Master lung pathology: normal anatomy, atelectasis, ARDS, and obstructive vs. restrictive diseases. Explore emphysema, asthma, & chronic bronchitis.
Normal Lung Structure & Respiratory Pathology Anatomy --- Normal Lung Structure Anatomy and Development Feature Detail --- --- Development Outgrowth from the ventral wall of the foregut Lobes Right lung: 3 lobes · Left lung: 2 lobes Airways Bronchi → Bronchioles (no cartilage/submucosal glands) → Terminal bronchioles → Acinus Acinus Functional unit distal to the terminal bronchiole; composed of respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli Alveolar Wall and Cell Types Cell / Component Detail --- --- Alveolar Wall Capillary endothelium + basement membrane + pulmonary interstitium (elastic fibers, collagen, fibroblasts, mast cells) Type I Pneumocytes Flat cells covering 95% of the alveolar surface Type II Pneumocytes Rounded cells; synthesize surfactant; progenitor cells for repair after injury Alveolar Macrophages Phagocytic cells within the alveolar space --- Atelectasis (Collapse) Definition: Loss of lung volume from inadequate expansion of air spaces → ventilation-perfusion imbalance. Type Cause Notes --- --- --- Resorption Total airway obstruction (mucus plugs, foreign bodies, tumors) Air distal to obstruction is absorbed Compression Fluid, blood, or air in pleural cavity (pleural effusion, pneumothorax) — Contraction (Cicatrization) Local or diffuse fibrosis preventing full expansion Irreversible --- Acute Respiratory Distress Syndrome (ARDS) Definition: Acute respiratory failure with bilateral opacities on imaging, not explained by cardiac failure. Involves Diffuse Alveolar Damage (DAD) . Pathogenesis - Triggers: Pneumonia, sepsis, aspiration, trauma - Mechanism: Endothelial and epithelial injury → vascular leakiness + loss of surfactant - Neutrophil Role: Macrophages release IL-8 → recruit neutrophils → release ROS and proteases → damage alveolar-capillary membrane Morphology Phase Features --- --- Acute Heavy, firm lungs; hyaline membranes (fibrin-rich edema + necrotic debris) lining alveolar ducts Organizing Proliferation of Type II pneumocytes + interstitial fibrosis --- Obstructive vs. Restrictive Lung Disease Feature Obstructive (e.g., COPD, Asthma) Restrictive (e.g., IPF, Sarcoidosis) --- --- --- Mechanism Increased resistance to airflow Reduced lung expansion/compliance FVC Normal or slightly decreased Significantly reduced FEV1 Significantly decreased Reduced proportionately FEV1/FVC Decreased ( 0.4 ) + goblet cell metaplasia Asthma - Hallmarks: Reversible airway obstruction, eosinophilic inflammation, smooth muscle hypertrophy - Atopic Asthma: IgE-mediated (Type I hypersensitivity) driven by TH2 cells (IL-4, IL-5, IL-13) - Morphology: Curschmann spirals + Charcot-Leyden crystals in sputum Bronchiectasis - Definition: Permanent bronchial dilation from destruction of muscle and elastic tissue due to chronic necrotizing infections - Associations: Cystic fibrosis, Kartagener syndrome, bronchial obstruction --- Chronic Interstitial (Restrictive) Lung Diseases Condition Key Features --- --- General Reduced lung compliance; "honeycomb lung" in end-stage disease IPF Progressive bilateral interstitial fibrosis; "usual interstitial pneumonia" (UIP) pattern Pneumoconioses Lung injury from inhaled mineral dusts (Coal, Silica, Asbestos) Sarcoidosis Multisystem disease; noncaseating granulomas; elevated ACE levels Hypersensitivity Pneumonitis Immunologically mediated; reaction to inhaled organic antigens (e.g., Farmer's lung)