Pathophysiology : Asthma


  • Primary response is chronic inflammation from exposure to allergens or irritants
    • Leading to airway bronchoconstriction, hyper-responsiveness, and edema of airways
    • Exposure to allergens or irritants initiates inflammatory cascade
  • Inflammatory mediators cause early-phase response
    • Vascular congestion
    • Edema formation
    • Production of thick, tenacious mucus
    • Bronchial muscle spasm
    • Thickening of airway walls
  • Early-phase response
    • As the inflammatory process begins, mast cells (found beneath the basement membrane of the bronchial wall) degranulate and release multiple inflammatory mediators.
      • IgE antibodies are linked to mast cells, and the allergen cross-links the IgE.
      • Inflammatory mediators such as leukotrienes, histamine, cytokines, prostaglandins, and nitric oxide are released.
    • Some inflammatory mediators have effects on the
      • Blood vessels, causing vasodilation and increasing capillary permeability (runny nose)
      • Nerve cells causing itching
      • Smooth muscle cells causing bronchial spasms and airway narrowing
      • Goblet cells causing mucus production
  • Late-phase response
    • Occurs within 4 to 6 hours after initial attack
    • Occurs in about 50% of patients
    • Can be more severe than early phase and can last for 24 hours or longer
    • If airway inflammation is not treated or does not resolve, it may lead to irreversible lung damage
    • Structural changes in the bronchial wall known as remodeling


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