Astma 2006-en

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Astma 2006-en

  1. 1. By – Dr. SAMIA FATIMA
  2. 2.  1. Eosinophils  2. Mast cells  3. T-lymphocytes  4. Neutrophils  5. Basophils
  3. 3. Acute inflammation Chronic inflammation Remodeling of airways Symptoms of bronchoconstriction Exacerbation nonspecific hyperreactivity Ongoing obstruction of airways
  4. 4. Pathogenesis of asthma
  5. 5. 1.Early phase  Inhaled Antigen  Sensitised mast cells on the mucosal surface  bronchoconstriction  Histamine bronchoconstriction, increased vascular permeability.  prostaglandin D 2  bronchoconstriction, vasodilatation.  Leucotriene C4,D4, E4  Increased vascular permeability, mucus secretion and bronchoconstriction.  Direct subepithelial parasympathetic stimulation  bronchoconstriction.
  6. 6. 2.Late phase  starts 4 to 8 hours later  Mast cell release additional cytokine  Influx of leukocytes(neutrophil,eosinophil)  Eosinophils are particularly important- exert a variety of effect
  7. 7. Bronchial inflammation Environment factor Genetic prediposition Bronchial hyperreactivity + trigger factors Cough, Wheeze, Breathlessness, Chest tightness Oedema BronchoC Mucus production Airways narrowing
  8. 8. MAST CELLS release histamine,cysteinyl-leukotrienes,cytokines,chemokines, growth factors and neutrophins causes bronchoconstriction MACROPHAGES AND DENDRITIC CELLs release cytokines,IL-10. dendritic cells are the antigen presenting cells EOSINOPHILS release of basic proteins and oxygen derived free radicals causes airway hyperresponsiveness
  9. 9. NEUTROPHILS increased numbers of activated neutrophils are found in sputum and airways of patients with severe asthma. T Lymphocytes Th2 cells release IL-5 eosinophilic inflammation IL-4,13 increased IgE formation
  10. 10. PRIMARY MEDIATORS 1.Th2 cells > IL 4,5 > IgE production & Mast cell recruitment 2.Histamine - bronchconstriction by direct and cholinergic reflex actions 3.ECF and NCF
  11. 11. Secondary mediators LT C4, D4, and E4. prolonged bronchospasm increased vascular permeability increased mucus secretion. Prostaglandins (D2) Bronchospasm Vasodilation PAF platelet aggregation granule secretion.
  12. 12. i. Inflammatory cell infiltration of the airways ii. Increased thickness of the bronchial smooth muscle iii. Partial or full loss of the respiratory epithelium iv. Subepithelial fibrosis v. Hypertrophy and hyperplasia of the submucosal glands and goblet cells vi. Partial or full occlusion of the airway lumen by mucous plugs vii. Enlarged mucous glands and blood vessels
  13. 13.  Acute bronchoconstriction  Swelling of bronchial wall Chronic production of mucous  Remodeling of airways walls

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