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PULMONARY PATHOLOGY

PULMONARY PATHOLOGY. Prof Frank Carey. General Approach. Understanding mechanisms of disease Emphasizing the role of the pathologist in diagnosis. Functional Classification of Lung Disease. Distinctive clinical and physiological features define: Obstructive lung disease

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PULMONARY PATHOLOGY

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  1. PULMONARY PATHOLOGY Prof Frank Carey

  2. General Approach • Understanding mechanisms of disease • Emphasizing the role of the pathologist in diagnosis

  3. Functional Classification of Lung Disease Distinctive clinical and physiological features define: • Obstructive lung disease • Restrictive lung disease

  4. Airway Narrowing/Obstruction • Muscle spasm • Mucosal oedema (inflammatory or otherwise • Airway collapse due to loss of support • (Localised obstruction due to tumour or foreign body)

  5. Main Categories of Obstructive Disease • Asthma • Chronic obstructive pulmonary disease (COPD/COAD/COLD)

  6. Chronic Obstructive Disease • Chronic bronchitis • Emphysema Symptomatic patients often have both

  7. Chronic Bronchitis Cough productive of sputum on most days for 3 months of at least 2 successive years • An epidemiological definition • Does not imply airway inflammation

  8. Chronic Bronchitis • Chronic irritation defensive increase in mucus production with increase in numbers of epithelial cells (esp goblet cells) • Poor relation to functional obstruction • Role in sputum production and increased tendency to infection

  9. Chronic Bronchitis • Non-reversible obstruction • In some patients there may be a reversible (“asthmatic”) component

  10. Normal vs. Chronic Bronchitis

  11. Small airways in Chronic Bronchitis • More important than traditionally realised • Goblet cell metaplasia, macrophage accumulation and fibrosis around bronchioles may generate functional obstruction

  12. Emphysema • Increase beyond the normal in the size of the airspaces distal to the terminal bronchiole • Without fibrosis The gas-exchanging compartment of the lung

  13. Emphysema (types) • Centriacinar (centrilobular) • Panacinar • Others (e.g. localised around scars in the lung)

  14. Emphysema • Difficult to diagnose in life (apart from in extremis) • Radiology (CT) can show changes in lung density • Correlation with function known from autopsy studies

  15. Emphysema • “Dilatation” is due to loss of alveolar walls (tissue destruction) • Appears as “holes” in the lung tissue

  16. Normal lung

  17. Centriacinar emphysema

  18. Panacinar emphysema 1

  19. Panacinar emphysema 2

  20. Emphysema How do these changes relate to functional deficit? • Poorly at macroscopic level • Better with microscopic measurement

  21. Normal

  22. Early emphysema

  23. Emphysema Impairs Respiratory Function • Diminished alveolar surface area for gas exchange • Loss of elastic recoil and support of small airways leading to tendency to collapse with obstruction

  24. Loss of surface area (emphysema)

  25. Loss of support on bronchiolar walls

  26. As disease advances…. Pa O2 leads to: • Dyspnoea and increased respiratory rate • Pulmonary vasoconstriction (and pulmonary hypertension)

  27. Epidemiology of COPD • Smoking • Atmospheric pollution • Genetic factors

  28. Pathophysiology of Emphysema High rate of emphysema in the rare genetic condition of a 1 antitrypsin deficiency • THE PROTEASE/ANTIPROTEASE HYPOTHESIS

  29. Elastic Tissue • Sensitive to damage by elastases (enzymes produced by neutrophils and macrophages) • a 1 antitrypsin acts as an anti-elastase Imbalance in either arm of this system predisposes to destruction of elastic alveolar walls (emphysema)

  30. Tobacco smoke….. • Increases nos. of neutrophils and macrophages in lung • Slows transit of these cells • Promotes neutrophil degranulation • Inhibits a 1 antitrypsin

  31. Bronchial Asthma A chronic inflammatory disorder characterised by hyperreactive airways leading to episodic reversible bronchoconstriction

  32. Asthma • Extrinsic - response to inhaled antigen • Intrinsic - non-immune mechanisms (cold, exercise, aspirin)

  33. Immunological Mechanisms Type I hypersensitivity - allergen binds to IgE on surface of mast cells • Degranulation (histamine) • muscle spasm • inflammatory cell influx (eosinophils) • mucosal inflammation/oedema • Inflammatory infiltrate tends to chronicity

  34. Pathology • Narrowed oedematous airways • Mucus plugs • Inflammatory cells (lymphocytes, plasma cells, eosinophils) • Epithelial cell damage

  35. Mucosal oedema

  36. Mucus plugs

  37. Mucus plug/inflammation

  38. Inflammation

  39. Inflammation/epithelial damage

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