Describe in detail the pathophysiological process of bronchitis

Describe in detail the pathophysiological process of bronchitis

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Acute bronchitis is an incendiary reaction to infections of the epithelium of the bronchi. In clinical nomenclature acute bronchitis suggests a self-limiting inflammation of the large trachea of the bronchi that is manifested by cough with no pneumonia (Kinkade & Long, 2016). The inflammatory reaction results in brochial epithelial damage, which results in airway hyper active responsiveness and phlegm production (Kinkade & Long, 2016). Epithelial cells shedding and desertification of the airway epithelium to basement membrane in combination with the existence of lymphocytic cellular infiltrate were exhibited after influenza virus mediated tracheobronchitis. Microscopic analysis has shown thickening of the brochial and tracheal mucosa analogous to the swollen areas (Kinkade & Long, 2016).

Hyper-excudation of the submucosal glands leads to obstruction of the airways from excessive phlegm. The most extrusive symptom is secretion production (Kinkade & Long, 2016). Acute bronchitis has a brief, acute duration that subsides with no long-standing effects.

Describe in detail the pathophysiological process of bronchitis
Describe in detail the pathophysiological process of bronchitis

Pulmonary function tests of patients with acute bronchitis shows brochial blockage analogous to asthma (Kinkade & Long, 2016). As the symptoms of acute bronchitis lessen, pulmonary function goes back to normal. Half of all individuals with acute bronchitis continue to cough for more than two weeks (Kinkade & Long, 2016). In a one-fourth of patients, cough can last for more than one month (Kinkade & Long, 2016). This is called postbrochitis syndrome. This phase possibly shows ongoing restoration to the bronchial walls after clearance of acute infection (Kinkade & Long, 2016).

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Chronic Bronchitis that recurs for years can precipitate severe complications in relation to hypoxemia and hypercapnic respiratory malfunction (Kinkade & Long, 2016). Protracted hypoxemia leads to cyanosis, polycythemia and pulmonary hypertension (Kinkade & Long, 2016). Pulmonary hypertension can successively lead to cor pulmonale which is a mutation in the structure and performance of the right side of the heart (Kinkade & Long, 2016). Chronic Bronchitis also raises the risk of acute bacterial and viral illness, the warning sign exacerbation of which may deteriorate overall respiratory health (Kinkade & Long, 2016).