Page 373 - Concise Pathology for Exam Preparation ( PDFDrive )

358 SECTION II Diseases of Organ Systems

• Burns
• Ionizing radiation
• Pulmonary embolization
• Inhalation of irritants
• Oxygen toxicity
• Smoke
• Gases and chemicals like ammonia, chlorine and nitrogen dioxide
• Chemical injury
• Heroin or methadone or barbiturate overdose
• Acetylsalicylic acid
• Thiazides
• Haematological conditions
• Multiple transfusions
• DIC
• Others
• Pancreatitis
• Uraemia
• Cardiopulmonary pass
• Hypersensitivity reactions

Gross Pathology

Heavy, red, boggy lungs, which ooze fluid on cutting

Microscopy
• Alveolar lining and pulmonary capillary endothelium are damaged.
• Alveolar walls are lined by a waxy hyaline membrane consisting of fibrin-rich oedema
fluid mixed with cytoplasmic and lipid remnants of necrotic epithelial cells.
• Type II pneumocytes proliferate to regenerate alveolar lining.
• Fibrin exudates organize and intra-alveolar fibrosis may ensue.
• Resolution is unusual; ARDS is commonly fatal.

X-ray
Shows diffuse bilateral infiltrates

Q. Define atelectasis. Enumerate and describe its various types.

Ans. Definition: Incomplete expansion of the lungs at birth (neonatal atelectasis) or collapse
of previously inflated lungs produces areas of relatively airless parenchyma.

Types:
1. Resorption atelectasis (Flowchart 13.2)
2. Compression atelectasis (Flowchart 13.3)
3. Contraction atelectasis:

Mucous plugs and exudates in smaller bronchi (seen in asthma, bronchitis, bronchiectasis, post-
operative states) and aspiration of foreign bodies.

Complete obstruction of airway

Resorption of air trapped in dependent alveoli, leading to resorption atelectasis
FLOWCHART 13.2. Mechanism of development of resorption atelectasis.

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