ABSTRACT
Asthma is characterized by fluctuating airways obstruction, with diurnal variation and nocturnal exacerbations. This manifests as the triad of wheeze, cough and breathlessness. These symptoms are due to a combination of constriction of bronchial smooth muscle, oedema of the mucosa lining the small bronchi, and plugging of the bronchial lumen with viscous mucus and inflammatory cells (Figure 33.1). Asthma is broadly categorized into non-allergic and allergic, but there is considerable overlap. In allergic asthma, which is usually of early onset, extrinsic allergens produce a type I allergic reaction in atopic subjects. Type I reactions are triggered via reaginic antibodies (IgE) on the surface of mast cells and other immune effector cells, especially activated Th2 lymphocytes, which release cytokines that recruit eosinophils and promote further IgE synthesis and sensitivity. Patients with non-allergic (late-onset) asthma do not appear to be sensitive to any single well-defined antigen, although infection (usually viral) often precipitates an attack. Inflammatory mediators implicated in asthma include histamine, several leukotrienes (LTC4/D4 and E4) 5-hydroxytryptamine (serotonin), prostaglandin D2, platelet-activating factor (PAF), neuropeptides and tachykinins. Increased parasympathetic tone due to local and centrally mediated stimuli also promotes bronchoconstriction.
