Pathophysiology · MU Sofia

82. Obstructive lung diseases (bronchial asthma) - etiology, pathogenesis, clinical manifestations.

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Topic 82 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 250 words (2 min of reading), with 15 flashcards.

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  1. Obstructive lung diseases (bronchial asthma) – etiology, pathogenesis, and clinical manifestations.

Obstructive lung diseases (bronchial asthma) – etiology, pathogenesis, and clinical manifestations.

Asthma is a chronic inflammatory disease of the airways characterized by reversible bronchial obstruction, airway hyperresponsiveness, and episodic symptoms.

Etiology

  1. 1 Extrinsic (allergic, atopic) asthma
  • Most common type, often starting in childhood.
  • Triggers:
  • Inhaled allergens: dust mites, pollen, animal dander.
  • Food allergens (less common).
  • Associated with:
  • Allergic rhinitis.
  • Eczema.
  • Positive family history (strong genetic predisposition).
  1. 2 Intrinsic (non- allergic) asthma
  • Usually adult onset.
  • Triggers:
  • Respiratory infections (especially viral).
  • Cold air, exercise.
  • Stress, strong odors.
  • Medications (aspirin —aspirin- exacerbated respiratory disease).
  1. 3 Occupational asthma
  • Due to workplace sensitizers (chemicals, dusts).
  1. 4 Drug- induced asthma
  • Aspirin and NSAIDs (by shifting arachidonic acid metabolism toward leukotriene production).

Pathogenesis

  1. 1 Initial sensitization phase (in allergic asthma)
  • Allergen exposure → uptake by antigen-presenting cells → activation of Th2 cells → B cells produce IgE antibodies.
  • IgE binds to mast cells → sensitization.
  1. 2 Re- exposure (early- phase reaction)
  • Allergen cross-links IgE on mast cells → degranulation → release of histamine, leukotrienes, prostaglandins → bronchoconstriction, mucus secretion, vasodilation.
  1. 3 Late- phase reaction
  • Recruitment of eosinophils, neutrophils, and Th2 cells → sustained inflammation, epithelial damage, and further hyperreactivity
  1. 4 Airway remodeling (in chronic asthma)
  • Smooth muscle hypertrophy.
  • Subepithelial fibrosis.
  • Goblet cell hyperplasia → increased mucus.

Clinical manifestations

Typical symptoms (episodic)

  • Dyspnea.
  • Wheezing (mainly during expiration).
  • Cough, often worse at night or early morning.
  • Chest tightness.

During attack

  • Prolonged expiration.
  • Use of accessory muscles.
  • Hyperinflated chest.
  • Tachypnea, tachycardia.
  • In severe cases ("status asthmaticus"): silent chest, severe hypoxia, possible respiratory failure.

Between attacks

  • Often asymptomatic, especially in early disease.

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