Acute bronchitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Overview

The pathologic process starts with the inoculation of tracheobranchial epithelium with invading organism, which leads to inflammation, thickening and increased mucus production.

Pathophysiology

Pathogenesis

The causative agent is transmitted through the large and medium size airway tracts.^[1]
Following transmission, the agent inoculates the tracheobronchial epithelium.
This process leads to inflammation, thickening, and increased mucus production in the airways compared to normal bronchi as shown below:

Normal Bronchi
Inflamed Bronchi

Microscopy

On microscopic analysis, epithelial-cell desquamation and denuding of the airway to the level of the basement membrane, in association with the presence of a lymphocytic cellular infiltrate, have been demonstrated.^[2]

References

↑ Gonzales R, Sande MA (2000). “Uncomplicated acute bronchitis”. Ann. Intern. Med. 133 (12): 981–91. PMID 11119400.
↑ WALSH JJ, DIETLEIN LF, LOW FN, BURCH GE, MOGABGAB WJ (1961). “Bronchotracheal response in human influenza. Type A, Asian strain, as studied by light and electron microscopic examination of bronchoscopic biopsies”. Arch. Intern. Med. 108: 376–88. PMID 13782910.

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[pmid11119400-1] Gonzales R, Sande MA (2000). “Uncomplicated acute bronchitis”. Ann. Intern. Med. 133 (12): 981–91. PMID 11119400.

[pmid13782910-2] WALSH JJ, DIETLEIN LF, LOW FN, BURCH GE, MOGABGAB WJ (1961). “Bronchotracheal response in human influenza. Type A, Asian strain, as studied by light and electron microscopic examination of bronchoscopic biopsies”. Arch. Intern. Med. 108: 376–88. PMID 13782910.

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