5th January 2024

Pathophysiology

Asthma is a complex disease with multigene association interacting with environmental exposure.

Pathophysiology of asthma involves two major elements: inflammation and airway hyper-responsiveness. The large airways and small airways of <2 micrometres are the sites of inflammation and airway obstruction.

Airway inflammation is secondary to interaction of inflammatory cell mediators and cells in the airways. An initial trigger causes release of inflammatory mediators, which leads to activation and migration of inflammatory cells. This inflammatory reaction is a T-helper type2 lymphocytic response. Other white cells involved are eosinophils, basophils, mast cells, macrophages, neutrophils, and natural killer cells. Neutrophils are important in near-fatal exacerbation of asthma. These cells cause changes in airways’ epithelium, tone, autonomic neuronal control and hypersecretion of mucus. They also alter the mucocilliary function and increase smooth muscle responsiveness.

Products of the inflammatory response induce smooth muscle contraction and airway hyper-responsiveness. Finally, airway smooth muscle in asthmatic people is increased in mass due to hypertrophy and hyperplasia.