegia
ii. Tuberculosis : Cold Abcess, Functional Organic
Collapse ofVertebral Column 1. Tone Hysterical rigidity Hypotonia or
3. Tumours may be present, clasp knife
but never hypoto- rigidity
i. Lipomas, Neurofibromas,
nia or clasp knife
Meningomas, Leukemia rigidity
ii. Metastasis causing fracture 2. Power Astasia abasia: Varies from
dislocation of ver tebral Inability to stand grade Oto
column. though the motor grade
4. Others : Aortic aneurysms power is normal in IV
recumbent position
compressing the vertebr al
column, fluorosis. 3. Involuntary Usually none Flexor spasms/
movements fasciculations
B. Extramedullary Intradural
4. Wasting Usually absent May be pres-
1. Arachnoiditis : Tuberculosis, ent
Syphillis,Pyogenic,Cryptococcus,
5. Sensations; None. Patient Present.
Toxoplasmosis, Fungal, Chemical
correlation does not burn or Sensory
2. Tumours:Lipoma,Neurofibroma, between sen- cut the anesthe- level usually
Meningoma sory tic skin. present with a
loss&known zone of hyper-
C. Intramedullary
anatomical esthesia
1. Syringomyelia distribution above.
2. Infection: Tuberculoma, Syphillis 6. Deep reflexes Normal or brisk Absent or brisk
(gumma)
7. Plantar response Never extensor Extensor
3. Tumour : Glioma, Lipoma
8. Sphincter Absent Maybe pres-
4. Trauma : Hematomyelia disturbances ent
5. Others : Hemangioma, A-V
Malformation Table 6.18 : Differences between Upper
Motor Neurone and Lower Motor
II. Due to Lower Motor Neuron Lesions Neurone Diseases
A. Anterior Horn Cells Upper Motor Lower Motor
1. Infections : Poliovirus, HIV, HTLV-1 Neurone Neurone
2. Motor Neuron Disease 1. Affection Muscle groups Individual
B. Roots muscles
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Table 6.19 : Localisation of the Spinal Cord Lesion in Paraplegia
Sensory system Motor system Reflexs
1. CI-C4 Sensory loss in the neck. Spastic quadriplegia. Trapezius Abdominals and Cremasteric lost.
involved. and sternomastoid may Plantars extensors. Deep jerks
be brisk.
2. CS-Tl Sensory loss above the manubri Wasting and weakness of the Abdominals lost, plantars Deep
um sterni and the upper limbs. muscles of the upper limbs. Spas jerks of the upper limbs lost, those
tic flexous, adduction. of the lower limbs brisk.
Paraplegia.
3. T2-L 1 Upper limb sensation normal. Wasting and weakness of the Abdominal lost, plantars exten
Sensory loss below the level of intercostals and/or abdominal sors. Deep jerks of upper limbs.
the lesion over the thorax and muscles and spastic paraplegia. Normal, those of lower limbs brisk.
abdomen. ED
4. L2-IS Upper limb sensation normal Wasting and weakness of flexors Abdominal and cremasteric pres
Sensory loss below the anterior and abductors of hip, exten ent.
superior iliac spine. sors of the knee & dorsiflexors Plantars-extensor. Upper
of the ankle. limb jerks normal.
K.J.absent. A.J. brisk.
5. 51-52 Sensory loss over the sole and Weakness and wasting of the Abdominals, cremasteric, upper
calves and lower posterior aspect gluteii, thigh, calf, peroneal and limb jerks & K.J. normal. Plantars
of the thigh. small muscles of the foot. lost A.J. lost.
6. 53-54 Saddle-shaped anesthesia urine No weakness but incontinence All normal, except anal
and feces. incout of and bulbocavernous which
are lost
7. Conus medul- Perianal anesthesia No paralysis, sphincter distur All normal, except anal and bulbo
laris bances common cavernous which are lost.
8. Cauda Equina Localisation of lesion depends upon the roots (between L2 and 55) involved.
Causes G. Miscellaneous:
A. Hereditary ataxias: 1. Paget's disease of bones
1. Friedreich's ataxia. 2. Multiple metastasis
2. Sanger Brown ataxia Lesions of the Spinal Cord
B. Infections:
Transverse Myelopathy: (Complete spinal cord tran
1. Syphilis section): When there is complete transection, all the
2. Tuberculosis motor and sensory functions below the level of spinal
3. Arachnoiditis cord damage are disturbed.
C. Vascular: Eel's disease 1. Sensory: All sensations (touch, pain, temperature,
D. Toxic: vibration and position) are impaired below the
1. SMON level of the lesion. Root pains or segmental
paresthesia may occur at the level of the
2. Alcohol
lesion. Localized vertebral pain (with tumors
E. Deficiency: and infections) may be present and may be of
1. Subacute combined degeneration localizing value.
2. Pellagra 2. Motor: Paraplegia (paralysis ofboth lower limbs)
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or quadriplegia (paralysis of all the four limbs) charac terized by paraplegia following
occurs below the level of the lesion. Initially, the vaccination. Recovery may occur.
weakness is flaccid and areflexic due to spinal 8. Compression myelitis: This is characterized
shock, later, hypertonic hyp erreflexic paralysis by subacute or gradual onset of one or more
occurs. features of transverse myelopathy. There is
At the level of the lesion, lower motor neurone usually presence of root pains due to irritation
signs (wasting, weakness, areflexia and paralysis) of the nerve roots at the level and sometimes
pain, tenderness, rigidity and deformity of the
occur due to damage to the anterior horn cells
vertebral column.
or their ventral roots.
9. Neoplasms: The spinal neoplasms may be
3. Reflexes: Below the level of the lesion there is intramedullary, extramedullary or extradural.
loss is superficial reflexes, extensor plantar and Differences between intramedullary and
brisk deep reflexes. extramedullary tumors are as follows:
4. Autonomic disturbances: Anhydrosis, trophic
skin changes, impaired temperature control, Multiple Transverse Levels
vasomotor instability, impotence and bladder Multiple transverse levels may occur in the following:
disturbances may occur. 1. Arachnoiditis
Causes 2. Multiple secondaries
1. Traumatic spinal cordinjuries: There is sudden 3. Multiple neurofibromatosis
onset of transverse myelopathyfollowing trauma. 4. Spinal angiomas
Recovery is usually uncommon. Electric shock, 5. Disseminated sclerosis
lightening or radiation expsoure may cause
spinal cord transection immediately or after Hemisection of the Spinal Cord
many years. 1. Sensory: Loss of pain and temperature on the
2. Viral transverse myelitis: There is an acute or opposite side and loss of position and vibration
subacute onset of transverse myelopathy with sense on the same side below the level of lesion.
tingling and numbness to start with. Recovery Hyperaesthethic band at level of lesion.
often occurs. 2. Motor: Spastic monoplegia of lower limb or
3. Tuberculous transverse myelitis: Refer hemiplegia may occur below the level of the
Tuberculosis of CNS. lesion on the same side. Segmental lower motor
4. Anterior spinal artery thrombosis: There is an neurone signs occur at the level of the lesion.
acute onset of transverse myelopathy but the 3. Reflexes: Below the level of the lesion on the same
posterior columns are not affected because they side, superficial reflexes are lost, deep reflexes
are supplied by the posterior spinal artery. are brisk and plantars are extensor.
5. Multiple sclerosis: This is common in young Causes: Extramedullary lesion
females between 20-40 years in age. There are
characteristically relapses and remissions of Lesions Affecting Spinal Cord
primary optic atrophy, paraplegia and Charcot's
Centrally
triad (staccato speech, intention tremors and
nystagmus). 1. Sensory: The decussating fibers of the
6. Post Infectious demyelination : This is spinothalamic tract conveying pain and
characterized by paraplegia after viral infections temperature sensations are affected initially
with neurotropic viruses like mumps, measles, causing analgesia and thermoanesthesia in a
rubella, chicken pox, small pox. Complete suspended bilateral distribution. Touch, position
recovery usually occurs. and vibration sensations are normal (dissociate
7. Pos t-vaccinial demyelination: This is anesthesia). Affection of the spinothalamic and
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Table 6.20 : Differences between Extra brain-stem (syringobulbia). It is common in
medullary and lntramedullary Tumors males between 25-40 years age. There is gradual
onset of the above signs. In addition, trophic
Extramedullary lntramedullary
changes, kyphoscoliosis and pes cavus occur.
Radiating Fumicular pain If syringobulbia occurs, there is affection of
1. Root pains Common Rare ninth, tenth, and eleventh cranial nerves,
2. Dissociate anes- Uncommon Common nystagmus and Horner's syndrome.
thesia 2. Hematomyelia: This resembles syringomyelia
3. Pyramidal signs Marked Not so marked but the onset is acute following injury and there
4. Wasting Minimal Marked
is involvement of all the four limbs.
5. Brown Sequard May occur Does not occur
3. Intramedullary tumors: This resembles
syndrome syringomyelia in presentation and is often
difficult to differentiate clinically.
6. Sphincter distur- Late Early
bances N .B: In acute central cord syndrome, after hyper exten
7. Trophic changes Minimal Marked sion injury of the neck, the patient becomes quadriplegic
due to cervical trauma but within a few hours regains
8. Spinal tender- May be present Usually absent
ness strength in the legs. However severe motor impairment
in the arms remains (man in a barrel syndrome) due
9. CSF proteins Raised Normal
to damage to the gray matter at the cervical spinal cord
10. Spinal deformi- Common Absent enlargement.
ties
3. Reflexes: Deep reflexes in the lower limbs may be the feet and ascending up the leg and then
brisk. Ankle jerk may be lost if there is associated involving the trunk.
peripheral neuropathy. The superficial reflexes 2. There is difficulty in walking and unsteadiness
are usually lost and plantar reflex is extensor. of gait which is more pronounced in darkness.
Causes: 3. There is ataxia and spastic weakness of legs with
profound distal loss of postural and vibration
1. Subacute combined degeneration of the spinal sense with bilateral extensor plantars.
cord: This occurs due to deficiency of vitamin B 12
4. L'Hermitte's sign is positive (due to posterior
usually after the fourth decade. There is usually
column involvement)
associated pernicious anemia and histamine-fast
achlorhydria. Neurological features are as below: 5. Co ncur rent peripheral neuropathy i s
evidenced b y loss o f ankle jerks impairment
2. Sub-acute myelo-optic neuropathy (SMON):
of superficial sensations in glove and stocking
This commonly occurs in the elderly patients who
pattern.
are habituated to take large doses of enteroquinol
for long periods. In addition to the above features, 6. M i l d i m p a i r m e n t of m e m o r y c a l l e d
there is optic atrophy. "megaloblastic maddness".
3. Pellagra: This is characterized by diarrhea, 7. Bilateral optic atrophy is seen in 5-10% cases.
dementia and dermatitis in addition to the above Table 6.21 : Neurological Features of
features. Subacute Combined Degeneration
4. Taboparesis: This is common in younger patient (SACO) of Spinal Cord
with history of exposure. There are always mental I. Motor System
changes and often Argyll Robertson pupils
1. Tone: Increased
present. 2. Power: Diminished
5. Friedreich's ataxia: This is a heredofamilial 3. Wasting: Absent
autosomal recessive disorder of early onset 4. Coordination: Normal
involving, in addition to the pyramidal tracts and II. Sensory System
posterior columns, spinocerebellar tracts (which 1. Vibration,joint sense: Absent
causes truncal ataxia, titubation, nystagmus and 2. Touch, temperature pain: Glove and Stocking
slurred speech), optic atrophy, kyphoscoliosis, pes pattern
cavus and cardiac abnormalities (cardiac failure, Ill. Reflexes
heartblock, bundle branch block, Twave changes).
1. Deep Jerks/ Ankle Jerks: Brisk lost
This is a steadily progressive disorder ultimately
2. Plantars: Extensions
leading to death due to intercurrent infection, 3. Abdominals: Absent
cardiac failure and complications of associated 4. Sphincters: Frequency, Urgency
diabetes.
Anterior Horn Cell Syndromes
6. Nutritional myelopathy: This is due to protein
calorie malnutrition and resembles subacute e.g. Poliomyelitis (AFP)
combined degeneration of the spinal cord. 1. Sensory: Normal
Skin changes of vitamin deficiencies are usually 2. Motor: There is diffuse weakness, atrophy and
evident. fasciculations in the muscles of extremities and
trunk. Muscle tone may be reduced or normal.
Subacute Combined Degeneration
3. Reflexes: Deep tendon reflexes are usually lost.
(SACO)
Causes
Clinical Features
1. Progressive muscular atrophy: (See motor
1. Presenting feature is tingling sensation in
neurone disease below).
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( 6 ) Central Nervous System
,.
muscular atrophy sclerosis
Motor System
a. Tone Diminished Increased Normal Increased
b.Wasting Marked Absent Of tongue Absent (Small Spastic)
c. Fasciculations Present Absent Over tongue Absent
d.Power Diminished Diminished Normal Diminished
2. Sensory system Normal Normal Normal Normal
3. Reflexes:
a. Deep Absent Brisk Normal Jaw jerk brisk
b.Plantars Flexors Extensor Flexor Extensor
c. Abdominals Normal Preserved til I late Normal Preserved till late
4. Cranial nerves
a. Palatal palsy Absent Absent Present Present Absent (good-
gag)
b. Slurred voice & Absent Absent Present Present (spastic and
Dysphagia speech)
5. Respiratory infection Absent Absent Common cause of Common cause of
death death
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1. Distribution of Distal or proximal. Asymmetrical, Distal Proximal. Bulbar Proximal Distal or along
weakness May involve neck or along nerve distri- Respiratory nerve distribution
flexors bution
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< 6 ) Central Nervous System
Table 6.24 : Diseases Affecting Myoneural Junction
Myasthenia gravis Carcinomatous myopathy Botulism
,.
(Eaton Lambert Syndrome)
3. Distribution of weakness Bui bar muscles Respiratory Mainly limb muscles with Bui bar muscles Respiratory
Muscles Proximal muscles aching muscles
6. Associated disease Pernicious anemia, Thymoma, Oat-cell carcinoma of lung Gastrointestinal symptoms
SLE
8. EMG Progressive fatigue Decremen- Improves with rapid, repeated Slight improvement with
tal Response stimulation Incremental repeated stimulation.
Response
9. Treatment Neostigmine, Steroids, Thy- Guanidine Guanidine, Polyvalent botulism
mectomy antitoxin.
,.
humeral
3. Distribution ofWeak- Proximal > Distal Pelvic Same as Duchenne Face, scapula and arms Pelvic and shoulder
ness > Shoulder gridle
6. Prognosis 2nd decade-bed Normal life span Normal life span Varies
bound
3rd decade-death
Wheel-chair at 8-14 yrs.
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Diphtheria Triorthocresyl Phosphate Neuropathy
A. Palatal palsy, unilateral or bilateral by second A. Onset: 10-20 days after ingestion of ginger
or third week (no palatal palsy seen in Guillain adulterated with triorthocresyl phosphate
Barre syndrome). B. Pain in the limbs with inconsistent sensory loss.
B. Paralysis of accommodation, usually bilateral, Wasting and weakness of the distal muscles with
rarely unilateral, by the third or fourth week. BILATERAL WRIST DROP AND FOOT DROP.
There is diminished vision for near objects C. Retrobulbar neuritis
(therefore unnoticed in myopics). Pupillary
response to light and accommodation is sluggish. Acute Myasthenia Gravis
External ocular movements are usually normal, (Refer to Pg. 340)
rarely sixth nerve weakness may be present.
C. Generalized polyneuropathy by sixth or seventh Polymyositis
week. A. Subacute, symmetrical weakness of the proximal
1. Weakness of the lower limbs more than and trunk muscles. Sometimes only the
upper limbs quadriceps and neck muscles are involved.
2. Glove and stocking anesthesia B. Pharyngeal and laryngeal muscles may be
3. Loss of postural sense and sensory ataxia involved leading to dysphagia and dysphonia.
4. Paralysis of diaphragm, larynx and pharynx C. OCULAR and FACIAL MUSCLES are usually
SPARED and in 75% distal muscle are spared.
5. Sphincters are normal and there may or
may not be impotency D. Fever, muscle pain and tenderness may be
D. present.
Cardiac involvement due to vagal palsy -
tachycardia, atrial fibrillation, premature beats E. Reflexes are usually depressed, but sometimes
and bundle branch block brisk. (Ifmarkedlyreducedthinkofcarcinomatous
polymyositis).
Botulism Cardiac involvement: Arrhythmias, myocardial
F.
A. Onset: Symptoms usually develop within 18-30 infarction and minor ECG changes.
hours after ingestion of tinned food. G. It is precipitated by sunlight, sulphonamides and
B. Gastrointestinal symptoms like nausea and minor systemic infections.
vomiting occur. In most cases there is severe
constipation due to paralysis of the intestinal Poliomyelitis
muscles A. Younger age group. Below 25 years.
C. Neurological symptoms B. Pre-paralytic stage - Fever, malaise, headache,
1. Paralysisofaccommodationand sometimes drowsiness, insomnia, sweating, flushing, facial
also of the light reflex congestion, anorexia, vomiting and diarrhea for
2. Paralysis of the external ocular muscles, a day or two.
ptosis, diplopia and nystagmus C. Severe pain in the back and limbs and muscle
3. Weakness of the jaw muscles, respiratory tenderness.
muscles and muscles of the trunk and limbs D. There is flaccid paralysis and wasting of one limb
4. Tendon reflexes are always normal. Plantars in asymmetrical fashion. Sometimes paralysis
are flexors. There is no sensory disturbance occurs in all the four limbs and trunk muscles.
and consciousness is preserved up to the The lower limbs are more affected than the upper,
end. and the quadriceps, peronei and tibial groups are
D. There is usually no fever, unless associated most affected. The affection is maximum within
respiratory tract infection. the first 24 hours.
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E. Bulbar muscles may or may not be involved and ness and fatiguability of skeletal muscles due to
ocular muscles are only very rarely involved. decrease in number of Acetylcholine receptors at the
neuromuscular junction due to antibodies. It is an
Periodic Paralysis autoimmune disorder.
Table 6.27 : Differential Diagnosis of A. Incidence : Common in men in 50s and 60s;
Periodic Paralysis women 20s and 30s; women more frequently
affected than men.
Hypokalemic Hyperkalemic
B. Clinical features
Inheritance AD AD
1. Onset is insidious or subacute, rarely acute
Onset Adolescence Early childhood
2. External ocular movements are weak. There
Frequency of Daily yearly 2-3/day may be unilateral or bilateral ptosis.
attacks
Pupils are always Spared
Duration of attacks 2-12 hrs 1-2 hrs-> 1 day
3. Facial: Weakness of orbicularis oculi is
Precipitating Anxiety, heavy Cold, emotion quite constant. Retractors of the angles
factors meal and rest after infection, rest after
exercise exercise and KCI
of the mouth suffer more than elevators
resulting in snarling smile.
Kleve! Kdecreased Increased or
Normal 4. Other cranial nerves: There is palatal palsy.
Involvement of the masseters prevents
Type of channel Ca channelopathy Na channelopathy
closure of mouth (hanging jaw sign).
Treatment KCI Acetazolemine There may be nasal speech and ultimately
Mexinifline
respiratory paralysis.
Infectious Mononucleosis 5. Limbs: Proximal weakness initially in the
shoulder girdle, later on may be generalized
A. Ascending sensory-motor paralysis.
6. The weakness is more in the evening and
B Fever, sore throat, skin and rash, splenomegaly disappears after a night's rest. Usually there
and lymphadenopathy are usually associated. is no wasting or loss of deep reflexes.
C. High levels of Epstein-Barr virus antibody titre 7. Muscle groups commonly involved in
and increased IgM and IgG levels. decreasing order are bulbar, neck, limb
Infective Hepatitis girdle, distal limb and trunk.
8. If respiratory muscles are affected,
Jaundice with peripheral neuropathy. mechanical ventillation may be required
This may also occur in alcoholism, nutritional defi and patient is said to be in a "Myasthenia
ciency and amyloidosis. crisis".
Brain-stem Lesions with Neuronal Shock C. Diagnosis
1. Clinically :
A. Usually sudden in onset
B. a. Breath Holding Time : Breath
Cranial nerves always involved along with flaccid
weakness of all four limbs, which may become counting are done to assess vital
spastic later capacity,
C. Vertigo and vomiting due to vestibular b. Forward arm abduction(> 5 mins),
involvement c. On sustained upward gaze increased
ptosis may occur,
-
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( 6 ) Central Nervous System
3. Anti MUSK Antibodies (muscle specific 2. Paleocerebellum: This is connected to the spinal
kinase) positive is 40% of negative cases. cord, for maintaining posture.
4. Tensilon test: Edrophonium 2 mg is given 3. Neocerebellum: This is connected to the cerebral
IV. If muscle power is improved within 30 cortex by pontine and olivary connections for
seconds and sustained improvement for 2-3 voluntary movements.
mintues test is positive. It can be repeated
with 8 mg if required. Connections
5. CT scan (To look for thymoma) Thymus is Through the superior peduncle (connects cerebellum
enlarged in 70% of MG cases. and midbrain):
6. Electrophysiological study. A. Afferent: Ventral Spinocerebellar tract- It arises
a. Repetitive nerve stimulation - from the nuclei on the medial side of the Clark's
decremental pattern. column, crosses on the opposite side, ascends up
to the midbrain and then again crosses, entering
b. Single fibre EMG - Increased
the anterior lobe of the cerebellum on the same
variability of interpotential interval. side. It receives impulses from the Golgi tendon
D. Treatment type IB. lt sends inhibitory impulses to the motor
1. Pyridostigmine Orally 30 - 120 mg every neurones.
4-8 hours, titrated individually for each B. Efferent: Cortico-pontocerebellar tract - It
patient. arises from the lateral lobes and via the superior
2. Corticosteroids : IV or oral peduncle crosses to the opposite red nucleus.
3. Plasma Exchange : Removes antibodies, From the red nucleus it goes to the ventrolateral
used in crisis. nucleus of the thalamus from where it goes to
4. Immunomodulators : Azathioprine, the cerebral cortex.
c yclophosphamide, mycophendlate Through the middle peduncle (connects cerebellum
mofetil, tacrolimus and pons):
5. Thymectomy : In patients under 60 years, Efferent: Cortico-pontocerebellar tract - Fibers from
improves symptoms. the cerebral cortex along the corticospinal tract pass
to the cerebellum with a relay in the nuclei of the pons.
E. Drugs contraindicated in MG :
Through the inferior peduncle (connects cerebellum
Antibiotics : Aminoglycosides, Quinolones,
and medulla):
Muscle relaxants: pancuronium, D Tubocuan,
Betablockers, local anaesthetics, quinine, as A. Afferent:
these worsen the muscle weakness. 1. Dorsal-spinocerebellar tract: From the
Clark's column situated deep in the
posterior horn, it enters the anterior lobe of
9 > Cerebellum the cerebellum via the inferior peduncle. It
receives afferents from the muscle spindle
Cerebellum is an infratentorial structure in the pos type IA.
terior cranial fossa, attached to the brain stem by the 2. Olivo c e r e b e l l a r t r a c t: F r o m the
superior, middle and inferior peduncles through which extrapyramidal system to the lateral lobes
nerve fibers enter and leave. It has two lateral lobes of the opposite cerebellum.
and a central vermis.
3. Vestibulocerebellar tract: From the vestibular
There are four nuclei in the cerebellum: nucleus to the flocculonodular lobe.
Dentiform, Emboliformis, Fastigious and Globosus. 4. Cuneocerebellar tract.
Functionally it can be classified as : B. Efferent:
1. Archicerebellum: T his is connected to the
1. Fastigiobulbar tract: To the reticular area
vestibular nuclei for maintaining equilibrium.
for the control of tone
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finger approaches the nose in the to focus his vision elsewhere, the eyes move
finger nose test. This results from the towards the point of fixation with quick
involvement of the cerebellar afferent jerks and there are slow return movements
pathways in their connection with the to the resting point. The movements are
red nucleus and thalamus. more marked and of greater amplitude
2. Dysmetria: Inability to arrest the when the patient looks towards the affected
movements at desired points due to side.
loss of ability to gauge the distance, 4. Vertigo: Objects move away from the side
speed and power of movement. of the lesion. Sense of rotation of the body
3. Dyssynergy: Defective coordination in same direction with intra cerebellar
of various muscles and muscle lesion and in opposite direction with extra
groups participating in a movement. cerebellar lesion.
Therefore there is decomposition of 5. Speech disturbance: Staccato, scanning or
movements and the act is broken explosive speech. Sometimes dysarthria.
down into its component parts.
Differential Diagnosis
4. Dysdiadochokinesia: T here is
disturbance of reciprocal innervation Trauma: History of trauma prior to the onset of cer
of agonists and antagonists. Hence, ebellar disorders.
there is loss of ability to stop one Encephalitis: Usually causes acute cerebellar signs.
act and follow it immediately by Disturbance of external ocular movements including
a diametrically opposite act. This nystagmus, are more prominent.
is seen when the patient attempts Cerebellar Abscess:
alternate successive pronation and
supination of the hand, rapid tapping A. Symptoms and signs of cerebellar ataxia
of the fingers or alternate opening and B. Symptoms and signs of septicemia
closing of fists. C. Symptoms and signs of raised intracranial
5. Rebound phenomenon: Failure of tension
antagonist to counter overshoot Posterior Inferior Cerebellar Artery Thrombosis:
movements totally. Wallenberg's syndrome (Lateral medullary syndrome).
C. Disorders of Gait It is characterized by a sudden onset of-
1. Broad base A. Vertigo, vomiting (vestibular nucleus
2. Reeling gait involvement)
3. Deviation to the side of the lesion B. Dysphagia (nucleus ambiguous)
4. Truncal ataxia C. Ataxia (inferior cerebellar peduncle)
5. Titubation D. Ipsilateral anesthesia of the face (descending
II. Of No Localizing Value tract of the V nerve)
1. Static tremors: Tremors at rest due to E. Contralateral anesthesia of the limbs and trunk
hypotonia. (spinothalamic tract)
2. Skew deviation: Homolateral eye turns F. Nasal twang, nasal regurgitation (ipsilateral 9th,
downward and inward and contralateral 10th and 11th cranial nerves)
eye turns upwards and outwards. G. Ipsilateral Homer's syndrome (Descending
3. Nystagmus: With the hemisphere lesion, sympathetic fibers)
the eyes at rest are deviated towards the H. Nystagmus and intention tremors (vestibular
unaffected side. When the patient attempts nerve and cerebellar fibers)
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PRACTICAL MEDICINE
Disseminated Sclerosis: Refer paraplegia Dejerine Thomas Olivopon To Cerebellar Atrophy
Drugs: Cerebellar ataxia follows ingestion of certain 1. Usually starts about 50-60 years of age
drugs as mentioned above. 2. Cerebellar signs
Craniovertebral Anomalies: 3. Mental changes
Refer Quadriplegia 4. Parkinsonian features
Friedreich's Ataxia: Refer Paraplegia 5. Deep reflexes brisk or depressed
Sanger Brown's Ataxia Lhermitte Lejomme's Olivorubrocerebellar Atrophy
1. Family history Clinically resembles Olivopontocerebellar atrophy.
2. Cerebellar signs Only distinguished on autopsy.
3. Optic atrophy Delayed Cerebellar Degeneration
4. Ophthalmoplegia Resembles Holmes' but starts at about 60 years.
Marie's Ataxia Cerebellar Neoplasms
1. Family history 1. Cerebellar signs of gradual onset.
2. Cerebellar signs 2. Signs of raised intracranial tension.
3. Pyramidal signs Cerebellopontine Angle Tumor (E.g. Acoustic
Roussy Levy Syndrome Neuroma)
1. Family history 1. Cerebellar signs on the same side
2. Cerebellar signs 2. 5th, 7th and 8th nerve affection on the same side
3. Polyneuropathy or on both sides. Corneal reflexes are often the
earliest to be affected
Refsum's Disease
3. Pyramidal signs on the same or on both sides
(Familial disease of phytanic acid metabolism)
4. Signs of raised intracranial tension
1. Family history
Alcoholic Cerebellar Degeneration: Acute or gradual
2. Cerebellar ataxia
onset of cerebellar signs in an alcoholic. It has to be
3. Atypical retinitis pigmentosa differentiated from the above conditions.
4. Peripheral neuropathy with thickened nerves
10 > Tuberculosis of
5. Deafness
6. Anosmia
A-beta Lipoproteinemia Nervous S--------
stem -
--
1. Cerebellar ataxia Tuberculosis can affect the nervous system in the
2. Pyramidal signs with absent deep reflexes following ways:
3. Acanthocytosis on peripheral smear I. Meningitis
A-alpha Lipoproteinemia (Tangier's Disease) II. Tuberculoma
1. Cerebellar ataxia III. Vasculitis causing infarcts
2. Orange or yellowish gray discoloration of tonsils IV. Tuberculosis of the spine causing Pott's paraplegia
3. Polyneuropathy V. Intraspinal granulomas
Holmes' Cerebellar Degeneration V I. Arachnoiditis
1. Starts in middle life (35-40 years) I. Tuberculous Meningitis (TBM)
2. Cerebellar signs A. Pathology
3. Pyramidal signs 1. Meninges: At the base of the
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( 6 Central Nervous System
brain, a mass of gelatinous exudate b) Hemiplegia and monoplegia
obliterates the cisterna pontis and c) Painful ophthalmoplegia
cisterna interpeduncularis and 4. Signs of meningeal irritation: Neck
extends anteriorly along the floor of stiffness, Kernig's sign. etc.
the third ventricle to cover the optic
5. In children: Progressive spasticity,
chiasma and distal ends of the internal
decerebrate state, convulsions, coma.
carotid arteries. The meninges over
There is a greater incidence of
the convexity of hemispheres are less
hydrocephalous, convulsions and
involved.
brainstem signs with decerebration
2. Brain: Diffuse brain involvement in children.
commonly occurs due to:
6. Of complications
a) Edema in the absence ofinfarction
b) Infarction more common in the D. Clinical Stages
middle carotid territory 1. Meningeal signs only, without
neurological involvement or impaired
c) Tuberculoma sensorium.
B. Relation of pathological lesions to signs 2. Meningeal signs with neurological
and symptoms involvement but without impaired
1. Meningeal exudate: sensorium.
a) Hydrocephalous. 3. Meningeal signs with neurological
involvement and impaired sensorium.
b) Cranial nerve palsy.
E. Effect of Treatment
c) Meningeal sign.
Antituberculous treatment modify the
2. Infection of brain substance: course of the illness. If the treatment
a) Clouding of consciousness. is started early, prompt and complete
b) Convulsions. remission occurs. If it is started late is not
c) Hypothalamic and brain stem of much avail. Although the patient may
recover, he may be left with sequelae.
signs.
F. Sequelae
3. Arteritis and vascular obstruction:
Focal neurological deficit. 1. Due to basal exudates:
4. Allergic or hypersensitive: Massive a) Hydrocephalous
brain edema and raised intracranial b) Cranial nerve palsy: Deafness,
tension in absence ofhydrocephalous. blindness and ophthalmoplegia
C. Clinical features 2. Due to spinal block: Paraplegia,
quadriplegia
1. Prodromal:
3. Due to arteritis: Hemiplegia
a) Listlessness, apathy, irritability,
headache 4. Miscellaneous:
b) Anorexia, nausea, vomiting, and a) Mental disturbances
abdominal pain b) Convulsions
c) Low grade fever c) Endocrine disturbances
2. Raised Intra-cranial pressure - d) Ectopic ossification of the hipjoint
Headache, vomiting, papilledema G. Treatment
3. Focal deficit: 1. Antituberculous Drugs:
a) Convulsions Those that diffuse freely through
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PRACTICAL MEDICINE
the blood-brain barrier are INH, individual foci and later by means of their
rifampicin, pyrazinamide, cycloserine conglomeration. Thus, tuberculomas are
and ethionamide. Drugs that diffuse formed which remain isolated or merge
only in the presence of meningeal together to form a solid mass.
inflammation are streptomycin and The ultimate evolution depends on hyper
ethambutol. A combination therapy sensitivity and immune responses. Healing
is given for at least 1-1/2 years total occurs by fibrosis and calcification which
of 18 months with two or three of impairs the oxygen supply to the organisms
the following: Streptomycin, Isonex, by obliterating their vascular channels.
Ethambutol, Rifampicin, Cycloserine, There is little participation of fibroblasts
Pyrazinamide and Ethionamide. till the lesion reaches the surface meninges.
2. Steroids: C. Site
a) Toreducepia-arachnoidadhesions I. Posterior fossa and brainstem
b) To reduce toxicity and give a 2. Supratentorial: Parietofrontal
feeling of well being 3. Intraventricular
3. Hydrocephalus: 4. Extradural intracranial: Rare
a) Ventriculo-atrial shunt D. Clinical Features
b) Anterior third ventriculostomy 1. Signs of raised intracranial tension
c) Deroofing the fourth ventricle 2. False localizing signs which may not
4. Spinal Block: be false localizing but due to multiple
lesions, predominant signs due to a
a) Oral steroids.
large mass and false localizing signs
b) Intrathecal 50 mg due to a smaller lesion elsewhere
hydrocortisone.
3. Focal signs
c) Intrathecal streptodornase and E. Investigations
streptokinase.
1. X-ray skull:
d) S u r g i c a l d e c o m p r e s s i o n
a) Irregular, broken, calcareous shell
arachnoiditis.
b) Raised intracranial tension
II. Tuberculoma
c) Lo b u l a t e d c a l c i f i c a t i o n,
A. Definition: Single or multiple lesions
radiolucent in the centre but
or tumor-like masses of characteristic
dense at the periphery
granulation tissue which produces
symptoms of a space-occupying lesion. d) Nodular calcification: Multiple
calcareous concretions grouped
B. Pathogenesis: Tuberculomas result from together
hematogenous spread of infection from
2. Angiogram:
lungs, lymph nodes, peritoneum, kidney,
bone, skin, etc. The early lesion appears in a) Tumor blush
the cortex or the subcortical region and b) Reduction in the caliber of the
consists of a central area of incipient or blood vessels traversing the tumor
frank necrosis surrounded by epithelioid
or giant cells. In some, polymorphs may
be seen.
Initially microscopic foci are multiple �
and around the perivascular area. The I. ,1 , 1',
Fig 6101 H1n9Pnhanc1ngle\1ons
lesion enlarges through expansion of the - - -
346
( 6 ) Central Nervous System
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PRACTICAL MEDICINE
348
( 6 ) Central Nervous System
2. Multifocal radiculomyelopathy (multiple Carotids and Vertebral arteries. Right carotid arises
levels) from the arch of the aorta and left carotid arises from
3. Ascending variety (resembling Guillain brachiocephalic which arises from the aortic arch.
Barre syndrome) Vertebrals arise from the subclavian arteries and the
B. Chronic two vertebrals join to form the basilar artery which
1. Slowly progressive over months or years, then bifurcates into two terminal branches-right and
resembles spinal tumors left posterior cerebralarteries. The carotid and vertebral
artery system join at the base of the brain to form the
2. Root pains -scattered, persistent or severe
circle of Willis.
3. Lower motor neurone signs in the lower
limbs with sensory level higher up The Anterior Cerebral Artery (ACA)
C. Myelogram ACA runs anteriomedially to the interhemispheric
1. Dye moves slowly with multiple filling fissure, where it joins the opposite ACA by anterior
defects and fragmentation.
Anterior
2. Total block with ragged or concave edge o------- Cerebral
or a pitch fork appearance.
3. Multiple filling defects.
4. Large area of candle glittering.
5. In cauda equina region rat-tail or bundle
of faggot stick appearance.
6. Multiple, small, rounded, clear areas of cyst
formation.
Prognosis Posterior
cerebrals
1. In early cases the prognosis is good with
treatment.
2. If there is a delay in the diagnosis irreparable
damage may occur.
Treatment
Anterior
A. Medical --....----inferior
cerebellar
1. Antituberculous drugs
2. Steroids: Prednisolone 60 mg for 1 month
followed by lower doses for 3 months
3. Intrathecal hydrocortisone 50 mg. twice
weekly
4. If Cryptococcal: Amphotericin B
B. Surgical
1. Decompression with laminectomy
2. Removal of the inflamed meninges
11 > Cerebrovascular
Diseases
Blood Supply of Cerebral Hemispheres
Fig. 6.1 02: Circle of Willis
Cerebral hemispheres receive blood supply from
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PRACTICAL MEDICINE
communicating artery (anterior portion of Circle of absent of treatment. In carotid territory if the
Willis - Fig. 6.71). ACA gives origin to progression has stopped for 24 hours, it is not
Medial lenticular branches which supply dorsal likely to progress. However in vertebro-basilar
1.
territory the deficit may progress for up to 72
aspect of the optic chiasma and hyp othalamus,
hours.
and the medial striate artery (Heubner's artery)
which supplies blood to the anteroinferior limb Transient lschemic Attacks (TIA)
of the internal capsule and anterior aspects of
putamen and caudate nuclei. TIAs are sudden episodes of focal non-convulsive
neurologic dysfunction that completely resolves within
2. Callosal branches which supply the septum 24 hours but mostly by 1 hr. They are vascular in etiol
pellucidum and the fornix. ogy and commonly last 2-15 mins and are followed
3. Hemispheric branches which supply the medial by complete recovery.
surface of the hemisphere and upper border of 1. TIA in Carotid system: This is characterized by
frontal and parietal lobes. one or more of:
The Middle Cerebral Artery (MCA) a) Ipsilateral amaurosis fugax
MCA supplies most of the lateral surface of the ce b) Contralateral hemiplegia
rebral hemisphere and deep structures of the frontal c) Contralateral hemianesthesia
and parietal lobes. It gives lenticulostriate arteries, d) Contralateral homonymous hemianopia
which nourishes the adjacent corona radiata, external
e) Aphasia
capsule, claustrum, putamen, part of globus pallidus,
body of the caudate nucleus and superior portion of 2. TIA in Vertebrobasilar system: This is
the anterior and posterior limbs of the internal capsule. characterized by one or more of the following:
Other branches are orbitofrontal and anterior temporal a) Bilateral or shifting motor or sensory
arteries. The main trunk then divides into proximal dysfunction
and distal group of arteries. b) Bilateral homonymous hemianopia
The Posterior Cerebral Artery (PCA) c) Diplopia, dysphagia or dysarthria by
PCA are the terminal branches of the Basilar artery itself are not considered TIAs, however
and supplies the occipital lobes, the inferomedial in combination with (a) or (b) should be
portions of the temporal lobes, medial ventral, lateral considered as vertebrobasilar TIAs.
ventral, posterior and superior thalamus, hippocampus Causes
fornices and psalterium.
I. Cerebral Infarction (85%): This may be due to
Cerebrovascular Syndromes a) Thrombosis: Due to atherosclerosis, syphilis
Stroke: It is a relatively abrupt onset of focal neurologi or TB
cal deficit resulting from diseases of arteries or veins b) Embolism: This involves predominantly
that serve the central nervous system. MCA and PCA. ACA and Basilar arteries
are not commonly involved. Embolus may
Types arise from
1. Completed stroke: It is the term applied to the 1. Heart: Myocardial infarction,
temporal profile of the stroke syndrome in which mural thrombus arrhythmias,
the deficit is prolonged and often permanent. valvular heart diseases, mitral valve
Most of them reach the maximum of neurological prolapse, prosthetic valves, infective
dysfunction within an hour of onset. endocarditis, marantic endocarditis,
2. Stroke in Evolution: It is the term applied to congenital heart disease, cardiac
the temporal profile in which the neurological tumors.
deficit occurs in a step wise or progressive 2. Extracranial Vasculature
fashion, culminating in a major deficit in the
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{ 6 ) Central Nervous System
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PRACTICAL MEDICINE
352
( 6 ) Central Nervous System
contralateral hemiplegia (Weber'.s ache is infrequent. Although they usually carry good
Syndrome) prognosis, multiple lacunae may cause pseudobulbar
2. lpsilateral oculomotor palsy with palsy and dementia.
contralateral cerebellar ataxia
Clinical Syndromes
(Nothnagel Syndrome)
3. Ipsilateral oculomotor palsy with 1. Pure motor hemiparesis: Lacunae in internal
contralateral rubral tremor / ataxia capsule or basis pontis causes opposite face
and contralateral hemiplegia and arm weakness more than leg. There is no
(Benediect's syndrome). aphasia, apractagnosia, sensory, cortical or visual
disturbances.
4. Combination of Nothnagel and
Benedikts syndrome is Claude's 2. Pure Sensory stroke: Lacunae in ventral lateral
Syndrome - Ipsilateral oculomotor nucleus of thalamus causes paresthesias and
palsy with contralateral ataxia and hemi-sensory loss on opposite side. Subjective
tremor. No hemiplegia. symptoms are much more than objective sensory
loss.
5. Parinaud'.s syndrome
3. Ataxic Hemiparesis: Lacunae in posterior limb
a) Supranuclearparalysisofelevation
ofinternal capsule or basis pontis cause weakness
b) Defective convergence predominantly in the legs and incoordination of
c) Convergence retraction nystag- the arm and legs without dysarthria and facial
mus involvement.
d) Lid retraction (Collier's sign) 4. Dysarthria - Clumsy hand syndrome: Lacunae
e) Skew deviation (Setting sun sign) deep in basis pontis causes supranuclear facial
palsy, dysarthria, deviation of the tongue and
f) Light near dissociation
loss of fine motor control of the hand.
6. Unilateral or Bilateral Internuclear
ophthalmoplegia Treatment of Acute lschemic Stroke and
7. Pseudoabducent palsy Transient lschemic Attack (TIA)
8. Peduncular hallucinations - often 1. Anti-hypertensive drugs: BP should not be
silent, mobile and colorful and lowered precipitously. BP must be lowered only in
frequently pleasurable severe cases (systolic BP> 200 mmHg). Usually
9. Decerebrate rigidity, Locked-in Calcium antagonists are preferred. Nimodipine,
syndrome and disturbances in a cerebroselective calcium channel blocker, can
consciousness. be used.
2. Intravascular volume must be maintained
Lacunar Infarctions
3. Osmotic therapy with mannitol may be given
Lacunae are small ischemic infarcts that range in to control edema of large infarcts, but isotonic
diameter from 30 - 300 µm and result from occlu volume must be replaced to avoid hypovolemia.
sion of the penetrating arteries, chiefly from anterior 4. Anticoagulants: Initially with heparin, including
choroidal, middle cerebral, posterior cerebral or basilar low molecular weight heparins.
arteries. The most frequent sites are putamen, bases
pontis, thalamus, posterior limb of internal capsule Thrombolysis
and caudate nucleus. The primary pathology is lipo Recombinant Tissue Plasminogen Activator (rtPA) is
hyalinosis of the arteries. approved for thrombolysis in acute stroke.
Long-standing hyp ertension and atherosclerosis are Dosage: 0.9 mg/kg - (10% as bolus, remaining over
common predisposing factors. TIAs shortly before 60 minutes) maximum of90 mg.
the onset of a lacunar stroke is frequent, but head-
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PRACTICAL MEDICINE
....
354
{ 6 ) Central Nervous System
6. Trunk ataxia more than ipsilateral Table 6.30 : Differences between
limb ataxia Hypertensive and Lobar Hemorrhages
7. Horizontal nystagmus with fast Hypertensive lobar
component towards the side of lesion hemorrhage hemorrhage
8. Small reactive pupils 1. Etiology Hypertension Vascular anomaly,
Blood dyscrasias, Tu-
9. Neck rigidity, slurred speech &
mors, Angiopathy, etc.
bilateral hyper-reflexia and Babinski
2. Site Putamen, thala- Parieto-temporal area
signs may be present.
mus, cerebellum occipital lobes (sub-
D. Pontine hemorrhage (5-7% of cases) and pons cortical white matter)
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PRACTICAL MEDICINE
...
356
( 6 ) Central Nervous System
due to release ofvasoactive substances from 6. Antiplatelet agents: Low dose Aspirin (75 to
blood into the subarachnoid space. Spasm 325 mg) and Ticlopidine have been used.
induced ischemia may lead to hemiparesis, 7. Anticoagulants: Warfarin when indicated.
cortical sensory loss, hemianopia, altered 8. Epsilon amino caproic acid (EACA) 24-48
consciousness and urinary incontinence. gm/day protects against recurrence of
3. Others: Hydrocephalus, cerebral edema hemorrhage by preserving the clot that
and convulsions, hyponatremia cerebral ultimately seals the bleeding point.
salt wating syndrome. 9. Management of unconscious patient: See
JI. Medical Coma
l. Pulmonary: Neurogenic pulmonary edema 10. Symptomatic treatment: Analgesics like
pneumonia, atelectasis, etc. dextro propoxyphene or paracetamol are
2. Cardiac: Cardiac arrhythmias like useful for severe headache.
premature beats, ventricular tachycardia, II. Surgical
ventricular fibrillation, etc. These are due to 1. Aneurysmectomy: If the berry aneurysm
stimulation of autonomic nervous system is on the surface of the brain, it must be
by subarachnoid blood. removed or ligated because there is a high
3. Others: Urinary tract infection, vaginitis, incidence of recurrence of the bleeding in
gastrointestinal hemorrhage, thrombo the second and third week.
phlebitis and SIADH 2. Hydrocephalus: VP shunt
Management 3. Newer Endovascular techniques - coiling
or clipping of aneurysms.
I. Medical 4. Angioplasty of cerebral vessels in case
l. Measures to reduce the raised intracranial of severe vasospasm when ischemic
tension: Mannitol 350 mg. intravenously symptoms appear despite of maximum
daily for 3-4 days, furosemide 40 mg orally medical therapy.
or glycerol 50-200 ml. orally daily are useful. 5. Internal carotid artery ligation: This is
Dexamethasone 4 mg 6 hourly parenterally done gradually over several weeks if the
also helps to lower the intracranial tension. aneurysm is not surgically accessible.
2. General Measures: Bed-rest (for atleast 3
weeks and about 6 weeks if surgery is not
contemplated), analgesics, stool softeners. 12 Parkinsonism
3. Antihypertensive drugs: If BP is high, it
should be lowered with appropriate drugs. Parkinsonism is a disorder of the extrapyramidal
BP should be lowered very gradually and system, characterized by tremor, rigidity, bradykinesia
not abruptly, as it will disrupt cerebral and postural disturbances.
autoregulatory reflexes.
Parkinson's Disease (Paralysis Agitans)
4. Nifedipine 10 mg sublingual is useful to
immediately lower the blood pressure, it Parkinson's disease (PD) most commonly affects
could be repeated after 10 to 15 minutes persons over the age of 55 years, and is characterized
up to 40-60 mg. Diazoxide and Sodium by : bradykinesia, rest tremor, rigidity and postural
nitroprusside are other useful drugs. instability. (Atleast two of these and a response to
However they have to be given IV and are levodopa should be usually present to make the di
hence not used nowadays. agnosis). The substantia nigra has two parts, the pars
5. Nimodipine 30 mg, tds, is the drug of choice reticulata (made up of nonpigmented cells) and the
as it is a specific cerebrovascular Calcium pars compacta (made of pigmented neurons).
channel antagonist. It is available IV also.
Pathophysiology: The disease is uncommon before the
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PRACTICAL MEDICINE
age of 40 years and there is a slight male preponderance. C. Vascular: Atherosclerosis and Hyperten
The Parsi community in Bombay had an age-adjusted sion.
prevalence ratio of 192/100,000, which is higher than D. Toxic: N-methyl-4-phenyl-tetradropyri
that in most other studies. The incidence of PD is less dine, (MTPT), Manganese carbon
in smokers but the cause of this is not known. monoxide, carbon disulphide, cyanide
The corpus striatum has a rich concentration of ace and methanol.
tylcholine (Ach). Ach is synthesized and released by E. Head-injury:
small striatal neurons, upon which it has an excitatory
G. Degenerative: Alzheimer's disease, Pick's
effect. Dopamine is synthesized by the pigmented
disease, Communicating hydrocephalous.
neurons (pars compacta) of the substantia nigra and is
transported via the nigrostriatal pathway to the corpus III. Parkinsonism Plus Syndrome:
striatum, where it has an inhibitory effect on striatal A. Sporadic:
neurons. It is thought that a functional equilibrium 1. Progressive supranuclear palsy
exists in the striatum between acetylcholine (which
2. Shy-Drager syndrome
is excitatory) and dopamine (which is inhibitory).
3. Striatonigral degeneration
In PD, there is a loss of pigmented neurons in the
substantia nigra in the midbrain and locus ceruleus 4. Parkinson's disease - amyotrophic
in the pons, with characteristic intracytoplasmic, lateral sclerosis
eosino-philic inclusion bodies (Lewy bodies) in the 5. Cortical - basal ganglionic degenera
surviving neurons. As a result, the dopamine content tion
in the corpus striatum is markedly decreased. At 6. Olivopontocerebellar atrophy
least 80% of the pigmented neurons in other parts of
B. Inherited:
the CNS and also of certain nonpigmented neurons,
especially in the nucleus basalis of Meynert (in the 1. Huntington's disease
substantia innominata). 2. Olivopontocerebellar atrophy
There may also be a decrease in other neurotransmit 3. Hallervorden - Spatz disease
ters like noradrenaline, 5 hydroxy-tryptamine (5 HT), 4. Neuroacanthocytosis
gamma-aminobutyric acid (GABA), enkephalins and
substance P. Clinical Features
The concentration of acetylcholine in the striatum is The progression of the disease is usually gradual over
preserved but in those with dementia, acetylcholine many years but occasionally it may be more rapid
content in the cerebral cortex is decreased, probably as over a few months.
a result of loss of neurons in the substantia innominata. 1. The initial symptom is usually tremor involving
Moreover, demented patients with PD, like those with one hand, which then spreads to involve the leg
Alzheimer's disease, also have a loss of somatostatin on the same side before becoming bilateral. It
neurons in the cortex. Low 5 HT concentrations in the may also involve the head and jaw. The tremor
brain, may contribute to the depression commonly is present at rest at a rate of 4-6 per second. It
seen in patients with PD. is absent during sleep. It is partially relieved
Etiology by complete relaxation, when the patient is in
a relaxed state of mind and during action. It is
I. Idiopathic: Primary or Paralysis Agitans. aggravated by anxiety. In some patients, there is
II. Secondary: also a faster, postural tremor at a rate of 7-8 per
A. D rugs: Reserpine, Phenothiazines, second. Other characteristics of parkinsonian
butyrophenones, Metoclopramide etc. tremor are supination - pronation of the forearm,
B. Infection: Encephalitis lethargica, AIDS, adduction-abduction of the thumb and flexion-
dementia complex, cysticercosis and extension of the fingers (which gives rise to the
Creutzfeldt - Jakob disease. 'pill rolling' tremor commonly seen).
358
( 6 ) Central Nervous System
6. Eye movements are usually normal except
for difficulty in convergence. There may be
some limitation of upward gaze and minimal
disturbances of saccadic and pursuit eye
movements.
7. The voice is slow, monotonous and oflowvolume.
8. Increased sweating and seborrhea is often noted
on the face. There is difficulty in swallowing,
especially later in the disease course, with
consequent dribbling of saliva.
9. The handwriting becomes small (micrographia)
and untidy.
10. Movements: Because of bradykinesia the patient
often sits still in one posture with little movement
for a long time. He may have difficulty in getting
up from the chair or bed and in the later stages
'
Fig. 6.103 :Mask l1keface in Parkinson1sm
-
even rolling over in the bed may not be possible.
- - ---� ·--· -
Voluntary movements become slow and the
2. Rigidity manifests symptomatically as stiffness of
patient takes a progressively longer time to
the muscles and mainly involves the neck, trunk
perform everyday activities like dressing and
and proximal parts of the limbs. It is described as
bathing. Repetitive movements like supination
'lead pipe' rigidity because the increase in muscle
- pronation of the forearm or tapping the floor
tone is present throughout the range of movement.
with the feet are slow and of low amplitude.
When tremor is super-imposed on the rigidity,
But sometimes, when the patient is agitated or
there is a 'cog wheel' effect, which is most easily
startled, he is capable of rapid movement but
elicited at the wrist and elbow.
this is only temporary.
3. Bradykinesia implies a difficulty in initiating
11. Constipation is very common and urinary
voluntary movement (such as getting up from
frequency and incontinence may also be present.
a chair) and a slowness of movement which
results in a progressive increase in the time taken 12. Gait: One of the earliest signs of Parkinson's disease
to perform daily activities. This is probably the is loss of arm swing while walking. The gait has
most disabling feature of Parkinson's disease. other characteristic features. 'Freezing' implies a
Moreover, spontaneous movements like arm difficulty in starting to walk (start hesitation) and
swing while walking are absent. also an inability to maneuver through narrow
4. Postural abnormalities manifest as a flexed passages such as through a doorway or around
posture of the trunk and limbs together with a an obstacle (gait hesitation). The gait is usually
difficulty in maintaining one's balance when that shuffling and slow. Some patients have a festinant
posture is disturbed by an external force. gait in that progressive steps become faster, as
though the patient is chasing his centre of gravity.
5. Face: The combination of these four cardinal
This may end in a fall.
features gives rise to characteristic signs and
symptoms. The face has a mask like appearance The posture is stooped with flexion of the neck,
with few spontaneous movements of expression trunk and limbs. The arms are adducted, flexed
and a staring appearance because of decreased at the elbow and wrist; there is ulnar deviation of
blinking of the eyes. On tapping the glabella, the the hand and flexion of the metacarpophalangeal
patient continues to blink with each tap (unlike joints with extension at the interphalangeal
in normal individuals where the blinking stops joints. When the patient is standing, a slight
after a few taps). push forwards or backwards may make the
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PRACTICAL MEDICINE
patient take a few steps in that direction to a postural tremor at a frequency of 5-8 per second,
keep his balance propulsion and retropulsion there usually being no tremor at rest. Other signs and
respectively) and the patient may even fall. This symptoms of Parkinson's diseases are absent. Charac
is because the patient is unable to make the slight teristically, alcohol reduces or abolishes the tremor and
postural adjustments normally required to keep beta blockers and primidone are also useful.
one's balance. Spontaneous falls are not frequent Patients with depression often have an expressionless
early in the disease. Postural hypotension may face, stooped posture and relative immobility and these
be present in a few patients. may be confused with PD. Moreover, depression is a
There are no objective sensory impairments common accompaniment of Parkinson's disease and
(other than an impairment of olfactory sensation some who ultimately develop PD have depression as
in some patients). Both the deep and superficial their presenting symptom. But in such cases, other
reflexes are normal and there is no significant features of PD will become manifest within a period
decrease in muscle power. of one year.
13. Cognitive and psychiatric complaints are common. Other causes of psychomotor retardation should be
Some of them may be side effects of drugs considered and these include the normal aging pro
(e.g., confusional states, hallucinations and cess, drug intoxication, systemic illness, frontal lobe
psychosis). About 40% of patients suffer from syndromes, akinetic mutism, catatonia, subcortical
depression even early in the disease. The patient dementia, normal pressure hydrocephalus and other
may also have difficulty in making decisions movement disorders.
and may become dependent on others. There is Blood and CSF examination and cerebral imaging stud
thought to be a premorbid personality type in ies such as CT and MRI scans are non contributory in
PD (introspective, rigid, diffident). The intellect making the diagnosis of PD but may be of use when
is usually well preserved but late in the disease there is a suspicion of other causes of Parkinsonism.
course about 15% of patient will develop frank Positron emission tomography (PET) scans, when
dementia (when dementia is defined by DSM-III available, will show a decreased uptake in the striatum
criteria). in patients with PD.
Progress and Mode of Death Staging
In most patients the disease progresses gradually over The Hoehn and Yahr Scale can be of use in assessing
about 10 years until they become wheelchair-bound the severity of the disease and to decide the line of
or bed ridden because of severe bradykinesia, rigid management.
ity and postural instability. Death may occur from Table 6.31 : Staging: Hoehn and Yahr
aspiration pneumonia, septicemia from urinary tract Scale
infection, decubitus ulcers or from secondary causes
Stage I Unilateral involvement
like vascular disease or neoplasia. Stage II Bilateral involvement but no postural abnor
malities.
Diagnosis Stage Ill Bilateral involvement with mild postural imbal
The diagnosis of Parkinson's disease is based on the ance; the patient leads an independent life.
Stage IV : Bilateral involvement with postural instability;
clinical symptoms and signs and by excluding other the patient requires substantial help
causes of Parkinsonism (secondary Parkinsonism and Stage V : Severe, fully developed disease; the patient is
Parkinsonism - plus syndromes). restricted to bed and chair.
Conditions which may initially be confused with PD I. Anti-Parkinsonism Drugs
are essential tremor and depression, which are far Drugs used in the treatment of PD (with the
commoner conditions. possible exception of deprenyl), do not alter the
Essential tremor is often inherited as an autosomal progression of the disease but they do enable the
dominant trait. It may appear at any age. It is mainly patient to remain independent and functional
for a longer period.
360
( 6 ) Central Nervous System
The decision as to when to start treatment and antiviral drug but in additio
n it
with what drugs depends on the predominant rele ase s sto red dop am ine
fro m
symptoms at that time, the functional capacity presynaptic terminals. Therefore
it is
of the patient and whether the patient is able only useful in the early stages of the
to carry out his occupation and activities of disease. The usual dose is 100 mg bid.
daily life with reasonable efficiency. The staging Side effects include ankle edema and
system of Hoehn and Yahr can be of use in livido reticularis (a reddish mottling
making this decision but the decision should of the skin of the lower extremities),
be individualized for each patient. both of which are not harmful) but
Drug treatment should be delayed as long as in higher doses it may cause an acute
confusional state.
possible, and when started, the dose of the
drug should be gradually increased until the 3. Deprenyl (selegiline) is a monoamine
required benefit is achieved. The goal should oxidase B inhibitor which inhibits the
be to relieve the symptoms to manageable levels catabolism of dopamine in the brain
and not necessarily to give complete relief from (unlike MAO-A inhibitors which
symptoms. This is because all the drugs have inhibit the catabolism of dopamine in
got side effects, both short term and long term, the peripheral tissues). It could retard
which are minimized by using smaller doses of the progression of PD as judged by
the drugs. the duration of disease after which it
Patients in stages I and II of the Hoehn and becomes necessary to start levodopa.
A.
When used in conjunc tion with
Yahr scale either require no treatment
levodopa, it decreases the amount
or may be treated with anticholinergics,
of levodopa required. Moreover, it
amantadine or deprenyl.
is also useful in the management of
1. The anticholinergics are mainly useful the long term side effects oflevodopa.
in decreasing the rest tremor. These Because of these properties, there is
drugs attempt to maintain the ratio a trend to use deprenyl early in the
between dopamine and acetylcholine course of PD. The average dose is 5
in the striatum. Commonly used to 15 mg/day given in divided doses
drugs are trihexyphenidyl (1 to 2 mg twice a day.
qid), benztropine (0.5 to 1.0 mg tid),
B. Patients in stage III, IV and V of the Hoehn
benzhexol hydrochloride (2 to 5 mg
and Yahr scale usually require levodopa.
qid) and orphenadrine (50 mg qid),
Anti-cholinergics or amantadine may
starting with a small dose. Frequent
be used in conjunction with levodopa
side effects are dryness of the mouth,
to increase its efficacy or relieve specific
constipation and slight blurring
symptoms like rest tremor.
of vision which are not harmful in
l. Levodopa is the cornerstone of drug
themselves. They should be used
therapy for Parkinson's disease. A
with caution in the elderly, as they
good response to the drug is seen
can cause acute urinary retention and
in at least 75% of patients. The most
confusion. They are contraindicated
beneficial effect is on bradykinesia
in patients with glaucoma as they may
and postural instability.
precipitate an acute rise in the intra
Dopamine does not cross the blood
ocular tension.
brain barrier but its precurs or
2. Amantadine is more effective than levodopa does. In the brain, levodopa
anticholinergics and is also useful is converted to dopamine by dopa
in decreasing the tremor. It is an decarboxylase, thereby replenishing
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PRACTICAL MEDICINE
the dopamine loss in the striatum. dopamine and are usually relieved by
When given alone, it is converted to the addition ofcarbidopa. In addition,
dopamine by dopa-decarboxylase domperidoneand taking the drug after
present in peripheral tissues and meals are also effective in relieving
only about 5% of the dose enters the the gastrointestinal side effects. An
brain. To prevent this, a peripheral
overdosage of levodopa can result in
decarboxylase present in peripheral
psychiatric and cognitive symptoms
tissues and only about 5% of the
dose enters the brain. To prevent (such as delirium, hallucination and
this, a peripheral decarboxylase psychoses) and dyskinesias.
present in peripheral tissues and MAO-A inhibitors ( used a s
only about 5% of the dose enters the antidepressants) are contraindicated
brain. To prevent this, a peripheral and sympathomimetics should be
decarboxylase inhibitor (either used with caution as these can cause
carbidopa or benserazide) is used in an acute rise in the blood pressure.
combination with levodopa. Such a Levodopa is contra-indicated in
combination markedly decreases (by patients with malignant melanoma
about 80%) the amount of levodopa
since levodopa is a precursor of
required.
melanin and may thus induce a
Plain levodopa tablets are available
recurrence of melanoma.
but most patients receive levodopa
carbidopa combinations (L-C). These At least 65% receiving plain levodopa
combination tablets are available or L-C (without dopamine agonists
as L-C 275 (250 mg levodopa; or deprenyl) develop long term side
25 mg carbidopa), L-C 110 (100 effects in varying severity after 2-5
mg levodopa; 10 mg carbidopa and years:
L-C Plus (100 mg levodopa; 25 mg a. Some patients, especially those
carbidopa). The combination of
with dementia, show a decreased
levodopa and benserazide (in a ratio
response to the drug. Increasing
of 4: 1) is not widely available.
the drug dose often results in an
L-C is started in small dose (e.g. acute confusional state.
half a tablet of L-C Plus tid or qid)
b. In the 'wearing-off' effect, the
and gradually increased every few
duration during which the drug
days to achieve the required benefit.
is effective becomes progressively
Even though the maximum dose of
less. In such cases, the total daily
L-C 275 is about 6 to 8 tablets/day,
dose should be given at more
there is a strong indication to use
frequent intervals (sometimes
dopamine agonists or deprenyl in
every 1 to 2 hours) with a conco
patients whose symptoms are not
mitant decrease in the amount of
adequately controlled by smaller
each dose.
doses oflevodopa. If a patient who is
on plain levodopa is to be started on c. In the 'on-off' effect, the patient
L-C, there should be at least a 12-hour fluctuates between 'on' periods
gap between the discontinuation of with activity (and often also
levodopa and the starting of L-C. dyskinesias) and 'off' periods
with akinesia and rigidity. These
Early side effects of levodopa are
fluctuations are unpredictable,
nausea, vomiting, cardiac arrhythmias sudden and not related to the
and orthostatic hyp otension. These timing of drug intake.
are due to peripheral conversion to
362
( 6 > Central Nervous System
Both the 'wearing-off' and 'on-off' 4 mg/day) given tid or qid acts
effects are often associated with both on D, and D2 receptors and
dyskinesias which take the form therefore may be more powerful
of choreoathetotic movements. with a longer duration of action
These side effects may be due to than bromocriptine. The side effects
defective absorption of levodopa are similar to those of levodopa
because IV administration of the except that abnormal involuntary
drug often results in a more stable movements are less prominent and
clinical state. neuropsychiatric side effects may
These late onset side effects of be more marked.
levodopa are difficult to treat. II. Other drugs:
The addition of deprenyl or 1. Since de pression i s a common
dopamine agonists together with accompaniment, itshould be identified and
a decrease in the dose oflevodopa treated with tricyclic antidepressants and/
may be of help and, the early or ECT when required. MAO-A inhibitors
introduction of either of these are contraindicated in patients receiving
drugs may delay and minimize levodopa as they may cause an acute rise
these side effects. Omitting in the blood pressure.
levodopa completely has not Psychiatric and cognitive symptoms such
been found to be useful and may as confusional states, hallucinations and
even be harmful because of severe psychoses are more common in elderly
akinesia postural disturbances patients who may also be demented. These
and rigidity which may result. symptoms are often caused or aggravated by
Experimentally, sustained-release the antiparkinsonian medication. In such
forms of L-C and subcutaneous cases, decreasing the dosage of the drug
administration of a dopamine can be of use and, if necessary, psychosis
receptors agonist (e.g. lisuride) can be treated with clozapine (which does
via an infusion pump, are being not have significant extrapyramidal side
tried to minimize these long term effects).
side effects. 2. Patients in whom a faster postural tremor
2. The dopamine receptor agonists are predominates will benefit from beta
bromocriptine, pergolide and lisuride. blockers (propranolol - 40 to 80 mg tid;
There are two known dopamine metoprolol) or primidone (50 mg HS,
receptors in the brain-D1 and D2 • increased gradually to a maximum of 250
Stimulation ofD, receptors increase mg/day).
intracellular cyclic AMP but the III. Regular exercise Program
same is not true on stimulation Parkinson's disease is usually a slowly progressive
of D2 receptors. D2 receptors are disease and this should be impressed upon the
more important in alleviating the patient and his relatives so that the patient is
motor symptoms of Parkinsonism encouraged to live an independent life for as
but stimulation of D 1 receptors long as possible. A regular exercise program
may produce additional benefit. and accessory aids, when necessary, will help
Bromocriptine acts only on D2 in achieving this objective. In the later stages,
receptors. The usual dose is 15 to the help of a physiotherapist will be of value.
30 mg/day given in divided doses
IV. Prevention of precipitating factors
(tid or qid), starting with a small
dose (2.5 mg HS). Pergolide (1 to Patients with PD have an aggravation of
363
PRACTICAL MEDICINE
symptoms if ther� is any super added illness and and metoclopramide block the dopamine
therefore infections should be promptly treated receptors) but anticholinergics are effective. The
and surgery avoided unless absolutely necessary. parkinsonian symptoms usually subside within
V. Surgery a few months after discontinuation of the drug.
Small surgical lesions of the globus pallidus 2. Infections: The patients with post encephalitic
or ventrolateral nucleus of the thalamus using Parkinsonism tend to be of a younger age
steriotaxic techniques reduces or abolishes group than those with idiopathic PD and the
the tremor and rigidity in the contralateral Parkinsonism symptoms are usually milder and
limbs but does not benefit the bradykinesia progression is slow. Moreover, other features such
and postural instability. At present it is rarely as oculogyric crisis, dyskinesias, tics, diplopia or
resorted to because of more effective drugs and other focal neurological deficits are frequently
the morbidity associated with the procedure. present. Response to levodopa is usually good.
But it may be used in exceptional cases where
the patient is young and has incapacitating 3. Vascular: Parkinsonism resulting from multiple
tremor and rigidity on one side of the body small infarcts have long standing, poorly
which are resistant to drugs. Adrenal medullary controlled hypertension and also other features
transplant to the corpus striatum was initially of multi-infarct dementia such as pseudobulbar
thought to be helpful but its value has not been palsy, exaggerated tendon reflexes, extensor
substantiated. At present, trials are on to the plantars and a short stepped gait, apart from
assess the usefulness of transplantation of fetal impairment of cognition. Response to levodopa
substantia nigra neurons. is poor.
Secondary Parkinsonism 4. Toxins: MPTP is converted in the glial
cells of the brain to MPP+ by the action of
1. Drugs: Reserpine (especially in large doses) monoamine oxidase B. MPP+ is then taken up
depletes dopamine from the nerve terminals into dopaminergic neurons via the dopamine
in the striatum while the neuroleptics
Table 6.32 : Parkinsonism - Plus Syndromes
Pathology Clinical
1. Multiple system atrophy Alpha Age of onset: 50 years
synucleinopathies
Median survival 6-9 years
Rigidity and akinesia predominate &tremor is less
Autoimmune involvement- postural hypotension, sweating, pedal
edema, syncope
Urinary involvement- urgency, retention, incontinence, impotence in
men
2 types of MSA (pl Parkinsonian symptoms predominant (cl cerebellar
symptoms predominant
Primary autonomic failure: Shy-Drager syndrome
2. Progressive supranvellar Tau gene mutations Age of onset: 6-7 decade
palsy (Steele Richardsons Survival: 5-10 years akinetic parkinsonism, unsteadiness, slowness, Falls
syndrome) occur early in disease.
No tremor
Eye: Supranuclear gaze palsy affecting down gaze first &then upward
gaze.
Some develop dementia
3. Corticobasal degenera- Tau gene mutations Allen limb- involuntary purposeless movements of a hand, rigid
tion ity, involuntary movements, myoclonicjerks, higher mental function
involvements
364
( 6 > Central Nervous System
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PRACTICAL MEDICINE
367
PRACTICAL MEDICINE
368
{ 6 > Central Nervous System
In extracerebral lesions altered consciousness suspected. If there is respiratory depression,
may be the earliest manifestation. stimulants like nikethamide (Coramine)
2. Subtentorial lesions: Coma can occur with may be given round the clock. Endotracheal
intrinsic brainstem lesions like cerebrovascular intubation may be required if secretions
accident by destruction of ARAS. Extrinsic cannot be adequately removed and if this
lesions cause compression either by the neuronal is required for more than 48-72 hours,
tissue damage or through herniation syndrome tracheostomy may be required.
leading to asymmetrical motor signs, cranial 2. Circulation: Patients with raised intracranial
nerve palsies, and vomiting. tension are usually hypertensives.
3. Extra-cranial disorders: Normal brain Sometimes, the patient may be unconscious
requires oxygen and glucose for its metabolism. and in shock. He must be adequately
Only 2 gm of glucose exists as reserve in hydrated with intravenous fluids. If
brain. Cerebral cortex and hippocampus are hypotension persists after adequate
most sensitive to glucose depletion. Thiamine hydration, venous cutdown and a CVP
and pyridoxine are required for glucose (central venous pressure) line must be
metabolism 3.3 cc of oxygen per 100 gm maintained. If it is normal or high in
brain tissue per min is required for normal presence of hyp otension, vasopressors
metabolism in brain. Mental changes occur like mephentermine or dopamine
when less than 2.5 cc of oxygen per 100 gm. hydrochloride may be given.
brain tissue per minute is available and coma 3. Nutrition: An unconscious patient can be
occurs when it falls to 0.2 cc. adequately nourished orally through the
The characteristic features of endogenous Ryle's tube. Whilst feeding, the patient
disorders leading to coma are: must be propped up, either by raising the
head end of the bed or using 2-3 pillows,
a. Decreasing level of consciousness precedes
to prevent aspiration. Daily 2000-2500
motor signs.
ml of fluids and about 1500-2000 calories
b. Motor abnormalities: There are three types are given with combination of milk, fruit
of motor abnormalities. juices, vegetable soups, rice kanji, aerated
i. Tremors - Coarse and irregular. waters and sugar. In uremia, fruit juices
ii. Asterixis - sudden asynchronous and coconut which contain large amounts
palmar flapping at the wrist which of potassium are restricted unless urine
are absent at rest and maximum output is adequate and serum electrolytes
with sustained posture. These occur do not show hyperkalemia. Similarly milk
probably because of the electrical is also restricted in uremia.
lapses in the controlling muscles. 4. Oral cavity: The mouth must be regularly
iii. Multifocal myoclonus - Unpatterned cleaned especially with glycerine borax
movements of the facial and proximal preferably 2-3 times a day. Oral infections
muscles of the limbs. and parotitis are very common if this care
is neglected. Secretions, if any, must be
Treatment regularly sucked with the help of suction
machine.
I. Management of the unconscious patient:
5. Urinary care: The patient usually passes
l. Respiration: A clear airway must be
urine in bed which would require repeated
maintained so that oxygenation of blood
changing of bedsheets. If this is not done,
and brain do not suffer. This is done by
bedsores and infections occur. Hence, in a
pulling the tongue forward and doing throat
male patient a condom catheter is passed
suction as often as required. Humidified
which would prevent bed soiling. However,
oxygen may be administered if hypoxia is
369
PRACTICAL MEDICINE
this is not possible in females. Again in some bedsore does develop, it must be dressed
unconscious patients there is retention of regularly with hydrogen peroxide and
urine. In such cases, a self retaining Foley's antibiotic dressings must be applied. The
catheter is put. Once a patient is put on a affected part must be kept free from pressure.
self retaining catheter, various measures to 8. Eyes: If the eyes of the comatose patient
prevent and treat urinary tract infection are remains open, exposure keratitis and
undertaken as follows: ulcerations may occur which can be
a. Catheter dressing must be done daily. prevented by putting antibiotic eyedrops
b. Bladder washes may be given if there in the daytime and ointment at night. The
is pyuria. eyes must be closed and if required padded
and bandaged.
c. Bladder exercises must be given after
a few days to prevent loss of tone If the eyes remain closed, the chance of
of bladder muscles by periodically exposure keratitis is not present but even
clamping the catheter for few hours. then the eyes must be cleaned 3-4 times
d. Urine must be sent regularly for with plain clean water.
routine and culture examination. If 9. Passivephysiotherapy: An immobile patient
urinary infection is present, urinary often develops stiff joints. To prevent this,
antibiotic syrup like co-trimoxazole, the limbs must be regularly moved at all
nitrofurantoin, chloram-phenicol joints for a few times through its complete
or ampicillin may be given through range. This may be repeated 2-3 times a day.
the Ryle's tube. Injectable gentamicin
II. Removal of the cause: Removal of the cause is
may be required for Pseudomonas
most important in therapeutics. They may not
infection.
be often obvious. However, if it is obvious and
6. Bowel: Comatose patients are often treatable it must be treated. A few examples are
constipated. This can be prevented or as follows:
treated by regular simple or saline enemas
1. Gastric lavage, analeptics and naloxone for
on alternate days. Ifthe patient has diarrhea,
narcotic poisons.
it must be promptly controlled with binding
2. Atropine and oximes for organo
mixtures, metronidazole, antibiotics
phosphorous poisoning.
or antimotility agents like loperamide.
3. Forced alkaline diuresis for barbiturate
Bedsores develop rapidly if patient remains
poisoning.
dirty in fecal matter. Nursing care to keep
4. Ice-baths in heat stroke.
perianal and genital region clean is of
utmost importance. 5. Removalofthepatientfromthecontaminated
atmosphere and administration of oxygen
7. Skin: The bed must be regularly made. and carbon dioxide in carbon monoxide
Bedsheets must be dry and whilst preparing poisoning.
the bed, creases should be avoided. If the
Srstem
the patient must be regularly turned and
kept on each side alternately and sometime ----
prone. Special care must be taken of the Syphilis usually affects the nervous system in the
pressure points. Alcohol and spirit must tertiary stage. However, it may show affection even
be used to clean the skin. This is followed in the secondary stage.
by liberal powdering. Neurosyphilis usually occurs 10-30 years after the
In spite of good care of skin, however, if the primary infection, hence it is more common between
the age of 30 and 60 years.
370
( 6 ) Central Nervous System
Males are affected more than females. In the terminal stages there may be incontinence
Neurosyphillis is rare but with the epidemic of HIV, of urine and stools and the patient may become
its incidence is increasing. bedridden.
II. Disturbance of Speech and Writing: Usually the
Classification patient has slurred speech. Grammar is affected
A. Parenchymatous: Direct affection of nervous due to mental changes. Words and sentences
system by spirochetes. may be wrongly used or omitted. There may be
1. GPI ( General paralysis of insane) nominal aphasia and echolalia. Patient may be
unable to write in a straight line and there may
2. Tabes dorsalis
be micrographia. The writing often depicts the
3. Primary optic atrophy mental state of the person. Spasticity and tremors
B. Meningovascular: Neurological involvement also affect the writing.
secondary to vascular affection III. Progressive Spastic Paraplegia: There is gradual
l. Cerebral form onset of weakness of both lower limbs due to
a) Cerebral thrombosis involvement of the motor cortex.
b) Vertical meningitis IV. Disturbance in Reflexes: Due to spastic paraplegia,
there is loss of abdominal reflex, brisk ankle and
c) Gummatous basal meningitis
knee jerks and extensor plantar reflex.
d) Encephalomalacia
V. Disturbance in Pupils: The patient may have small,
e) Gumma unequal or irregular pupils. There may be Argyll
2. Spinal form Robertson or reverse Argyll Robertson pupils.
a) Acute transverse myelitis VI. Tremors: Tremors in GPI are conspicuous on
b) Meningomyelitis voluntary movements. They are coarse tremors
c) Hypertrophic, cervical, best seen in the facial muscles, especially lips
pachymeningitis and tongue, and in the outstretched hand.
d) Erb's spinal paralysis VII. Congestive Attacks of GPI: Also called
apoplectiform episodes, these are characterized
e) Amyotrophy
by sudden focal neurological deficit. Hemiplegia
f) Radiculitis is the commonest. There may be hemianopia,
g) Gumma aphasia, apraxia, monoplegia, paraplegia or
h) Caries of the spine quadriplegia. There may also be transient loss
of consciousness.
General Paralysis of Insane (GPI)
Recovery is usually complete within a week.
Site of Lesion: Diffuse involvement of the cerebral CSF Picture: Increased proteins with moderate pleo
cortex cytosis: 15-100 cells. Colloidal gold curve is paretic.
CSF VDRL is positive.
Clinical Features
I. Mental Changes: These are the earliest symptoms Treatment
and the earliest change is usually impairment of I. Penicillin: Benzathine penicillin 2.4 mega units
intellectual efficiency. There is loss of power to intramuscular, per week for 4 weeks. It may be
concentrate, impairment of judgment, memory repeated after 4 to 6 months.
defects }ability of mood leading to imbecility. II. Convulsive shock therapy for psychiatric
This is the simply dementic form. symptoms.
In the grandiose type there is a sense of euphoria
III. Fever or malarial therapy used commonly in the
and delusions of grandeur.
past, and for some resistant cases in the recent
The other emotional states commonly seen are past is no longer advocated.
mania, depression, paranoid and schizophrenia.
371
PRACTICAL MEDICINE
Pulmonary Embolism
433
PRACTICAL MEDICINE
Hypertranslucency
Opaci1k-s (cw in number
Lxtrcmd) numerous op.icnu:s
Ca"·"·' Ca""" .
'
Tuberculosis, Varicdla. • • • •
H1stoplasmos1s, Metastases, • . • • •
, • •
Metastases,
Alvcolar m1cro
Sarcoidosis
OQ • •. .
lithiasis,
·. ·.. . .....
.
Metastases
Cau.,e,
Sarcon.los1s,
Pncumocomos1s,
��::�
Alveolar micro-
d1�llSC.
l'nl'tlmO
con1os.is
Chest PA Chest PA
Opocities\\lth assoc:iatcd
lymph nodes
Cuuu.,
Tu�rculosis.
S:uco1dosis.
Histoplasmos1s,
Mct.i.stascs.
Silicosis
Causes
Unilateral
1. Pleural:
a) Pneumothorax
b) Contralateral pleural thickening (apparent,
Miliary Mottling (Refer X-ray Pg. 161) hyper-translucency)
2. Pulmonary:
Causes
a) Unilateral obstruction
A. Infection: b) Bullae
1. Bacterial: Disseminated tuberculosis,
c) Eventration of the left dome of the
broncho-pneumonia, brucellosis, etc.
diaphragm
2. Fungal: Histoplasmosis, coccidioidomy
3. Chest wall
cosis, blastomycosis, etc.
a) Mastectomy
B. Allergic: Tropical eosinophilia, Loeffler's
syndrome, drug reaction b) Absent pectoral muscle
434
( 9 ) Radiology
Bilateral Bilateral
l. Pleural: Bilateral pneumothorax l. Pregnancy
2. Pulmonary: 2. Obesity
a) Emphysema 3. Ascites
b) Bronchial asthma 4. Large abdominal mass
c) Bullae 5. Abdominal distension
3. Cardiac 6. Infants
a) Primary pulmonary hyp ertension
b) Ebstein's anomaly
c) Fallot's tetrad with pulmonary atresia
435
PRACTICAL MEDICINE
2. Sarcoidosis F. Miscellaneous:
3. Lymphomas 1. Lipoma, mesothelioma
4. Leukemias 2. Mediastinal abscess
5. Metastasis 3. Cardiac aneurysm or tumor
Causes
A. Pulmonary I Parenchymal Calcification:
I. Diffuse:
1. Infection: Tuberculosis, abscess,
histoplasmosis, varicella, pneumonia
2. Tumor: Hamartoma, pulmonary
A-V aneurysm, metastasis from
osteogenic sarcoma
3. Unknown: Broncholiths, alveolar
micro-lithiasis
4. Silicosis
5. Hemosiderosis (long standing mitral
stenosis)
6. High density (post-lymphography,
baritosis, stannosis)
II. Solitary
1. Infection: Tuberculosis, histoplasmo
B. Aorta: sis
1. Aneurysm 2. Hamartoma (popcorn calcification)
2. Unfolding B. Cardiac Calcification:
3. Anomalous origin of the great vessels 1. Aortic arch
C. Cysts: 2. Constrictive pericarditis
3. Valves or valve rings
1. Dermoid teratoma
4. Thrombi and myxomas
2. Cystic hygroma
5. Coronary arteries
3. Bronchogenic cyst
C. Mediastinal Calcification:
4. Pleuro-pericardial cyst
1. Lymph glands: Tuberculosis, sarcoid,
5. Meningocele pneumoconiosis
D. Thymus: 2. Tumors: Teratoma, dermoid, thyroid
1. Enlargement adenoma
2. Tumor D. Pleural Calcification:
E. Esophagus: I. Diffuse
1. Achalasia cardia 1. Infection: Tuberculosis, pyogenic
2. Hiatus hernia empyema
3. Enterogenous cyst 2. Asbestosis
436
< 9 > Radiology
II. Focal (Subpulmonic plaques) Pulmonary Plethora
1. Asbestosis Dilated vessels throughout the lung fields
2. Talcosis
E. Chest Wall Calcification:
1. Ribs (Bone islands, Costal cartilages)
2. Muscles and soft tissue (Cysticercosis,
Guinea worm, Dermatomyositis)
3. Phleboliths
F. Egg Shell Calcification:
1. Silicosis
2. Coal workers Pneumoconiosis
3. Sarcoidosis
Causes
1. Left ventricular failure
2. Valvular heart diseases: MS, Ml, AS, AI
Causes:
1. Recurrent pulmonary emboli
2. Chronic pulmonary disease
3. Long standing left heart disease
4. Left-right shunt
Causes:
Causes:
1. Fallot's tetrad. Fallot's triad, Truncus arteriosus 1. Left sided heart failure
2. Severe pulmonary stenosis 2. Cor-pulmonale
3. Pulmonary emboli
437
PRACTICAL MEDICINE
438
< 9 > Radiology
the superb natural contrast of air is less generously
available. Plain-X-ray abdomen must be evaluated
as follows:
1. Lung bases and diaphragm: For basal pneumonia,
pleurisy, gas under the diaphragm
2. Extraabdominal soft tissues: (An incarcerated
hernia may be the cause of patient's bowel
obstruction)
3. Skeletal structures: Lumbar vertebra, vertebral
pedicles, spleen and kidneys may be visualized
4. Fat and muscle plane: Psoas muscle
5. Solid organs: Liver, spleen and kidneys
6. Gas shadow in stomach and colon
7. Calcification
8. Intraperitoneal air and fluid
Paralytic lleus
Diffuse fluid and gaseous distension ofsmall and large
bowels and if the plate is taken in upright position,
air and fluid levels may be present at the same level.
Causes: Peritonitis, drug effect, bowel ischemia, trauma
Bowel Obstruction
Proximal to the lesion the gut is distended with gas
and fluid, distally the gut is empty. The upright X-ray
shows step-ladder distribution.
439
PRACTICAL MEDICINE
Causes
1. Perforation of a viscus
2. Following abdominal surgery
3. Tubal insufilation test
4. Peritoneal dialysis
5. Infection of peritoneum by gas formi ng
organisms
Calcification in Abdomen
Causes:
1. Fecaliths
2. Phleboliths
3. Calcified lymph nodes
4. Calculi: Renal, biliary, pancreatic, splenic
5. Calcified fetus
6. Liver: Amebic abscess, tuberculosis, calcified
hydatid cyst, histoplasmosis, brucellosis
7. Calcification of abdominal wall, cysticercosis
8. Pancreas: Chronic pancreatitis
9. Suprarenal: Addison's disease, neuroblastoma
10. Splenic: Splenic cyst
Preparation
Three days preceding the investigation, the patient is
put on a low-residue diet. The patient is given deflatu
lant medication like methyl polysiloxane or activated
charcoal and mild purgation e.g. bisacodyl or castoroil
on the night previous to the day of procedure. Patient
is kept fasting overnight.
TECHNIQUE: AP view of abdomen is taken while
the patient is in a state of full inspiration. Another
antero-posterior view is taken by centering the tube
on pubic symphysis. Alternatively both the areas may
ows merge with each other. If there is free gas in the be covered in the same film.
peritoneal cavity it will ascend in standing position INTERPRETATION: In a normal person the psoas
and lie between the diaphragm and the liver density. shadows are seen running obliquely downwards from
440
(9 > Radiology
Small Kidney
1. End stage renal disease
2. Chronic pyelonephritis
3. Hypoplastic kidney
4. Renal artery stenosis
There can be unilateral agenesis of kidney causing
absence of renal shadow on that side. Alternatively
the kidney may be ectopic (e.g. Pelvic).
441
PRACTICAL MEDICINE
442
( 9 > Radiology
5 Barium Studies
inspiration the portal to esophageal venous pressure
falls, hence blood flows from portal to esophageal veins
Details of the gastrointestinal tract can be studied if which become varicose because of poor submucosal
the gastrointestinal tract is filled with radio-opaque support.
substance like barium.
Appearance
For the barium meal, the patient swallows a suspension
of radio-opaque barium sulfate, whilst the radiologist 1. On esophagoscopy: Blue rounded projections
observes its passage on the fluorescent screen, or on the under the mucosa.
TV monitor of an image intensifier. Films are taken 2. On barium swallow: Long thin, evenly spaced
to provide a permanent record of any abnormality lines of normal mucosa disturbed by the varices
discovered. The barium enema is used in the diagnosis as filling defects in the regular contour of the
of diseases of the large intestine and rectum. Barium esophagus.
suspension is introduced into the rectum as an enema
and manipulated around the colon to the cecum. Hiatus Hernia
1. On plain X-ray a ring shadow containing a fluid
Esophageal Varices level and superimposed on the cardiac shadow.
Situation: In the submucous and subepithelial layers 2. Barium studies show esophagus and the cardiac
by anastomosis of left gastric and short gastric veins end of the stomach protruding up through the
with the esophageal veins. normal hiatus.
Causes:
I
1. Portal hyp ertension --.,-..-� - ·-· Fig.
·--
9.23 · Hiatus hernia
- ---��- - -- --
2. Cirrhosis of liver Achalasia Cardia
3. Transiently in viral hepatitis 1. Esophagus is dilated
4. Alcoholic 2. There is an area of smooth narrowing just distal
Mechanism: The exact mechanism is not known. With to the dilated segment
443
PRACTICAL MEDICINE
3. Gas shadow is absent in stomach on plain X-ray Gastric Ulcer
abdomen
1. A constant projection from the main barium
shadow in the stomach due to ulcer crater. It is
conical with apex pointing outwards from the
stomach.
2. Some small craters and those below the incisura
ulnaris may be seen as small spherical opacities
surrounded by a transradiant zone. There may be
some deformity or interruption of rugal pattern
nearby due to surrounding edema. The average
gastric ulcer crater will be invisible radiologically
after about 4 weeks. However, healing takes about
6 weeks. A recurrent ulcer crater on a new site
will probably heal with greater ease than one on
the old site, where scar tissue and poor blood
supply will be factors delaying healing.
Carcinoma of Esophagus
Irregular narrowing ofthe lumen with slight proximal
dilation.
444
< 9 > Radiology
3. Ifit is seen en face after compression, it appears as 2. Slow initial emptying of stomach after barium
an isolated spot, the surrounding edema causing meal, in spite of periods of vigorous peristalsis.
a translucent area. Slow final emptying with a large barium residue
4. If the ulcer is chronic, the rugae may converge after 6 hours.
towards it giving a stellate appearance. 3. In severe cases, stomach is dilated.
5. If the ulcer is large, barium may remain in the
Causes of Delayed Gastric Emptying
crater after the rest of the cap has emptied.
1. Pyloric stenosis
2. Physiological upset following vomiting caused
by distaste for barium
3. Emotional upset due to grief, anxiety or even
upsets associated with asthma and migraine
lleocecal Tuberculosis
1. Filling defects or absence of filling of caecum
due to spasm
2. Irregular contour, persistent narrowing of the
ileum and cecum or shortening of the ascending
colon
3. Irregular lumen with contractions and dilatations
4. Multiple fluid levels
5. Calcification of mesenteric lymph nodes may
be present.
Crohn's Disease
1. A localized narrowing with irregularity of colon
wall. (Absence of concave indentations of the
two ends of narrow area).
445
PRACTICAL MEDICINE
Ulcerative Colitis
Neoplasm of Colon
1. An area ofnarrowing ofthe coloniclumen which
may be eccentric or annular.
2. A concave indentation of the lumen just beyond
the narrowing.
446
< 9 > Radiology
447
PRACTICAL MEDICINE
Osteopaenia-,c) :r:�)
\· ·�. •, .. ·,
4
":'imberger's/ -·.
sign
[]
Scurvy 0 Healed
In scurvy there is adequate calcium but lack of osteoid Sub� Periosteal
peri Scurvy:
tissue. reaction Metaphyseal
osteal Lifted
1. Epiphysis: The epiphysis has a dense margin lucency
hemo
with radiolucent centre (ring sign or halo sign of rrhage Uneven
Wimberger).
2. Metaphysis: the white line of metaphysis is wider
, Fig 9.35 Scurvy
than normal. 'Scurvy zone' lies between the bone I
f
and the white line. Widened � Metaphyml
.-., Fraying.
� & \ ,ptay;ng&
...._,
/ wth
3. Diaphysis: There is uniform demineralization P ate
widening
Cott��I
of the bone. The cortex is thinned out giving the loss of
Sp
Zone of
bone a uniformed ground-glass appearance with provisional
calcification
penciled outline. Angular lateral bony spurs are
present. These are defects in the cortex at the Rachitic
junction of diaphysis and metaphysis (angle sign). rosary
Bowing
4. Subperiosteal hemorrhages may occur which of
libia
may lift the periosteum. It may calcify sometimes.
Rickets
Croniotabes:
Aattening of
• �:t!�
etum on Zone
1. Epiphysis: The epiphysis lacks a bony cortical of provisional
the occiput
margin and appears indistinct. There may be Thickening of \�alcifica!ion.
frontal bone (& \�sclerosis,
epiphyseal separation which is more common Metaphyseal
parietal bones)
in renal rickets. lucency
448
< 9 > Radiology
and distally concave (cupping). The zone of Osteoporosis
calcification instead of forming a well-defined
Demineralization of bone with thin cortices and
white line, is irregular and of low density. Its
delicate medullary trabeculae.
end appears arranged in longitudinal rows
(fraying or streaking). Cortical spurs from the Causes:
metaphysis may grow towards the displaced
epiphysis resulting in deformity. I. Endocrine: Cushing syndrome, thyrotoxicosis,
hypogonadism
3. Diaphysis: There is generalized decalcification
of the bones resulting in increased radiolucency 2. Metabolic: Mucopolysaccharidosis, homocys
between the diaphysis and epiphysis. tinuria
4. Green-stick fractures with bending and 3. Deficiency: Famine, scurvy, hyp ocalcemia
deformities may occur. 4. Bl o o d diseases: Leukemia, myel oma,
lympho-sarcoma, secondaries, histiocytosis
Osteomalacia 5. Drugs: Heparin, steroids
Definition: Osteomalacia is a disorder characterized 6. Idiopathic
by failure of the bony matrix to mineralize normally 7. Osteomalacia
and promptly.
Osteosclerosis
Features
1. Generalized decalcification of the bone Causes
2. Vertebral bodies are biconcave (cod-fish I. Fluorosis
vertebrae) 2. Secondariesfrom malignancy of prostate, breast,
3. Looser'szones or pseudo-fracture may be present. bronchus, gut and Hodgkin's disease
They are 1-3 mm wide transradiant zones 3. Marble bone disease
extending 1 cm into the bone at right angle to
4. Osteopoikilosis
the cortex and look like incomplete fracture.
They occur in ischio-pubic rami, axillary borders 5. Mastocytosis
of the scapula, ribs, femur, humerus and lower
third of tibia and fibula
4. Deformities of limb and pelvis (triradiate pelvis)
may be present.
5. If chronic renal failure is the cause of osteomalacia
there may be sub-periosteal bony erosions in
middle phalanges and sclerosis of the vertebral
end plate (rugger jersey spine).
Bony Metastasis
1. Erosion without bone reaction or periosteal new
Looser's zones bone formation
paenia Pseudo or 'Milk 2. In the vertebrae it may cause vertebral collapse
mans fractures with intact disc space
Fig 9 37 .Osteomalac1a 3. Sclerosing bony metastasis have to be
distinguished from Pager's disease
449
Table 9.4 : Differences between
Sclerosing Metastasis and Paget's
Disease
Sc/erasing
metastasis
Paget's disease
f Inter·
osseous
ligament
lcification
Fluorosis
Annulus
sification
Large
u
PRACTICAL MEDICINE
M
teophytes J /
Large bony
excrescences
and periosteal
reaction
Fluorosis
1. Osteosclerosis of the spine and pelvis
2. Ground-glass appearance of the bones
Rheumatoid Arthritis
3. Calcification ofthe interosseous membrane ofthe
forearm, intervertebral ligaments, sacrospinous Peri-articular
and sacrotuberous ligaments osteopenia
Joint space
widening
450
9 > Radiology
Septic Arthritis
1. Joint effusion with joint swelling
2. Rapid loss of cartilage and subchondral bone
Psoriatic Arthritis
M surface
VJ� erosion Sclerosis ecrcased
joint
c) space
Ankylosis
Erosion
Disc
;§
cal�ific
"Bamboo
Spino.,.-m
nIIt
atrnn
yndesmo
phytes
Gout
1. Capsular swelling leading to gross destruction
451
PRACTICAL MEDICINE
In children: Acromegaly
1. Widened sutures
1. The long bones are wide, thick, with coarse bony
2. Prominent convolutional markings trabecular pattern & tufting of the terminal
3. Erosion of posterior clinoids. Sella turcica is phalanges.
---
shallow
[]�=--
Frontal sinus
In adults: enlargement Acromegaly
& bossing �
1. Erosion of posterior clinoids ...... Tufting
Osteoarthritis
2. Silver beaten appearance (Fig 9.47) Increased
�_
Jomt space
� Broad bones
Osteopaenia
�
ance
Prognathism
Prominent
tendinous
attachments
Increased
heel-pad
thickness
Pituitary tum ur
Pituitary gland Coronal
� CT Brain
Sphenoid sinus
452
< 9 > Radiology
2. The vault of the skull is increased in thickness,
paranasal sinuses are large, mandible shows
prognathism and malocclusion ofteeth and sella
turcica is widened, deep and ballooned.
lntracranial Calcification
Pathological lntracranial Calcification
I Intracerebral. Localised
Infection-Tuberculoma
abscess, cysticercoi,is
1\tmour-meningioma,
(0
1 . • )
glioma. teratoma
metastases: Other
haematoma. cavernous
angioma
a
�
ky calcif•
ication-Glioma
Skul l PA Skull PA
Surface Calcification
Meningeal Subdural
Haematoma
TB meningitis
Curvilm ar.
concavo-
convex
calc1ficahon / \
Hydrocephalus �
453
PRACTICAL MEDICINE
c:;�::.':t
5L'""
Abnormal body
1. Infections: Tuberculosis,hydatidcyst,cysticercosis
Punched-out
r?�,
and toxoplasmosis ost�ytic
lesions
Y,<ongbon"
..:=__J-....:=:,
collapse
arteriosclerosis, AV malformations
3. Tumors: Meningioma, dermoid, cranio
pharyngioma, etc.
4. Miscellaneous: Sturge Weber syndrome, tuberous
sclerosis, hypoparathyroidism.
Thalassemia
1. Skull: The diploic space is widened with lack of
definition ofthe outer table. In severe cases, outer
table cannot be defined and the bony trabeculae
tend to be arranged at right angles to the inner
table giving hair-on-end appearance.
2. Long bones: The medullary cavity is wider
with coarse trabeculae and thinned out cortex.
This is best seen in phalanges which may lose
its biconcave shape and become rectangular or
biconvex.
454
1 > Endotracheal Tube with 0.5 mm increments. The cuffed tubes are avail
able in 4.0 to 10.0 mm sizes with 0.5mm increments.
Sterilization
The India Rubber tubes can be boiled or autoclaved.
The PVC or Portex tubes are available in gamma ir
radiated packs for single use.
Uses
1. Cardiopulmonary arrest to carry out artificial
respiration
Fig 10 1 · Endotracheal tubew1th a cuff
- - ---- - -- - --
-
2. Respiratory failure due to severe pneumonia,
It is a tube made oflndia Rubber, Portex (polyethylene)
chronic obstructive lung disease and respiratory
or Polyvinyl chloride (PVC). The Portex and PVC
muscle paralysis (Gullian Barre syndrome,
tubes are softer and less irritant to the mucosa. They
myasthenia gravis, bulbar poliomyelitis, etc.)
have a radio-opaque line along their length to assess
the exact location of the tube. The tube has a smooth 3. To secure the airway and clear secretions to
atraumatic tip. The end ofthe tube isbeveled. The bevel prevent aspiration in unconscious patients
usually faces left. There is also a sub terminal opening 4. To administer general anesthesia.
(eye) on the right in order to inflate the right lung. 5. To suction the trachea in newborns in case of
There is a 1 cm graduation along the tube to indicate meconium aspiration
the depth ofinsertion. There is also a 2 cm mark (called
the Vocal Cord Guide) at the distal end which helps in Method
placement of the tube beyond the vocal cords. The patient is kept in supine position with the cervi
The endotracheal tube may be cuffed or uncuffed. cal spine flexed and the head extended at the atlanto
The cuffed tubes have a cuff at the distal end which occipital joint. Standing at the head of the patient,
can be inflated through a smaller tube which runs the laryngoscope is inserted into the oral cavity and
alongside the endotracheal tube or is embedded in the vocal cords are visualised. The Endotracheal tube
its wall. There is also a pilot balloon with a one-way (with the cuff deflated), with the bevel facing left, is
valve on the proximal end of the smaller tube which inserted through the vocal cords until the cuff passes
helps to assess the pressure ofair injected into the cuff. through the cords. The Ambu bag is now connected
to the endotracheal tube and ventilation is started.
Endotracheal tubes may be for oral or nasal insertion.
Bilateral air entry is checked for by 5 point ausculta
Sizes tion (left and right anterior chest wall, left and right
lateral chest wall and epigastrium).
The size indicates the internal diameter of the tube in
mm. Uncuffed tubes are available in sizes2.5 to 10.0 mm If there is bilateral equal air entry, the cuff is inflated
with 3-4 cc ofair and the endotracheal tube is fixed with
-
PRACTICAL MEDICINE
456
< 1 0 > Instruments
Tracheostomy tube may be of Portex or rubber, cuffed
or without cuff. A metal tube is also available which
does not have a cuff.
The metal tube is used when permanent tracheostomy
is required as following laryngectomy. It has an inner
tube which be changed and cleaned.
The Protex tube has a cuff which can be inflated by
injecting air through the outer tube. The balloon gets
inflated and secures the tracheostomy tube in posi
tion. A plastic attached to the tube has ribbons which
secures the tube around the neck.
Indications
l. Laryngeal spasm as in tetanus. Fig. 10.3: Laryngoscope
2. Prolonged artificial ventilation is required.
cephalad than in adults. The blade has a slot at the base
3. Airway obstruction due to trauma, tumor or
where is attached onto the handle. It can be fixed at 90
secretions.
degrees to the handle. It has a long shaft which used
Complications to compress the soft tissues of the oral cavity and the
pharynx. It has a blunt and slightly bulbous tip which
l. Tracheomalacia
is used to elevate the larynx.
2. Infection
The light source is usually a small light bulb which
3. Trauma to airways
fits onto a socket on the blade and lights up when the
4. Collapse of the lung
blade is locked onto the handle and fixed at 90 degrees.
Uses of cuffed tracheostomy tube
Uses
l. Prevents leak of gases during positive pressure
ventilation 1. To pass an endotracheal tube
2. Prevents aspiration 2. To visualize the upper airway upto the vocal
cords (Direct Laryngoscopy)
3. Secures the tube in place
Procedure
Duration
Patient is placed in supine position with the cervical
Tracheostomy can be kept for 15-20 days.
spine flexed and the head extended at the atlanto oc
Refer Pg. 502 cipital joint. Standing at the head end of the patient,
the handle of the laryngoscope is held in the left hand
3 > Lar�ngosco�e
and the mouth of the patient is opened with the right
-------- hand. The blade of the laryngoscope is passed into the
It consists of a handle and a blade with a light source. oral cavity and the tip is placed between the base of
The handle has a rough surface for a better grip. It is the tongue and the epiglottis. The soft tissues of the
usually short to prevent the handle from abutting the oral cavity and pharynx are then elevated with upward
chest or breasts. The handle also contains the batteries movement of the handle of the laryngoscope in order
which are required for the light source. to visualize the vocal cords.
The Blade can be of two types: straight blade (Miller) At this time, a second helper provides Cricoid Pressure
or curved blade (Macintosh). The straight blade is (Sellicks maneuver). The thyroid cartilage is located
preferred in infants and children younger than 8 and the hard tissue just below it is the cricoid carti
lage. Using the thumb and index finger, firm pressure
years since the larynx is situated more anteriorly and
is applied over the cricoid cartilage. This blocks the
457
PRACTICAL MEDICINE
.
.
esophagus with the firm cartilage of the trachea. It 1L/min-24%
.
also allows the larynx and vocal cords to be visual 2L/min-28%
ized more easily. 3L/min-32%
With the vocal cords in view and the helper apply 4L/min- 36%
ing cricoid pressure, the endotracheal tube is passed
between the vocal cords. The proper tube placement 5 L/min- 40%
is confirmed by five point auscultation. Only after 6-10L/min- 44%
confirmation of proper tube placement and inflation Oxygen Mask can provide upto 60% oxygen at 6 to
of the balloon, is the cricoid pressure removed. 10L/min
Sterilization Oxygen Mask with Reservoir can provide 90 to 100%
oxygen. There is a corrugated tube or reservoir bag
The blade and the handle (with the batteries removed)
are sterilized by soaking in a solution of gluteraldehyde attached to the mask in which oxygen is concentrated
followed by properly rinsing them with warm water to deliver a higher percentage of oxygen to the patient.
and drying the instruments with a clean soft cloth. 6L/min- 60%
7L/min - 70%
Complications
• 8L/min - 80%
1. Local tissue injury that is to the lips, gums, teeth,
• 9L/min - 90%
tongue, palate pharynx, larynx or esophagus.
• 10L/min- nearly 100%
2. Dislocation of the cervical vertebra in case of
vigorous mobilization of the neck. Precautions
3. Aspiration of a detached tooth, blood clots or Patientswho are unconscious or in coma may vomit and
the bulb of the laryngoscope. aspirate the vomitus in case a tight fitting mask is used.
4. Vagus nerve irritation causing changes in heart Refer to Chapter 11, Pg. 503 Oxygen Therapy.
rate and blood pressure.
458
( 10 > Instruments
Plastic
actuator body 8 > Rotahaler
Mouthpiece
Mouthpiece
cover
Raised
'square'
hole
Fig 10.4 :Metered dose inhaler Fin
The advantages over oral or parenteral drug admin
istration are that there is a rapid onset of action, a
s maller dos e of drug is required, there is a lower
incidence of side effects , the inhaler is easier to carry Fig. 10.6 · Rotahaler
and it is cost-effective.
This is a dry powder inhaler (DPI) which is breath
The biggest disadvantage with this method is that cor activated. The Rotacap is inserted into the raised square
rect coordination from the patient is required. hole. On rotating the base, the two halves of the Rotacap
The patient is adviced to rinse his mouth after each use separate and can be seen through the transparent body.
in order to prevent oral candidial infections. The patientthen puts the mouthpiece between his teeth,
s eals his lips around it and breathes in through the
mouth as deeply as possible. The rotahaler is easier to
7 > Spacehaler manipulate than the MDI and is specially suitable for
children, elderly, arthritic patiens. The disadvantages
This consists of a smooth plastic cylinder, at one end of are that it requires a minimal inspiratory flow rate of
which is mouthpiece through which the patient inhales about 28 litres/min and since it is difficult to assemble
the drug and at the other end the metered dose inhaler in breathless or handicapped patients .
is placed. The procedure is like Metered Dose Inhaler.
Opening for
exhaled air 9 Nelson's Inhaler
Ir--er
�')
nist
Notches This is an earthenware inhaler which is filled up to the
base of the spout with three quarter cold water. The
glass mouthpiece is boiled and inserted in the cork s o
that it points in a direction opposite to the spout. The
patient inhales through the mouth only and exhales
through the nose. The drug used is tincture benzoin,
menthol, eucalyptus or pine. The inhaler is covered
by a flannel bag which fits it. It is useful in respiratory
chamber Mouth piece
ailments and coryza.
Fig. 10.5: Spacehaler
459
PRACTICAL MEDICINE
Indications
It is used to provide Intermittent Positive Pressure
Ventilation
Procedure
When the bag is squeezed, air is driven into the lungs
of the patient via the face mask, endotracheal tube or
tracheostomy. The pressure release valve prevents
10 > Ambu Bag {Self high pressure ventilation thus preventing barotrau
inflating Ventillation
mas. On releasing of the pressure the bag re-inflates
automatically. The recoil of the chest causes the air to
�a_gl_ _ leave the lungs by the one-way expiratory valve. The
Ambu Bag has to be cleaned after each use by soaking
it in a disinfectant solution and then properly rinsing
and drying it.
Fig.10.8.Ambu bag
--- --------�-- -----·---
The AMBU Bag (Ambulatory Manual �reathing!lnit)
has the following parts:
1. Outlet (mask is attached to this end)
2. Two Valves
• One-way Expiratory Valve (to prevent
expirated air from entering the bag)
Pressure Release Valve or Pop offValve (set
Flange Bite portion
at 30 - 45 cm of Hp)
Fig. 10.9. Oropharyngeal Alfway
3. Self inflatable rubber bag (refills automatically - -- - - - - ---
after compression) The oropharyngeal airway is a plastic or metal instru
4. Two Inlets ment. It has 3 part: the flange, the bite portion and
the body. The flange is a circular flat part at the oral
Oxygen Inlet (for connection to the oxygen
end which prevents the airway from entering the oral
source)
cavity. The bite portion is a straight firm part between
• Air Inlet (left open or attached to an oxygen the flange and body. It is at the level of the teeth and
reservoir) prevents the patient from biting the airway and causing
Oxygen Delivery obstruction to the air channel. The body is curved and
rests over the tongue and with the tip facing the larynx.
No Oxygen Source- Delivers 21 % Oxygen (Room The nasopharyngeal airway is made of plastic or rub
air) ber. It is longer and has a flange and a body. The body
With Oxygen Source but Without Oxygen is curved to fit in the nasopharynx.
Reservoir - Delivers 40% Oxygen The metal airways are sterilized by autoclaving or
With Oxygen Source and Oxygen Reservoir boiling. The plastic airways are disposable and meant
Delivers nearly 100% Oxygen for one time use.
460
( 10 ) Instruments
> Mouth
point the airway is rotated 180 degrees, the concavity
is directed inferiorly and the airway is slipped into 12 Gag
place over the tongue.
In children it is better to use a tongue depressor be
fore inserting the airway in the correct position. The
airway must not push the tongue backward and block
the airway. It is then secured in place using adhesive
Fig. 1 O 1 O: Doyen's mouth gag
I
tape attached to the bite portion.
. -- - -- ---- - --- -- - - - -- -- - - - . -
The size of the nasopharyngeal airway is assessed by Types
measuring the distance form the tip of the nose to the
1. Doyen's: Opening maintained with a ratchet.
tragus of the ear and adding 2.5 cm to it. It is lubricated
well and inserted into any nostril gently until it rests 2. Mason's: Opening maintained with a screw.
in the pharynx. It is then fixed in place. 3. Ferguson's: Opening maintained with a ring.
Complications Uses
1. Oropharyngeal Airway 1. To open the mouth in an unconscious patient
for oral toilet and to free the airway.
• If the airway too long it may obstruct the
2. To prevent tongue bite in an epileptic patient
larynx by pushing down the epiglottis
during attack.
against the posterior pharynx
If the airway too short it may push the 3. In fibrous ankylosis of the temporomandibular
tongue backwards and cause obstruction joint, to open the mouth during oral surgery e.g.
tooth extraction, tonsillectomy etc.
• Vomiting may be stimulated in a conscious
or semiconscious patient.
461
PRACTICAL MEDICINE
,
and a rubber bulb. The asepto syringe has one tapering
end to be fitted into the catheter and one broad end to
I Fig.10.11 :Tongue depressor be fitted with the rubber bulb. When the bulb is pressed,
the air goes out and when released the fluid is sucked
Uses into it. It can be sterilized by autoclaving or boiling.
1. To examine the throat and oral cavity e.g. tonsils, Uses
palatal movements, posterior pharynx
1. Bladder wash
2. To examine the gag reflex.
2. Irrigation of wounds or cavities
3. To test for the spasm of the masseter muscle
in a suspected case of tetanus (captive tongue Procedure
depressor).
The solution used for bladder wash (Potassium Per
4. To open the mouth in an unconscious patient
manganate, Silver Nitrate or Betadine) is sucked into
for suction or oral toilet.
the asepto syringe by placing its tapering end into the
solution and squeezing and releasing the bulb. The
Fig.10 12:Trocarandcannula
Uses Catheter
1. To withdraw thick fluid form the body cavity
e.g. ascitic tapping, when thick pus is suspected.
(It is not required routinely as ordinary needles Fig.10.14. Simple rubber catheter
are adequate)
This is also known as Nelatons or Robinson Catheter.
2. To aspirate pus in amebic abscess of the liver. It is a simple catheter made oflndia Rubber. It is closed
3. For suprapubic aspiration of urine from the at one end and has an eye at one end (sub-terminal
bladder. opening). It has a single lumen. Sizes available are 1
to 12. It can be sterilized by autoclaving or boiling.
Bulb a) Urinary
It consists of a glass syringe with a capacity of 100 ml 1. Acute retention ofurine: To relieve bladder
162
( 10 ) Instruments
by evacuating urine from it. It cannot be It is also available as a siliconized tube which is more
retained in the bladder. inert and non irritant than the latex tube. There may
2. For bladder washes also be a triple lumen catheter in which the third lu
men is used for irrigation of the bladder.
3. To inject chemotherapeutic agents into the
bladder e.g. Thiotepa, BCG It is available in a gamma irradiated sterile pack cov
ered with a plastic sheath. It is to be used only once.
4. To collect urine from the bladder for Urine
Culture Testing Sizes
5. To differentiate between retention of urine
The most commonly used sizes are in the 'French
and anuria
system' indicated by the letter F. Sizes 8 F to 30 F are
b) Non Urinary available in even numbers. IF= 0.3 mm.
Common sizes used in males: 16, 18.
1. Oxygen Catheter: A thin simple rubber
catheter can be used as a nasal oxygen Common sizes used in females: 14, 16.
catheter Other systems of caliberations are the English (E),
2. Tracheal/ Laryngeal toilet or suction American and German (Benique).
3. Oral suction Balloon Capacity
4. Enema or High bowel wash: Larger bore,
The balloon can be filled from 5 to 50 cc. The maxi
simple rubber catheter
mum capacity is indicated on the smaller channel.
5. Calorie Test: To infuse the warm or cold Over-filling with saline can lead to rupture of the
fluids into the ear balloon, and a constant urge to defecate due to pres
6. Tourniquet: It can be used as a tourniquet sure on the rectum.
Uses
17 > Foley's Self-retaining Urinary
Catheter 1. Acute retention of urine: To relieve it and to
Balloon inflation tip differentiate it from anuria
2. UMN or LMN bladders: To prevent incontinence
3. Transverse myelitis: To prevent over-distention
and atrophy of the detrussor fibers during
Urinary drainage tip Catheter
neuronal shock. After neuronal shock, it is
Fig. 10 15 Foley's self-retaining catheter clamped and released at serially increasing
intervals for training the automatic bladder.
It is a double lumen, self retaining, disposable, sterile
(Ref. Ch. 6: Urinary Bladder)
and ready to use catheter. It is made of latex. It has a
sub-terminal balloon and an eye on one end and the 4. Ruptured urethra: For railroading to splint the
other end is bifid. The catheter has two lumens, one urethra
big one for the passage of urine and the other smaller 5. Following prostate surgery: As a hemostat
one for inflation of the balloon with sterile normal 6. Instilling chemotherapeutic agents into the
saline. The inflated balloon makes the catheter 'self bladder e.g. Thiotepa, BCG
retaining' by resting at the bladder neck. The bifid end
7. Supra-pubic cystostomy
has two channels, one is for the passage of urine and is
connected to the urosac bag and the other is smaller 8. For monitoring urine output in cases of shock,
and connected to the balloon through the smaller burns, renal failure, etc.
lumen. The smaller channel has a valve which prevents 9. To give bladder washes
the injected fluid from coming out. 10. To obtain urine for culture sensitivity testing
463
PRACTICAL MEDICINE
Urinary
1. Suprapubic cystostomy
2. Condom catheter in males, along with a condom
3. Self retaining catheter in females (Foley's
Catheter is preferred)
Disadvantages
1. It is highly irritant and thus cannot be used for
Fig 10.18 Urosac bag
long periods
-------------------
2. It can be difficult to remove due to difficulty in This is a calibrated bag with markings to indicate
straightening the flower. the volume filled. It has a 2 liter capacity. It has two
3. The flower might get detached. This needs tubes. The tube on the top is connected to the urinary
cystoscopic or ultrasonographic removal. catheter and has a non- return valve. The second tube
is at the bottom or side and is used to empty the urine
collected in the bag. It is kept closed otherwise. It is
disposable, sterile and ready to use.
465
PRACTICAL MEDICINE
70Cms (3)
Base
Procedure Sizes
Available in sizes 8 to 22 French in even numbers, 8
The tip of the tube is lubricated. The tube is introduced
466
( 10 ) Instruments
being the smallest and 22 being the largest diameter. closes the epiglottis and allows the RT to pass into the
Regular Adult sizes are 14 - 16 F. esophagus. The RT gently pushed further until the 2nd
mark is at the nostril.
Uses
Confirm the RT is in place by the following methods
Diagnostic and then secure it with adhesive tape:
Upper gastro-intestinal bleeding: In cases of Aspirating Gastric contents from the RT
hematemesis or malena, the RT is inserted and Injecting air through the RT while simultaneously
gastric fluid is aspirated to diagnose upper GI auscultating the epigastrium
bleeding. Putting the nasal end of the RT into a bowl of
GastricAnalysis: To diagnose peptic ulcer disease, water. If the RT is in the trachea, there will be
Zollinger Ellison syndrome, achlorhydria, etc. air bubbles.
Poisoning: Aspirate sent for analysis Tracheal intubations will result in coughing as
Exfoliative cytology: For diagnosis of stomach the RT irritates the trachea or bronchi.
cancer Plain X Ray of the Abdomen will show the radio
Tuberculosis in children: Acid Fast Bacilli (AFB) opaque line along the RT and the lead shots.
in the aspirate in children who cannot produce
Precautions
sputum or swallow it. Early morning aspiration
is preferred. RT Feeding: The patient has to be propped up. There
• Tracheo-esophageal fistula: In newborns, there should be 2 hours between feeds. Before feeding, as
will be an obstruction to the passage of the RT pirate the gastric content to check if at least one third
or the RT will coil up in the blind esophagus. the contents have been emptied or not. If not, the feed
should be delayed. The RT should be flushed after the
Therapeutic feeding. The patient should be propped up for at least
• Enteral feeding of nutrients or drugs for patients half an hour after the feed.
who cannot ingest it orally
Complications
Gastric lavage or stomach washes in case of
poisoning and hematemesis. 1. Epistaxis, rhinitis
• Gastric decompression in intestinal obstruction, 2. Pharyngitis
paralytic ileus, acute gastric dilation, peritonitis 3. Esophagitis,esophageal perforation,rupture and
or post operatively. bleeding of esophageal varices
In acute cholecystitis or acute pancreatitis: to 4. Reflux esophagitis since lower esophageal
give rest to the bowel sphincter is incompetent
Contra Indications 5. Gastritis,gastric bleeding (ifover-zealous suction
• done rapidly)
Corrosive poisoning
6. Aspiration pneumonia if tracheal insertion not
• Kerosene poisoning
detected
Procedure 7. Hypokalemic, hypochloremic, metabolic
With the patient sitting up, the more patent or larger acidosis if overzealous suction
nostril is selected. It is properly cleaned and then
23 > Sengstaken-Blakemore
anesthetized by instilling lignocaine jelly. The RT is
removed from the pack and the tip is lubricated with
---Tube (S.B. Tube)
lignocaine jelly on it.
The tip is now gently pushed along the floor of the nose
It is a 50 cm long latex tube. Its distal end has 4 sub
and the patient is encouraged to swallow as the tube
terminal holes for gastric aspiration. It has 2 balloons
passes into the throat and into the esophagus. This
467
PRACTICAL MEDICINE
25 > Record Syringe and The B.D. needle has a bevel, body and shoulder. The
number of the needle varies inversely with the thick
Needle ness. The lower the number, the thicker is the needle,
e.g. number 18 needle has a thickness of 1/lS'h of an
I-
inch.
10 5
The needle can be fitted directly to the nozzle or can
be locked together by applying a metallic Leur Lock
to the needle which prevents slipping of the needle. If
the syringe has a Leur Lock, it cannot be autoclaved
It consists of a piston made of metal and a glass body or boiled since it is metal.
with a long tapering nozzle that is also made of metal.
It derives its name from the fact that for the first time in Uses of Syringes
the history ofmedicine, something could be recorded. 1. 2 cc Syringe:
It is available in sizes 2, 5, 10 and 20 cc.
a. Injection: To administer drugs
Advantage eg. Analgesics-(Paracetamol, Deriphyllin),
Antibiotics- (Gentamycin), Vitamins
The piston does not come out of the body and break. (Vitamin K, Vitamin B complex, etc.),
others- (diazepam)
Disadvantage
b. Aspiration of blood for Arterial blood gas
It cannot be autoclaved as it is partly glass and partly analysis
metallic. The cement between the glass and the metal 2. 5 cc Syringe:
melts on autoclaving and as glass and metal expand
a. Injection - to administer drugs
differently, the syringe can be damaged. Hence, they
e g . A n t i b i o t i c s (s t r e p t o m y c i n ,
are rarely used today.
cephalosporins, chloroquine), Analgesics
(diclophenac), local anesthesia, Vaccine
469
PRACTICAL MEDICINE
·�1
27 > Tuberculin Sy_rlng!!___
sodium bicarbonate); Antibiotics
(crystalline penicillin, cefalosporins)
• Chemotherapy
• Vaccines- Antirabies Vaccine
l�·E "
r....mw+iM·iiM··i:HW··-,
Sclerosants in sclerotherapy
• Exchange Transfusions
To inject Air into a Ryle's tube to check It is a lee syringe with a blue piston.
if it is in the stomach Uses
To inflate the bulb of the Foley's
Mantoux Test to inject old tuberculin (OT) or purified
catheter with saline or distilled water
protein derivative (PPD) intra-dermally in a dose of
Preparing diluted solutions e.g. 1:100 0.1ml containing STU (tuberculin units). It may also
or 1:1000 solutions be used to give test doses before giving a drug.
b. Aspiration
• Blood Collection
Bone Marrow Aspiration
• Fine Needle Aspiration Cytology
4. 20 or 50 cc Syringe:
a. Injection:
Chemotherapy Fig 10.26: Insulin syringe
'.
Aminophylline 0.25gms in 20cc of It is a 1ml syringe made of plastic or glass with a white
10% Dextrose IV or red piston. It is available in graduations of 40, 80 or
Feeding through the Ryle's Tube 100 units. It is available with or without a 26 number
Injecting fluid or blood in case of needle attached. It is disposable, sterile and ready to use.
hypovolemic shock
Uses
b) Aspiration
1. To inject Insulin (insulin is available in 40, 80
Pleural Fluid, Pericardia! Fluid or
or 100 units per ml hence the calibrated needle
Ascitic Fluid Aspiration
makes insulin administrations easier)
Blood Collections
2. Mantoux testing (to inject the tuberculin-OT or
• Stomach Washes PPD)
Uses of Needles 3. To give BCG, TT, DPT or Hepatitis vaccination
1. No. 12 -16: Aspiration of thick fluids or pus, 4. To give intra-dermal test dose (before giving
bone marrow aspiration certain drugs like penicillin)
2. No. 18: Blood collection from donors, I.V. fluids, 5. Allergy testing
aspiration of fluids from body cavities 6. To give drugs: Inj. Adrenaline0.5- 1 ml, Vitamin
3. No. 20 - 21: Blood collections (small amounts, K 0.1 ml in a newborn
routinely), l.V. Fluids 7. To collect blood for Arterial Blood Gas Analysis
4. No. 22 - 23: l.M. injections, F.N.A.C.
5. No. 24: l.M. injections in children
470
< 10 > Instruments
471
PRACTICAL MEDICINE
Uses
===�
Blunt obturator - ./ 1. Pleural malignancy
2. Tuberculosis
> Trucut
Jamshidi biopsy needle
35 Needle
Inner
notcbed�=:====::'...__------_J
otbun.tor
,. Adjustable stop
Fig.10.33:Trucut needle
This needle has sliding knife edge and is used for
Fig. 10.31: Bone marrow asp1rat1on needle
Kidney or Liver Biopsy. It is less traumatic and helps
2. Guard 2 ems from the tip. (Guard prevents to obtain a better specimen.
through and through penetration of the bone)
3. Stilette
36 > Southey's Tube and
___,__]
Needle
� > Pleural Bio��edlL
Cutting
edge,. --mtl 11 M
Fig.10.34: Southey's tube and needles
•Guard These are tiny needles put together in a tube. Each
needle has shoulder to which a thread can be tied. The
other end is pointed and the body is hollow.
It was used in the past to remove edematous fluid
Notch Knob from the cutaneous tissue. The disadvantage was the
•
severe infection which sometimes followed. Now with
diuretics, this is an obsolete needle.
Ounter Inner Trocar St1llete Punch
cannula cannula biopsy
> Tournigu_e____
needle
Parts Uses
472
( 10 ) Instruments
38 > Venesection Needle the tube, the tube is kinked. The scalp vein needle is
fixed with adhesive tape to the skin. The tube is then
flushed with saline or 0.5ml of heparin. When used in
children, the hand has to be splinted to prevent move
ment since movement can cause counter-puncture.
This is a needle with a cannula. Just above the tip it Complications
is bulbous, to which a polyethylene tube snugly fits.
• Counter-puncture detected by hematoma
(The other end of the polyethylene tube is pushed in
(swelling) formation just distal to the scalp vein
the vein after venesection). As the name suggests it is
needle or by resistance felt during flushing with
used during venesection.
saline or heparin
: Fig 10.36.ScalpVeinneedle
473
PRACTICAL MEDICINE
Sizes
14 -24 G in even increments. Smaller the number,
larger the bore of the needle.
Uses
To get venous access for a longer period (48 - 72 hours)
for the administration of intravenous fluid, intravenous
drugs, blood and blood products, multiple fluids or
drugs together �-- �--- Fig.- 10.38:
---
Three way
-- --- ---
Complications
43 > I. V. Set
Counter-puncture: Detected by hematoma
The I.V. Set has three parts: the proximal limb, Murphy's
(swelling) formation just distal to the scalp vein
chamber and the distal limb. The proximal limb has a
needle or by resistance felt during flushing with
saline or heparin
Thrombophlebitis due to infection or irritation
by drugs or fluids
Uses
It is commonly connected to an I.V. Cannula Fig. 10.39 IV Set with Murphy's chamber
- - - -- - - --- -- --- -.
474
( 10 ) Instruments
sharp pointed tip which is used to puncture the outlet Precautions With Murphy's Chamber
of the I.V. Fluid bottle or bag.
Before connecting the I.V. Set to the venous access, the
The Murphy's chamber is a glass chamber that is used regulator should be fully opened and the fluid should
to regulate the flow of fluid by adjusting the number be allowed to fill the Murphy's chamber up to a certain
of drops falling per minute. level and fill the tubing. This drives all the air in the
The distal limb is consists of a long tubing with a nozzle tubing out and prevents air embolism. The fluid level
at the end which is attached to the venous access ( scalp in the Murphy's Chamber will prevent the air from the
vein, angiocath or three-way). It also has a regulator proximal part to enter the venous access. Thus a fluid
which is used to adjust the rate of flow through the level should always be maintained.
Murphy's chamber. There may be a rubber tip just at
1. Macrodrip Set
The Murphy's chamber is normal. 16 drops
constitute 1ml. Clinical thermometer is used to record temperature.
In a clinical thermometer there is a constriction just
Uses beyond the bulb. When the thermometer bulb is placed
1. Fluid administration such as colloids in the mouth, mercury within expands and this force
(albumin, hemaxcele, Dextran) or of expansion is great enough to force the expanding
crystalloids (normal saline, ringer lactate, mercury past this constriction. The part of the mercury
DNS) which has expanded beyond the constriction remains
in position and indicates patient's temperature. The
2, I.V. drug administration (antibiotics, iron,
mercury must be jerked back into the bulb before the
etc.)
thermometer is used again.
2. Microdrip Set Clinical thermometer is calibrated over the range
95-108°F, since the body temperature does not vary
The Murphy's chamber has a thin needle coming
much from its normal values of98.4°F. Since the bulb
into it from the top. 16 micro drops constitute
is thin and small, the thermometer is quick acting,
1ml.
reaching the body temperature in about 1 min. The
Uses : Accurate small quantities of drugs quantity of mercury used is small and the capillary
have to be given I.V. (nitroglycerine, sodium tube must therefore have a very fine bore. To enable
nitroprusside, dopamine, dobutamine, adrenal the thermometer to be read, the front of the glass is
ine, noradrenaline, insulin, heparin, etc.) shaped so as to produce a magnified image of the thread.
3. Blood Transfusion Set After being washed and wiped it should be stored in
a glass jar partly filled with a disinfectant like 70%
The Murphy's chamber has a filter in it to filter isopropyl alcohol with 1% iodine. The jar should have
out any clots. a piece of cotton wool at the bottom.
Uses Recording the temperature:
Transfusion ofblood and blood products (whole After cleaning the thermometer and shaking it to bring
blood, packed cells, platelets, fresh frozen plasma, the column of mercury down to about 2° below nor-
cryoprecipitate, coagulation factors, etc.)
475
....;...
PRACTICAL MEDICINE
476
< 10 ) Instruments
Uses 12 inches. Double lumen tubes are ideal. The bell is
usually 1 inch in diameter and the diaphragm is 11/2
For proctoscopic examination to diagnose condition
inches in diameter.
like hemorrhoids, anal fistulas, anorectal strictures
or ulcers and for internal banding of hemorrhoids. Uses
Procedure The stethoscope is used in auscultation of the chest or
abdomen. The bell is used for low frequency sound 30
The patient is placed in the left lateral position. The
to 150 Hz= S3, S4, MDM and the diaphragm is used
upper leg is flexed and the lower leg is extended. Per
for high frequency sound> 300 HZ= Sl, S2, clicks,
rectal examination is done to exclude painful pathology
OS, systolic murmur, early diastolic murmurs.
ofthe anus and anal canal. The assembled proctoscope
is lubricated and inserted in the anus in the direction
47 > Stethosco�e
contains the central line, the guide wire, introducer,
- - -
- ---- needle and dilator.
1. The guide wire is a slender wire which is used
to cannulate the vein first. Its tip is curved into
a T shape so as to make it non traumatic and
also so that the tip is not caught in any valves
in the veins. It is threaded into the introducer,
which is spiral, making the long guide wire
easier to handle.
2. The needle is usually 18 or 20 No. and is hollow
so that the guide wire can go through it.
3. The dilator is usually a plastic device with a
tapering tip which can be cannulated over the
guide wire in order to dilate the site of puncture
allowing the central line to be passed without
Fig. 10.43: Stethoscope resistance into the vein.
The stethoscope was invented by Laenec. This was a
Catheter Through Sheath Technique
wooden instrument. Electronic and magnetic stetho
scopes are also available. They usually contain a needle, sheath and the central
It has a dual chest piece with a valve that allows switch venous catheter.
ing from the bigger diaphragm to the smaller bell. 1. The Needle is a large bore needle, No. 16. The
There is tube connecting the chest piece to the binaural needle can be inserted into the sheath.
connector and earpieces. The tubing length should be 2. The Sheath is made ofpolyethylene and is shorter
than the needle so that the tip of the needle
477
PRACTICAL MEDICINE
protrudes out of it when the needle is inserted saline. The catheter is secured in place with a suture
into the sheath. and a sterile dressing is given.
3. The Central Venous line is similar to the one
above but it also has an inner wire to prevent it Method of Insertion of the Needle
from kinking while being inserted into the vein. According to the Site Selected:
478
PRACTICAL MEDICINE
Complications
I. Serious arrhythmias may occur if the patient
has been receiving digoxin.
2. Hypertension and pulmonary edema may
sometimes occur.
3. Burning of the skin of the chest wall may occur
if adequate jelly is not applied.
F,g 11 1 Card1overs1011
480
< 11 ) Procedures
papilledema) because of the risk of herniation of 4. Puncture: A lumbar puncture needle with a
brain through foramen magnum, and damaging stilette is introduced after 2-3 minutes into the
the vital medullary centres causing death. anesthetized space, with the cutting edge of the
2. Marked spinal deformity bevel in the direction parallel to the fibers of
the ligamentum flava. The needle is introduced
3. Local infections
(slightly upwards and forwards at 5° to avoid
4. Suspected cord compression injury to the disc) through the resistance
Procedure of supraspinous ligament. The interspinous
ligament is then easily negotiated. At about 4-7
1. Position: The patient is placed on his side at the cm, the firmer resistance of ligamentum flavum
edge of the bed with the knee drawn up and the popping sensation as the dura is breached. The
head flexed. It can also be done with the patient stilette is then withdrawn and the fluid is collected
sitting and bending forward. slowly in 4-5 bulbs for biochemical, cytological
2. Site: In the 3rd lumbar space. This space lies in and serological tests.
the plane which joins the highest points on the 5. Seal: The needle is withdrawn and the puncture
iliac crest. The skin over the back from the lower mark is sealed with a tincture benzoin seal
thoracic vertebrae to the coccyx is sterilized with 6. Post-procedure orders:
Cetavlon, ether, iodine and spirit. The part is
draped. a. Plenty of fluids are to be taken by mouth.
3. Local anesthesia: The skin to be punctured is b. Head low position, with half to one block
infiltrated with 5 ml of2% lignocaine. Infiltration to prevent headache
is done up to ligamentum flava. c. Salicylates, if headache
Problems
I. Dry Tap
A. The needle is blocked: Re-insert the stilette
to dislodge any flap of dura that may have
blocked the needle.
B. Faulty technique: Repeat the procedure.
Fig. 11 2: Position for lumbar p uncture w ith patient lying C. Subarachnoid block
1
down :
II. Bloodstained CSF
A. Trauma to the spinal blood vessels.
B. Subarachnoid hemorrhage.
6 To distinguish between these two conditions. CSF
must be collected in 2 parts is separate test tubes. The
appearance of more blood in one sample compared
to the other suggests trauma; in subarachnoid hemor
rhage it is uniform.
Complications
1. Headache is the commonest problem. To mini
Fig 11 3:Sect1onof the spi11alcordshow1n9L P.11eedle111 mise this, plenty of fluids should be taken orally,
the third lumbar space l Skin, 2 Sup1asp1nous lig,m1cnt, head-low position is to be given and salicylates
3 Ligamentum flavum, 4 lntersp1nous l1gament, 5 Dura
if required. In neurosyphilis, headache never
mater, 6.Vertebral body, 7. Disc, 8 Pmterior 10119,tud,nill
ligament. occurs following lumbar puncture.
1
481
PRACTICAL MEDICINE
Appearance Clear /Colourless Turbid Clear or Slightly opaque Clear Clear Clear
Pressure 60-lSOmm t t N t torN
ofCSF
Proteins 20-40mg% ttt ttt t tt t
Sugar 40-70mg% J..H HJ.. N -1, N
Chlorides 720-750mg% -1, -1, N -1, N
482
( 11 ) Procedures
4. Tumors near the cauda equina, around D. Malignant cells: Cerebral or spinal
the ventricles and acoustic neuroma. malignancy
III. Proteins
A. Increased:
1. Meningitis
4 > Cisternal Puncture
2. Encephalitis including poliomyelitis Cisternal puncture is aspiration of C.S.F from the
cisterna magna by puncturing in midline, half an inch
3. Disseminated sclerosis
above the second cervical vertebra.
4. Guillain Barre syndrome
5. Neurosyphilis Indications
6. Spinal cord compression 1. Diagnostic: Same as for lumbar puncture.
7. Intra-cranial tumor Lumbar puncture is preferred to cisternal
puncture. If L.P has been traumatic or if there
8. Cerebral arteriosclerosis
is spinal deformity and LP is difficult, cisternal
B. Decreased: (Not known) puncture is done.
IV. Sugar 2. Spinal block: When there is spinal block
A. Increased: demonstrated by a myelogram from below,
1. Diabetes mellitus myodil is introduced also from above after a
cisternal puncture to know the upper limit of
2. Following I.V glucose administration
the block.
3. Encephalitis
B. Decreased: Meningitis Contra-indications: Same as for L.P.
V. Chlorides Procedure
A. Increased: (Not known)
1. Position: The patient is placed on his side at the
B. Decreased: edge of the bed with his head flexed.
1. Purulent and tuberculous meningitis 2. Site: In the mid-line halfan inchabove the second
2. Systemic hypochloremia cervical vertebra and in the plane of the tip of
VI. Cells the mastoid. Hair is shaved over the back of the
A. Polymorphonuclear leucocytosis: head below external occipital protuberance and
the part is sterilized with Cetavlon, ether, iodine
1. Pyogenic meningitis.
and spirit.
2. Acute syphilitic meningitis 3. Local anesthesia: The skin and the subcutaneous
3. Acute poliomyelitis (early stage) tissues are punctured with 1 % lignocaine
4. Epidural abscess 4. Puncture: The cisternal puncture needle with
B. Lymphocytosis: calibrations and short bevel is introduced in the
1. Meningitis-tuberculo us, viral, midline, half an inch above the second cervical
syphilitic and late stages of pyogenic vertebra. It is pushed for about 4-5 ems in the
plane of tragus and nasion when it enters cisterna
2. Encephalitis
magna and CSP comes out.
3. Poliomyelitis-later stages
484
CARDIOVASCULAR DRUGS
INOTROPIC DRUGS
Drug/Dose Action Side Effects Uses
1. DIGITALIS
Rapid 1. It increases the force of systol- Cardiac: Premature beats atrial 1. Congestive cardiac failure
a) DIGOXIN 1.5 mg ic contraction and decreases and ventricular tachycardia and 2. Left ventricular failure
initially 0.5 mg 6 hrly till the oxygen expenditure for a fibrillation. Heart blocks, sinus 3. Atrial fibrillation and flutter
digitalization given work output. bradycardia 4. Premature beats
b) DIGITOXIN 0.4 mg 2. Heart rate is decreased. Gastrointestinal: Anorexia, 5. Supra-ventricular
orally0.2 mg.6 hrly till 3. Conduction through the A.V. nausea, vomiting (of central tachycardias
digitalization node and Purkinje's fibers is origin} and diarrhea
Contra-indications:
c) OUABAIN depressed. Neurological:
1. High output states
I.V. ultra-short acting 4. Refractory period of atria and 1. Vertigo
2. Partial heart (AV) block
II. Slow ventricles is decreased and 2. Visual hallucinations, colour
that of AV node is increased 3. Ventricular tachycardia
a) DIGOXIN 0.25 - 0.5 mg. vision defects and blurring
(QT interval shortens). 4. Constrictive pericarditis
initially 0.25 mg/day till 3. Headache
It acts by inhibiting the sodi- 5. Myocarditis/Diphtheria
digitalization 4. Neuralgic pains
um-potassium ATPase. 6. Hypersensitivity
b} DIGITOXIN 0.2 mg Miscellaneous:
This causes faster release of 7. WPW syndrome
initially 0.2 mg. 8 hrly 1. Skin rashes, eosinophilia
till digitalization calcium which enhances the 8. Hypokalemia
2. Gynecomastia
111. Mointenancedose
automaticity, contractibility
ectopic pacemaker activity. 3. Premature labour with ECG
a) DIGOXIN 0.25 mg/day changes in fetus
10-20 µgm/kg body wt
b} DIGITOXIN 0.1-0.2
mg/d
2. AMRINONE
0.5 µg/kg IV bolus injection It inhibits the enzyme phospho- 1. Hypotension on IV Cardiacfailure
followed by 2 to 20 µg/kg/ diesterase which metabolises administration Now withdrawn due to toxicity.
min infusion cyclic 3,5 AMP to the inactive cy- 2. Myocardial ischemia Mega studies have shown
MILRINONE clic 5 AMP. Causes vasodilata- 3. Thrombocytopenia increased mortality
tion with fall in systemic vascular
resistance. It increases the force
of contraction & velocity of relax-
ation of cardiac muscle.
VESNARINONE Inhibits phosphodiesterase (as
60 mg/day orally above}. Enhances influx of Ca ions
through Ca-channels
3. DOPAMINE
2.5-20 µg/kg/min. It is a direct beta-1 agonist which 1. Nausea, vomiting 1. Cardiogenic shock
Up to 4 µg/kg/min: Renal stimulates the heart and causes 2. Angina, palpitations 2. Chronic refractory congestive
dose renal, mesenteric and cerebral 3. Arrhythmia (less than with cardiac failure
4-10 µg/kg/min: lnotropic vasodilation. Low doses increase catecholamines} 3. Low doses in renal failure
dose with J3 action renal blood flow, but large doses Contra-indications: 4. Dilated Cardiomyopathy
>10 µg/kg/min: a+ J3 action stimulate alpha receptors causing
1. Pheochromocytoma
vasoconstriction and reduction of
renal blood flow. 2. VF/ V T
The other drugs used in heart failure are ACE inhibitors, vasodilators and diuretics, which are discussed elsewhere.
PRACTICAL MEDICINE
4. DOBUTAMINE
2.5-10µg/kg/min. rate or It increases the cardiac output As dopamine, but causes less 1. Cardiogenic shock
peripheral vascular without increasing the heart tachycardia as it does not heart 2. Chronic refractory congestive
release endogenous nor-actions. failure epinephrine. cardiac failure
Contra-indications: HOCM 3. Dilated Cardiomyopathy
ANTI-ARRHYTHMIC AGENTS
1. CLASS IA AGENTS
b) PROCAINAMIDE Similar to quinidine, but safer for Cardiac: Similar to quinidine Similar to quinidine
0.25-0.5 gm 4-6 hrly. orally. IV use. Torsades de pointes
100 mg.1V stat&every4min. Extra-Cardiac Drug Interactions: Absent with
Total dose 1 gm. 1. Intolerance, skin rash digoxin or warfarin
250-500 mg IM 6 hrly. 2. GI: Nausea, vomiting,
Therapeutic serum levels: diarrhea
8-12µg/ml 3. Agranulocytosis
Toxic level 30µg/ml 4. Lupus like syndrome/SLE
5. Psychosis
6. Exacerbation of myasthenia
d) MORICIZINE Inhibits the rapid rise of action 1 . Dizziness Not effective for ventricular
200 mg. 8 hrly potential (phase 0) 2. Postural hypotension tachycardia & utility for atrial
up to 900 mg/day 3. Nausea vomiting tachycardia needs further study
2. CLASS 18 AGENTS
558
( 15) Drugs
b) PHENYTOIN SODIUM 1. Depresses ventricular auto- 1. I.V. Phenytoin causes local 1. Digitalis-induced arrhytmias
1 gm IV given at< 50 mg/min maticity. phlebitis due to alkaline because it does not increase
followed by 100 mg every 8 2. Accelerates AV conduction. diluent A.V.block
hrly 3. Does not decrease conduc- 2. Hypotension 2. Premature beats
Therapeutic serum levels tion velocity like quinidine or 3. Gum hypertrophy 3. SVTand VT
10-20 µg/ml. procainamide. 4. Megaloblastic anemia 4. Ventricular arrhythmia after
Toxic levels : 20 µg/ml. 5. Cerebellar ataxia GA and surgery
6. Nystagmus 5. Congenital QT syndrome
7. Lupus (when � blockage has failed)
6. Epilepsy with arrhythmias
3. CLASS IC AGENTS
b) ESMOLOL
(Ultrashort acting) As Propranolol (As propranolol) Useful for emergencies
5 gm in 500 ml dextrose 0.5 Due to ultrashort action, very few Effect occurs in 2 min and after
mg/kg over 1 min, folowed by side effects. termination of infusion recovery
50 µg/kg infusion over 4min, from beta blockade occurs in
followed by 1 mg/kg over 4 10-20min.
min upto 2 mg/kg
559
PRACTICAL MEDICINE
to 200mg daily or alternate tion of the cardiac action paten- 3. Slate-grey discoloration of 2. Refractory paroxysmal
days or 300-400mg IV slowly tial skin &retinal pigmentation tachyarrhythmias
over 1/2 3 min orin a c;frip. 4. Bradycardia, hypotension and 3. Atrial flutter and fibrillation
conduction defects 4. VPC's
5. Extrapyramidal effects, 5. Recurrent cardiac arrest
pripheral neuropathy, vetigo,
insomnia etc.
6. Pulmonary Fibrosis
7. Liver damage
8. Hypo- &hyperthyroidism
b) BRETYLIUM
5 - 10mg/kg IV bolus; Adrenergic neuron blocking 1. Hypotension 1. Life threatening ventricular
IV 0.5-2 mg/min. agent. It increases ventricular 2. Nausea and vomiting arrhythmias
80-160mg oral 12 hrly fibrillation threshold. 2. CPR
c) SOTALOL
80to 320mg orally Non selective p adrenergic Similar to Propranolol Life threatening ventricular
every 12 hrly receptor antagonist that also pro- Torsades de pointes arrhythmias
longs cardiac action potentials by
inhibiting delayed rectifies and
other K• currents
6. CLASS IV AGENTS
VERAPAMIL 1. Causes coronary dilatation 1. Constipation 1. SVT:Atrial tachycardia,
40or80mgTDSorally and reduces myocardial oxy- 2. Hypotension Atrial fibrillation
OR gen consumption. 3. Vertigo 2. Premature beats
5 mg - 1O mg IV for paroxys- 2. Interferes with inward dis- 4. Nervousness 3. IHD:Angina
mal atrial tachycardia placement of clacium & de- 4. Hypertension
lays the conduction within AV
node
7. MISCELLANEOUS
a) ADENOSINE Purine analogue ideal for Re-en- 1. Facial flushing Re-entrant supra ventricular
6- 12 mg IV as a rapid bolus, try tachycardia 2. Dyspnea and chest tachycardia
followed by 12 mg after 2 min 1. Inhibits sinus node automa- discomfort Interaction
if no effect. ticity 3. Nausea &light headedness 1. Effects antagonized by
30mg (10ml amp) 2. Prolongs AV nodal refractori- 4. Sweating theophylline and caffeine
ness 2. Effects potentiated
by dipyridamole &
carbamazepine
b) ISOPRENALINE 1. Enhances the rhythmicity of 1. Palpitation, flushing 1. Second degree A.V. block
2 mg in 5CO ml 5% dextrose sinus, nodal and ventricular 2. Headache 2. Ventricular tachycardia with
OR 10-15 mgQDS sub- pace-makers 3. Angina block
lingually. 2. Enhances A.V. conduction
3. Increases heart rate and car-
diac output.
ANTI-ANGINAL AGENTS
1. NITRATES
GLYCERYL TRINITRATE Increases coronary blood flow de- 1. Headache, halitosis 1. Angina pectoris
SL 0.15 to 0.6 mg. creased oxygen consumption of 2. Methemoglobinemia 2. Pulmonary hypertension
Buccal 1 mg every 3 to 5 hr. the heart by decreasing the pre- 3. Glaucoma 3. Cyanide poisoning
Sustained release 2.5 to 9 mg load and afterload. 4. Hypotension and syncope 4. Paroxysmal nocturnal dyspnea
2 to 4 times a day. Contra-indications 5. As spasmolytic
Ointment - 2%4to8 hr. 1. Acute myocardial infarction 6. Achalasia cardia
I.V. 5 µg/min. 2. Severe anemia 7. Chronic stable angina
DISC/TTS patch (2.5-1Smg) OD 8. Portal hypertension
ISOSORBIDE DI NITRATE ERYTHRITYL TETRANITRATE prophylaxis
Sublingual 2.5 - 10mg every 5,15 mg TDS upto 30-60mg
2 to 3 hrs. Sustained release PENTA-ERYTHRITOL
40-80mg every8to 12 hr PENTA NITRATE
Oral 10to40mg every 6 hr 20-40mg8D
ISOSORBIDEMONONITRATE
10mg, 20mg,40&60mg SR
560
< 15) Drugs
Drug/Dose Action Side Effects Uses
2. K-CHANNEL OPENERS
3. BETA-BLOCKERS
4. CALCIUM BLOCKERS
ANTI-HYPERTENSIVE AGENTS
1. DIURETICS (Refer Pg. 567)
561
PRACTICAL MEDICINE
2. BETA-BLOCKERS
3. CALCIUM ANTAGONISTS
a) NIFEDIPINE Refer Pg. 562 Refer Pg. 562 Hypertension and Refer Pg. 562
20 mg.BD
5 mg sublingually in hyper
tensive emergencies
d) NITRENDIPINE Similar to Nifedipine but Ion- Similar to Nifedipine Hypertension and Refer Pg. 562
20-40mg0D ger acting and more specific for
coronary and peripheral blood
vessels.
e) AMLODIPINE Similar to Nifedipine but longer Similar to Nifedipine Hypertension and Angina
2.5-lOmgOD action
f) NICARDIPINE Similar to Nitrendipine but short- Similar to Nifedipine Hypertension, hypertensive crisis
60-90 mgBD er acting and Angina
g) ISRADIPINE Similar to Nitrendipine. Dose has Similar to Nifedipine Hypertension, hypertensive crisis
5-20mg0D to be reduced in elderly & in kid- and Angina
ney and liver damage.
562
< 15) Drugs
Drug/Dose Action Side Effects Uses
4. ACE INHIBITORS
b) ENALAPRIL Similar to captoprll but longer Lesser than captopril, longer Same as above
2.5 - 20.mg OD acting. acting.
c) LISINOPRIL Similar to captopril but longer Similar to Captopril but ageusia Same as above
5 - 40 mg.OD acting and more effective. &thrombocytopenia does not
occur. Cough, headache and
diarrhea more with Lisinopril.
e) RAMIPRIL 2.5-20 mg OD Similar to Captopril. Dose adjust- Similar to Lisinopril. Same as above
ment reqd. in renal failure Lesser cough.
j) TRANDOLAPRIL 1-40D
6. VASODILATORS
563
PRACTICAL MEDICINE
c) SODIUM NITROPRUSSIDE Relaxes both arteriolar and ve- Retching apprehension, twitch- 1. Hypertensive emergencies
200µg/min. nous smooth muscles without ing, hypothyroidism, methemo- 2. Acute coronary syndromes
SO mg of powder is to be any effect on the uterus or GI globinemia. with hypertensive crisis
tract. It reduces the oxygen con- Hypotension, diaphoresis, nau-
dissolved in 500 ml of 5%
sumption of myocardium. The ac- sea, vomiting, dizziness, tinnitus,
dextrose just prior to
tion is rapid in onset and of short blurred vision.
administration. duration. Hence the hypotensive
It is light sensitive and effect is reversible on stopping
a paper bag over the IV the drug. It is useful in presence
container is necessary. It is of Ml, pulmonary edema and dia-
given at 200 ug/min. betes where diazoxide is contra-
0.5-8 µg/kg/min IV drip indicated. It should not be used>
3-4 days.
d) MINOXIDIL 1. Similar to hydralazine, but Pulmonary hypertension, hyper- 1. Hypertension
2.5 -40 mg BO or ointment longer acting. It causes fluid trichosis, headache 2. Baldness (Alopecia), specially
retention, hence it has to be ointment
combined with a diuretic.
2. Potassium channel opener.
7. ALPHA BLOCKERS
NON-SELECTIVE a BLOCKERS
a) TOLAZOLINE They are alpha-adrenergic block- 1. Flushing, palpitation, sweat- 1. Peripheral vascular disease
25mg t.d.s. ing agents. ing. 2. Diagnosis and treatment of
orally or SO mg S.C. They cause peripheral vasodilata- 2. Postural hypotension.
pheochromocytoma
b) PHENTOLAMINE tion and increase force of contrac- 3. Nausea, vomiting, diarrhea,
5 mg I.M. or l.V. tion of myocardium. aggravation of peptic ulcer 3. Shock; Because blood flow
c) PHENOXYBENZAMINE 4. Precipitates myocardial to certain critical areas rather
10-50 mg OD or BO orally infarction. than B.P. is the important fac-
tor in survival from shock
4. Raynaud's syndrome
5. Scorpion bite
6. Male sexual dysfunction
SELECTIVE a BLOCKERS
a) PRAZOSIN Direct relaxant of the vascular Same as above but less likely to 1-6.Same as above
0.5 mg twice a day smooth muscles and alpha- produce reflex reflex tachycardia 7. Benign Prostatic hypertrophy
maximum 5 mg oral. receptor blockade. Selective (BPH)
5-20 mg in BPH blocker of a 1 receptors. First dose 8. Hypertension
hypotension.
b) TERAZOSIN Same as above As above Hypertension
1 mg at bedtime Long acting Prostatic hypertrophy
max 10 mg/day oral.
c) DOXAZOSIN Same as above As above Same as above
1-2mg0Dupto 16mg Long acting
e) INDORAMINE: 20 mg BD Same as above As above Prostatic hypertrophy
8. CENTRALLY ACTING DRUGS
a) ALPHA METHYL DOPA 1. Catecholamine synthesis 1. CNS: Headache,drowsiness, 1. Drugofchoicein Pregnancy
250 mg-2000 mg. inhibitor: Inhibits dopa de depression, Parkinsonism induced hypertension
It is safe during pregnancy carboxylase which normally 2. CVS: Precipitates C.C.F. 2. Hypertension
inhibits the conversion of 3. Hemo lyticanemia
dopa to dopamine & nor 4. Miscellaneous: Diarrhea,
adrenaline & thereby reduces
loss of libido, bradycardia.
sympathetic tone (vascular
resistance). Contra-indicati ons:
2. Converted to alpha methyl 1. Pheochromocytoma
noradrenaline which dis 2. Liver disease
places noradrenaline from 3. With MAO inhibitors
the granule stores. It acts as a
false neuro-transmitter and
due to its lesser potency pro
duces relative hypotension.
3. Similarto clonidine
564
( 15) Drugs
c) MOXONIDINE 1. Selective imidazole agonist (1- Similar but far lesser side effects Hypertension,esp. with obesity,
agonist) than clonidine diabetes and hyperlipidemia
2. Co-stimulates et-2 receptors
3. Similarto clonidine
9. CATECHOLAMINE DEPLETORS
RESERPINE Catecholamine depletor: The Due to sympathetic blockade: Hypertension, rarely used due
(An alkaloid from Rauwolfia) exact mechanism is not known. 1. Salivation, nasal congestion, to side effects.
0.25-1 mg orally It depletes 5 H.T. from CNS and cutaneous vasodilatation.
0.5-2.5 mg I.M. or I.V. catecholamines from peripheral 2. Increased gastric secretion
sympathetic nerve endings in and peptic ulcer.
Orally,action takes 4 weeks.
cluding that of heart and various
I.V.,action in 10 min 3. Orthostatic hypotension,
other sites in the body. It prevents
I.M. action in 2 hrs bradycardia.
granular uptake (reversible) as
well as granular storage (irrevers Central action:
ible) of catecholamines. If given 1. Weight gain and increased
after MAO inhibitors or with it, it appetite.
causes hypertension. 2. Mental depression.
3. Parkinsonism.
4. Feminization & impotence.
Allergic: Thrombocytopenia.
a) GUANETHIDINE 1. Inhibits the transmission of 1. Due to sympathetic blockade: Hypertension, rarely used due
1Omg or 25 mg tablets noradrenaline at sympathetic Postural hypotension, to side effects.
once a day upto 100 mg/day nerve terminals. diarrhea, nausea,vomiting,
2. Depletes noradrenaline parotid tenderness and nasal
stores at sympathetic nerve congestion
endings. 2. Impotency: Impotence,failure
3. Blocks the re-uptake of nor to ejaculate
adrenaline by sympathetic 3. CNS: Mental depression.
nerve endings. 4. Polyarteritis nodosa.
Contraindicated in:
1. Pheochromocytoma
2. Severe IHD
3. CVA
b) BETHANIDINE Similar to guanethidine, but Similar to guanethidine, but diar- Hypertension,rarely used due to
5-lOmg BD shorter duration of action. rhea is rare. side effects.
565
PRACTICAL MEDICINE
ANTI-THROMBOTIC AGENTS
1. STREPTOKINASE Plasminogen activator. 1. Bleeding 1. Acute myocardial infarction
7.5-15 lakhs JU 1.V. Plasminogen is the inactive en 2. Anaphylaxis 2. Deep vein thrombosis
Loading dose 2.5-5.0 lakhs JU zyme in plasma which binds to 3. Allergy 3. Pulmonary embolism
followed by rest of the dose fibrin during the formation of 4. Hypotension 4. Arterial thrombosis or embo-
over 6 hrs. thrombus. This binding ensures 5. Hemorrhagic stroke lism
2. UROKINASE fibrinolytic properties on the 5. Acute peripheral arterial
6. Fever, rash, pruritus, wheeze
2.5-7.5 lakhs JU 1.V. plasminogen-plasmin system. occlusion
7. Arrhythmias
Loading dose 2.5 IU over 10 Contra-indications: 6. Occlusion of AV cannulae
mins followed by 5 lakhs JU 1. Active bleeding 7. Acute ischemic stroke
over next 60 mins 2. Bleeding diathesis 8. Acute coronary syndromes
3. TISSUETYPE 3. Recent trauma like unstable angina
PLASMINOGEN ACTIVATOR/ 4. Recent surgery/neurosurgery
ALTEPLACE {TPA)
5. Recent invasive procedure
10 mg 1.V. bolus followed by
6. Recent GI or genito-urinary
50 mg over next 1 hour bleeding
4. ANISTREPLASE 7. Recent prolonged CPR
(ACYLATED PLASMINOGEN 8. Stroke or TIA in past 1 year
STREPTOKINASE ACTIVATOR
9. Historyof brain tumor,
COMPLEX -APSAC) 30 units
aneurysm or AVM
I.V. bolus over 2 mins
10. Active peptic ulcer
5. TENECTPLASE 0.53 mg /
kg IV over 10 seconds single 11. Pregnancy
dose 12. Uncontrolled severe
6. RETEPLASE (rPA) 10 million hypertension
units bolus IV over 2 - 3 min
utes. Repeat after 1 0 minutes
HEPARINS/ APROTININ
1. HEPARIN (conventional) 1. Anti-thrombin action. 1. Allergic and Anaphylactic Anticoagulant action starts im
(Refer Pg. 566 for PE/DVT) 2. Anti-prothrombin action. reaction: Asthma, urticaria mediately, reaching peak in 5-10
10,000 units 1.V. followed by 3. Anti-thromboplastin. 2. Hemorrhage from various minutes & is normal in 2-4 hrs.
5000 1.V. 6 hourly. Susequent 4. Anti-polymer action of fibrin sites 1. Acute coronary syndromes:
doses depend on clotting monomer. 3. Alopecia unstable angina, AMI
time. CT should not exceed 5. Lipoprotein lipase: 4. Diarrhea 2. Pulmonaryembolism
12 min. Pitkin menstruum 3. Deep vein thrombosis
Heparin activates lipoprotein 5. Osteoporosis: (on a dose of
is a repository form of cone. 15,000 units per day for over 6 4. Perioperative DVT prophylaxis
lipase which inhibits lipemia.
heparin 20,000-40,000 units months)
Since lipemia inhibits fibrino- 5. DIC. 6. Evolving stroke/TIA
in dextrose-gelatin-acetic-
lysis, heparin increases fibri- 7. L A or LV clot
acid base.
nolytic activity
a) DALTEPARIN 1. Molecular weights vary from Similar to heparin but far lesser 1. Domiciliary or outpatient
2500 - 10000 IU; S.C./1.V. 4000 to6500 heparin
b) ENOXAPARIN 20-40 mg S.C. 2. Longer duration of action 2. Similar to heparin
c) REVIPARIN SODIUM 3. Predictable response
1432 IU; S.C. 4. Lesser interaction with plate-
d) PARNAPARIN lets
3200-6400 IU; S.C./1.V. 5. Minimal action against
e) NADROPARIN 3075 IU; S.C. thrombin
f ) TINZAPARIN 6. Similar to heparin
3. APROTININ
10,000 - 20,000 Units 1.V. Plasmin inhibitor Hypersensitivity reactions 1. Reduction of perioperative
followed by 5,000 - 10,000 blood loss during open
units 1.V. 6 hrly till satisfactory cardiac surgery.
response 2. Traumatic/hemorrhagic
shock, Septic shock
3. Fulminant pancreatitis
566
( 15 > Drugs
DIURETICS
1. LOOP DIURETICS
a) F UROSEMIDE Acts on all sites of nephron, ex- 1. Hypokalemia, hypona- 1. Acute left ventricular
40-100 mg upto 2 gm cept distal tubules. It causes loss tremia, hypochloremia failure
orally, J.M. or J.V. of Na, K, chloride, Ca, Mg & phos- 2. Hyperglycemia 2. Edema disorders
phates. Water is lost along with
3. Skin rashes 3. Forced diuresis e.g. Barbitu-
sodium. JV furosemide rapidly rate poisoning, etc.
4. Bone marrow depression
causes pooling of blood in pe-
5. Pancreatitis 4. Cardiac failure (CCF)
ripheral deep veins. This effect
occurs before diuresis & is impor- 6. Ototoxicity 5. Acute renal failure
tant in treatment of pulmonary 7. Precipitation of Hepatic 6. Anti-hypertensive
edema and acute LVF. encephalopathy
2. THIAZIOES
3. POTASSIUM SPARING
b) TRIAMTERENE Acts directly on the distal tubule. 1. Hyperkalemia 1. Edema disorders with diuret-
25-100 mg/day. Depresses the excretion of 2. Diarrhea ics.
potassium but increases the 3. Dry mouth 2. Pseudo - aldosteronism.
excretion of sodium and chloride.
4. Skin rash
c) AMILORIDE HYDRO- Acts on proximal & distal tubule Similar to triamterene Similarto triamterene.
CHLORIDE 5-10 mg/day
567
PRACTICAL MEDICINE
5. OSMOTIC DIURETICS
(ADRENALINE) 0.5-1.0 ml S.C. 1. Increases the rate, force of 1. Pallor, palpitation, tremors, 1. Anaphylactic shock
or l.M. 1:lOOOin 1 ml contraction& cardiac output anxiety, headaches 2. Cardiac resuscitation
2. Adrenaline stimulates adenyl 2. Angina\ pains 3. Bronchial asthma
cyclase and increases 3-5' cy 3. Arrhythmias in patients with 4. Control of hemorrhage like
clic AMP which causes bron infarction epistaxis or following tooth
chodilatation. 4. Sudden hypertension extraction
3. Causes contraction of radial 5. With local anesthetics, re
muscles of iris causing pupi\ duces its systemic absorption,
lary dilatation. prolongs its action&reduces
4. Constricts blood vessels and systemic side effects.
controls local bleeding 6. Open angle glaucoma
568
( 15) Drugs
2. ATROPINE Blocks the muscarinic effects of 1. Dry mouth, dysphagia, 1. Preanesthetic medication
ATROPINE SULFATE acetylcholine as it has the same constipation, paralytic ileus 2. Organophosphorus poisoning
0.5 mg/ml and 6 mg/ml affinity for muscarinic receptors 2. Urinary retention. 3. Bradyarrhythmias
0.5 mg tablets. as acetylcholine but poor intrinsic 3. Blurred vision and precipites 4. Motion sickness
activity of glaucoma.
OXYPHENONIUM 5. Colic and dysmenorrhea
10mg orally, 4. Allergic dermatitis. 6. Peptic ulcer: Reduces HCI
GLYCOPYROLLATE Precautions: secretion and smooth
1. In elderly it precipitates glau muscles spasm.
coma and urinary retention (if 7. Parkinsonism:To relieve
enlarged prostate).
tremors and rigidity.
2. In chronic lung diseases. it
8. To produce mydriasis & cy
dries up secretion
cloplegia (e.g. fundus exam)
569
PRACTICAL MEDICINE
PROPANTHELINE Decreases gastric acid secretion. Less than atropine 1. Peptic ulcer
15 mg thrice a day Increases gastric emptying time, 2. Abdominal colic
30 mg at bedtime oral allows antacid to at on gastric
PIRENZEPINE mucosa for long time.
100 mgBDS orally
HOMATROPINE Paralyses the iris and ciliary mus- Less than atropine 1. Pre anesthetic medication
1 to 2% eye drops mydriasis cle. Produces 2. OPC poisoning
and cycloplegia 3. Funduscopic examination
Duration 24 to 48 hrs. 4. lritis
5. Break adhesions between
iris and ciliary body
EUCATROPINE Same as above Less than atropine Sa me as above
2%to 5%eye drops Duration 12 to 24 hrs
4. BETA-2 STIMULANTS
SALBUTAMOL Beta-2 stimulant. It is resistant Nervousness,drowsiness, 1. Bronchial asthma.
100,200,400 µg inhalation to inactivation by COMT and has Weakness and tremors. 2. To delay delivery in premature
2- 4 mg orally tds longer duration of action. labour.
SALMETEROL 25 µg/puff 3. Hyperkalemic periodic
1-2 puffsBD paralysis
TERBUTALINE
5 mg tds orally; 0.25 mg SC or
5 g/min1V
ISOETHARINE, FENOTEROL
CARBUTEROL, IBUTEROL
RIMITEROL, PIRBUTOL,
RITODRINE
570
( 15) Drugs
,.
5, METHYL XANTHINE DERIVATIVES
7. CORTICOSTEROIDS
,.
c) KETOTIFEN
1 mgB.D.
1 mg/5 ml syrup
Cromolyn analogue.
Inhibits antigen induced release
of chemical mediators especially
,.
Drowsiness, dizziness,
headache 2.
Prophylaxis of childhood
asthma
Allergic rhinitis
histamine and SRS-A. Inhibits 2. Dry mouth, nausea vomiting 3. Allergic conjunctivitis
bronchial, nasal, ocular and der- 3. Increased appetite and 4. Allergic dermatitis
mal response to histamine. weight gain 5. Desensitize,
Interferes with eosinophil de- 4. Thrombocytopenia with
granulation and chemotaxis and antidiabetic drug
hence reduces inflammation
9. LEUKOTRIENE BLOCKERS
10. ANTI-CHOLINERGICS
571
PRACTICAL MEDICINE
2. POTASSIUM IODIDE 1. Acts reflexly as well as directly 1. lodism: Nasal catarrh, Expectorant
300mg. to increase the respiratory se conjuntival swelling,edema
POTASSIUM CITRATE cretions. of eyelids lacrimation,
VASICINE 2. Liquifies thick viscid sputum. increased respiratory tract
secretions, edema & ulcers of
larynx, headache, skin rash
2. Hypothyroidism and goitre.
4. DEXTROMETHORPHAN Same as codeine, but safer Same as codeine, but safer Same as codeine,but safer
10-20 mg TDS. Max 120 mg
ANTI-ALLERGIC DRUGS
1. ANTI-HISTAMINICS
A. DIPHENHYDRAMINE (DPH)
They inhibit the action of
histamine releases on GI tract,
,.
CNS: Sedation,fatigue,las-
situde, tinnitus, diplopia and
,. Allergic disease: Urticaria,hay
fever,rhinorrhea,pruritus.
25-75 mg orally, 10 mg IM. uterus, blood vessels and euphoria. 2. Hypnotic (DPH,PM)
B. PHENIRAMINE MALEATE (PN) salivation. They have no effect on 2. Anti-cholinergic: Dryness 3. In lytic cocktail (PM) to
25-75 mg orally bronchospasm, hypotension and of mouth,blurring of vision, produce hypothermia.
gastric secretion. tremors, impotence and 4. Parkinsonism (DPH)
C. CHLORPHENIRAMINE
retention of urine. 5. Motion sickness (PMC)
MALEATE (CPN)
5.20 mg orally or IM. 3. GI: Nausea, vomiting, epigas- 6. Cardiac arrhythmia (A,DPH)
tric distress.
D. PROMETHAZINE (PM) 7. Vertigo (PMC)
4. Skin: Rash, photosensitivity.
12.5-25 mg orally 8. Drug-induced dystonias
5. Hemopoietic: Blood dyscra- (extra-pyramidal reactions)
E. PROMETHAZINE (PMC)
sias. (DPH,PM)
25-75 mg orally.
F. ANTAZOLINE (A) 50-100 mg
572
< 15) Drugs
Drug/Dose Action Side Effects Uses
5. CETIRIZINE Potent and highly selective H 1- 1. Headache, dizziness, drowsi- 1. Allergic rhinitis
10 mg OD orally histamine receptor antagonist ness 2. Urticaria
without anti-cholinergic and anti- 2. GI discomfort
serotoninergic actions
SEROTONINERGIC AGENTS
1. CYPROHEPTADINE 1. It has anti-5 HT2, anti- 1. Drowsiness, dizziness 1. Pruritus in allergic dermatitis,
4-20 mg/day histaminic, atropine-like anti- 2. Dry mouth urticaria,etc.
cholinergic, anti-tremor and 3. Mental confusion,headache, 2. Seasonal and perennial
anti-convulsant properties. ataxia pollenosis.
2. Directly stimulates 3. To stimulate appetite
hypothalamic appetite center 4. Post-gastrectomy dumping
3. Stimulates hypothalamic CRH syndrome
release 5. Carcinoid syndrome
4. Suppresses aldosterone 6. Rarely in refractory pituitary
Cushing's disease
7. Rarely in refractory idiopathic
aldosteronism
573
PRACTICAL MEDICINE
4. TRAMADOL Weak agonist of all opioid Similar to opioids 1. Moderate to severe pain
50-100mg TDS/QDS receptors speciallyµ receptors 2. Post-operative pain
100 mg S.C.,I.M. or I.V.
7. NALORPHINE Partial agonist of the nalorphine 1. Nausea, vomiting, miosis, 1. Effective antidote to
HYDROBROMIDE type sweating, pallor etc. morphine and other opioid
5-lOmglM 2. Respiratory depression compounds overdose
2. Opioid de-addiction
3. With morphine, for opioid
withdrawal syndrome
574
15 > Drugs
,.
Drug/Dose Action Side Effects Uses
,.
2. PARACETAMOL Similar analgesic and anti-pyretic Hemolytic anemia Similar to salicylates, but more
2-5 gm/day in actions as salicylates 2. Skin rash potent anti-pyretic without:
divided doses 3. Renal damage G.I. irritation or
4. Liver damage 2. Acid-base and electrolyte
5. Methemoglobinemia imbalance.
6. IBUPROFEN Analgesic, anti-pyretic and anti- Similar to a,pirin but less potent
inflammatory properties similar
,. Acute gout
200-400 mgTDS 2. Rheumatoid arthritis
to aspirin 3. Ankylosing spondylitis
4. Osteoarthritis
1 2. ENFENAMIC ACID Similar to Aspirin Similar to Aspirin but less gastric Analgesic, antipyretic and anti-
1.2-2.4 gm/day upset. inflammatory agent.
13. TOLMETIN Similar to lndomethacin Similar to lndomethacin. Similar to lndomethacin but less
potent.
14. PIROXICAM Similar to Aspirin Similar to Aspirin but less G.I. Similar to Aspirin
10-20 mg OD (analgesic) upset
20-40 mg OD (anti-
inflammatory)
15. TENOXICAM Similar to Aspirin Similar to Aspirin but less G.I. Similar to Aspirin
20mg -0D orally side-effects
16. ALCOFENAC Similar to Piroxicam. but more Similar to Aspirin Similar to Aspirin
1 gmTDS potent
,.
50 mg twice a day orally
1 8. KETOROLAC It inhibits cyclo-oxygenase and Renal toxicity Analgesic, but also has anti-
10-20 mgTDS the formation of prostaglandins. 2. Hypersensitivity pyretic and anti-inflammatory
Is peripherally acting analgesic. properties.
575
PRACTICAL MEDICINE
19. COX-2 INHIBITORS 1. Superselective cyclo-oxygen- Lesser than other NSAIDS 1. Pain
NIMESULIDE ase type-II (Cox-2) blocker 2. Similar to other NSAIDS
100 mg BD/TDS 2. Weak inhibitor of prostaglan-
MELOXICAM dins
7.5-15 mg BD/TDS 3. Potent anti-inflammatory
4. Anti-histaminic
5. Inhibits superoxide anion for-
mation
6. Inhibits release ofTNF-a
7. Anti-cytokine
DRUGS IN MIGRAINE
1. ERGOT ALKALOIDS 1. Vascular: Potent vasoconstric- 1. Vascular:Thrombosis, 1. Acute attack of migraine
a) ERGOTAMINETARTARATE (ET) tor directly (ET) or by alpha gangrene (ET,DHE)
- 1-2 mg; max. 6 mg/day or 12 blockade (DHE). They also 2. Nausea, vomiting 2. Migraine prophylaxis (MS)
mg/wk orally have 5 HT antagonistic activi- 3. Intra-uterine fetal death 3. Post-partum hemorrhage
b) DIHYDROERGOTAMINE (DHE) ty with partial 5 HT1 agonistic (EM,MM) (EM,MM)
- 1 mg S.C. action. 4. Uterine rupture (EM,MM) 4. Uterine involution (EM)
c) ERGOMETRINE MALEATE (EM) 2. Oxytocic action on the uterus 5. Retroperitoneal fibrosis (MS) 5. Hypertension (Hydergine)
- 0.5 mg I.V. 3. Hyperperistalsis 6. Orthostatic hypotension (oral
d) METHYLERGOMETRINE (MM) DHE)
- 0.25-0.5 mg orally or
0.2 mg S.C./1.M./I.V.
e) METHYSERGIDE (MS) -
1-2mg orallyTDS
2. SUMATRIPTAN S HTl receptor agonist 1. Flushing, neck pain, dizziness, 1. Acute attack of migraine
6 mg S.C. or 100 mg orally tingling 2. Status migrainosus
2. Can precipitate coronary 3. Cluster headache
ischemia 4. Refractory headache
3. Allergy and rash
576
( 15) Drugs
ANTI-EPILEPTIC DRUGS
1. DIPHENYLHYDANTOIN Inhibits the spread of seizure dis- 1. Intolerance: Rash 1. Grand mal epilepsy
SODIUM charge in brain by decreasing in- 2. Gum hypertrophy 2. Psychomotor and focal
100mg tds;4 mg - 8 mg/kg. traneuronal sodium. 3. Cerebellar ataxia seizures
PHENACEMIDE It restores the balance between 4. Megaloblastic anemia 3. Cardiac arrhythmias
Analogue of phenyl hydantoin; the excitatory glucamate path- 5. Nausea, vomiting 4. Trigeminal neuralgias
Used in psychomotor epilepsy way and inhibitory GABA path- 5. Diabetic neuropathy
6. Aplastic anemia
way and causes anti-epileptic
METHOIN ETHOTOIN 7. Hirsutism 6. Chorea
action
8. Osteomalacia Does not sedate the patient
9. Facial coarsening
577
PRACTICAL MEDICINE
10. CLONAZEPAM Similar to diazepam. 1. Drowsiness Petit mal and myoclonic seizures.
0.5 mg tablets; 4-8 mg/day 2. Ataxia, dyskinesias
3. Hyperexcitability
4. Hypotension
11 .SODIUM VALPROATE It acts by inhibiting GABA trans- 1. Nausea, vomiting, diarrhea Grand mal, petit mal, myoclonic
200 mg/day initially then aminase, thus increasing the con- 2. Liver damage and psychomotor epilepsy. It is
600-1600 mg/day centration of GABA, an inhibitory 3. Interferes with platelet less effective in partial seizures.
transmitter in the CNS aggregation. It increases phenobarbital and
4. Drowsiness decreases phenytoin blood levels
on simultaneous administration
5. Weight gain
6. Loss and curling of hair
7. Teratogenic
12. GABAPENTIN Increases release of GABA Same as sodium valproate Partial seizures resistant to other
900to 1800 mg/day in three therapy.
divided doses
13. TIAGABINE GABA reuptake inhibitor Headache, dizziness, somnolence Add-on drug for partial seizures
4-12mgTDS with or without secondary
generalisation
14. VIGABATRIN GABA transaminase inhibitor, in- 1. Weight gain Refractory epilepsy
500 mg; dose 1-3 g/day creases brain GABA 2. Drowsiness, diplopia
3. Depression, memory
disturbances
1 S. LAMOTRIGINE Blocks the influx of Sodium ions. 1. Nausea, headache, ataxia 1. Partial and generalised
150-SOOmgBD Antagonist of NMDA glutamate 2. Skin rash secondary seizures
receptor 3. Steven Johnson syndrome 2. Lennox-Gestant syndrome
17. SULTHIAME Sulphonamide derivative 1. Nausea, anorexia, weight loss 1. Temporal lobe epilepsy
100-600 mg/day 2. Apathy, ataxia, blurred vision 2. Myoclonic epilepsy
3. Photophobia, psychosis, 3. Refractory grand mal epilepsy
paresthesia
4. Kidney damage
18. TOPIRAMATE Blocks sodium channels through 1. GI side effects Refractory epilepsy
300-600 mg/day GABA 2. Same as newer anti-epileptics
578
( 15) Drugs
MUSCLE RELAXANTS
1. DIAZEPAM Centrally acting muscle relaxant Refer Pg. 577 Refer Pg. 577
2-10 mg tds orally
2. MEPHENESIN Acts on the entire neuraxis and 1. Anorexia, nausea, vomiting 1. Myalgia
1-2gm orally causes muscle relaxation 2. Dizziness, diplopia, 2. Arthralgia
0.5-1 gm 1.V. nystagmus, ataxia 3. Myositis
3. Respiratory depression 4. Spastic neurological disorders
4. Hemolysis
5. Changeof hair colour
3. BACLOFEN Acts on the pre-synaptic mecha- 1. Drowsiness, lassitude, 1. Relief of flexor spasm
5 mg TDS increased upto 80 nisms and reduces the release of hallucination, depression 2. Reduce tonic flexor dystonia
mg/day excitatory transmitter. 2. Blurred vision of lower limbs in spinal
3. GI disturbances spasticity
3. Refractory hiccups
4. DANTROLENE It reduces the calcium release 1. Dizziness, drowsiness, fatigue 1. Spasticity
25 mgTDS upto 300 mg/day. into the sarcoplasm and thus the and weakness 2. Malignant hyperpyrexia
muscle contraction is weakened. 2. Diarrhea 3. Neuroleptic malignant syn
3. Hepatotoxicity dromes (NMS)
S. D-TUBOCURARINE It combines with the receptors 1. Hypoxia and respiratory Muscle relaxant
6-lOmg lV on the motor end-plate and thus paralysis
(1 ml=3mg) blocks the action of acetylcholine 2. Hypotension
by Competitive blockade 3. Esophageal ulceration due
to paralysis of esophageal
sphincter and regurgitation
of gastric juice
6. GALLAMINE Similar to D-Tubocurarine 1. Respiratory paralysis Muscle relaxant
1 mg/kg IV 2. Hypotension, tachycardia and
cardiac arrhythmias
7. SUCCINYLCHOLINE Acts as a partial agonist of acetyl- 1. Cardiac arrest and ventricular Muscle relaxant
0.1-0.5 mg/kg IV choline arrhythmias
2. Respiratory failure
3. Muscle soreness
8. ALCURONIUMCHLORIDE Same as D-Tubocurarine Same as D-Tubocurarine Same as D T- ubocurarine
0.04 - 0.08 mg/kg 1.V. Does not release histamine
ATRACURIUM, DOXA Does not block ganglia
CURIUM, MIVACURIUM,
ROCURINIUM
9. PANCURONIUM Same as above Same as above More potent than
0.04 - 0.08 mg//kg 1.V. D-Tubocurarine
10. VECURONIUM Same as above Same as above Same as above
80 - 100 µg/kg I.V.
11. BOTULINIUM TOXIN Binds irreversible to cholinergic Uncommon and not serious Spastic disorders like spasmodic
TYPE A presynaptic sites torticollis, hemifacial spasm,
blepharospasm, laryngospasm.
ANTI-PSYCHOTIC DRUGS
1. PHENOTHIAZINES 1. Reduces the incoming 1. Intolerance: Skin eruptions, 1. Major Psychosis: Schizophre
CHLORPROMAZINE sensory stimuli by acting visceral yellowish brown or nia
10,25,50,100 mg. tablets. on brain-stem recticular purple pigmentation due 2. Aggressive behavioral disor
Dose: 100-1500 mg formation. to melanin or melanin-like ders in children.
2. Modifies the functions of the substance 3. Anti-emetic (depresses
25 mg/ml l.M.
limbic system. 2. Anticholinergic effects chemo-receptor trigger zone)
FLUPHENAZINE
3. Causes chemical blockade of 3. Thrombocytopenia and 4. Anti-hiccup
2.5·1Omg orally
noradrenaline, dopamine and aplastic anemia 5. To include hypothermia
(3-4 div.doses) 5 HT, decreasing the sympa- 4. Intra-hepatic cholestasis.
PERPHENAZINE 6. Muscle relaxant in tetanus
thetic activity in hypothala- 5. CNS: Drowsiness, restlessness.
12.5-50mg 7. Pre-anesthetic medication
mus. Parkinsonism, hypothermia
every 2-4 weeks 8. Senile psychosis
6. Endocrine: Gynecomastia, 9. Manic depressive psychosis
weight gain, impotence, NB: Potentiates analgesic
lactation & mental irregulari drugs like morphine and
ties. Aggravation of diabetes phenobarbitone.
mellitus.
579
PRACTICAL MEDICINE
7. RESPERIDONE Atypical anti-psychotic drug 1. Dyskinesias like akathisia 1. Psychosis -typical & atypical
1-2 mg/day which blocks D2, 5HT, a2 and Hl 2. Lesser than others 2. Schizophrenia
receptors
SEDATIVES/ HYPNOTICS
1. CHLORDIAZEPOXIDE Exact mechanism is not known. 1. Drowsiness, lethargy 1. Anxiety
10-30 mg/day It probably acts on the limbic sys- 2. Allergic reactions 2. Withdrawal of alcohol in
tern and the brain-stem reticular 3. Blood dyscrasias alcoholics
system. It probably also acts on 4. Tolerance 3. Epilepsy
the neurons containing GABA in- 4. Pre-anesthetic medication
5 May produce bizarre
creasing the concentration of the
· reactions with MAOI,
latter. This may be responsible for
xant and anti-convul- barbiturates, alcohol and
:�:�; ;:� amitriptyline.
t
7. BUSPIRONE Acts mainly on the 5HT-1a recep- Dizziness and Drowsiness Anxioselective for anxiety state
5-lOmgTDS tors. Interacts with dopaminergic without sedative, hypnotic,
D2 receptors muscle relaxant and anti
convulsant properties
580
( 15) Drugs
10. BARBITURATES Barbiturates inhibit the neuronal 1. Intolerance: Nausea, vomiting 1. As a sedative and hypnotic
PHENOBARBITONE uptake of GABA or may stimu- 2. Allergic: Urticaria, angio- 2. Anti-convulsant, Grand-ma I
30 mg -400 mg orally or I.M. late the release of GABA which edema. 3. Anesthesia (Thiopental) and
depresses CNS. REM sleep is sup- 3. Megaloblastic anemia in prenesthetic medication.
pressed. Depresses respiration by 4. Tolerance habituation and 4. Potentiation of action of
abolishing neurogenic, chemical addiction analgesics like salicylates
& hypoxic drive. It causes hypo-
s. Aggravates petit mal and 5. Injaundice, to increase the
tension by:
may cause excitement and enzyme conjugation ofbilirubin
11.GLUTETHIMIDE It induces hypnosis without an- 1. Mydriasis, paralytic ileus, dry- Sedative and hypnotic
0.5-1.o gm orally algesics, anticonvulsant or anti- mouth
tussive action. It suppresses REM 2. Respiratory depression
sleep 3. Hypotension
4. Tremors, spasticity and
brisk jerks or peripheral
neuropathy. Psychosis.
5. Addiction
6. Blood dyscrasias
581
PRACTICAL MEDICINE
ANTI-DEPRESSANTS
1. MAO-INHIBITORS
2. TRICYCLIC ANTIDEPRESSANTS
,.
BUPROPION 200-300 mg hypotension
,.
depression to hypomania
6. MIANSERIN It blocks the presynaptic alpha Drowsiness, ataxia and Anti-depressant without anti-
10-30mg t.d.s adrenoceptors and increases the dizziness cholinergic and cardiotoxic
turnover of brain nor-adrenaline. 2. Weight gain effects.
Unlike amitriptyline it does not 3. Agranulocytosis Similar to tricyclics.
prevent the peripheral re-uptake 4. Patients may swing from
of nor-adrenaline depression to mania
5. May raise blood sugar
,. ,.
concentration
,.
BUPROPION 200-300 mg hypotension
582
( 15 > Drugs
ANTI-PARKINSONISM DRUGS
1. BENZHEXOL Atropine-like action reduces seb- 1. Confusion, delirium, Parkinsonism even in the
2 mg daily upto orrhea, sialorrhea, rigidity and hallucinations presence of cardiac lesion and
10-30 mg/day tremors. 2. Urinary retention hypertension.
3. Blurred vision, glaucoma
4. Dry mouth, paralytic ileus
2. CYCRIMINE CHLORIDE Similar to benzhexol Similar to benzhexol, but lesser 1. Parkinsonism. Along with
5-1 Omg but as high as side-effects. phenothiazines to counter
45 mg can be used extrapyramidal effects.
7. LEVA-DOPA Increases dopamine content of 1. On and off phenomenon Idiopathic and arteriosclerotic
3-6 gm daily (Gradually the basal ganglia by being con 2. Anorexia, nausea, vomiting Parkinsonism responds well. Post
increased). verted to dopamine. It improves 3. Behavioural: Depression, encephalitic, less well tolerated
akinesia, tremors, rigidity, seb agitation, confusion, and drug induced does not
orrhea, sialorrhea, aphonia and restlessness, hallucinations, respond at all.
memory. It makes the patient delusions and suicidal
alert and interested in the sur tendencies
roundings. 4. Choreiform movements
5. Palpitation, tachycardia,
arrhythmias, postural
hypotension.Increased AV
conduction.
8. CARBI-DOPA Inhibits dopa decarboxylase By itself carbi-dopa does not In Parkinsonism, used with
Tablets of 25 mg. carbi-dopa which coverts L-dopa to dopa cause any side-effects. However L-dopa, it decreases the
with 250 mg L-Dopa mine in the GI tract, hence more it does not prevent the following requirement of L-dopa with out
BENSERAZIDE L-dopa is available to cross blood side effects of L-dopa. affecting the therapeutic effect.
Tablets combined with brain barrier and concentrate in 1. Orthostatic hypotension
L-Dopa basal ganglia. Since carbi-dopa 2. Involuntary movements
does not cross blood-brain bar 3. Adverse mental effects
rier it does not prevent L-Dopa
Dopamine in CNS.
583
PRACTICAL MEDICINE
,.
Drug/Dose Action Side Effects Uses
10.SELEGINE It is a MAO-B inhibitor which in- None so far known It is supposed to increase the life-
SmgBD hibits Dopamine catabolism. It expectancy and halt the progress
is an anti-oxidant which reduces of Parkinson ism.
nigrostriatal neuronal death.
DRUGS IN STROKE
1. ANTI-PLATELET AGENTS
5. Diabetic angiopathy
6. Post Coronary Stent
,.
7. Post CABG (Bypass surgery)
584
( 15) Drugs
ANTIBACTERIAL AGENTS
SULFONAMIDES
1. SULFONAMIDES Due to structural similarity with 1. Intolerance: 1. Meningococcal meningitis.
a) SULFADIAZINE: PABA it competes with and prob- a) Serum sickness. 2. Bacillary dysentery.
2-3 gm initial. ably substitutes the latter in bac- b) Anaphylactoid reaction. 3. Urinary tract infection.
1 gm 4-6 hrly. later. terial metabolism. It inhibits folic c) Steven Johnson syndrome 4. Chancroid.
acid synthetase which converts
b) SULFADIMIDINE: as above. 2. Urinary tract: 5. Trachoma and inclusion
PABA to folic acid, resulting in
c) SULFAMETHIZOLE Renal colic and stones due to conjunctivitis.
folk acid deficiency and injury to
10-200 mg 4-6 hrly. bacterial cell. This injured cell can precipitation of the drug in 6. H. influenza meningitis
d) SULFAMETHOXYPYRIDAZINE: be easily phagocytosed. It is inef- tubules. 7. Intestinal sterilisation prior to
300 mg 12 hourly fective in presence of pus and tis- 3. Hemopoietic: surgery on colon.
e) SULFAPHENAZOLE: 1 gm. sue breakdown products which a) Agranulocytosis, 8. Ulcerative colitis.
initially, then 0.5 gm. 12 hrly. contain large amounts of PABA. aplastic anemia, 9. Resistant malaria, nocardiosis,
f ) SULFAGUANIDINE: 3-6 gm 6 Similarly, Procainamide, Procaine thrombocytopenia. toxoplasmosis.
hrly. and Amethocaine which yield b) With G6PD deficiency- 10. Prophylaxis of bacillar
g) SALAZOPYRINE: 0.5-1.0 gm. PABA, antagonise sulfonamides. lntravascular hemolysis. dysentery, meningococcal
h) MEFENIDE HYDROCHLORIDE: c) In fetus and neonates- meningitis
2.5%with 1%Methyl eel- Kernicterus
lulose cream. 4. Miscellaneous:
i) SULPHASUXAZOLE: 2 gm a) Goitre and hypothyroidism
585
PRACTICAL MEDICINE
QUINOLONES
1. NALIDIXIC ACID It interferes with the synthesis of 1. Nausea, vomiting, diarrhea Effective against gram-negative
1 gm6hrly DNA. 20% of the drug is present 2. Allergy, fever, rash, pruritus, urinary tract infection, especially
in active form in urine which is an eosinophilia, urticaria with E. coli, Proteus, Klebsiella,
adequate antibacterial concen- 3. CNS: Headache, malaise, Aerobacter and occasionally
tration. Excretion of free drug is drowsiness, myalgia, Pseudomonas.
increased in alkaline urine. convulsions Contra-indicated in:
4. Hemolytic anemia 1. Cerebral atherosclerosis,
5. Respiratory depression Parkinsonism, Convulsions.
2. Impaired hepatic and renal
function.
2. NORFLOXACIN Similar to Nalidixic acid 1. Nausea vomiting, 1. Urinary tract infection
400 mg BD for?-10 days one 2. Drowsiness, dizziness, light- 2. Gonorrhea.
hour before or two hours headedness
after food. It loses its potency if combined
with Nitrofurans or antacids but
not Ranitidine/cimetidine
3. ENOXACIN - 200- 400 mg BD Similar to Norfloxacin Similar to Norfloxacin Gonorrhea, UTI
CINOXACIN - 500 mg BD
ACROSOXACIN - 300 mg OD
4. CIPROFLOXACIN It inhibits DNA gyrase 1. Cardiac arrhythmias 1. Effective against gram
250-500 mg TDS orally or 200 2. Oral candidiasis negative organisms including
mg IVB-12 hourly x 10-14 3. Hallucination, dizziness pseudomonas.
days 4. Interstitial nephritis 2. Bacterial gastroenteritis
3. Typhoid fever
4. Septicemia
S. Osteomyelitis
6. Pneumonias,chronicbronchitis
7. STDs, e.g. gonorrhea,
chancroid
8. Tuberculosis, esp. drug
resistant strains
s. PEFLOXACIN As above As above As above
400mg BD x 10-14days
BETA-LACTAMS
1. PENICILLIN Interferes with the cell wall syn- 1. Anaphylaxis. 1. Pneumococcal,
Na-K salt ofBenzyf Penicillin: thesis of gram-positive bacteria. 2. Serum sickness syndrome streptococcal, taphylococcal,
5 lakh units/ml. l.M./1.V. This makes the cell membrane 3. Skin rashes, hemolytic meningococcal, gonococcal
Procaine Penicillin Forte: 5-1O vulnerable to damage by sol- anemia, hematuria, infections
lakh units I.M. daily. utes in the surrounding media. albuminuria. 2. Syphilis
Benzathine Peniciffin: 2-4 Cell walls of gram-negative ba- 4. Jarisch-Herxheimer reaction. 3. Diphtheria, tetanus, anthrax,
mega units I.M. once every 3 cilli are complex, hence very high Cl. welchii, plague.
5. Superinfection.
weeks. concentrations of the drug are 4. Actinomycosis, pasteurella,
required to inhibit cell wall syn- 6. local pain, erythema, listeriosis
thesis. induration.
5. Prophylaxis of Rheumatic
fever, Gonorrhea, Syphilis
586
< 15) Drugs
Drug/Dose Action Side Effects Uses
3. CLOXACILLIN 5-10 times more potent than Allergic reactions. Penicillin-resistant staphylococcal
0.5-1 gm. 4-6 hrly. Methicillin. infection.
DICLOXACILLIN
FLUCLOXACILLIN
4. AMPICILLIN As penicillin, but less active Similar to Penicillin 1. Urinary tract infection.
250-500 mg. 6 hrly. against gram-positive organisms 2. Respiratory infection.
AMOXICILLIN and more sensitive against gram 3. Meningitis.
Twice as potent as negative organisms. It is inactivat- 4. Endocarditis.
Ampicillin. ed by Penicillinase, therefore not
5. Biliary and intestinal
effective against Staphylococci
TALAMPICILLIN diseases.
resistant to benzyl penicillin.
PIVAMPICILLIN
6. PIPERACILLIN Broad spectrum penicillin active Similar to Penicillin. Pseudomonas and other gram
15-20g/day against Pseudomonas aeruginosa negative organisms
AZOCILLIN Neonatal meningitis
MEZLOCILLIN
B. LINCOMYCIN It inhibits the 50 S site on the bac- 1. Pseudomembranous colitis 1. B.fragilis infection
SOOmgTDS terial ribosomal RNA 2. Nausea, Vomiting.Jaundice 2. Malaria
CLINDAMYCIN 3. Bone-marrow suppression 3. Toxoplasmosis
lSOmgQDS 4. Fever, rash, arthritis. 4. Pneumocystis carinii
MACROLIDES
1. ERYTHROMYCIN Inhibits protein synthesis in bac 1. Allergic reaction: 1. Infective endocarditis, (4-6
1-2 gm/day. terial cell. Fever, rash, urticaria and gm)
Binds to 50 s ribosomal subunit. lymphadenopathy. 2. Diphtheria carriers.
2. Nausea, vomiting, epigastric 3. Prophylaxis of rheumatic
pain. fever, streptococcal infection
3. Cholestatic hepatitis. 4. Allergy to penicillins
5. Upper RTI
6. Pneumonia, also atypical
7. Vaginitis (chlamydia)
8. Wound, burn infections,
impetigo, eczema, acne.
2. ROXITHROMYCIN As above As above 1. As above
150 mg B.D. x 5 days 2. Active against Legionella,
mycoplasma, H. influenza
3. AZITHROMYCIN As above As above As above
250 -500 mg OD x 3 days
588
( 15) Drugs
AMINOGLYCOSIDES
1. STREPTOMYCIN 1. Combines with ribosomes 1. Injection abscess. 1. Tuberculosis
0.75 gm/day IM x 3 months and interferes with m-RNA- 2. Anaphylaxis. 2. Bacteremia and SBE
in TB. Streptomycin sulfate ribosome combination, 3. Ototoxicity(vestibular>coc 3. Plague
tablets 0.5-2.0 gm orally as inducing it to manufacture hlear)-lmbalance, tinnitus, 4. Brucellosis
intestinal antiseptic peptide chains with wrong vertigo 5. Tularemia
amino-acids, which destroys 4. Nephrotoxicity
the bacterial cell. Binds to SO s 6. Urinary tract infection
5. Circumoral paresthesia 7. Respiratory tract infection
ribosomal subunit.
6. Curarimimetic and 8. H. influenza meningitis
2. Inhibits enzymes involved in
aggravates myasthenia 9. Intestinal anti-septic-gut
Krebs cycle and xanthine oxi-
dase. It is bactericidal. 7. Eosinophilia, rash sterilization
8. Drug fever 1O.Chanchroid, granuloma
9. Drug resistance inguinale
2. KANAMYCIN Similar to streptomycin As above. Damage more to 1. Septicemia and SBE with
0.5-1.5 gm/day for maximum cochlear than vestibular division gram-negative organisms.
10 days. ofVIII nerve. 2. MDR-TB
3. GENTAMYCIN Similar to streptomycin but also 1. As for streptomycin. Pneumonia, septicemia and
80 mg. 8 hrly. I.M. 5 mg, intra- effective against Pseudomonas 2. Dizziness. meningitis due to Pseudomonas,
thecally. aeruginosa. Proteus, Klebsiella, Aerobacter,
Staphylococcus Streptococcus,
Salmonella etc.
4. TOBRAMYCIN Similar to gentamycin Similar to gentamycin but less Four times more active
3-5 mg/kg IM in three divided nephrotoxic than gentamycin against
doses Pseudomonas.
TETRACYCLINES
1. TETRACYCLINES 1. Chelates calcium and magne- 1. Intolerance 1. Plague
1-2 gm/day orally. sium. 2. Nausea, vomiting, diarrhea 2. Cholera
IM orlV. 2. Inhibits essential enzyme sys- 3. Superinfection 3. Bacillary dysentery
terns of the organisms. 4. Hepatic dysfunction 4. Amebic dysentery
3. Interferes with phosphoryla- 5. Fanconi-like syndrome 5. Urinary tract infections
tion of glucose. 6. Permanent yellow staining of 6. VD: Syphilis, Gonorrhea
4. Suppresses the bacterial pro- teeth Chancroid, G. inguinale
tein synthesis by interfering 7. Benign intracranial 7. Mycoplasma pneumonia
with transfer RNA. (Bacterio- hypertension in infants 8. Chlamydia infections, LGV,
static).
Trachoma, Psittacosis
589
PRACTICAL MEDICINE
5. Binds to 30s ribosomal sub- 8. Bone: Reduce linear growth 9. Rickettsial infections
unit of bones in fetus. 1 O. Spirochetal: leptospirosis
9. Aggravate peptic ulcer in 11. Actinomycosis, Anthrax
uremia by inhibiting ureas of 12. Diagnostic test in Neoplasms:
gastric mucosa,which breaks Tetracyclines given for 5
urea to ammonia (latter days, Malignant cells exhibit
serves to reduce (gastric brilliant yellow fluorescence
acidity) under UV light
CHLORAMPHENICOL
1. CHLORAMPHENICOL Interferes with protein synthesis 1. Intolerance 1. Typhoid fever
1-3gm/day. of bacteria. 2. Bone marrow depression 2. Urinary tract infection
3. Superinfection 3. H. influenza meningitis
THIAMPHENICOL 4. Liver damage 4. Plague
is the other analogue 5. Grey baby syndrome-in 5. Gram-negative septicemia
neonates and infants and5BE
6. CNS: Peripheral neuritis, optic
neuritis,cochlear damage,
convulsions, depression,
ophthalmoplegia
ANTI-TUBERCULOUS DRUGS
1, RIFAMPICIN Macrocyclic antibiotic. 1. Liverdamage Tuberculosis.
450 -600 mg/day orally Inhibits DNA-dependent RNA 2. Influenza-like reaction Other uses:
(10 mg/kg) polymerase thus stopping the 3. Intolerance: Fever,skin 1. leprosy and ENL
expression of bacterial genes. rash,diarrhea,leucopenia, 2. Meningococcal carrier
BACTERICIDAL. eosinophilia,ataxia,dizziness 3. Staphylococcal septicemia
4. Orange-red colour to urine, 4. Herpes zoster
feces, sputum 5. H. influenza
It is metabolized in liver. Hence, 6. Brucella
in liver disease the concentration
7. Mycetoma
is raised.
8. Qfever
9. Legionella
10. Chlamydia
4. ETHAMBUTOL Not known. BACTERIOSTATIC. 1. Optic nerve damage 1st line supplemental agent-TB
25 mg/kg x 12 wks. Acts mainly against rapidly grow- 2. Anaphylactic reaction only Crosses BBB and is equally
15 mg/kg x 11/2 yrs. at night ing organisms. 3. Nausea,vomiting concentrated in CSF and plasma.
4. Confusion, headache
5. PYRAZINAMIDE Not known. BACTERICIDAL.Nico- 1. Toxic hepatitis on 7th day. Intensive chemotherapy regimen
500-750 mg BD (25 mg/kg) or tinamide analogue Acts in acidic 2. Hyperuricemia,gout, drug
MORPHAZINAMIDE environment also. polyarthralgia
(more potent) 3 gm/day orally 3. Skin rashes and
(500 mg tablet) photosensitivity.It may
cause bright red-brown
discoloration of skin.
590
( 15) Drugs
7, CYCLOSERINE Broad-spectrum antibiotic 1. CNS: Weakness, tremors Reserve second line agent
1-2gm daily Inhibits the synthesis of the bac- ataxia, convulsion, slurred
terial cell wall. speech, brisk jerks and ankle
clonus.
2. Insomnia, psychosis.
8. VIOMYCIN Complex polypeptide antibiotic Similar to streptomycin Inhibits 90% strains of MDR-TB
1 gm twice a week I.M.
10. AMIKACIN/KANAMYCIN BATERICIDAL to extracellular or- Similar to streptomycin. Not effective against viomycin
1-1.5 gm. l.M. x 60 days. ganisms. Refer Pg. 589 resistant organisms.
11. THIACETAZONE Not known. BACTERIOSTATIC. l. Anorexia, nausea, vomiting. HIV-associated TB. It is also
AMITHIOZONE V. cheap. 2. Skin rashes, Steven Johnson useful in Leprosy. It crosses BBB
150mg daily Banned by WHO due to side- syndrome. producing equal concentration in
effects. 3. Bone-marrow, kidney and CSF and plasma inflammation.
liver damage.
12. PARA-AMINO SALICYLIC Interferes with utilisation of para- 1. GI: Anorexia, nausea, Low level of anti-TB activity.
ACID(PAS) amino benzoic acid by the my- vomiting, diarrhea. ·Reserve drug.
12-15 gm/day orally. cobacterium. Sulfonamides also 2. Intolerance: Fever, s�in rash,
PAS granules 4 gm 8 hourly act in similar fashion, but are not lymphadenopathy.
useful because tubercle bacillus 3. Hemopoietic: Leucopenia,
accommodates PAS or PABA but eosinophilia, ataxia.
rejects sulfonamides. 4. Hepatic damage.
5. Acute renal failure.
6. Myxedema, Loeffler's
syndrome
13. ETHIONAMIDE Derivative of INH. Like INH and 1. Nausea, vomiting, diarrhea, 1. Crosses BBB and achieves
200 mg b.d. up to 1 gm. daily. PZA it inhibits protein synthesis. metallic taste good CSF concentration,
2. Toxic hepatitis specially in MDR-TB
3. CNS:As lNH 2. It is also useful in Leprosy.
4. Skin rashes, alopecia 3. Atypical mycobacteria
5. Pellagra-like syndrome
6. Hypothyroidism
14. CLARITHROMYCIN Macrolide sp. in macrophages Nausea, vomiting, bitter taste Atypical mycobacteria
250-500 mg OD and excellent activity against
atypical mycobacteria
ANTI-LEPROSY DRUGS
1. DAPSONE Similar to sulfonamides. 1. Allergy: Dermatitis, drug 1. Leprosy: Improvement
DIAMINODIPHENYL Bacteriostatic fever. occurs within 4-8 months.
SULFONE (DDS) Inhibits bacterial folic acid syn- 2. Nausea, vomiting. Morphological Index (Ml)
25 mg/wk: 4 wks. thesis. 3. Hemolytic anemia in G6PD becomes zero in 5 months
50 mg/wk: 4 wks. deficiency patients. (with Rifampicin, Ml becomes
100 mg/wk: to continue, 4. Anemia, zero in 5 weeks).
orally for 3-lOyears. methaemoglobinemia, 2. Dermatitis herpetiformis
agranulocytosis, 3. Pneumocystis carinii
5. Hepatitis, goitrogenesis. 4. Malaria
6. Nephrotic syndrome 5. Cutaneous leishmaniasis
591
PRACTICAL MEDICINE
ANTI-AMOEBIC DRUGS
,. DEHYDROEMETINE Causes degeneration of nucleus 1. Local reaction; Pain, weakness 1. Amebiasis (Extra-intestinal)
and reticulation of cytoplasm of of muscle. 2. Paragonimus westermani
30-60 mg. l.M. or SC daily at
night for 10 days. the trophozoites which arrests 2. GI disturbances: Nausea, (lung fluke) infestations
its multiplication and leads to its vomiting, diarrhea. 3. Emetic
phagocytosis. No action on cysts. 3. CVS: Tachycardia, 4. Fascioliasis
hypotension, myocarditis, 5. Giardiasis
pericarditis. 6. C1.1taneous leishmaniasis
2. QUINOLINE 1. Interferes with the essential 1. Nausea, vomiting, diarrhea Diiodo is more useful in acute
DERIVATIVES enzyme system of the para- 2. Fever, chills, skin eruptions. dysentery against trophozoites
a. DIIODOHYDROXYQU/NOLINE site. 3. Headache, vertigo, S.M. O.N. whereas lodochlor is more useful
b. / ODOCHLORHYDROXYQUIN- 2. Halogenates its proteins. in cyst passers.
OLINE 1. Amoebiasis (Intestinal).
1-2 gm/day x 20 days. 2. Moniliasis.
0.75 gm/day x 1O days 3. Trichomonas vaginitis.
592
( 15) Drugs
9. TETRACYCLINES Intestinal bacteria manufacture Refer Pg. 589 The return of bacterial flora to
1-2 gms/dayx 10 days certain metabolites and vitamins pretreatment level often leads to
or PARAMOMYCIN on which the protozoa thrives. a relapse. Hence it is useful only as
25 mg/kg x 1O days. Tetracyclines alter the bacterial an adjuvant.
flora creating a medium unfavor-
able for the growth of amebae.
Other drugs: DIHYDROXY STILBAMIDINE, ALLOPURINOL (Refer Pg. 577),PAROMOMYCIN (Refer Pg. 589), AMPHOTERICIN B, STIBOPHEN
ANTI-MALARIAL DRUGS
1. QUININE 1. Schizonticidal hence useful as 1. ldiosynchrasies: Flushing, 1. Malaria.
QUININE BISULFATE OR malarial suppressant. pruritus,bronchospasm,ITP, 2. Myotonia congenita.
HYDROCHLORIDE 2. Quinidine-like action on the agranulocytosis 3. To prevent nocturnal muscle
300-600 mg/day orally. heart. 2. Cinchonism:Tinnitus nausea, cramps
QUININE DIHYDROCHORIDE 3. Analgesic, muscle relaxant. headache, visual impairment, 4. Diagnosis of myasthenia
300-600 mg I.M. or I.V. 4. Smooth muscle relaxant. deafness,vertigo. gravis which is aggravated by
5. Curarimimetic on skeletal 3. Backwater fever: Fever, quinine 600 mg 2 hourly for 3
muscles. hemoglobinuria and acute doses.
renal failure. 5. As a Sclerosing agent.
2. CHLOROQUINE Acts by inhibiting the incorpora- Refer Pg. S92 Useful against erythrocytic from
1 gm stat; 0.5 gm after 8 hrs. tion of phosphatesinto the RNA of P. falciparum and vivax and
0.5 gm x 2 days and DNA of Plasmodium. It also gametocytes of P. vivax. It has
Dose: 1 tab = 250 (150 mg has anti-inflammatory anti-hista- no effect on sporozoites and
base); 4 tab stat followed by minic, local anesthetic and myo- persistent tissue forms.
2 tab; After 8 hours followed cardial depressant action.
by 2 tabs; Daily on Day 2 & 3;
Total dose (150 mg base)
4. PRIMAQUINE Probably acts by affecting the 1. Epigastric distress. Malaria. (it should not be
15 mg/day x 14 days metabolic functions of the mito- 2. lntravascular hemolysis in G6 combined with mepacrine or
chondria of gametocytes. It is ef PD deficiency. proguanil as they potentiate its
fective against gametocytes of all 3. Anemia,leucopenia, toxicity).
species. methemoglobinemia.
593
PRACTICAL MEDICINE
s. PROGUANIL Prevents the reduction of folic- Free from side effects in Malaria.
300-600 mg initially acid by the plasmodium which therapeutic doses.
300 mg daily x 5 days. interferes with the nucleic acid In large doses.
CHLORPROGUANIL synthesis causing arrest in eryth- 1. GI disturbances
200 mg once a week to be rocytic schizony. It is schizontici- 2. Reduces gastric acidity
continued for 4 weeks after dal to P. vivax and falciparum. It
3. Depresses myocardium
leaving Malarial area. prevents development of gam-
etes in the gut wall of mosquito. 4. Leucopenia.
5. Hematuria
6. CYCLOGUANIL Protects against P. vivax and falci- Similar to proguanil Long acting anti-malarial.
,.
5 mg/kgl.M. parum for 3 months or longer due Disadvantages:
to slow release of active moiety Development of resistant
from repository strains.
2. Secondary folic acid
deficiency
,.
once a wk and one week prior restlessness confusion or Precautions
to and 4 weeks after leaving seizures Avoid in pregnancy/lactation
endemic area for prevention 2. Avoid with betablockers
3. Quinine should be used with
caution if mefloquine is used
as prophylaxis
9. HALOFANTRINE Unknown mechanism. Nausea, vomiting.Do not Malaria: P.falciparum and P.vivax
(250 mg) 2 TDS x 1 day use in pts.receiving quinine,
chloroquine or quinidine
ANTI-HELMINTHIC AGENTS
1. NICLOSAMIDE Vermicidal. No side effect except mild GI 1. Teniasis
1 gm early morning on empty Inhibits anaerobic phosphoryla- disturbances 2. H.nana
stomach repeated after 1 hr. tion of ADP by mitochondria of 3. D.latum
Purge after 1/2-1 hr. parasite.
2, MALE FERN Filicic acid in it, acts by paralysing 1. Nausea, vomiting, diarrhea T. solium, saginatum and H. nana.
(Oleoresin of Aspidium) the muscles of the parasites. 2. Headache, vertigo, tremors
Fat-free diet for 2 days Saline fits, hyperreflexia.
purgative the previous night. 3. Optic atrophy, Xanthopsia
(1 ml in capsule) 3-6 ml 2 hrs 4. Respiratory depression.
later purge
5. Myocardial depression.
6. Increased unconjugated
bilirubin
7. Renal tubular necrosis.
594
< 15 > Drugs
Drug/Dose Action Side Effects Uses
4. PIPERAZINE CITRATE Reduces the formation of succi- 1. Nausea, vomiting, diarrhea. 1. Ascariasis
For ascariasis 5 gm. single nate in the worm leading to flac- 2. Urticaria. 2. Oxyuriasis (thread worm)
dose (5 ml=750 mg). cid paralysis of the worm. Patient 3. Cerebellar ataxia, vertigo,
easily expels the paralysed worm. convulsions, blurred
vision, paresthesia.
6. BEPHENIUM HYDROXY Produces contracture of the mus- Nausea, vomiting, diarrhea. 1. Ascariasis.
NAPHTHOATE cle of the parasite. 2. Ankylostomiasis.
5 gm for adults. 3. Trichostrongylus oriental is.
2.5 gm for children
No food for 2 hrs. after the
drug.
7. MEBENDAZOLE It causes a selective and irrevers- Rarely abdominal discomfort and 1. Ascariasis.
100 mg b.d. x 3 days. ible inhibition of glucose uptake diarrhea. 2. Ankylostomiasis.
600mg t.d.s. x 21 days in in helminths resulting in their im- In higher doses 3. Trichuris trichura.
hydatid cyst. mobilisation and death. 1. Arthralgia 4. Enterobius vermicularis.
2. Dizziness, headache 5. Listeriosis
6. Tenia saginatum & solium.
7. Hydatid cyst.
10. THIABENDAZOLE Interferes with metabolic path- 1. Anorexia, nausea, vomiting, 1. Ascariasis.
25 mg/kg x 3 days. way essential for the worms. epigastric distress. 2. Ankylostomiasis.
2. Drowsiness, dizziness. 3. Thread worms.
3. Skin rash, pruritus. 4. Strongyloids.
5. Trichiniasis.
6. Trichuriasis.
14. HEXYL RESORCINOL Not known. lrritantto skin and mucous 1. Ascariasis.
Fat-free meal on previous membrane. 2. Ankylostomiasis.
night. On empty stomach 1 3. Dwarf tapeworm.
gm. swallowed 2 hrs. later. 4. Giant lung fluke.
saline purge. No food for 5 5. Thread worm.
hrs. Repeat every 3-7 days for
6. Whipworm.
3 courses.
7. Fish tapeworm.
8. Spermicide in contraceptive
jelly.
595
PRACTICAL MEDICINE
,.
Drug/Dose Action Side Effects Uses
,.
4. Hepatic or renal damage.
17. HYCANTHONE Stimulates the uptake of 5 HT Nausea, vomiting. S.haematobium and S. mansoni.
4 mg/kg orally x4 days. by non-neuronal tissue of the 2. Hepatotoxic.
2-3 mg/kg I.M.x4days. worm. It interferes with the lay- 3. Mutagenic.
ing of eggs, induces separation of 4. Minimal ECG changes.
paired worms and produces de-
generative changes in the worms
leading to death.
19. NIRIDAZOLE Destroys the vitellogenic glands 1. Reversible T wave changes 1. S. japonicum and S. mansoni.
25mg/kg x 7 days. of the female in the liver. Destroys (ECG) 2. Guinea worm.
the testes in males. The male is 2. Agitation, confusion, 3. · Amoebiasis.
immobilised in connective tissue. convulsions, hallucinations 4. Cutaneous leishmaniasis.
3. Hemolysis if G6PD deficiency
4. Nausea, anorexia.
20. ANTIMONY COMPOUNDS Destroys the larvae inside thova. ,. Hepatic damage. 1. S. haematobium.
Stibophen 1.5ml. I.M. on 2. Renal damage. 2. Leishmaniasis.
first day,2.5ml. next day. 5 3. Arrhythmia.
ml.on 3rd day up to 75ml.
Stibocaptate 3 0-50mg/kg up
,.
to2.5gm.
21. DIETHYL CARBAMAZINE Sensitises the microfilaria so 1. Anorexia, nausea, vomiting Lymphatic filariasis-Loa Loa,
1 00mg t.d.s.x21 that they become suceptible to 2. Allergic reactions. W. bancrofti, W. Malayi
phagocytosis and are fixed by the 3. Fever, headache 2. Tropical eosinophilia.
R E cells in liver sinusoids. 4. Pruritus with constitutional 3. Onchocerciasis and B.malayi
Microfilaricidal. symptoms (Mazzotti reaction, 4. Visceral Larva migrians
seen withOnchocerciasis)
,.
3. Blindness 3. Scabies
,.
Piperazine citrate ,.
Tetrachlorethylene. ,.
Piperazine citrate. ,. Lucanthone
2. Mebendazole. 2. Bitoscanate. 2. Pyrantel 2. Hycanthone.
3. Bephenium hydroxynaphtho- 3. 4-lodothymol. 3. Pyrvinium pamoate. 3. Trivalent antimony
ate 4. Bephenium hydroxynaphtho- 4. Thiabendazole. 4. Metrifonate.
4. Tetramisole. ate. 5. Mebendazole. 5. Dichlorovos.
5. Hexylresorcinol. 5. Thiabendazole. 6. Hexylresorcinol. 6. Niridazole.
6. Thiabendazole. 6. Mebendazole.
7. Diethylcarbamazine 7. Hexylresorcinol.
8. Pyrantel.
596
< 15 > Drugs
Drug/Dose Action Side Effects Uses
,.
Tapeworm Fllarlasls Guinea worms
ANTI-FUNGAL AGENTS
1. GRISEOFULVIN Acts as purine analogue and
interferes with the nucleic acid 2.
,. Nausea, vomiting, diarrhea. ,. Superficial fungal skin
infections: Teniasis capitis,
500 mg/day in 4 divided Photosensitivity.
doses synthesis. It disrupts the fungal 3. CNS: Headache, paresthesis, barbae, corporis, cruris, pedis,
spindle formation. It tightly binds vertigo, insomnia, blurring. manus
keratin and make epidermis resis- peripheral neuritis. 2. Onychomycosis
tantto fungal infection. 4. Superinfection.
5. Others: Gynecomastia,
pigmentation, proteinuria,
antabuse-like action.
,.
hypomagnesemia
6. ITRACONAZOLE Same as fluconazole Less toxic than ketoconazole Same as above and
100 mg, 200 mg BD, OD Onychomycosis, Sporotrichosis
SAPERACONAZOLE
597
PRACTICAL MEDICINE
,.
4. Pancytopenia
ANTI-VIRAL AGENTS
1. ACYCLOVIR Viral thymidine kinase converts ,. Phlebitis. Useful for systemic, ophthalmic &
,.
5-10 mg/kg IV 8 hourly. 3% acyclovir to acycloguanosine 2. Light headedness, nausea, mucocutaneous infection with
topical ophthalmic ointment, monophosphate which is phos- sweating and hypotension. Herpes simplex virus 1 & 2
in paraffin base phorylated to triple phosphate, 2. Varicella zoster virus.
a potent inhibitor or viral DNA 3. Prophylactically in
polymerase. immunocompromised host.
2. FAMCYCLOVIR Inhibits viral DNA polymerase 1. Headache ,. Herpes zoster
PENCYCLOVIR Spectrum:HSV-l,HSV-2,VZV, HBV 2. Nausea 2. Recurrent genital herpes
8 hrly. 3. Diarrhea 3. Resistant hepatitis B infection
,.
0.5% drops or ointment ap- incorporated in viral and host for topical use 2. Post-herpetic neuralgia
plied every 1-2 hrs. DNA Gastrointestinal ulceration 3. HSV keratitis
2. Bone-marrow depression
6. TRIFLURIDINE Pyrimidine nucleoside. lrrevers- Systemic toxicity 1. HSV keratitis
Topical ible inhibition of thymidylate syn- 2. Drug-resistant HSV
thetase and to some extent DNA mucocutaneous infections
,.
polymerase
7. SORIVUDINE Inhibits viral synthesis Toxic in high doses. Causes liver Herpes zoster
,.
Spectrum: VZV, HSV-1, EBV and testicular tumors in rodents. 2. Varicella infections
8. VIDARABINE Purine analogue. It inhibits viral Fluid overload 1. Herpes simplex
10-15 mg/kg/day I.V. 3% eye DNA polymerase. 2. Anemia, leukopenia 2. Varicella-zoster
ointment 3. Thrombocytopenia 3. HSV keratitis
,.
4. Neurotoxicity 4. Neonatal herpes simplex
598
( 15) Drugs
10. FOSCARNET Inhibits viral DNA polymerase 1. Nephrotoxic CMV retinitis in AIDS
Spectrum:HSV, VZV, HIV, CMV 2. Hypocalcemia
3. Hypomagnesemia
4. Hypo/ hyper phosphatemia
12. AMANTIDINE Interfereswith viral uncoating.Jn 1. CNS: Dizziness, anxiety, 1. Influenza A prophylaxis & Rx
lOOmgBD hibits ion channel function on M2 insomnia, difficulty in 2. Early parkinsonism
matrix protein on influenza virus concentration. (Reserve drug)
INTERFERON p tion through effect on B lym- confusion 4. CML, hairy cell leukemia, NHL,
INTERFERON y phocytes 6. Taste disturbances multiple myeloma, renal cell
5. Inhibits onset of delayed hy- 7. Thyroid, lupus and hemolytic carcinoma
persensitivity anemia INTERFERON{3:
Multiple sclerosis
INTERFERONr
Chronic granulomatous disease
1. ZIDOVUDINE (AZT, Nucleoside analogue. Acts by in- 1. Anemia 1. Patients with AIDS or ARC
Azidothymidine) 300 mg corporating itself into DNA of the 2. Granulocytopenia 2. Patientswith HIV infection
BO Monotherapy: Only for virus, thereby stopping the repli- 3. Cardiomyopathy CD4 +counts< 500/uL and
prevention of maternal-fetal cation process. The resulting DNA 4. Lactic acidosis plasma viremia > 20000
transmission of HIV is incomplete and cannot create a 5. Hepatomegalywith steatosis copies of HIV RNA.Im I
In combination: 200 mg TDS new virus. 6. Headache, nausea, fatigue, 3. Prevention of maternal-fetal
or 300 mg BOS malaise transmission of HIV
2 DIDANOSINE (ddl, 2'3' Dide- Nucleoside analogue 1. Pancreatitis Alone or in combinationwith AZT
oxyinosine) Action same as Zidovudine 2. Peripheral neuropathy for treatment of HIV infection
In combination: 3. Abnormal liver function tests in patientswith CD4 +counts<
200 mg BOS ifwt > 60 kg 4. Lactic acidosis 500/uL
125 mg BOS ifwt< 60 kg 5. Hepatomegalywith steatosis
Taken on empty stomach
3. ZALCITABINE (ddC, 2' 3' Nucleoside analogue 1. Peripheral neuropathy 1. In combinationwith AZT for
dideoxycytidine) Action same as Zidovudine 2. Pancreatitis treatment of patientswith
In combination: 3. Lactic acidosis CD4+ counts< 500/ul
0.75 mgTDS 4. Hepatomegalywith steatosis 2. As monotherapy for
Not to be usedwith ddl or 5. Oral ulcers advanced disease that is
antacids progressing despite AZT or
patients intolerant to AZT
4. STAVUDINE (d4T, 2'3' dide- Nucleoside analogue 1. Peripheral neuropathy 1. Adults intolerant to approved
hydro-3'-dideoxythymidine) Action same as Zidovudine 2. Pancreatitis therapies
In combination: 3. Lipoatrophy 2. Patientswhose disease is
30 mg BOS 4. Lactic acidosis progressing despite other
5. Hepatic steatosis therapies
5. LAMIVUDINE
(3TC, 2'3' dideoxy-3'-thiacyti-
Nucleoside analogue
Action same as Zidovudine
1. Peripheral neuropathy
2. Pancreatitis
,. In combinationwith
othernucleoside analogues
dine) 3. Hepatotoxicity fortreatment of HIV infection
Only in combination: 2. Hepatitis 8, C infection
150 mg BOS
599
PRACTICAL MEDICINE
1. NEVIRAPINE Stops HIV production by binding 1. Skin rash In combination with nucleoside
Monotherapy: Orally 200 mg directly to reverse transcriptase 2. Hepatotoxlcity analogues for treatment of
OD for 14 days then 200 mg and prevents conversion of RNA progressive HIV infection
BDS to DNA
In combination: 200 mgBOS
4. ETAVIRINE
1. SAQUINAVIR MESYLATE Acts on last stage of viral life cy- 1. Nausea In combination with other
In combination: (taken within de. Inhibits protease enzyme and 2. Diarrhea, headaches antiretroviral agents for
2 hrs of full meal) 1000 mg+ prevents HIV-1 from being 3. Hyperglycemia treatment of HIV infection when
100 mg ritonavirBDS successfully assembled and re- 4. Fat redistribution, lipid warranted
leased from the infected CD4+ abnormalities
T cell
600
( 15) Drugs
1. ENFUVIRTIDE Interferes with binding of HIV to 1. Local injection skin reaction Patients with persistent viremia
In combination: its receptor or co- receptor or with 2. Bacterial pneumonia rate after treatment with other ARV
90 mg SC lnj. BDS the process of fusion increased agents
3. Hypersensitivity reactions
INTEGRASE INHIBITOR
CCR5 ANTAGONIST
ALCOHOL
,. ETHYL ALCOHOL 1. Systemic actions are toxic and
not discussed here.
1. Acute alcoholism 1. Systemic: Methyl alcohol
poisoning
Loading dose 0.6 g/kg 10 g/ 2. Chronic alcoholism
hr infusion in methyl alcohol 2. Local actions: irritant, germi- 3. Alcohol related systemic 2. Local: Symptomatic treatment
poisoning. cidal, astringent, antiseptic, damage for fever, antiseptic (70%
and cosmetic/cooling effect. cone), prevention of bed
3. 1 gm of alcohol= 7.1 calories, sores, wash out phenol
but these are empty calories. 3. Local inj. to destroy ganglia
e.g. trigeminal neuralgia
4. Percutaneous ethanol inj. as a
sclerosant e.g. autonomously
functioning solitary thyroid
nodules.
2. DISULFIRAM 1. Interferes with oxidation of 1. Nausea, vomiting Alcohol de addiction, should be
100-200 mg daily 800 mg on acetaldehyde formed during 2. Metallic taste given in hospital only.
day 1 CARBIMIDE alcohol metabolism 3. Headache, drowsiness,
2. Inhibits dopamine beta-oxi- cramps
dase, thus depletes catechol- 4. Severe acetaldehyde reaction
amines
ANTI-MALIGNANCY AGENTS
,. CYCLOPHOSPHAMIDE
SO mg. tablet.
1. Damages the nuclei of grow- 1. Anorexia, nausea, vomiting
ing and multiplying cells. This 2. Bone marrow depression
1. Lymphomas and Hodgkin's
disease.
100-200 mg powder in vial for affects hemopoietic system, leading to anemia, leucope- 2. Acute leukemias.
injections I.M. or I.V. 2-3 mg/ epithelial tissues, germinal nia and thrombocytopenia 3. Bronchogenic carcinoma.
kg. In combination therapy epithelium of the gonads and 3. Depress spermatogenesis 4. Multiple myeloma.
with other drugs150 mg for hair follicle. Latter causes alo- in males. Amenorrhea in 5. Ovarian carcinoma and semi-
5 days every1S-30days for6 pecia. females. nomas.
courses. 2. It suppresses the antibody 4. Fetal abnormalities if given
6. lmmunosuppressant as in
production and immune re- during pregnancy. steroid resistant nephrosis,
sponse. 5. Hemorrhagic cystitis. transplantation, etc.
7. Mycosis fungoides.
2. MELPHALAN Similar to cyclophosphamide 1. Bone marrow depression Multiple myeloma
2 mg tablets4-6 mg for 2. Nausea vomiting
3 weeks repeated after1 3. Alopaecia.
month. 4. Oral ulceration
3. CHLORAMBUCIL Similar to cyclophosphamide Similar to cyclophosphamide Chronic lymphocytic leukemia
5-10 mg for 3 weeks. but no alopecia or hemorrhagic
cystitis
601
PRACTICAL MEDICINE
10. VINCA ALKALOIDS Inhibits mitosis at metaphase. 1. Nausea, vomiting, 1. Acute lymphoblastic
VINCRISTINE constipation leukemia (vincristine).
1.4 mg/sq.m 2. Alopecia. 2. Hodgkin's lymphoma
VINBLASTINE 3. Neurotoxicity: Peripheral (Vinblastine)
0.1 mg/kg body wt. neurits, cranial nerve palsy, 3. Choriocarcinoma
ataxia, tremors, mental (Vinblastine).
depression, marrow
depression (more with
Vinblastine).
11. RUBIDOMYCIN It acts by inhibiting DNA-depen- 1. Bone-marrow depression. Acute myeloblastic leukemia in
40 mg/m/day. I.V. dent RNA synthesis. 2. Allergic reaction. combination with Vincristine and
3. Myocardial depressant. prednisolone.
12. ADRIAMYCIN Binds to DNA and inhibits DNA 1. Myelosuppression. 1. Acute lymphoblastic
20-30 mg/day for 2-3 days. synthesis. Binds myocardial DNA 2. G.I. disturbances & stomatitis leukemia.
which may cause cardiomyopa- 3. Alopecia. 2. Lymphoblastic
thy. 4. Cardiomyopathy. lymphosarcoma.
13. BLEOMYCIN Causes DNA nicking. Inhibits DNA 1. Pneumonitis leading to 1. Epidermoid carcinoma of skin,
10-20 units I.V. or I.M. or S.C. ligases important for DNA replica- pulmonary fibrosis. respiratory & oral cavity &
twice a week. tion, recombination and repair. 2. Dermographic and sclero- genito-urinary tract.
derma-like skin changes. 2. Lymphomas.
14. MITHRAMYCIN Interferes with RNA synthesis. 1. Myelosuppression. 1. Embryonic cell carcinoma of
25 ug/kg/day. l.V. for 1 day. 2. Liver and kidney damage. testis
3. Bleeding due to suppresssion 2. Hypercalcemia of malignancy
of clotting factors. 3. Paget's disease
15. o'-p DDD (Mitotane) It gets selectively concentrated in 1. Anorexia, nausea, lethargy, Malignant neoplasms of adrenal
8-1 Ogm orally for4-8 wks. adrenal cortex and destroys it. drowsiness. cortex.
followed by 4 gm as mainte- 2. Addison's disease.
nancedose.
602
( 15) Drugs
17. CYTOSINEARABINOSIDE Inhibits DNA polymerase, dur- 1. Nausea, vomiting. 1. Acute myeloid leukemia.
2-4 mg/kg IV for 2 days ing the 'S' phase of the cell cycle. 2. Bone marrow depression. 2. Hodgkin's disease and
Maintenance dose 1 mg/kg/ Suppresses humoral and cellular lymphoma.
week S.C. immunity.
19. CARMUSTINE (BCNU) It acts by alkylation of DNA and 1. Myelosuppression 1. Hodgkin's disease
other nucleoproteins and the car- 2. Nausea, vomiting 2. Meningeal leukemia
bamylation of lysine residues on 3. Pulmonary fibrosis 3. Tumours of the brain
proteins. 4. CNS toxicity.
20. PROCARBAZINE It causes degradation of DNA and 1. Myelosuppression 1. Hodgkin's disease
50-300 mg 2-3 times a day protein synthesis. 2. Nausea, vomiting, CNS 2. Oat cell carcinoma of lung
toxicity
3. Hypertension with tyramine
containing food due to MAO
inhibition.
21. CISPLATJN It binds to DNA, nuclear and cyto- 1. Renal impairment 1. Solid tumours
20-30 mg daily upto 1SO mg plasmic proteins. 2. Nausea, vomiting 2. Testicular tumours
I.V. 3. Anaphylaxis 3. Ovarian carcinoma
4. Hearing loss for high
frequency
22. PACLITAXEL Inhibits microtubule formation 1. Suppresses bone marrow 1. Ovarian and breast cancers
35 mg/sq.m. 2. Myalgia 2. Lung, esophagus, head and
3. Cardiotoxicity neck cancers
23. ETOPOSIDE Plant glycoside which arrests cells 1. GI toxicity 1. Lymphomas, acute leukemias
50-100 mg/sq.m. inG2 phase 2. Myelos�ppression 2. Testicular & bladder cancers
3. Neuritis 3. Trophoblastic disease
4. Small cell lung cancer
24. FLUTAMIDE Anti-androgen, anti-estrogen GI toxicity, Mucositis, CNS 1. Advance CA prostate
250 mgTDS disturbances 2. Refractory hirsutism
25. HYDROXYUREA DNA inhibitor; inhibits ribonucle- 1. Myelosuppression 1. CML, myeloma, P. vera
30-80 mg/kg oside diphosphate reductase. 2. Skin and GI disturbances 2. Thrombocytosis
3. Neurological disturbances 3. Sickle cell anemia HIV/AIDS
HEMOPOIETIC DRUGS
1. HEPARIN Refer Pg. 566
2. PROTAMINE SULFATE Because it is a strongly basic com- Hypotension, dyspnea, To neutralise the excess anti-
(1% solution). 1 mg neutral- pound it neutralises the acidic bradycardia, flushing and feeling coagulant effect of heparin.
ises 100 units of heparin. It is group in heparin thereby abolish- of warmth. Protamine sulfate itself has
given slowly I.V. not to exceed ing the anticoagulant activity. anticoagulant activity and hence
50 mg over 10 minute. its dose should not exceed 50 mg.
over 10 mins.
3. COUMARIN-DERIVATIVES: 1. Suppress the formation of 1. Hemorrhage. Oral anti-coagulant action takes
BISHYDROXYCOUMARIN factors II, VII, IX and X from liv- 2. Allergic manifestations. 2-3 days to occur and remains
(WARFARIN) (5 mg. tablets) er by blocking the utilisation 3. G.l.upset. for 2-3 days after the drug is
10-20 mg. oral for 3 days of vitamin K due to structural 4. Alopecia. withdrawn.
followed by further dose similarity.
depending on Prothrombin 2. Uricosuric by interfering with
time and International the renal tubular reabsorp-
Normalized Ratio (INR) tion of urate.
603
PRACTICAL MEDICINE
4. EPSILON AMINO It blocks the activation of Plas- 1. Nasal stuffiness. Excessive fibrinolysis as in
CAPROIC ACID (EACA) minogen by competitive block- 2. Abdominal discomfort, abruptio placentae, post-partum
5 gm. initially followed by 1 ade and thus reduces the fibrino- nausea, vomiting, diarrhea. hemorrhage, snakebite, etc.
gm. 1 hrly. l.V. till satisfactory lytic activity. 3. Skin rash.
response. 4. Hypotension.
7. PARENTAL IRON Same as above. 1. Local pain, inflammation and 1. Failure to absorb oral iron.
Iron dextran, lron-carbohy- discoloration of skin. 2. Intolerance to oral iron.
drate complex. 50 mg/ml. of 2. Anaphylaxis, Headache 3. Exhausted iron stones when
elemental iron I.M. 20 mg/ml fever, arthralgia, tachycardia, daily iron loss exceeds the
of elemental iron I.V. flushing, circulatory collapse absorption of oral iron.
and even death. 4. Severe iron deficiency
anemia in late pregnancy.
5. Unreliable patient.
8. VITAMINK Vit. K is essential for blood coagu- 1. Anaphylaxis following. l.V 1. AdultVit K deficiency
2.5 - 25 mg orally OR lation (Biosynthesis of prothrom- administration (malabsorption syn.,
0.5 - 1 mg SC or IM OR bin, factors VII, IX and X) and pro- 2. Hemolytic anemia obstruction.jaundice,
0.5 - 25 mg IV ( < 1 mg/min) tein C and Protein S. 3. Hyperbilirubinemia malnutrition)
4. Kernicterus 2. Vit K deficiency in infants
following acute diarrhea
3. Neonatal Vit K deficiency
4. Bleeding state during oral
anticoagulant therapy.
11. MOLGRAMOSTIM (GM-CSF) Granulocyte -macrophage colony 1. Mild and transient 1. Lymphomas
5-10 mcg/kg/day stimulating factor 2. AML- post-chemotherapy
3. Adjuvant to cancer
chemotherapy or gangciclovir
4. Myeloblastic syndromes
5. Aplastic anemia
Other drugs are: Cyanocobalamin and Folic acid (Refer Pg. 13)
CHELATING AGENTS
1. DIMERCAPROL SH groups of Dimercaprol bind 1. Vomiting 1. Poisoning due to arsenic,
(British Anti Lewisite) the metals (As, Hg, Cu, Au, Bi, Ni) 2. Tachycardia, sweating, rise in bismuth, mercury, nickel
300 mg/day I.M. BP 2. Lead poisoning as adjuvant
SUCCIMER- Chemical analog 3. Inflammation of mucous 3. Wilson's disease, copper
of dimercaprol orally membranes poisoning: as an adjuvant to
4. Cramps poisoning: as an adjuvant to
penicillamine.
2. CALCIUM DISODIUM EDE- Exchanges Calcium for metals like 1. Proximal tubular necrosis 1. Lead poisoning
TATE Pb, Zn, Mn, Cu, Cd. The complex is 2. Anaphylaxis 2. Poisoning with zinc, copper,
1 gm IV over 1 hr, b.d. for 3 to 5 then excreted in urine. 3. Acute febrile reaction iron, manganese & radio-
days active metals- plutonium etc.
3. Porphyria
604
( 15 > Drugs
3. d- PENICILLAMINE Chelates Cu, Hg, Pb, Zn. 1. Anorexia, nausea, loss of taste 1. Wilson's disease
250 mg b.d. to q.i.d. 1 hr sensation 2. Copper poisoning
before or 2 hrs after meals 2. Rash 3. Mercury, lead poisoning
ACETYL d-PENICILLAMINE 3. Renal toxicity 4. Cystinuria and cystine stones,
1 gm total dose t.d.s./q.i.d. 4. Bone marrow depression hemosiderosis
5. Rheumatoid arthritis and
scleroderma
6. Primary biliary cirrhosis
4. DESFERRIOXAMINE Forms a stable complex with fer- 1. Allergic reactions l. Iron overload: in patients
0.5-1 gm/day IM in iron over- ric iron. This is excreted in urine. 2. Cramps who receive repeated blood
load DTPA and L1 are other 3. Pain in abdomen transfusions, e.g thalassemia
iron chelators 4. Fever 2. Hemachromatosis
5. Dysuria 3. Acute iron toxicity
s. TRIENTINE 400-800 mg t.d.s Similar to d-penicillamine Similar to d-penicillamine, but Wilson's disease
before meals less toxic
2. CLOMIPHENE CITRATE Ovulation inducer. Inhibits nega- l. Rare, Abd. pain, bloating, 1. Anovulatory infertility
50 mg from day 5 for 5 days tive feedback mechanism which blurred vision, multiple 2. Male infertility
suppresses release ofGNRH. pregnancies.
3. OCTREOTRIDE Synthetic analogue of soma- 1. Veryfew 1. Acromegaly
0.05-0.1 mg S.C. BO tostatin 2. Local pain,GI 2. Gut endocrine tumors
Growth hormone inhibitor 3. Hematemesis
4. After pancreatic surgery
4. GROWTH HORMONE Somatropin stimulates growth 1. Veryfew l. Short stature due toGHD
4, 12, 16,361U esp. in children with GH deli- 2. Unmasks hypothyroidism 2. Short stature due to
0.1 IU/kg/day SCat night ciency. 3. Lipo-atrophy CRF,Turner's synd. & other
Anabolic action. 4. Urticaria secondary causes
3. Catabolic states like burns,
critical care
4. Pan-hypopituitarism;
aging; andropause (male
menopause)
5. AdultGHD
s. DESMOPRESSIN Vasopressin analogue which acts 1. Water intoxication 1. Cranial diabetes insipidus
2-4 mcglday SC/IV BD on V2 receptor linked adenyl cy- 2. Dilutional hyponatremia 2. Pituitary neurosurgery
Nasal spray 20-40 mcg/day clase system on the collecting 3. Nausea, headache, nasal 3. Nocturnal anuresis
TERLIPRESSIN tubule. congestion, epistaxis 4. Renal function testing
1-2 mg lV 4. Vasopressin is cardiotoxic 5. Hemophilia A, von
VASOPRESSIN Willebrand's disease
5-20 IU SC/IV 6. Bleeding esophageal varices
605
PRACTICAL MEDICINE
7. THIOAMIDES They inhibit the organic binding 1. Allergic: Skin rash fever 1. Hyperthyroidism
Propylthiouracil of iodine,both iodination of tyro- arthralgia,lymphadenopathy 2. To induce hypothyroid state in
Up to 600 mg.qds. sine as well as coupling of lodoty- 2. Blood: Leucopenia, conditions like severe angina
Methimazole 5-20 mg/day rosines. agranulocytosis, or intractable cardiac failure.
8. IODIDES The exact mechanism is not 1. lodism: Skin rash,rhinorhea, 1. Pre-operative in thyroid
Sodium or Potassium 6-10 known. It rapidly shuts off the re- lacrimation,salivation. surgery to reduce vascularity.
mg/day. lease of thyroid hormone which 2. Goitre and myxedema. 2. To control hyperthyroidism
gets stored in the colloid material 3. Precipitate thyrotoxicosis. rapidly e.g. CCF.
of thyroid.
9. RADIOACTIVE IODINE Radio-active iodine emits gamma 1. Hypothyroidism. Hyperthyroidism. The effect
5-10 ug. on empty stomach. and beta rays. Beta rays destroy 2. Genetic damage. becomes apparent by 3-4 wks.
thyroid follicles and produce ti- 3. Thyroid car�inoma. and is maximum after 3-4 months.
brosis. 4. Damage to fetal thyroid if
given during pregnancy.
606
( 15 > Drugs
11. ESTROGEN & ITS 1. Major estrogen in premeno- 1. Endometrial hyperplasia and 1. Hormone replacement
DERIVATIVES pausal women malignancy therapy
CONGUGATED ESTROGENS 2. Addition of 17-a-ethyl gp en- 2. Ca breast 2. Menopause
0.625 mg0D hances oral activity 3. Thrombosis 3. Oral contraception
ETHNYL ESTRADIOL 0.01, 3. Promotes endometrial 4. Hypertension 4. Endometriosis
0.02, o.os mg, growth thickening, stratifica- 5. Nausea,vomiting 5. Dysfunctional uterine
E2GEL tion & cornification of vagina 6. Fluid retention, wt.gain, bleeding
TRAN5DERMAL 4. Inhibits anterior pituitary increased appetite 6. Carcinoma breast, prostate
THERAPEUTIC SYSTEM 5. Capillary dilation, fluid reten- 7. Depression 7. Osteoporosis
ESTRADIOL 0.025, 0.05, 0.1 mg/day tion 8. Decreased libido, impotence 8. Atrophic vaginitis
ESTRIOL 1 mg, 2 mg 6. Protein anabolism 9. Fungal infection
17-� ESTRADIOL 3 mg per 5 gm gel 7. Contraception
ESTRADIOL VALERATE 10 mg/ml
12. PROGESTERONE and PRO- 1. Progesterone prepares uterus 1. GI disturbances 1. Premenopausal syndrome
GESTROGENS for receiving the fertilised 2. Acne, breast discomfort 2. Anovulation- amenorrhea
NATURAL MICRONISED ovum & suppresses uterine 3. Fluid retention,edema, 3. Benign mastopathy
PROGESTONE 100 mg capsi motility. weight gain 4. Menopause
HYDROXYPROGESTONE 2. Can inhibit ovulation, 4. Rash, depression 5. Threatened,habitual abortion
CAPROATE prolonged uterotrophic 5. Hepatotoxic 6. Luteal phase defects
250-500 mg IM weekly effects, stimulates luteal 6. Virilisation 7. Mild to moderate endometriosis
MEDROXYPROGESTERONE action 7. Thromboembolism 8. Contraception
ACETATE 3. Some androgenic & anabolic 8. Ectopic pregnancy 9. DUB, Menorrhagia,
5-10 mg daily 5-10 days orally effects but no estrogenic Metropathia hemorrhagica
150 mg depot every 12 weeks effects. 10. Dysmenorrhagia
DYDROGESTHONE 10 mg
BDS/TDS
ALLYLOESTENOL 5-10 mg OD
NORETHISTERONE 5-20 mg
ORALLY
13. TESTOSTERONE & ITS Male sex hormone 1. Water,Na and K retention 1. Hypogonadism
DERIVATIVES 2. Anabolic 2. Impotence
TESTOSTERONE DEPOT 3. Virilisation 3. Gynecomastia
100,250 mg IM 3-weekly 4. CNS effects 4. Delayed puberty
DIHYDROTESTOSTERONE GEL 5. Stunting of growth 5. Controversial: aging,
2.5 gm eunuchoidism, sexual
MESTRALONE 25 mgTDS frigidity, aplastic anemia,
menorrhagia, metropathia
hemorrhagica.
3. SULFONYLUREAS 1. Stimulate the release and syn- 1. Allergic reaction: Skin rash, 1. Maturity onset diabetics who
(Before food) thesis of insulin. leucopenia, aplastic anemia. are without complication and
a. Tolbutamide 0.5-1 2. Prolonged use stimulates the 2. Goitre. with FBS less than 300 mg%.
gm.TDS proliferation of islet cells. 3. Potentiates action of ADH. 2. Diabetes insipidus
b. Chlorpropamide 3. Inhibits gluconeogenesis and 4. Cholestatic jaundice. (Chlorpropamide).
0.25- 0.5 gm TDS glycolysis. 5. Increased risk of mortality 3. Diagnosis of insulinomas and
C. Glibenclamide from cardiovascular deaths. diabetes.
5-20 mg OD or BDS
d. Glipizide
5-20 mg OD or BDS
e. GLICAZIDE40-80 mgTDS
f. GLIMPERIDE 1-2 mg OD
4. BIGUANIDES (after food) 1. Stimulate the peripheral utili- 1. Bitter metallic taste, nausea, 1. Obese, type II diabetes
a. Phenoformin : 25 mg. sation of glucose. vomiting, abdominal 2. Adjuvant in juvenile diabetics
tablets up to 8 tablets per 2. Correct insulin insensitivity of discomfort. who have marked fluctuations
day. muscles. 2. Lethargy, weakness, wt. loss. of glucose levels. Biguanides
b. Metformin: 500 mg 3. Interferes with glucose ab- 3. Anaphylactic reaction. help to smoothen the control
tablets upto 8 tablets per sorption. 4. Lactic acidosis. of blood sugar by insulin.
day. 850 mg BD 4. Inhibits insulin degradation. 5. Decreases hepatic glycogen, 3. Insulin resistance
inhibits lipogenesis and 4. Polycystic ovarian syndrome
increases fibrinolytic activity
of plasma.
s. A LPHA GLUCOSID ASE Alpha glucosidase inhibitor. 1. Flatulence and abdominal 1. NIDDM
INHIBITORS Interferes with absorption of glu- bloating 2. IGT
A C A RBOSE case from the gut. 2. Transient transaminitis 3. Adjuvantto insulin in type I
50 to 100 mg given
with each meal
VAGLIBOSE, MIGITOL
6. GLITAZONES Activates PPAR"'Y (perioxime pro-
liferation activated receptor)
1. Hepatotoxicity ,. Insulin resistance
(INSULIN SENSITISERS) 2. Hypoglycemia 2. Type 2 DM
TROGLITAZONE (banned} 3. GI Intolerance 3. Polycystic ovarian syndrome
ROSIGLITAZONE 2,4, 8 mg
PIOGLITAZONE given with meal
7. MEGLITINIDES Non-sulyphonyl urea, acts on a 1. Hypoglycemia 1. Adjuvant in Type 2 DM
REPAGLINIDE 0.5, 1, 2 mg special receptor on the beta cell 2. Headache 2. Diabetics with erratic eating
NATEGLINIDE given with meal habits (dose only with meal}
3. Fasting states
4. Chronic renal insufficiency
8. INCRETINS
1. INCRETIN MIMETICS Long Acting GLP 1 Agonist 1. Nausea, vomiting, stomach Type 2 DM: Monotherapy as
a. Exenatide: 5- 10 mcg SC discomfort initial treatment or Combination
twice a day, 1 hour before 2. Headache therapy
meals 3. Hyperglycemia
b. LIRAGLUTIDE: 1.2-1.SMG 4. Pancreatitis, Nesidioblastosis
SC once a day (rare)
2. INCRETIN ENHANCERS Dipeptidyl peptidase (DPP} IV In- 1. Nausea Type 2 DM: Monotherapy as
(DPP IV INHIBITORS} hibitors 2. Headache initial treatment or Combination
a. Vildagliptin, 50mg twice 3. Hypersensitivity and Skin therapy
a day Reactions
Sitagliptin, 100 - 200 mg
per day
608
< 15 > Drugs
Drug/Dose Action Side Effects Uses
2. FIBRATES It reduces VLD L, LDL production Increases the risk of gall stones. 1. Type lll,IVand V
GEMFIBROZIL in the liver. hyperlipidemias.
300,600 mg BD or TDS 2. Hypertriglyceridemia
BEZAFIBRATE
200-400 mg TDS
FENOFIBRATE micronised
3. CLOFIBRATE It inhibits the hepatic synthesis 1. Nausea, diarrhea,weight gain. 1. To reduce plasma lipid.
2-3 gm/day. of cholesterol and transfer of tri 2. Allergy 2. Atherosclerotic arterial
glycerides from the liver to the 3. SGOT may rise disease.
plasma. 4. Displaces drugs like 3. Angina.
tolbutamide & coumarin
derivatives from their plasma
binding sites & hence the
dose of these drugs must be
reduced.
4. PROBUCOL Lowers both LDL and HDL choles- 1. Diarrhea Type Ill,IV and V hyperlipidemias.
terol. 2. Prolonged QT,
3. Liver damage.
GASTRO-INTESTINAL DRUGS
1. ALUMINIUM HYDROXIDE 1. Al (OH)3 combines with HCI 1. Constipation. 1. Non-systemic antacid
Al (OH)3 4-8ml. hrly. orally. in stomach forming AICl3 and 2. It prevents absorption of astrigent and demulcent.
H20; thus neutralizing acid. phosphates which may rarely 2. To prevent phosphate reab
2. It has astringent and demul lead to osteomalacia. sorption as in chronic renal
cent properties, by which it 3. It interferes with the failure or phosphatic renal
forms a protective coating absorption of tetracyclines, calculi.
over ulcer. corticosteroids, iron, 3. To control bile salt diarrhea
anticholinergic drugs, etc. 4. To treat ectopic calcification.
2. MAGNESIUM TRISILICATE Similar to Aliminium hydroxide Diarrhea 1. Antacid
2-4gm/day 2. Cathartic
3. SODIUM BICARBONATE 1. NaHC03 combines with HCI 1. Systemic alkalosis. 1. Systemic antacid.
NaHCO, 2 gm. 2 hrly. in stomach to from NaCl 2. Retention of sodium. 2. Metabolic acidosis.
2. Eructations due to CO, liber 3. Rarely it may precipitate 3. To render urine alkaline in
ated during neutralisation peptic perforation in a urinary tract infections or
gives a sense of abdominal patient with gastric ulcer to prevent precipitation of
discomfort. This is carmina due to distension caused by sulfonamides or uric acid.
tive action. liberated co,. 4. Locally: Antipruritic lotion. for
mouth or eye wash, douche,
enema, and to loosen wax in
the ears.
4. CARBENOXOLONE Exact mechanism not known. 1. Water and sodium retention 1. Peptic ulcer.
50-100 mg TDS for 48weeks. 1. It probably acts by stimulat which may precipitate cardiac 2. Aphthous ulcer (Lozenges
ing mucus secretion. failure and hypertension. containing S mg).
2. It also stimulates collagen ac 2. Hypokalemia.
tivity and epithelisation at the 3. Headache.
base of the ulcer. 4. Heart-burn.
5. H2-RECEPTOR ANTAGONISTS 1. Abolishes histamine stimu 1. Blood dyscrasias. 1. Peptic ulcer.
CIMETIDINE 1000 mg/day lated gastric and acid secre 2. Skin rash 2. Esophagitis
RANITIDINE 300 mg/day tion and flushing 3. Hepatotoxicity 3. Stress ulcers
FAMOTIDINE 40 mg/day 2. Inhibits gastric H2 receptors, 4. Gynecomastia. 4. Zollinger Ellison syndrome
ROXATIDINE ACETATE this reduces basal, 24 hours 5. VPBs,AVblock 5. Gastro-oesophageal reflux
and nocturnal acid secretion
75 mg BDS x 8weeks 6. Decreased libido N.B. Has no anti-androgen action.
as well as Pepsin
Reduce to 75 mg on alt. days 7. Leucopenia Does not interfere with hepatic
2. Has mucosal protective ac- drug metabolism.
if Cr clearance 20-50 ml/min.
tion
6. PROTON PUMP INHIBITORS It causes irreversible inactivation Reduced acidity in stomach may 1. Duodenal and gastric ulcer
OMEPRAZOLE of H-K-ATpase. This prevents the predispose the person to enteric 2. Zollinger Ellison syndrome
20 mg daily up to 600 mg for exchange of K with H and thus infections. 3. Reflux esophagitis.
4-8weeks reduces the secretion of H and in 4. Mastocytosis
LANZOPRAZOLE 30 mg OD creases pH in stomach.
5. Multiple endocrine neoplasia
PANTOPRAZOLE
609
PRACTICAL MEDICINE
19. DIPHENOXYLATE ATROPINE Inhibit intestinal motility. Hence Paralytic ileus. Anti-diarrheal.
5 mg. diphenoxylate they reduce"intestinal hurry�
0.20mg. atropine
20. DIMETHYPOLY Acts as a defoaming agent thus Non-toxic. Flatulence, bloating and
SILOXANE allowing easy escape of gases distension.
40mg tabletsTDS from GI tract.
610
< 15 > Drugs
Drug/Dose Action Side Effects Uses
21. LOPERAMIDE It interacts with the acetyl cho- 1. Dry mouth. Acute and chronic diarrhea.
4 mg initially followed by 2 line release at the nerve endings 2. Nausea.
mg after each loose stool up and intra-mural ganglia causing 3. Drowsiness.
to 16 mg in 24 hrs. sustained inhibition of peristaltic
activity.
22. METOCLOPRAMIDE Increases the resting tone of the 1. Extra-pyramidal reactions, 1. Functional GI disorders
10 mg TDS orally gastroesophageal sphincter and usually transient and 2. Vomiting.
10 mgl.M. stimulates co-ordinated gastric disappear within 24 hrs. on 3. Non-Ulcer dyspepsia
movements to speed up gastric stopping the drug. 4. Pre-anesthetic medication
emptying. It blocks dopaminergic 2. Gynecomastia Galactorrhea 5. Persistent hiccough
receptors. 3. Diarrhea, dizziness, skin rash 6. Gastroparesis due to diabetes,
scleroderma, etc.
23. DOMPERIDONE Antagonises the inhibitory effects 1. Dry mouth, thirst, diarrhea Similar to.Metoclopramide. Extra
10 mg three to fourtimesa of dopamine and enhances gas- 2. Galactorrhea & gynecomastia pyramidal reactions do not occur
day before food. tric motility.This enhances gastric 3. Skin rash as it does not cross the blood
emptying and prevents vomiting. 4. Headache. brain barrier.
24. CISAPRIDE Acts at the myenteric plexus of Mild, related to GI tract. No 1. Delayed gastric emptying
10-40 mg/day 15 min before the gut causing increased release endocrine or extra-pyramidal 2. Non-ulcerdyspepsia
meals. of acetylcholine. It increases gas- effects. 3. Reflux esophagitis
tric and intestinal motility and 4. Chronic constipation
lowers esophageal pressure.
25. BILE SALTS Choleretic agents; therefore dis- 1. Diarrhea 1. Medical dissolution of gall
CDCA 10-15 mg/kg/day solve gall stones. 2. Hepatotoxicity stones, sp. cholesterol &
URSODEOXYCHOLIC ACID radiolucent stones
13-15 mg/kg/day. 2. Primary biliary cirrhosis
ELECTROLYTES
1. POTASSIUM Hyperkalemia: cardiac arrhyth 1. Hypokalemia: Diabetic ketoacidosis, severe diarrhea hypokalemic
IV (2 meq/ml): only given in a mias neuromuscular effects. periodic paralysis
drip. 2. Forced alkaline diuresis: barbiturate poisoning
3. Glucose-potassium-insulin drip for Ml
4. With IV fluids
5. Paralytic ileus
Oral (syrup) 1. With non potassium-sparing diuretics
2. With digoxin therapy
3. Mild hypokalaemia
611
PRACTICAL MEDICINE
PLASMA EXPANDERS
1. DEXTRAN 1. Cheaper than other plasma 1. May interfere with blood 1. Uses as substitutes for plasma:
Dextran-150 expanders. grouping and cross matching e.g. burns hypovolemic shock,
Dextran-70 2. Action lasts for 24 hours 2. Can cause hypersensitivity endotoxic shock, extensive
Dextran-40 3. Dextran-40 decreases RBC 3. Can disturb coagulation and trauma
sludging and improves mi- plateletfunction. 2. Temporary replacement for
crocirculation blood loss.
4. Can be stored for many years.
2. Degraded gelatin 1. Does not interfere with blood 1. More expensive Same as above. Can be used for
(Hemaccel) grouping and cross matching priming heart-lung machines and
2. Hypersensitivity is rare. dialysis machines.
612