PBL Session 3Rosshini Jagatheswaran
Describe thePATHOGENESIS ofbronchial asthmaMUST KNOWLearning Outcome
How T helper cells work?
TH2cellssecrete cytokines IL-4, IL-5, IL-13stimulate B cells to produce IgE and otherantibodies. IL-4 stimulates the pr...
Sensitization to Allergen• Inhaled allergens• TH2– dominated response• IgE productions• Eosinophil recruitment• Release of...
Allergen-Triggered Asthma• Re-exposure• Ag-induced cross linking of IgE bound to IgEreceptors on mast cell• Mediators rele...
• Leukotrienes- constriction of bronchi  bronchospasm- increased mucus production  mucosalaccumulation• Histamine- incre...
Late Phase• Recruited leukocytesinitiate late phase• Mediators releasefrom endothelium,epithelial cells,leukocytes• Eosino...
Comparison of a normal bronchiolewith that in a patient with asthma• Increase in the number of mucus-secretinggoblet cells...
POP-QUIZWhich T Helper Cell plays an importantrole in bronchial asthma?What happens after IgE binds to themast cell in the...
Some factors released by eosinophils inthe late phase causes damage to theepithelium. Give 2 examples of thefactors.Give 2...
THANK YOU
Pathogenesis of bronchial asthma
Pathogenesis of bronchial asthma
Pathogenesis of bronchial asthma
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Pathogenesis of bronchial asthma

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Pathogenesis of bronchial asthma

  1. 1. PBL Session 3Rosshini Jagatheswaran
  2. 2. Describe thePATHOGENESIS ofbronchial asthmaMUST KNOWLearning Outcome
  3. 3. How T helper cells work?
  4. 4. TH2cellssecrete cytokines IL-4, IL-5, IL-13stimulate B cells to produce IgE and otherantibodies. IL-4 stimulates the production of IgE IL-5 activates locally recruited eosinophils IL-13 stimulates mucus secretion frombronchial submucosal glands and alsopromotes IgE production by B cells
  5. 5. Sensitization to Allergen• Inhaled allergens• TH2– dominated response• IgE productions• Eosinophil recruitment• Release of granules and mediators
  6. 6. Allergen-Triggered Asthma• Re-exposure• Ag-induced cross linking of IgE bound to IgEreceptors on mast cell• Mediators released – histamine, leukotrienes• Tight junctions between epithelial cells open• Antigen enter mucosa• Mucosal mast cells activated• Eosinophil release other mediators
  7. 7. • Leukotrienes- constriction of bronchi  bronchospasm- increased mucus production  mucosalaccumulation• Histamine- increased vascular permeability  swelling &redness  edema- increased mucus production  mucosalaccumulation• Eosinophilic chemotactic factor- Chemotaxis of eosinophils accumulation ofeosinophils
  8. 8. Late Phase• Recruited leukocytesinitiate late phase• Mediators releasefrom endothelium,epithelial cells,leukocytes• Eosinophils  MBP,ECP – damageepithelium
  9. 9. Comparison of a normal bronchiolewith that in a patient with asthma• Increase in the number of mucus-secretinggoblet cells in the mucosa and hypertrophy ofsubmucosal mucus glands  Accumulation ofmucus in the bronchial lumen• Recruitment of eosinophils & macrophagesintense chronic inflammation• Thickened basement membrane• Hypertrophy & hyperplasia of smooth musclecells
  10. 10. POP-QUIZWhich T Helper Cell plays an importantrole in bronchial asthma?What happens after IgE binds to themast cell in the first phase-sensitizationphase?Leukotrienes causes …?Upon re-exposure of Ag, what happensafter binding of IgE?
  11. 11. Some factors released by eosinophils inthe late phase causes damage to theepithelium. Give 2 examples of thefactors.Give 2 differences of a normalbronchiole and bronchiole of anasthmatic patient.
  12. 12. THANK YOU
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