Pathophysiology : Asthma

Pathophysiology

• 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