Asthma Pathology
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Direct answer
Asthma is a chronic inflammatory airway disease with variable, reversible airflow obstruction and hyper-reactivity, driven by TH2 lymphocytes, IgE and eosinophils in the allergic (atopic) form. The asthmatic airway shows oedema, smooth muscle hypertrophy, goblet cell hyperplasia with tenacious mucus plugs, a thickened subepithelial basement membrane and an eosinophil-rich infiltrate; sputum contains Curschmann spirals (twisted mucus casts) and Charcot-Leyden crystals from eosinophil granule proteins. Attacks are triggered by allergens, infections, exercise, cold air, aspirin and occupational agents, and status asthmaticus — unremitting attack — can be fatal.
What you must remember
- Immunology: sensitisation produces IgE via TH2-derived interleukin-4, eosinophil recruitment via interleukin-5 and mucus secretion via interleukin-13; mast-cell mediators cause early-phase bronchospasm, and late-phase cellular inflammation sustains it.
- Atopic (extrinsic) versus non-atopic (intrinsic): childhood allergic asthma with family history versus adult-onset disease, often triggered by respiratory infections or drugs; aspirin-sensitive asthma completes the Samter triad with nasal polyposis.
- Mucus plugging: overstuffed goblet cells and mucous glands fill airways with viscid plugs that contain shed epithelial clusters (Creola bodies) and branching mucus casts.
- Charcot-Leyden crystals: bipyramidal crystals of eosinophil granule protein in sputum; Curschmann spirals are twisted mucous casts of small airways — both classic sputum findings.
- Remodelling: subepithelial fibrosis producing a thickened basement membrane, smooth muscle hypertrophy and angiogenesis, explaining fixed obstruction in long-standing disease.
- Fatal asthma pathology: lungs overinflated with small dark airways plugged by mucus, accompanied by eosinophils and hypertrophied smooth muscle; death is from asphyxia.
- Management direction: inhaled corticosteroids as controller therapy with bronchodilators and stepwise escalation per current guidance, plus trigger avoidance; biological agents target severe allergic and eosinophilic disease.
Common confusion
Asthma is separated from COPD by complete reversibility, diurnal variability, eosinophilic inflammation and onset in youth — yet the two coexist as asthma-COPD overlap. Within asthma, the early phase (minutes, mast-cell mediators, bronchodilator-responsive) differs from the late phase (hours, TH2-cell driven, steroid-responsive). Do not confuse Charcot-Leyden crystals (eosinophil protein, bipyramidal) with Curschmann spirals (mucus casts, spiral shaped); naming the right structure in sputum is a recurring one-mark decision.
Exam-focused takeaway
Stems show a child with wheeze after dust exposure and a strong family history (atopic asthma), an adult with polyps and aspirin sensitivity, or a sputum photograph with spiral casts. Questions test the interleukin-TH2 axis, the histological triad of mucus, smooth muscle and basement-membrane thickening, and the sputum crystals. Link each microscopic finding to its mechanism and management responds to phase — bronchodilator early, steroid late.
Frequently asked questions
Which cells dominate asthmatic airway inflammation?
TH2 lymphocytes orchestrating eosinophils and mast cells through interleukins 4, 5 and 13 in allergic disease.
What are Curschmann spirals and Charcot-Leyden crystals?
Twisted mucous casts of small airways and bipyramidal crystals of eosinophil granule protein respectively, both found in asthmatic sputum.
Why is the basement membrane thickened in asthma?
Subepithelial fibrosis from chronic inflammation deposits collagen beneath the epithelium — a key feature of airway remodelling that contributes to fixed obstruction.
What is the Samter triad?
Asthma, chronic rhinosinusitis with nasal polyps and aspirin sensitivity, due to abnormal arachidonic acid metabolism.
What is status asthmaticus?
A severe, prolonged attack unresponsive to standard therapy, risking exhaustion, hypercapnia and death from asphyxia.