INTERNAL DISEASE-RESPIRATORY SYSTEM

BRONCHIAL ASTHMA
Definitions: allergic disease which is manifested by paroxysmal attacks

Etiology and pathogenesis:

It is a ployaetiological disease. It can be provoked by a) External agents( exogenic allergens) b) Internal agents( endogenic allergens which depends on the infection of airways) Exogenic allergens: It can be provoked by: a)odours- flowers, hay, petrol, perfumes, carpet, pillow dust b) foods- eggs, crabs, strawberries c) Memory of it or by remembrances of the conditions under which the allergens acted the past Endogenic allergens: Microbial antigens that are formed during various inflammatory processes, such as sinusitis, chronic bronchitis, chronic pneumonia. Products of decomposition of microbes and tissue proteins forming due to proteolytic process at the inflammatory focus can act as allergens Factors that cause bronchial asthma: a)hereditary- constitutional factors b)climate such as during spring and autumn c)response of the parasympathetic nervous system to the stimuli received from various exteroceptors and interoceptors d)hyperexcitation of the vagus nerve centers e)development of the pathological reaction in the afferent receptors of the bronchial walls f)hypersensitivity to local irritants

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Evidence of bronchial asthma: Importance of partial B-adrenergic blockade in the pathogenesis of the bronchial asthma and reduced activity of cyclic adenosine monophosphate during attacks of the disease. Finally hormonal shifts which are connected to adrenal glands. It is confirmed by effect of corticosteroid therapy on the course of the disease. Atopic bronchial asthma: Provoked by allergic reaction occurring in the bronchial tissue. There are three stages: a)immunological: antigen combines with the specific antibodies(IgE fixe on mast, plasma, and lymph cells) b)pathochemical: histamine, serotonin, and slow acting substance anaphylactin are released from these cells as a result of degranulation and alteration c)pathophysiological: spasm develop in the bronchi along with the oedema of bronchial mucosa

Clinical picture:
There are two types of attack: a) Dyspnoea( short attack of asthma) b) Status asthmaticus( prolonged attack of asthma Dyspnoea: Arise suddenly, gradually increase in strength, and last from a few minutes to several hours or days Status asthmaticus: a)patient assume forced position, breath often whistling and noisy, mouth opened, and nostrils flare out b)veins of the patient swollen during expiration and normal during inspiration c)patient cough with thick sputum during peak of an attack d)the chest expands during attack and the accessory muscle are involved e)percussion gives bandbox sound

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f)lower margin of the lungs below normal and mobility of lower border is limited during respiration g)auscultation reveals many whistling rales h)tachycardia is observed i)blood test shows moderate lymphocytosis and eosinophilia j)X- ray shows high translucency of the ling fields and limited mobility of diaphragm

Course:
Attacks can be rare like once a year or several years. It can also develop a more severe course with frequent and grave attacks. Concurrent chronic bronchitis, pneumosclerosis cause corresponding changes. Sometimes the patient may die during attack.

Treatment:
a)should be identified and eliminated whenever possible b)removal of causative stimulus like allergens c)symptomatic therapy should be given if pathogenic therapy is not effective d)can give subcutaneous injection like adrenaline hydrochloride and ephedrine solution e)can give intravenous injection like euphylline f)can prescribe broncholytics g)remedial exercises and health-resort therapy

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ACUTE PNEUMONIA
DEFINITION
PNEUMONIA is an acute inflammation of the lungs developing independently or as a complication in other disease

SUSCEPTIBILITY
MEN are more susceptible than WOMEN, especially severe in CHILDREN and ELDERLY patients.

ETIOLOGICAL CLASSIFICATION
1. 2. 3. 4. BACTERIAL pneumonia (pneumococcal, staphylococcal, streptococcal, etc.) VIRUS (influenza virus, viruses or ornithosis, psittacosis) MYCOTIC (candidiasis, etc.) Pneumonia causes by GASES, VAPOURS, DUSTS, etc.

CLINICAL MANIFESTATIONS Vary depending on the initial bodys sensitivity

I. II. III. IV. Hyperergic Cyclic character of its course Frequent affection of the whole lobe of lung (with pleural involvement) Special character of effusion due to a markedly impaired permeability of the vessel wall

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BRONCHOPNEUMONIA
Also known as LOBAR PNEUMONIA, synonym: FOCAL CATARRHAL

MORPHOLOGY
Affected separated lobules of lungs; the foci may be located in various parts of both lungs simultaneously (mostly in the lower part of the lung) Occurs mostly in CHILDREN and the AGED, usually during cold seasons (spring, autumn, winter)

ETIOLOGY
i. ii. iii. iv. BACTERIAL FLORA (pneumococci, streptococci, staphylococci) VIRUSES (in influenza, nithosis and psittacosis) Decrease body IMMUNOLOGICAL PROPERTIES (overcooling, acute respiratory disease, etc.) Can develop against the background of CHRONIC DISEASE OF THE LUNGS (bronchiectasis, chronic bronchitis) due to hematogenic infection in purulent inflammatory disease (sepsis, after operation, etc.)

Inhalation of suffocating or irritating GASES or VAPOURS (benzene, toluene, benzene, etc.) or other toxic substances can provoke the onset to bronchopneumonia.

PATHOGENESIS
INFLAMMATION extension of inflammatory process from the bronchi and bronchioles to the pulmonary tissue INFECTION get inside the pulmonary tissue via bronchi, frequently peribronchially (by lymph ducts and interalveolar septa) LOCAL ATELECTASIS occurs in obstruction of the bronchus by a MUCOPURULENT PLUG Obstruction of bronchial patency can be caused by a sudden bronchospasm and edema of the bronchial mucosa, inflammation (bronchitis), etc.

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CLINICAL PICTURE
I. II. III. Result of PHYSICAL EXAMINATION : the same as in acute bronchitis (at the onset) Acute bronchitis with high temperature and symptoms of more severe disease COUGH, FEVER, DYSPNOEA If the inflammatory focus is at the periphery of the lung and the inflammation involve the pleura, PAIN IN THE CHEST during coughing and deep breathing may occur Fever usually remittent and irregular; temperature often subfebrile (may be normal in the middle-aged or old patient) Objective examination sometimes reveals MODERATE HYPERAEMIA of the face and CYANOSIS of the lips. ACCELERATE RESPIRATION 25 to 30 per minute RESPIRATORY LAGGING of the affected side of the chest PERCUSSION SOUND lose resonance (presence of large focus, also in confluent pneumonia) AUSCULTATION bronchial breathing, dry and moist rales, crepitation X-RAY reveals indistinct densities; in confluent pneumonia the densities are spotted ( mostly in lower border of lungs); shadow of lung root expanded due to enlarged lymph nodes SPUTUM mucopurulent, first tenacious but later more thin, sometimes there are traces of blood, but not rusty. Contain a large number of leukocytes, macrophage and columnar epithelium. BLOOD COUNT mild neutrophilic leukocytosis, moderately increased ESR

IV. V. VI. VII. VIII. IX.

X.

XI.

COURSE
Usually more protracted and flaccid than pneumonia. Prognosis is favorable with appropriate treatment.

INTERNAL DISEASE-RESPIRATORY SYSTEM

ACUTE LOBAR PNEUMONIA

Frequently in patient who had PNEUMONIA in their past history

ETIOLOGY
I. II. III. Frenkel pneumococci (type I and II, less frequent type III and IV) Fridlaender diplobacillus, Pfeiffers baccilus, streptococcus, staphylococcus etc. Acure mostly after SEVERE COOLING Main portal of infection is bronchogenic, less frequent lymphogenic and hematogenic CONGESTION OF LUNG in cardiac failure, chronic and acute diseases of upper airways, avitaminosis, overstrain and other factors promote the onset of pneumonia

IV.

CLINICAL PICTURES
A. ONSET of disease (general condition : grave) i. SHAKING CHILLS (1-3 HOURS) ii. SEVERE HEADACHE iii. FEVER (39-40OC) iv. PAIN ON THE AFFESTED SIDE v. COUGH (dry at first, after 1-2 days rusty sputum expectorated) B. GENERAL EXAMINATION i. HYPEREMIA of the cheeks ii. DYSPNOEA iii. CYANOSIS iv. HERPES on the lips and nose v. The affected side of the chest lags behind the respiratory act vi. VOCAL FREMITUS is slightly exaggerated over the affected lobe vii. LUNG SOUND vary, depend on the distribution of the process, stage of disease viii. PERCUSSION SOUND shortened, often with tympanic effect because liquid and air are simultaneously contained in the alveoli ix. VESICULAR BREATHING decrease, BRONCHOPHONY increase, so-called INITIAL CREPITATION is present

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C. HEIGHT of the disease (red and grey hepatization stages) i. Grave general condition ii. General toxicosis iii. Accelerated & superficial RESPIRATION (30-40 per min) iv. TACHYCARDIA (100-200 bpm) v. DULLNESS over the affected lobe of lung vi. BRONCHIAL RESPIRATION vii. Exaggerated VOCAL FREMITUS AND BRONCHOPHONY viii. BRONCHIAL BREATHING inaudible

Resolution stage
1) 2) 3) 4) 5) 6) 7) 8) 9) 10) 11) 12) 13) The exudate thins air again fills the alveoli to decrease dullness of the percussion sound, tympany increases bronchial breathing lessens Crepitation is heard again (crepitus redux) bcz the alveolar walls separate as air fill them Moist rales are heard Exaggerated vocal fremitus, then bronchophony, and finally bronchial breathing disappear The leucocyte count increases to (15000-25000 per microliter) Neutrophils account for 80-90% of leucocytes Eosinophils decreases and disappear in grave cases Relative lymphopenia and monocytosis are observed The ESR increases The red blood does not change

Sputum is tenacious during the congestion period; slightly crimson and contains much protein, a
smaller number of leucocytes, erythrocytes, alveolar cells, and macrophages. In the stage of red hepatisation sputum is scants and rusty; it contains fibrin and a higher num of formed element. In the stage of grey hepatisation leucocyte count in the sputum increases significantly; the sputum becomes mucopurulent. The leucocytes are converted into detritus, which is found in the sputum; many macrophages are also found. Pneumococci, staphylococci, Friendlaender diplobacilli can be detected in the sputum.

X-ray changes in the lungs depend on the stage of the disease. The lung pattern is first
intensified, then dense foci develop, which later fuse. The shadow usually corresponds to the lung
lobe. The lung becomes normally clear in 2 or 3 weeks. Dynamics of the X-ray changes depends on the time of the therapy is begun. 8

INTERNAL DISEASE-RESPIRATORY SYSTEM

Course and Complications

1) 2) 3) 4) Fatal outcome: 20-25% Parapneumonic pleurisy : pleurisy dvlp before the resolution of pneumonia Metapneumonic pleurisy : after resolution Others: myocarditis, meningitis, focal nephritis

Treatment of pneumonia
1) 2) 3) 4) 5) 6) 7) 8) 9) 10) Patient hospitalised Food rich on vitamins and easily assimilable Antibiotics : IM-penicillin; 4-6 times/day streptomycin; tetracyclin Sulpha drugs : sulphadimezine, sulphaethidole, sulphadimethoxine Oxygen therapy Coffein and Camphor : treat vascular insufficiency Digitalis and Strophanthine : in the presence of heart failure Expectorants : given during the resolution of pneumonia Cups, mustard plaster, physiotherapy : eliminate residual effect of pneumonia Resp exercises : improve lung ventilation

Prophylaxis
- mainly in strengthening and hardening of the body

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PULMONARY ABSCESS
-pulmonary melting of the lung tissue encircled by an inflammatory swelling
* pat anat: characterised by the presence of a single or multiple purulent foci that may be found on one or both lungs. After the abscess opens, a cavity is formed which is surrounded by inflammatory infiltration. Acute abscesses are surrounded by a thin ridge of the inflamed tissue. Chronic abscess are encapsulated in fibrous tissue.

a) Aetiology & Pathogenesis

1) Coccal flora (strepto, staphy, pneumococcus) 2) Sometimes associated by saprophytic auto infection of the upper airways. 3) Purulent process in the lungs develops mostly as an outcome of pneumonia or complicated bronchiectasis. 4) Primary abscess arise in wounds to the chest, aspiration of foreign bodies, and after operation on the upper airways 5) Can develop by hematogenic or lymphogenic routes 6) Suppuration of echinococcal cyst in the lung 7) Necrotisation of lung tissue : due to local disorder in blood circulation causing formation of cavity in the case of lung infarction or in the presence of the degrading tumour.

b) Clinical Picture
2 periods; before and after opening of an abscess i) General Before the opening chills weakness cough with sputum pain in the chest fever : from moderate to hectic dyspnoea detect pain on intercostal space of affected side can observe unilateral thoracic lagging corresponding to inflammation vocal fremitus depends on the location of the inflammatory focus (remains unchanged in deep localisation of inflammatory focus) can determine loss of resonance (dull sound) on the affected side a. in small deep abscess does not reveal any abnormalities b. superficial abscess : resp over affected side is decreased and vesicular c. sometimes : harsh breathing + dry rales are heard a. Neutrophilic leucocytosis : 15000-20000 per microliter b. ESR increases c. Study of sputum is not specific Does not differ from pneumonia or tuberculosis infiltration : a large focus of increased density with rough and indistinct margins is determined 10 a. b. c. d. e. f. a. b. c.

Palpation

Percussion Auscultation

Blood picture

X-ray picture

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ii)

Opening of the purulent abscess into the bronchus - starts with the opening of the purulent abscess into the bronchus accompanied by the sudden release purulent sputum (sometimes with odour) - expectorations may be 200ml to 2L a day. General Palpation Percussion Auscultation patient looks feverish if pleura is involved : unilateral thoracic lagging is observed on the affected side tympany is determined in the presence of large and superficial abscess a) resp can be either bronchovesicular or bronchial amphorical : if large cavity containing air communicated with the bronchial lumen b) resonant moist moderate and large bubbles rales can be heard over a limited area c) in the presence of concurrent diffuse bronchitis, intense rales interfere with the location of the abscess. a) ESR increase b) in grave cases : hypoferric anaemia develops c) sputum on standing- : separates into 3 layers : upper (foamy and mucous), middle (liquid,serous), and bottom (pus) microscopy of the sputum : presence if the elastic fibres. * if absent : termination of degradation of the lung tissue bacteriological flora; mostly containing cocci a) increased translucency; b) variation of the liquid level can be observed with the variation of the patients posture. c) If the draining bronchus is at the bottom of the cavity, the liquid level is undeterminable. d) The abscess cavity is surrounded on all sides by a border of inflamed tissue with a diffuse outer contour

Blood picture

X-ray picture

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INTERNAL DISEASE-RESPIRATORY SYSTEM

Course
Development and healing of lung abcess depends on location of cavity, conditions for its emptying and concurrent complications. Chronic disease of lungs promote pulmonary suppuration. Complications; 1)rupture of abcess into haemorrhage 2)pulmonary haemorrhage 3)development of pulmonary abcess 4)metastases of abcess into brain, liver,etc.

Treatment
bed rest antibiotic and sulpha drugs is given. Penicillin and streptomycin in large doses over long period. Therapeutic bronchoscopy is used to remove pus from cavity and to administer antibiotics directly into it. Symptomatic treatment consists of prescribing expectorants and broncholytics which liquefy sputum. Paetient should find a posture where best withdrawal of sputum and mantain this posture for 30min 2 to 3 times per day. If therapy is ineffective, surgical treatment.

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INTERNAL DISEASE-RESPIRATORY SYSTEM

Pleurisy (inflammation of pleura)

Divided into;
Dry pleurisy (pleuritis sicca) and pleurisy with effusion (pleuritis exudativa).

Character;
Serous,serofibrinous,purulent,haemorrhagic

Etiology and pathogenesis

Serous and serofibrinous; TB,pneumonia,rheumatism. Purulent process in pleura may be caused by pneumococci, streptococci, staphylococci, etc. Haemorrhagic pleurisy arise in TB of pleura, bronchogernic cancer, injuries in chest. Most pleurisy are secondary to disease of lung. It usually develops as reaction to pathological changes. Serous pleurisy arise as allergic reaction. Purulent pleurisy is a complication of bronchopneumonia; inflammation may extend to pleura or it may become abcess. Inflamation will attended by increased permeability of wall of affected capillaries.

Reactivity of Body;
In dry pleurisy, fibrin participates from exudates and deposits on pleura. Serous pleurisy may become infected to convert to purulent; exudates becomes turbid and contains many leucocytes. Purulent pleurisy develops abruptly in pericarditis, perioesophagitis, etc.

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INTERNAL DISEASE-RESPIRATORY SYSTEM

Clinical picture of Dry pleurisy

Pain in chest, stronger pain during breathing and cough. Cough is dry, temperature is subfebrile. Respiration is superficial. Lying on affected side lessens the pain. Percussion fails to detect any changes except decreased mobility of lung border on affected side. X ray picture show limited mobility of diaphragm because the patient spares the affected side of chest. Blood picture remain unchanged but moderate leucocytosis is observed in some cases.

Course
Patient recovers completely in 1 or 3week.

Clinical picture of Pleurisy with effusion

patient suffer from fever, pain , dysponea. cough is mild. Patients general condition is grave, attended with high temperature with pronounced circadian fluctuations, chills, signs of general toxicosis. The affected chest usually lags behind in respiratory movements. Vocal fremitus is not transmitted at area of accumulation. (For below,Refer figure page 183) Percussion produces dullness. Upper limit of dullness is S-shaped curve (Damoiseaus curve). The effusion occupies the area, which is a trangle both anteriorly and post. The Damoiseau curve is formed because exudates in pleurisy with effusion freely accumulate in lateral portions of pleural cavity, mostly in costal-diaphragmatic sinus. Transudate presses the lung and Damoiseau curve is not determined.

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2 triangles can be determined by percussion in pleurisy with effusion; the Garland triangle(on affected side), is located between the spine and Damoiseau curve. The Rauchfuss-Grocco triangle on healthy side is a kind of extension of dullness determined on the affected side. The triangle is due to displacement of mediastinum to healthy side. Left sided pleurisy with effusion is characterize by absence of Traube space.

Auscultation
Respiration auscultated slightly above the effusion level is usually bronchial due to compression of lung and displacement of air from it. The heart is displaced by the effusion toward the healthy side.(tachycardia) Arterial pressure decreased,dizziness, faints, etc. *Additional info From the internet; Ellis-Damoiseau curve
Curve-fitting compaction is data compaction accomplished byreplacing data to be stored or transmitted with an analytical expression. Examples of curve-fitting compaction consisting ofdiscretization and then interpolation are: 1. 2. Breaking of a continuous curve into a series of straight linesegments and specifying th e slope, intercept, and range foreach segment Using a mathematical expression, such as a polynomial or atrigonometric function, and a single point on thecorresponding curve instead of storing or transmittin g theentire graphic curve or a series of points on it.

Exploratory puncture is necessary to determine the properties of exudates for accurate diagnosis. During initial stage of the disease, the blood picture shows mild leucocytosis and eosinophilia. The ESR increased. TB pleurisy is characterized with lymphocytosis, while rheumatic pleurisy is neutrophilosis.
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PLEURISY
COURSE
Depend on aetiology Pleurisy in rheumatism Pleurisy with effusion complicating pneumonia Pleurisy with effusion (tuberculosis) 2-3 weeks (with appropriate treatment) Mild course Protracted (long time)

Development of coarse adhesions interferes with resorption of effusion (encapsulated pleurisy). Followed by: 1) Sunken chest 2) Absence of diaphragmatic mobility on affected site 3) Displacement of mediastinal organs toward affected site 4) Permanent pleural friction Prolonged purulent process result in amyloidosis of internal organs

TREATMENT
1. Therapy of main disease i. Rheumatism salicylates, amidopyrine, corticosteroids ii. Pneumonia- sulpha drugs, antibiotics iii. Tuberculosis- PASA,phthivazide,canamycin 2. Symptomatic therapy i. General strengthening vitamins ii. Desensitizing preparations iii. High-calorie diet 3. Thermal procedures accelerate resolution i. Compresses ii. Diathermy

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INTERNAL DISEASE-RESPIRATORY SYSTEM 4. Evacuation of effusion WHY: if pleural fluid not resorbed during 2-3 weeks HOW o Purulent exudates obligatory to remove o Slow to avoid collapse o 0.5-1 L removed and antibiotics injected into pleural cavity o To accelerate resorption, give diuretics o In presence of cardiac failure cordiamine, strophantine o To prevent pleural adhesion remedial exercise

PROPHYLAXIS
1. Early diagnosis 2. Active treatment of rheumatism, TB, other disease 3. Strengthening of body (exercise, cool shower)

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INTERNAL DISEASE-RESPIRATORY SYSTEM

CHRONIC PNEUMONIA
AETIOLOGY: result of protracted bronchopneumonia
1. 2. 3. 4. Frequent recurrent inflammations in bronchi & lungs Influenza epidemics Inhalation of harmful chemicals Smoking

PATHOGENESIS:
Auto immune process Acute, subacute diseases of lungs --------------------> chronic Inoculation test for causative agents: streptococci, staphylococci, pneumococci If pneumonia cured incompletely, inflammatory process becomes slow to give focal/diffuse pneumosclerosis. Patients may form I. Bronchiectasis II. Emphysema III. Respiratory insuffiecieny

CLINICAL PICTURE:
1. 2. 3. 4. Dyspnoea Subfebrile temperature Permanent cough with expectoration of purulent or mucopurulent sputum Mild leucocytosis

GENERAL INSPECTION:
1. Percussion: fail to reveal a loss of resonance over affected side (due to concurrent emphysema) 2. Auscultation: fine & moderate moist rales, sometimes against background of dry diffuse rales 3. X-Ray examination: a. Interlobar septa thickened b. Lung pattern at inflammation region intensified c. Lung root changed (enlarged lymph nodes)

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INTERNAL DISEASE-RESPIRATORY SYSTEM

COURSE:
1. FIRST STAGE a) Protracted pneumonia lasting 6 weeks b) Chronic bronchitis concurrent with relapsing pneumonia 2. SECOND STAGE a) Frequent exacerbations of inflammation in lungs b) Alternating with prolonged remissions in presence of symptoms of pneumosclerosis, lung emphysema, bronchiectasis 3. THIRD STAGE a) Marked symptoms b) Frequent exacerbations c) Pronounced functional disorders of external respiration and circulation

TREATMENT
1. Combined treatment WHAT: broad-spectrum antibiotics used with frequent alternation WHY: prevent microbial resistance Antibiotics + sulpha drugs is effective Corticosteroids with antibiotics suppress auto-immune process 2. Bronchial draining HOW: giving expectorants

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INTERNAL DISEASE-RESPIRATORY SYSTEM

BRONCHIECTASIS
Dilatation of bronchi 1. Primary (congenital) 2. Secondary (various disease of bronchi, lungs, pleura)

AETIOLOGY:
In children 1. 2. 3. 4. 5. Repeated acute bronchitis Whooping cough Measles Diphtheria Tuberculous bronchoadenitis

In adults 1. Acute diffuse bronchitis (develops against chronic relapsing bronchitis, non-resolved pneumonia, lung abscess) 2. Recurrent pneumonia 3. Pulmonary tuberculosis

PATHOGENESIS
1. 2. 3. 4. 5. 6. 7. 8. Inflammatory process extends onto muscular layer of bronchial wall Muscle fibers destroyed Bronchus tone lost Walls become thin Absence of ciliated epithelium promotes accumulation of sputum in lumen, upsets draining f(x) Stimulated chronic inflammation Inflamed site first granulated, later CT develops and disfigures bronchus Severely affected bronchi dilate during intense coughing

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INTERNAL DISEASE-RESPIRATORY SYSTEM

CLINICAL PICTURE
depends on size of bronchiectasis, degree of affection, activity of inflammatory process, presence of emphysema in lungs, degree of functional disturbances of external respiration Bronchiectasis in upper lobe Draining f(X) of bronchi intact Bronchiectasis in lower lobe Sputum expectorated with difficulty

1. Cough with expectoration of seromucopurulent or purulent sputum (foul smelling) a. Daily: 50-500mL b. Maybe blood c. Cough paroxysmal d. Morning - Sputum accumulated at night 2. Haemoptysis 3. Dyspnoea 4. Excess sweating 5. Weakness 6. Headache 7. Dyspepsia 8. Deranged sleep and appetite 9. Wasting 10. Exacerbate (worse) during wet and cold weather a. Body T rise b. Leucocytosis c. ESR increase

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INTERNAL DISEASE-RESPIRATORY SYSTEM

GENERAL INSPECTION:
1. 2. 3. 4. 5. Acrocyanosis Oedematous face Terminal phalanges of fingers become clubbed Nails resemble watch glass Chest :normal or emphysematous

Percussion sound-pulmonary, with bandbox tone (concurrent emphysema) Respiration: harsh or decreased vesicular breathing- emphysema On bronchiectatic area:dry, fine, moderate bubbling non-conconant rales Pleura friction: if inflammation already spreads to pleura X ray examination: -increased translucency of lungs -deformation of lungs pattern -presence of bands in the lower lobes of lungs

COURSE
3 stages of the diseases: Initial Moderately pronounced Terminal / final Characters of final stage: Chronic right ventricular heart failure Amyloidosis of the liver Amyloidosis of the kidneys

TREATMENT
Broad-spectrum antibiostics- give intramuscularly, intratracheally, inhalation Broncholytics and anti-allergic, expecorants: to improve the draining functions of the bronchi Cardiac therapy: for concomitant right-ventricukar failure Oxygen therapy Exercises

PROPHYLAXIS
Regular medical check-ups of patients with chronic bronchitis and pulomnary fibrosis Control of other harmful environmental effects: smpking, industrial hazards

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INTERNAL DISEASE-RESPIRATORY SYSTEM

EMPHYSEMA OF THE LUNGS

AETIOLOGY AND PATHOGENESIS
Most common causes: Obstructive bronchitis Occupational lung diseases Can occur in mechanical distension of the lungs or in the heavy physical exertions associated with retention of breath

CLINICAL PICTURE
Dyspnoea Increases in cold seasons, in chills, exacerbation of bronchitis Usually expiratory Intrathoracic pressure increases Neck vein dilates and swollen If associated with heart failure: during inspiration, vein remains swollen INSPECTION: Odematoes face, cyanotic mucosa, cheeks, nose and ear lobes, skin greyish Terminal halanges clubbed- nails like watch glass Chest-barrel shape Supraclavicular fossa levelled and protrude over the clavicles Accesory muscles actively involved in respiration PERCUSSION: Bandbox sound heard Descending lower borders of the lungs and limited mobility of lower boders AUSCULTATION diminished vesicular respiration heard diffuse dry rales- if there is concurrent bronchitis X RAY EXAMINATION translucent picture if lungs lungs borders lowered mobility of diaphragm limited residual volume increases in emphysema maximum lung ventilation and vital capacity decrease cardiac rhythm increases minute blood volume increase erythrocyte count increases

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INTERNAL DISEASE-RESPIRATORY SYSTEM

COURSE
emphysema of lungs usually progresses slowly

TREATMENT AND PROPHYLAXIS

remedial exercises in presence of cardiac failure: digoxin, ATP smoking control

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