Internal Medicine Form 1:

Answers with explanations from UpToDate

1. E. Vancomycin : here ceftazidime covers gm -ve & vanco will do gm +ve.

EXP: Central venous catheter (CVC) use has increased substantially, and associated infections have
become a frequent complication of catheter use. CVC infection rates are highest with short-term
noncuffed, nontunneled hemodialysis and multilumen catheters, and lowest with subcutaneous central
venous ports.

catheter-related bacteremia can arise from one of two sources [13]:

Migration from the skin along the outside of the catheter into the bloodstream. The Dacron cuff in
tunneled catheters typically incites an inflammatory response with fibrosis that, in turn and in time, may
create a mechanical barrier to migration of bacteria from the skin along the outside of the catheter.

Direct inoculation from a biofilm containing pathogenic micro-organisms that may form on the inner
surface of the catheter

Most catheter-related infections are caused by staphylococci and gram-negative bacilli; therefore,
antibiotics commonly used in antibiotic lock therapy (ALT) include vancomycin, cefazolin, ceftazidime,
ciprofloxacin, and gentamicin.(UPTODATE).

2. (A) ALS: AMYOTROPIC LATERAL SCLEROSIS:

The diagnosis of ALS is suggested when there are progressive symptoms consistent with upper and
lower motor neuron dysfunction that present in one of four body segments (cranial/bulbar, cervical,
thoracic, and lumbosacral) followed by spread to other segments over a period of months to years. The
course is not relapsing and remitting, but rather is insidiously progressive. Involuntary weight loss and
muscle wasting unrelated to nutrition may also occur.

Physical examination

Lower motor neuron signs include weakness, atrophy and fasciculations.

Upper motor neuron signs include the following:

Increased tone and increased extremity deep tendon reflexes .

The presence of any reflexes in muscles that are profoundly weak and wasted
Pathologic reflexes such as crossed adductors, a jaw jerk, or Hoffman sign .

The syndrome of pseudobulbar affect, which consists of inappropriate laughing, crying, and/or forced
yawning

The Babinski sign (reflex great toe extension, often with fanning of the small toes, with lateral plantar
stimulation) is present in about one-half of patients with ALS , but is a definitive indicator of upper
motor neuron pathology when present . Lateral plantar stimulation normally produces reflex toe flexion
without other leg or foot movement. Triple flexion occurs when plantar stimulation produces reflex
great toe extension, flexion of the knee, and flexion of the hip.
3.(A) Ig A defeciency : Recurrent sinopulmonary infections

Autoimmune disorders

Gastrointestinal infections and other intestinal disorders

Allergic disorders

Anaphylactic transfusion reactions

4. c. obtain CT without consent.

5. Warfarin :
Anticoagulant therapy is effective in reducing the risk of systemic embolization in patients with
nonvalvular atrial fibrillation (AF). Anticoagulation with warfarin, dabigatran, rivaroxaban, apixaban, or
edoxaban reduces this risk by almost 70 percent, and should be considered for most nonvalvular AF
patients.

recommendations for anticoagulant therapy in patients with nonvalvular AF are as follows

For patients with a CHA2DS2-VASc score 2 chronic anticoagulation (Grade 1A).

For patients with a CHA2DS2-VASc score of 1,The risk factor present may influence decision making.
Age 65 to 74 years is a stronger risk factor than the other features conferring a CHA2DS2-VASc score of
1.

For patients with a CHA2DS2-VASc of 0 =we suggest no anticoagulant therapy (Grade 2C). Patients
who are particularly stroke averse and who are at low bleeding risk may reasonably choose
anticoagulation.

6. a. ACTH STIMULATION TEST

adrenal insufficiency : Pt has hypotension, hyponatremia, hyperkalemia.

most patients with adrenal insufficiency have the following:

Chronic malaise,Lassitude,Fatigue that is worsened by exertion and improved with bed rest
Weakness that is generalized, not limited to particular muscle groups,Anorexia

Weight loss, hypotension,

7.E LACTIC ACID .

8.H RHABDOMYOLYSIS : HERE ITS THE ONLY OPTION I THINK WOULD LEAD TO BLOOD IN URINE.

9. E, GIVE IV 0.9%SALINE

10. C, INDOMETHACIN, acute gout here

treat most patients able to take an oral medication with a nonsteroidal antiinflammatory
drug (NSAID).
An oral low-dose colchicine regimen may be used in patients who are able to take an oral
medication but who have contraindications to NSAIDs (eg, moderate or more severe
chronic kidney disease [CKD], active peptic ulcer disease, or a history of
NSAID-intolerance
In patients with contraindications to the use of both NSAIDs and colchicine, we prefer
intraarticular, oral, or parenteral glucocorticoids, depending upon the number of involved
joints, the experience of the clinician with joint injection techniques, and the need, if
present, for parenteral rather than orally administered.
11. B Drug reaction is the only option left here as rest all are negative.
Drug fever: Clinicians are universally aware of the common occurrence of fever caused by drugs,
although reliable data on incidence are not available. Fever can be the sole manifestation of an adverse
drug reaction in 3 to 5 percent of cases. The risk of developing drug fever increases with the number of
drugs prescribed, especially in elderly patients. Patients with HIV infection also appear to have an
increased susceptibility to drug reactions of all types, including fever. Failure to recognize the etiologic
relationship between a drug and fever often has undesired consequences including extra testing,
unnecessary therapy, and longer hospital stays.(See 'Introduction' above).

Drug fever can be defined as "a disorder characterized by fever coinciding with administration of a
drug and disappearing after the discontinuation of the drug, when no other cause for the fever is
evident after a careful physical examination and laboratory investigation." (See 'Definition' above).

The mechanisms of drug fever are multiple and, in many cases, are poorly or incompletely understood.
However, most authorities classify drug-related fevers into five broad categories:

Hypersensitivity reactions, including the drug reaction with eosinophilia and systemic symptoms
(DRESS) syndrome

Altered thermoregulatory mechanisms

Reactions that are directly related to administration of the drug

Reactions that are direct extensions of the pharmacologic action of the drug

Idiosyncratic reactions (see 'Mechanisms' above)

Drug fever is usually a diagnosis of exclusion. The first assumption of most clinicians is that fever is due
to infection, which may not always be easy to exclude. Connective tissue diseases or malignancy, which
are other causes of fever of unknown origin, are also often difficult to exclude. (See 'General clinical
issues' above).

Rash, when present, may be a valuable clue to the presence of drug fever, but its absence should not
deter the clinician from suspecting the diagnosis. (See 'Presence of rash' above).

The timing of the onset of fever in relation to beginning the drug and the pattern of fever are
frequently not helpful in making a diagnosis. The median time to onset is about eight days but varies
from less than 24 hours to many months. Similarly, the pattern of fever may vary from a low-grade fever
without other associated symptoms to a "hectic" pattern with chills and rigors. (See 'Fever patterns'
above).

The white blood cell count can be elevated with accompanying eosinophilia in drug fever, but these
findings occur in less than 20 percent of cases. The erythrocyte sedimentation rate is usually increased,
but this is a nonspecific finding. Unexplained disturbance of liver function and/or renal impairment can
provide clues to the diagnosis. If urine microscopy reveals pyuria, a stain for eosinophils can be
performed and may be positive, especially in interstitial nephritis caused by beta-lactam antibiotics. (See
'Laboratory investigations' above).

In the majority of patients, the only way to know if a patient has a drug fever is by stopping the drug(s).
The usual approach is to discontinue the most probable offending drug first, followed sequentially by
cessation of other drugs if fever persists. Discontinuing all medications at once may eliminate the fever
but may also put the patient at some risk from the underlying disease and prevent identification of the
causative drug. In most but not all cases, resolution of drug fever will occur within 72 to 96 hours of
discontinuing the offending drug. (See 'Cessation of the drug(s)' above.)

12. a. Barium swallow.

Suspect zenkers diverticulum here

Zenker's diverticula are usually discovered in older adults, although they have been described in
children. Most patients present after the age of 60 (often above age 75), having had symptoms
ranging from weeks to years. For unclear reasons, the majority of patients are male .

Transient oropharyngeal dysphagia may be noted early in the course. The openings of large ZD
are often aligned with the axis of the pharynx such that food is preferentially diverted into the
diverticulum. When the pharyngeal sac becomes large enough to retain contents such as
mucus, pills, sputum, and food, the patient may complain of pulmonary aspiration, foul breath,
gurgling in the throat, appearance of a mass in the neck, or regurgitation of food into the mouth.
Marked weight loss and malnourishment can occur in patients with longstanding dysphagia. The
ZD may become so large that its retained contents may push anteriorly and completely obstruct
the esophagus.
13.b oral corticosteroids.
If after initial home treatment the patient has symptoms or signs suggestive of a severe
exacerbation (eg, marked breathlessness, inability to speak more than short phrases, use of
accessory muscles) or a peak flow less than 50 percent of baseline, he or she should seek
urgent medical attention. Patients may be advised by their clinician to take a dose of oral
glucocorticoids (eg, prednisone 40 mg) on route to the emergency department.

14. D. OSMOTIC DIURESIS.

15.B. GLUTEN SENSITIVE ENTEROPATHY.

The classic definition of celiac disease or gluten-sensitive enteropathy includes the following
three features: villous atrophy; symptoms of malabsorption such as steatorrhea, weight loss, or
other signs of nutrient or vitamin deficiency [7]; and resolution of the mucosal lesions and
symptoms upon withdrawal of gluten-containing foods, usually within a few weeks to months.
Patients with classic disease present with diarrhea, weight loss, or malabsorption, and possess
antibodies against gliadin and especially tissue transglutaminase.

Gastrointestinal manifestations Patients may present with classic signs, including diarrhea
with bulky, foul-smelling, floating stools due to steatorrhea and flatulence.

16. E .DO NOT ADMINISTER, MEDICALLY CONTRAINDICATED.

17. A. 0 %.

18. D sarcoidosis
Hilar adenopathy + uveitis + ppd negative .

19. e. weight reduction.

20.Mineralocorticoid Excess
Nonsuppressible (primary) hypersecretion of aldosterone is an underdiagnosed cause of
hypertension. The classic presenting signs of primary aldosteronism are hypertension and
hypokalemia. The most common subtypes of primary aldosteronism are:

Aldosterone-producing adenomas (APAs)

Bilateral idiopathic hyperaldosteronism (IHA; bilateral adrenal hyperplasia)

21. D. Kallamans Syndrome.

Congenital GnRH deficiency primarily is a disease of males, with the male-to-female ratio being
approximately 5:1, and can present at any age. The presenting signs and symptoms are a
function of the age-related period of reproductive activity.

During the neonatal period, boys with GnRH deficiency can present with
micropenis and/or cryptorchidism due to the silence of their
hypothalamic-pituitary-gonadal axis during this period; approximately one-half of boys
with microphallus have isolated GnRH deficiency as the underlying diagnosis. In
comparison, newborn girls have no obvious abnormal findings that might provide clues
to the diagnosis.

During childhood, which is physiologically characterized by a latency period of

reproductive activity, the lack of sense of smell in some patients (anosmia) or the
presence of skeletal abnormalities such as cleft lip/cleft palate or syndactyly (in patients
with mutations in the FGF signalling pathway) generally are the only way the diagnosis
can be made. This association of IHH with anosmia is referred to as Kallmann
Syndrome.

At puberty, patients of both sexes can present with a variable failure to undergo sexual
maturation and establish a clear-cut growth spurt (eg, primary amenorrhea in girls

Physical findings The body habitus of adolescent patients failing to undergo puberty
often is eunuchoidal, with arm span exceeding height by 5 cm or more. This finding
reflects the delayed closure of the epiphyses of long bones caused by hypogonadism
during puberty.

In women, secondary sexual characteristics are often completely absent, with little or no
breast development or axillary hair.

Men have little or no beard and body hair development, no increase in bulk of the
muscles, and failure of the voice to deepen.

In both sexes, some pubic hair can be present because adrenarche, with its concomitant
small amounts of adrenal androgen and estrogen secretion, is characteristically normal
22. Paradoxical Pulse:
Systemic blood pressure is not constant but varies slightly from heart beat to heart beat and
between inspiration and expiration. Normally, the systolic blood pressure decreases by less
than 10 mmHg during inspiration, but a decline of this magnitude is not detectable on
examination of the peripheral pulse. Moderate to severe cardiac tamponade, and occasionally
constrictive pericarditis, induce hemodynamic changes that enhance the inspiratory fall in
systolic blood pressure. This exaggerated drop in systemic blood pressure during inspiration is
termed pulsus paradoxus

23. B. Chronic volume overload on right ventricle. Pulmonary Hypertension .

he initial symptoms of PH are the result of an inability to adequately increase cardiac output
during exercise [2,3]. These include exertional dyspnea, lethargy, and fatigue. Additional
symptoms emerge as the PH progresses and right ventricular hypertrophy and failure
developThese include the following:

Exertional chest pain (ie, angina) is usually due to subendocardial hypoperfusion caused
by increased right ventricular wall stress and myocardial oxygen demand. However, it is
occasionally caused by dynamic compression of the left main coronary artery by an
enlarged pulmonary artery; this risk is greatest for patients with a pulmonary artery trunk at
least 40 mm in diameter [4-6].
Exertional syncope is due to the inability to increase cardiac output during activity or
reflex bradycardia that is secondary to mechanoreceptor activation in the right ventricle.
Peripheral edema is due to right ventricular failure, increased right sided filling cardiac
pressures, and extracellular volume expansion.
Anorexia and/or abdominal pain in the right upper quadrant due to passive hepatic
congestion.

Uncommon symptoms include cough, hemoptysis, and hoarseness (Ortner's syndrome). The
hoarseness is caused by compression of the left recurrent laryngeal nerve by a dilated main
pulmonary artery.

Examination Patients with PH may develop the following physical signs as they progress
from PH alone to PH associated with right ventricular failure:

The initial physical finding of PH is usually increased intensity of the pulmonic component
of the second heart sound, which may become palpable. The second heart sound is
narrowly split or single in patients with preserved right ventricular function
As right ventricular hypertrophy develops, a prominent A wave may emerge within the
jugular venous pulse. This may be accompanied by a right-sided fourth heart sound and
either a left parasternal heave or a downward subxiphoid thrust.
Right ventricle failure (or a right bundle branch block) widens the splitting of the second
heart sound. Auscultation may reveal a holosystolic murmur of tricuspid regurgitation and,
 occasionally, systolic ejection murmur and, in more severe disease, a diastolic pulmonic
regurgitation murmur.

24. A CT Scan of abdomen.

25. A activation of renin angiotensin system

The presence of an upper-abdominal bruit with a diastolic component that lateralizes toward
one side is highly suggestive of renal artery stenosis.

26. E Biopsy and culture of lung mass.Have a doubdt here I think this would be right if we
want to confirm m.avium here.

27. D. Administer 50% dextrose in water : as hypoglycemic episode here.

28. F Gilberts Syndrome - Clinical manifestations of Gilbert's syndrome include icterus secondary
to a mild, predominantly unconjugated hyperbilirubinemia (normal levels in these patients are < 3
mg/dl). Those patients who are symptomatic tend to have nonspecific complaints, including malaise,
fatigue, or abdominal discomfort. Certain events, such as hemolysis, fasting or consuming a fat-free
diet, physical exertion, febrile illness, stress, or fatigue are thought to be triggers for hyperbilirubinemia
in patients with Gilbert's syndrome.

29. A acute hepatitis

30. c. ciprofloxacin :
31.A. Aortic Dissection :
32.
Intravenous acyclovir therapy.

33. A . Alveolar arterial Mismatch.

34. A. Bone metastasis.

35. D Increased bone turm over : pagets here.

PDB is characterized by abnormalities of the osteoclast [38]; there are accelerated bone turnover and
abnormal bone remodeling. Both genetic and environmental causes are thought to contribute to its
pathogenesis. Inheritance appears to be autosomal dominant with variable penetrance, and multiple
genetic loci have been associated with PDB. The majority of patients with PDB are asymptomatic.
Symptoms are usually due to overgrowth of the affected bone. Pain may arise directly, from a pagetic
lesion in bone, or from secondary causes, including osteoarthritis, fracture, nerve impingement, or,
rarely, tumor.
Osteosarcoma is a rare, usually fatal complication of PDB, which typically presents in those with
longstanding skeletal disease. Such patients may report increased bone pain that is poorly responsive to
medical therapy, local swelling, and, less often, a pathologic fracture. Giant cell tumors may arise in
pagetic bone and are usually benign. Laboratory findings, which reflect increased bone turnover and are
typical of untreated disease, include elevated levels of serum alkaline phosphatase (sAP) and
bone-specific alkaline phosphatase (bAP). The degree of elevation generally reflects the extent and
activity of the disease, although this is not always the case. A normal or minimally elevated AP may be
seen in more limited disease.
Plain radiographs reflect the abnormal bone turnover characteristic of disease. A predominantly
osteolytic lesion may be seen early in disease. Over time, however, there is evidence of an osteoblast
response, and the bone thickens and enlarges, with thickened cortices marked by tunneling and
accentuated trabeculae at one or more affected skeletal sites. In late disease, there may be dense bone
by plain film, with little evidence of remodeling by biochemical parameters. Increased uptake is seen
focally at the sites of active pagetic bone lesions on radionuclide bone scanning. Bone scintigraphy is
more sensitive than plain radiography, particularly in early disease.
. We obtain a baseline radionuclide bone scan to document the extent and locations of skeletal
involvement; we perform radiographs of affected sites to identify impending fractures, potential
malignant lesions, osteoarthritis, or other bone abnormalities.

36.B Cardiomyopathy
37. E. Recurrent pulmonary emboli here ..there are subsegmental perfusion
defect seen.
38. Pyelonephritis
acute uncomplicated pyelonephritis is suggested by fevers, chills, flank pain, costovertebral
angle tenderness, and nausea or vomiting, with or without the typical symptoms of cystitis

39. E Renal tubule.

40. a. Observation only
41. B. Give isoniazid in asymptomatic tb with negative cxr findings.
42. E aortic valve replacement .
43. B. Measurement of Serum Cholestrol.
44. c. 7Measurement of Serum Ferritin Conc , Hemochromatosis here
Dark brown color - Mild elevation in liver enzymes - S3 - hyperglycemia.

All these manifestations point toward Hemochromatosis

Also, about the OA

UTD
"One report noted an increased frequency of heterozygous carriage of the hemochromatosis HFE gene
allele (C282Y) in older people with OA of the hands compared with healthy young controls"

45.C, Malignant Transformation of epithelial cells

46.D.Fat embolism.
47. E, Ventricles , VT is common after MI.
48.E, Ingested spores ,C difficile is highly transmissible via the fecal-oral route by
ingestion of spores.

49. B. oral acyclovir, Herpetic whitlow.

50.D. Sytemic broad spectrum antibiotics.