Episodic, reversible bronchoconstriction with airway hyperresponsiveness and inflammation.
Wheeze, dyspnea, chest tightness, cough (often at night)
Atopy: eczema, allergic rhinitis, family history
Allergic (atopic) mechanism
Allergen → Th2: IL-4 (IgE switch), IL-5 (eosinophils), IL-13 (mucus).
Early phase: IgE cross-linking on mast cells → histamine, leukotrienes · late phase: eosinophils, major basic protein
Type I hypersensitivity
Viral infection, exercise, cold air, aspirin (AERD), occupational agents, GERD, β-blockers.
Aspirin blocks COX → arachidonic acid shunted to leukotrienes
Asthma + nasal polyps + aspirin reaction
Mucus plugs, eosinophils, smooth muscle hypertrophy, thickened basement membrane, goblet cell hyperplasia.
Curschmann spirals (shed epithelium), Charcot-Leyden crystals (eosinophil protein)
Chronic remodeling → partly fixed obstruction
Obstructive PFTs reversing with bronchodilator (FEV1 ↑ ≥ 12% and 200 mL).
Normal baseline? → methacholine challenge
DLCO normal or ↑
Severe attack not responding to treatment; pulsus paradoxus.
Tiring muscles → CO₂ climbs back to "normal" or high
Normal/↑ PaCO₂ during an attack = impending failure
SABA rescue; ICS controller; LABA only with ICS; montelukast; biologics: omalizumab (IgE), mepolizumab (IL-5), dupilumab (IL-4Rα).
Target the Th2 cascade
Eosinophilic severe asthma → anti-IL-5
Bronchiectasis — definition
Permanent bronchial dilation after necrotizing inflammation destroys muscle and elastic tissue.
Chronic infection + impaired clearance → vicious cycle
Copious foul purulent sputum, hemoptysis, clubbing; tram-track / signet-ring sign on CT
Cystic fibrosis, primary ciliary dyskinesia (Kartagener: situs inversus, sinusitis, infertility), post-infection (TB, measles, pertussis), obstruction (tumor, foreign body), ABPA, immunodeficiency.
Kartagener: dynein arm defect · ABPA: hypersensitivity to Aspergillus in asthma/CF
Complications: AA amyloidosis, cor pulmonale