Asthma Pathology
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Direct answer
Reversible, episodic bronchoconstriction on a background of chronic airway inflammation defines asthma, and its pathology is allergic in most cases: sensitised mast cells armed with IgE degranulate within minutes of antigen exposure (the early phase, driven by histamine and leukotrienes), while an eosinophil-rich late phase returns four to eight hours later. Over years the airway remodels — thickened reticular basement membrane, hypertrophied smooth muscle and goblet cell hyperplasia — which explains why inhaled corticosteroids are maintenance therapy, not rescue therapy. Sputum and histology in severe disease show Curschmann spirals (twisted mucus casts of small airways), Charcot-Leyden crystals (bipyramidal eosinophil proteins) and Creola bodies (shed epithelial clumps). Death in status asthmaticus comes from mucus plugging, not bronchospasm alone.
What you must remember
- Early phase: antigen cross-links surface IgE on mast cells, releasing histamine, tryptase, leukotriene C4 and prostaglandin D2 within minutes — bronchospasm, oedema, wheeze that peaks by 30 minutes.
- Late phase: eotaxin and interleukin-5 recruit eosinophils four to eight hours later; this phase, not the early one, responds to corticosteroids.
- Remodelling: subepithelial type III collagen deposition beneath a thickened basement membrane, smooth muscle hypertrophy, goblet cell and submucosal gland hyperplasia — structural, and only partly reversible.
- Fatal asthma morphology: overinflated lungs that fail to collapse on opening the chest, tenacious mucus plugs occluding bronchi, Curschmann spirals and Charcot-Leyden crystals microscopically.
- Triggers worth naming: aeroallergens, exercise (dry cold air), respiratory viruses, cold air, drugs, occupational isocyanates and emotional stress.
- Samter triad: asthma, nasal polyposis and aspirin sensitivity — cyclooxygenase-1 inhibition diverts arachidonate to leukotriene synthesis.
- Treatment logic: short-acting beta-2 agonists rescue; inhaled corticosteroids suppress inflammation and the late phase; leukotriene modifiers suit aspirin-sensitive and exercise-induced disease; omalizumab (anti-IgE) and anti-interleukin-5 agents for severe refractory disease.
Early and late phases of one asthma attack
Watch a cat-allergic student enter a house with a cat. Within ten minutes she wheezes: inhaled antigen bridges IgE on submucosal mast cells, and preformed histamine plus newly generated leukotriene C4 contract bronchial smooth muscle and evoke mucosal oedema — the early-phase fall in peak flow that a salbutamol inhaler reverses cleanly. She feels well by evening, but at midnight the peak flow drops again without any fresh exposure. That is the late phase: cytokine-activated endothelium has recruited eosinophils and Th2 lymphocytes, which damage epithelium and heighten reactivity for days. A single steroid dose taken early blunts the second wave — the physiological justification for the steroid component in every preventer regimen. Repeated cycles of such injury lay down collagen beneath the basement membrane and bulk up the smooth muscle, so the airway that began merely twitchy becomes structurally narrow. Management, at bottom, is interrupting that loop before remodelling wins.
Samter, sputum and the exam
Aspirin-exacerbated respiratory disease supplies the classic integrated question: the asthmatic with nasal polyps who collapses after a tablet of aspirin has lost cyclooxygenase-1 activity, shunting arachidonic acid toward leukotriene synthesis — hence leukotriene receptor antagonists work particularly well. On the diagnostic side, remember that spirometry between attacks can be normal; bronchial provocation with methacholine demonstrating hyperreactivity then settles the label. And in the pathology viva, the three named findings — Curschmann spirals, Charcot-Leyden crystals and Creola bodies — are expected in one breath from a sputum slide or a post-mortem bronchus.
Frequently asked questions
Which cells and mediators drive the early phase of an asthma attack?
IgE-armed mast cells releasing histamine, tryptase and leukotriene C4 within minutes of antigen exposure, causing bronchospasm that peaks by about 30 minutes.
What is airway remodelling in chronic asthma?
Thickened subepithelial basement membrane from collagen deposition, smooth muscle hypertrophy and goblet cell hyperplasia — structural change explaining fixed component and steroid maintenance.
What are Curschmann spirals and Charcot-Leyden crystals?
Twisted mucus casts of small bronchi and bipyramidal crystals of eosinophil-derived protein respectively — the two sputum findings pathologists name in asthma.
What constitutes Samter triad?
Asthma, nasal polyposis and aspirin sensitivity, arising from leukotriene overproduction when cyclooxygenase is inhibited.
Why do lungs in fatal asthma fail to collapse at autopsy?
Diffuse mucus plugging of small and large airways traps air distally, leaving overinflated lungs that remain expanded when the pleural cavities are opened.