Pathogenesis of asthma

Pathogenesis of asthma

1. Pathogenesis Of Bronchial Asthma

2. Pathology Mucosa-Activated Eosinophils, T lymphocytes, mast cells. Thickening Basement membrane- Subepithelial collagen deposition. Lumen has Epithelial cells(Desquamation). Mucous plug(Mucous glycoproteins-Goblet cells; P lasma proteins- leaky bronchial vessels). Vasodilation, blood vessels. Narrowed, erythematous and edematous .

3. Cells Mast Cells-Initiation. Sensitivity by binding specific IgE . Macrophage-Activated by IgE . Dendritic cells-Major Antigen Presenting Cells. Eosinophils-Characteristic of Asthma . Basic Proteins and ROS AHR. Growth Factors Remodelling and exacerbations. Neutrophils-Severe Asthma and during exacerbations. T lymphocytes-Recruitment and survival of Eosinophils. Maintenance of Mast cells. T H 2 predominant. IL-5, IL-4 and IL-13. Structural cells-Epithelial cells(TSLP, IL-25 & IL-33), Fibroblasts and Airway smooth muscle cells.

4. “Mediator Soup”

5. Effects Of Inflammation Airway Epithelium-Loss of Barrier, Enzymes & Relaxant Factor; exposed Sensory Nerves. Fibrosis -Basement Membrane Thickening Sub epithelial Type 3 & 5 collagen deposition. TGF- β . Severe patients within airway wall. Airway Smooth Muscle- Responsiveness to constriction. Response to β agonist. PDGF/Endothelin-1 Hypertrophy and Hyperplasia . Vascular Response- Mucosal blood flow. Angiogenesis (VEGF). Microvascular leak. Mucous Hypersecretion -IL-13. Hyperplasia of Submucosal glands and Goblet cells. Neural Regulation- Neurotrophins . Substance P. Hyperalgesia. Reflex c holinergic contraction. Airway Remodelling. Airway Hyperresponsiveness -Excessive Bronchoconstriction. Direct and Indirect.

6. Summary

7. References Harrison’s Principles of Internal Medicine, 19E. Robbins & Cotran Pathologic Basis Of Disease, 9E .

8. Thank You