Pathophysiology of bronchial asthma, Biology

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Pathophysiology

Asthma result from several physiological alterations, including altered immunologic response, increased airways resistance, increased lung-compliance, impaired mucociliary function. Asthma resulting from the antigen-antibody reaction in which chemical mediators such as histamine, eosinophilic factor etc. caused constriction of smooth muscles of both the large and small airways resulting in bronchospasm, increased capillary permeability resulting in mucosal oedema and increased mucus production.

Bronchospams causes increased airway resistance and obstruction to air flow in and out of lungs. The lung become hyperinflated resulting in increased lung compliance. The increased mucus production can cause formation of mucus plugged which can further block the airway. Impaired mucocilliary function, hypertrophy of mucus-secreting glands, thickened mucus and slowed ciliary movement are common findings in persons with asthma. During an attack, increased mucus production combined with slowed clearance of mucus due to decreased ciliary movement results in increased water loss from mucus. Mucus becomes viscous, forming a mucus plug which may block airways.

Increased airway resistance and hyperinflation can increase the work of respiratory muscles resulting in muscle fatigue and exhaustion. Resulting hypoventilation in severe cases lead to respiratory acidosis, and even death.


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