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Describe bronchial asthma with its types, pathogenesis and morphology.

Pathology · 2nd Professional — Para-Clinical

Definition

Bronchial asthma is a chronic inflammatory disorder of the airways characterised by reversible airflow obstruction, bronchial hyper-responsiveness, and recurrent episodes of wheeze, breathlessness, chest tightness and cough.

Type	Mechanism	Features
Atopic (extrinsic, allergic)	Type I IgE-mediated hypersensitivity	Begins in childhood; family history of atopy; raised serum IgE and eosinophils; positive skin prick tests; associated with eczema and rhinitis
Non-atopic (intrinsic)	Non-immune triggers	Adult onset; normal IgE; negative skin tests; triggered by respiratory infection, cold, exercise, stress
Drug-induced	Aspirin-sensitive — shunting of arachidonic acid to leukotrienes	SAMTER triad — asthma, aspirin sensitivity and nasal polyps
Occupational	Sensitisation to a workplace agent	Isocyanates, flour, wood dust; symptoms improve away from work

Pathogenesis

Allergen in a sensitised airway cross-links IgE on mast cells → early (immediate) phase — 30 to 60 minutes → histamine, leukotrienes C4/D4/E4, prostaglandin D2 → bronchospasm, oedema and mucus → late phase — 4 to 8 hours → TH2 cells release IL-4, IL-5 and IL-13; eosinophils are recruited → Eosinophil major basic protein damages the epithelium → Repeated cycles → airway remodelling — permanent and only partly reversible

Morphology

Overinflated lungs with widespread mucus plugging of bronchi and bronchioles; the plugs may be coughed up as casts
Curschmann spirals — whorled mucus casts of small airways
Charcot–LEYDEN crystals — needle-shaped crystals of eosinophil membrane protein (galectin-10)
Creola bodies — clusters of shed epithelial cells
Airway remodelling — thickened basement membrane (subepithelial fibrosis), smooth muscle hypertrophy and hyperplasia, goblet cell and submucosal gland hyperplasia, and increased vascularity
Eosinophil-rich inflammatory infiltrate throughout the wall

CLINICAL PEARL

Airway remodelling is why asthma is not simply reversible bronchospasm. Repeated inflammation thickens the basement membrane and hypertrophies the smooth muscle, and those changes do not reverse with a bronchodilator. This is the reason inhaled corticosteroids, which suppress the inflammation, are the controller, while bronchodilators only relieve symptoms.

Applied Aspects

Diagnosis rests on demonstrating reversibility — a rise in FEV1 of 12% and 200 mL after a bronchodilator, or diurnal variability in peak flow
Inhaled corticosteroids are the cornerstone; relying on a bronchodilator alone leaves the inflammation untreated and is associated with worse outcomes
Status asthmaticus — severe unremitting attack; a silent chest, exhaustion, a normal or rising PaCO2 and confusion are signs of imminent respiratory arrest, not of improvement
Inhaler technique and adherence explain most "resistant" asthma, and should be checked before treatment is escalated
Biological agents — omalizumab (anti-IgE), mepolizumab (anti-IL-5) — for severe eosinophilic and allergic asthma
Identify and avoid triggers — dust mite, cockroach, pets, mould, tobacco smoke, and in India biomass smoke and outdoor air pollution
Distinguish asthma from COPD — asthma is reversible, often begins in childhood, varies day to day and has eosinophilic inflammation; COPD is largely irreversible, begins later, is progressive and has neutrophilic inflammation
Beta-blockers may precipitate severe bronchospasm and are avoided; cardioselective agents are used cautiously when genuinely indicated

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