In this article, we will discuss about the Pathophysiology of Bronchiectasis. So, let’s gets started.
The most widely accepted pathogenesis of infectious bronchiectasis is the vicious cycle hypothesis according to which increased susceptibility to infection and poor mucociliary clearance result in microbial colonization in the bronchial tree. Inherited conditions such as cystic fibrosis or dyskinetic cilia syndrome can cause impaired mucociliary clearance, and it has been proposed that even a single severe infection can result in significant airway damage and poor secretion clearance. The presence of microbes leads to chronic inflammation with consequent airway wall damage, continued impairment of secretion and microbial clearance, and ongoing propagation of the inflammatory cycle.
The classical studies of the pathogenesis of bronchiectasis from 1950s demonstrated significant small-airway wall inflammation and large-airway wall destruction as well as dilatation, with loss of elastin, smooth muscle, and cartilage. The inflammatory cells in the small-airways release proteases and other mediators such as reactive oxygen species and proinflammatory cytokines that damage the large-airway walls. Furthermore, the ongoing inflammatory process in small-airways results in airflow obstruction.
It is thought that antiproteases such as α1 antitrypsin play an important role in neutralizing the damaging effects of the neutrophil elastase and in enhancing bacterial killing.
Bronchiectasis and emphysema have been observed in patients with α1 antitrypsin deficiency.
The mechanism for noninfectious bronchiectasis includes immune-mediated reactions that damage the bronchial wall (associated with autoimmune conditions such as Sjogren syndrome and rheumatoid arthritis).
Traction bronchiectasis refers to dilated airways arising from parenchymal distortion as a result of lung fibrosis (eg. post-radiation fibrosis or idiopathic pulmonary fibrosis).
Source: Harrison’s Principles of Internal Medicine
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