Pathogenesis of Asthma
The airway obstruction in asthma is due to a number of factors which include: 1) bronchospasm; 2) edema of the airway; 3) increased mucus secretions; 4) cellular, especially eosinophilic, infiltration of the airway walls; and 5) injury of the airway epithelium. Formerly, it was thought that bronchoconstriction due to smooth muscle contraction in the airway was the major contributing factor in airway obstruction with asthma. Recently, however, it has been appreciated that the obstruction of the airways in asthma, especially in its chronic form, is primarily due to an inflammatory process.
The mast cell and its contents are more important in the acute bronchospasm caused by the reaction to inhaled irritants, allergens, and possibly exercise. More important in the chronic inflammation associated with asthma is the eosinophil which contains proteins that damage the epithelium of the airway. Neurogenic influences on the pathogenesis of asthma have led to the cholinergic theory. The cholinergic reflex plays a role in the acute bronchoconstrictive response to the inhalation of irritants. Recent interest in neurogenic mechanisms of asthma have focused on neuropeptides that are secreted by sensory nerves. These substances have vascular permeability and mucus secretory activity, bronchoconstrictor activity, and a bronchial vascular dilation effect. These cause narrowing of the airway and increased resistance to airflow. The chest x-ray changes seen in these patients include hyperlucency of the lung fields and hyperinflation characterized by wide intercostal spaces and flattened diaphragm.