Pathology of lung

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Pathology of lung

Transcript of Pathology of lung

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Pathology of lung

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Atelectasis

Loss of lung volume due to inadequate expansion of air spaces

1. Resorption

2. Compression/passive/relaxation/flaccid

3. Contraction /Cicatriztion

4. Non obstructive/micro

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Acute lung injury

Spectrum of endothelial and epithelial pulmonary lesions

Acute onset of dyspneaB/l pulmonary edemaHypoxemiaNo LHFPathology of vasculature- alveolar

capillary membrane damage Non cardiogenic pulmonary edema

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Acute injury can be

1. Direct injury- Pneumonia,aspiration of gastric contents

2. Indirect injury- sepsis,severe trauma with shock

3. A/c injury----------- ARDS

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ARDS

Diffuse alveolar capillary and epitrhelial damage

1. Respiratory insufficiency

2. Cyanosis

3. Severe arterial hypoxemia-not responding to oxygen therapy

4. Progress to mutisystem organ failure Neutrophils hav a imp role in ARDS

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Destructive forces are counter acted by anti proeases, oxidents ,etc

Degree of tissue injury depends on balance of two

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Emphysema

1. Centri acinar/centri lobar- in smokers-

2. Pan acinar/pan lobar- ass. With alpha 1 anti trypsin deffi.

3. Distal acinar/para septal- adj. to scarring, fibrosis,atelectasis

4. irregular- associated with scarring- assymptomatic

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C/C Bronchitis

Persistent productive cough for 3 consecutive months for 2 consecutive years

Three types1. Simple c/c bronchitis-productive cough—

mucoid sputum—air flow not obstructed2. C/C asthmatic bronchitis-hyper responsive

airways—intermittent bronchospasm and wheezing

3. C/C obstructive bronchitis-associated with emphysema

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Asthma

Air way remodeling ADAM33

1. Thickening of basement membrane of bronchial epithelium

2. Edema & inflammatory infiltrate in the bronchial walls,with a prominnce of eosinophils and mast cells

3. An increase in size of submucosal glands

4. Hypertrophy of bronchial smooth muscles

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Bronchiectasis

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Pneumonia

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Two types

1. Broncho

2. Lobar Mostly occurs by aspiration of

pharyngeal flora Lower lobes/ right middle lobes are

mostly affected

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1. Community- acquired Acute pneumonia-pyogenic org.

2. Community acquired atypical pneumonia-virus, mycoplasma, candida

3. Nosocomial- pseudomanas,gram neg.

4. Aspiration – anerobic

5. Chronic – Mtb

6. Necrotizing pneumonia and lung abcess-Anerobic + pyogenic

7. Pneumonia in the immunocompramised host – chlamydia, aspergillosis, CMV

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Complications of pneumonia

Lung abscess Empyema- suppurative materials may

accumulate in the pleural cavity Bacterial dissemination leading to

meningitis,arthritis, infective endocarditis Complications are much more with

serotype 3 pneumococci

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Atypical pneumonias

Acute febrile respiratory d/s characterized by patchy consolidation of lungs, largely confined to alveolar septa and pulmonary interstitium

Atypical-moderate amounts of sputum, absence of physical finings of consolidation,only moderate inc in WBC coun,lack of alveolar exudate

Mostly by Mycoplasma pneumoniae

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Lung Abscess

Suppurative destruction of lung parenchyma with central area of cavitation

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Good Pasture’s syndrome

RPGNHaemorrhagic interstitial pneumonitis

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Lung tumours

1. Squamous cell carcinoma/epidermoid carcinoma

2. Adinocarcinoma-bronchial derived, acinar,papillary,broncioloalveolar,solid

3. Small cell carcinoma-oat cell, intermediate

4. Large cell carcinoma,undiff,giant cell, clear cell

5. Others- combined small cell carcinoma,Adenosquamous carcinoma

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Adenocarcinoma has replaced SCC as the most common primary lung tumour

Most common in women,non smokers,persons younger than 45yrs

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Therapeutic classification

1. Small cell lung cancer (SCLC)

2. Non small cell lung cancer (NSCLC)

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