Pulmonary pathology

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Pulmonary Pathology, Part I

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Pulmonary pathology

  1. 1. Respiratory Pathology By: Noel C. Santos, M.D.
  2. 2. General Categories • Congenital Anomalies • Atelectasis • Pulmonary Vascular Disorders • Pulmonary Infections • Obstructive and Restrictive Diseases • Pulmonary Tumors • Diseases of the Pleura
  3. 3. Congenital Anomalies • Agenesis or Hypoplasia • Tracheal and Bronchial Anomalies: atresia, stenosis, TE fistula • Vascular Anomalies • Congenital Lobar Overinflation (emphysema) • Foregut cysts: bronchogenia, esophageal, enteric • Congenital Pulmonary Airway Malformation – Hamartomatous lesion, 5 types • Pulmonary Sequestrations: extralobar, intralobar
  4. 4. Atelectasis • Airless: incomplete expansion or collapse • Acquired –Resorption or Obstruction –Compression –Contraction
  5. 5. Pulmonary Vascular Disease • Edema – Hydrodynamic or cardiogenic – Microvascular Injury • Adult Respiratory Distress Syndrome – Diffuse Alveolar Damage • Impair respiratory function • Predisposes to infection
  6. 6. Pulmonary Edema • Hemodynamic Edema –Increased HP • Microvascular Injury –Injury to capillaries of alveolar septa –Important contributor in the development of ARDS
  7. 7. ARDS • Diffuse alveolar capillary damage • Respiratory failure • Arterial hypoxemia refractory to O2 therapy • Several causes: sepsis, trauma, cancer, inhaled gases • Differs from Hyaline Membrane of the Newborn – deficient surfactant
  8. 8. ARDS • Mechanisms: –Oxygen-derived free radicals –Aggregation of activated neutrophils –Activation of lung macrophages –Loss or damage to surfactant
  9. 9. Pulmonary Embolism, Hemorrhage & Infarction • Occlusion of pulmonary circulation • Predisposing factors: bed-ridden, risk-associated conditions, etc. • Embolic from other sites: deep veins of legs • Potential consequences: size, site, cardiovascular status – Respiratory compromise – Cardiovascular compromise
  10. 10. Pulmonary Hypertension • Normal: 1/8 of mean systemic pressure • ¼ or above is Pulmonary HPN • Primary or Idiopathic • Secondary – lung disease, left-sided heart disease, recurrent emboli • Endothelial dysfunction and injury with trigger mechanisms – persistent vasoconstriction
  11. 11. • Impaired defense mechanisms • Lowered general resistance of the host – Loss or suppression of the cough reflex – Injury to the mucociliary apparatus – Interference with the phagocytic or bactericidal action of alveolar macrophages – Pulmonary congestion and edema – Accumulation of secretions Pulmonary Infections
  12. 12. • Defects in innate immunity and humoral immunodeficiency →Pyogenic infections • Cell-mediated immune defects →intracellular microbes →very low virulence
  13. 13. Pulmonary Infections • Morphology – Lobar Pneumonia – Lobular Pneumonia or Bronchopneumonia – Atypical Pneumonia – Necrotizing Pneumonia and Lung Abscess • Where? – Community Acquired – Hospital Acquired or Nosocomial Infection • Time/Duration: Acute and Chronic • Etiologic Agent • Immunocompromised Host • Aspiration Pneumonia
  14. 14. Necrotizing Pneumonia and Lung Abscess • Anaerobic bacteria with or without mixed aerobic infection • S. aureus, K. pneumoniae, S. pyogenes. Type 3 pneumococcus
  15. 15. Pulmonary Tuberculosis
  16. 16. Aspiration Pneumonia • Markedly debilitated patients • Unconscious • Repeated vomiting • Abnormal gag and swallowing reflexes • Partly chemical and partly bacterial (more than one organisms; aerobes>anaerobes) • Necrotizing, fulminant course • Abscess formation as one of complications
  17. 17. Pneumonia in Immunocompromised Host • CMV, P. carinii, M. avium- intracellulare • Invasive aspergillosis and candidiasis • “Usual” bacteria, viral and fungal organisms
  18. 18. Chronic Obstructive Pulmonary Disease (COPD) –Increased resistance to air flow Restrictive Pulmonary Disease –Reduced expansion of the lung parenchyma
  19. 19. COPD’s • Emphysema • Chronic Bronchitis • Bronchial Asthma • Bronchiectasis
  20. 20. Emphysema • Abnormal enlargement of air spaces distal to the terminal bronchioles • Destruction of septal walls • Decreased surface area of functional pulmonary segments • Classification: 1. Centriacinar 2. Panacinar 3. Paraseptal 4. Irregular
  21. 21. Centriacinar Emphysema • Destruction and enlargement of the central or proximal parts of the acinus • Upper lobes and apices • Smokers
  22. 22. Panacinar Emphysema • Uniform destruction and enlargement of the acinus • Basal zones of the lung • Alpha1-antitrypsin deficiency
  23. 23. Paraseptal Emphysema • Mostly the distal acinus • Near the pleura and adjacent to fibrosis • Leads to pneumothorax
  24. 24. Irregular Emphysema • Irregular involvement of the acinus • Associated with scarring Others:  Bullous Emphysema  Interstitial Emphysema
  25. 25. Emphysema • Imbalance between proteases and their inhibitors • Tobacco – recruit neutrophils, stimulate release and enhance activities of enzymes, inactivation of antitrypsin
  26. 26. Chronic Bronchitis • Persistent productive cough • At least 3 months • At least 2 consecutive years • Morphology: hyperemia and edema of mucous membranes, mucinous secretions and casts, hypertrophy of mucous glands with airway plugging, inflammation and fibrosis, squamous metaplasia/dysplasia
  27. 27. Bronchial Asthma • Increased responsiveness to various stimuli • Paroxysmal contraction of airway passages –Extrinsic (Reagin-mediated, Allergen) –Intrinsic (Idiopathic or precipitated by other factors, non-atopic or non-reaginic)
  28. 28. Bronchial Asthma (cont.) • Overinflated lungs with patchy atelectasis • Occlusion respiratory passages • Edema, bronchial inflammation, hypertrophy of bronchial muscles & mucous glands • Curschmann’s spirals and Charcoat-Leyden crystals
  29. 29. Bronchiectasis • Chronic necrotizing infections • Abnormal & permanent dilatation of airways • Cough, fever, purulent sputum • Obstructive respiratory insufficiency
  30. 30. Bronchiectasis (cont.) • Atelectasis, diminished elastic forces • Distal airways, lower lobes: dilatations – cylindrical, fusiform or saccular • Spectrum of inflammation (mild to necrotizing), fibrosis • May lead to abscess formation • Complications: cor pulmonale, metastatic abscesses, systemic amyloidosis • associated with bronchial obstruction, congenital/hereditary conditions, immotile cilia syndrome, necrotizing pneumonia
  31. 31. Restrictive (Interstitial) Lung Disease • Clinical: dyspnea, decreased lung volumes and compliance • Radiologic: diffuse infiltrates, ground-glass shadows • Pathologic: diffuse, chronic inflammation and/or fibrosis of alveolar interstitium
  32. 32. Interstitial Lung Disease • Pathogenesis: – Initial Event: injury to epithelium/endothelium via inhaled or blood-borne toxins/agents – Early Acute Changes: alveolitis – proinflammatory and fibrogenic substances – Late Effects: interstitial fibrosis
  33. 33. Interstitial Lung Disease • Idiopathic • Pneumoconioses • Granulomas • Hypersensitivity Pneumonitis • Pulmonary Eosinophilia • Bronchiolitis Obliterans – Organizing Pneumonia • Diffuse Pulmonary Hemorrhage • Pulmonary Alveolar Proteinosis
  34. 34. Idiopathic Pulmonary Fibrosis • Progressive pulmonary fibrosis • Hypoxemia, progressive resulting in pulmonary insufficiency, cor pulmonale and cardiac failure • 30 – 50 y/o; immune complex • Early Stages: interstitial & intra-alveolar edema, interstitial infiltration by leukocytes, type II pneumocyte proliferation • Intermediate Stages: interstitial & intra-alveolar fibrosis • End Stages: spaces lined by epithelium & separated by inflammatory fibrous tissue (HONEYCOMB LUNG)
  35. 35. Pneumoconioses • Inhalational disorders: mineral dusts, organic dusts, fumes and vapors • Factors: – Amount: concentration, duration, clearance mechanisms – Size, shape, buoyancy (1 to 5 μm) – Physicochemical reactivity and solubility: quartz, highly soluble (toxic), resist dissolution
  36. 36. Pneumoconioses • Carbon Dust – Coal Workers’ Pneumoconiosis • Silicosis (mining, sandblasting, metal grinding, manufacture of ceramics) • Asbestosis –Chrysotile: curled, flexible serpentine –Crocidolite: brittle, straight amphiboles
  37. 37. Coal Workers’ Pneumoconiosis (CMP) • Anthracosis: small harmless • Simple CWP: macules • Complicated CWP or Progressive Massive Fibrosis (PMF): severe fibrosis and scarring with disabling respiratory insufficiency
  38. 38. Silicosis • Promotion of persistent inflammation and fibrosis • Release of oxidants, cytokines, growth factors (fibroblast proliferation and collagen deposition) • Collagenous nodules, coalesce, calcification and/or blackening • Hyalinized whorls of collagen, scant inflammation, birefringent silica particles
  39. 39. Asbestosis • Diffuse interstitial fibrosis with asbestos bodies • Pleural Reactions: benign effusions, fibrous pleural adhesions, dense fibrocalcific plaques • Mechanisms: – Release of enzymes, toxic free radicals – Release of fibrogenic cytokines and growth factors – Direct stimulation of fibroblast collagen • Bronchogenic carcinoma and Malignant mesothelioma
  40. 40. Granulomas • Infectious: Tuberculosis, fungal • Non-infectious: Sarcoidosis, foreign bodies • SARCOIDOSIS: – Unknown etiology, F>M – Non-caseating granulomas – Asymptomatic to debilitating – Elevated serum IgG and calcium
  41. 41. Hypersensitivity Pneumonitis • Immunologically-mediated • Inhaled dusts or antigens – Farmer’s lung: actinomyces spores in hay – Pigeon’s breeder’s lung: feathers, excreta – Humidifier/Air-conditioner: HS, asthma, allergic bronchopulmonary aspergillosis – Idiopathic chronic eosinophilic pneumonia: focal consolidation of lymphocytes and eosinophils; steroid responsive
  42. 42. Bronchiolitis Obliterans – Organizing Pneumonia • Response to chronic infectious or inflammatory injury of the lungs • Cough, dyspnea, recent RTI • Loose fibrous tissue plugs within bronchioles and organizing pneumonia • Improve gradually or with steroid therapy
  43. 43. Diffuse Pulmonary Hemorrhage • Goodpasture’s syndrome – Necrotizing, hemorrhagic interstitial pneumonitis with progressive GN – Ab’s against BM • Idiopathic pulmonary hemosiderosis – Chronic, episodic hemorrhage – Unknown etiology – Heavy hemosiderin deposition w/fibrosis • Vasculitis-associated hemorrhage – Wegener’s granulomatosis, SLE, HS angiitis
  44. 44. Pulmonary Alveolar Proteinosis • Obscure etiology • Radiologically: diffuse pulmonary opacification • Pathologically: dense, amorphous, PAS-positive lipid- laden material in intracellular spaces • Clinically: respiratory difficulty (cough, sputum containing gelatinous materials) • Intraalveolar exudate: surfactant-like material, necrotic alveolar macrophages and type II cells • Exposure to irritating dusts and chemicals; immunocompromised
  45. 45. Respiratory Pathology By: Noel C. Santos, M.D.

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