ASTHMA

Asthma and chronic obstructive pulmonary disease (COPD) show several similarities in their clinical features.

Asthma is a chronic disorder of the airways that is characterized by reversible airflow obstruction and airway inflammation, persistent airway hyperreactivity (AHR) and airway remodeling. The pathogenesis of asthma involves several processes. Chronic inflammation of the bronchial mucosa is prominent, with infiltration of activated T-lymphocytes and eosinophils. This results in subepithelial fibrosis and the release of chemical mediators that can damage the epithelial lining of the airway. Many of these mediators are released following activation and degranulation of mast cells in the bronchial tree. Some of these mediators act as chemotactic agents for other inflammatory cells. They also produce mucosal edema, which narrows the airway and stimulates smooth muscle contraction, leading to bronchoconstriction. Excessive production of mucus can cause further airway obstruction by plugging the bronchiolar lumen. See Fig 1

Fig 1 Inflammatory mediators in Asthma: Activation of mast cells results in secretion of several mediators that contribute to the pathogenesis of asthma. These mediators produce bronchconstriction and initiate both the acute inflammatory response and attract cells responsible for maintaining chronic inflammation. IL, interleukin; GM-CSF, granulocyte and macrophage colony-stimulating factor; PG, prostaglandin; TNF, tissue necrosis factor; IFN interferon

Category: Pharmacology Notes