Bronchitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | |||
* '''[[Acute bronchitis]]:''' | *'''[[Acute bronchitis]]:''' | ||
:Inflammatory response of the bronchial epithelium to | :Inflammatory response of the bronchial epithelium to infectious agents or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa. | ||
*'''Chronic bronchitis:''' | *'''Chronic bronchitis:''' | ||
:Halmark features include:[[hyperplasia]] (increased number) and [[hypertrophy]] (increased size) of the goblet cells ([[mucous gland]]) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. | :Halmark features include:[[hyperplasia]] (increased number) and [[hypertrophy]] (increased size) of the goblet cells ([[mucous gland]]) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction. | ||
===Microscopy=== | |||
*'''Acute bronchitis''' caused by [[influenza virus]] shows an epithelial-cell desquamation in association with the presence of a lymphocytic cellular infiltrate<ref name="pmid13782910">{{cite journal |vauthors=WALSH JJ, DIETLEIN LF, LOW FN, BURCH GE, MOGABGAB WJ |title=Bronchotracheal response in human influenza. Type A, Asian strain, as studied by light and electron microscopic examination of bronchoscopic biopsies |journal=Arch. Intern. Med. |volume=108 |issue= |pages=376–88 |year=1961 |pmid=13782910 |doi= |url=}}</ref>. | |||
*'''Chronic bronchitis''' On microscopic histopathological analysis there is infiltration of the airway walls with [[Inflammation|inflammatory]] cells, particularly CD8+ T-lymphocytes and neutrophils<ref name="pmid15047950">{{cite journal |vauthors=Baraldo S, Turato G, Badin C, Bazzan E, Beghé B, Zuin R, Calabrese F, Casoni G, Maestrelli P, Papi A, Fabbri LM, Saetta M |title=Neutrophilic infiltration within the airway smooth muscle in patients with COPD |journal=Thorax |volume=59 |issue=4 |pages=308–12 |year=2004 |pmid=15047950 |pmc=1763819 |doi= |url=}}</ref>. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airways. Further progression leads to [[metaplasia]] and [[fibrosis]] of the lower airway. The consequence of these changes is a limitation of airflow<ref name="pmid19494220">{{cite journal |vauthors=Cosio MG, Saetta M, Agusti A |title=Immunologic aspects of chronic obstructive pulmonary disease |journal=N. Engl. J. Med. |volume=360 |issue=23 |pages=2445–54 |year=2009 |pmid=19494220 |doi=10.1056/NEJMra0804752 |url=}}</ref><ref name=kc>Kumar P, Clark M (2005). ''Clinical Medicine'', 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.</ref><ref name="pmid22029978">{{cite journal |vauthors=McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, Wright AC, Gefter WB, Litzky L, Coxson HO, Paré PD, Sin DD, Pierce RA, Woods JC, McWilliams AM, Mayo JR, Lam SC, Cooper JD, Hogg JC |title=Small-airway obstruction and emphysema in chronic obstructive pulmonary disease |journal=N. Engl. J. Med. |volume=365 |issue=17 |pages=1567–75 |year=2011 |pmid=22029978 |pmc=3238466 |doi=10.1056/NEJMoa1106955 |url=}}</ref>. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 14:29, 16 September 2016
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
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Bronchitis Main page |
Overview
Bronchitis is the inflammatory response of the bronchial epithelium to infections or irritants. The pathophysiological finding seen with acute bronchitis include: thickening, inflammation and increased mucos production. When process becomes chronic, decreases in the bronchial mucociliary function leads to airway clogging by debris and copious mucus secretion.
Pathophysiology
Pathogenesis
- Inflammatory response of the bronchial epithelium to infectious agents or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa.
- Chronic bronchitis:
- Halmark features include:hyperplasia (increased number) and hypertrophy (increased size) of the goblet cells (mucous gland) of the airway, resulting in an increase in secretion of mucus which contributes to the airway obstruction.
Microscopy
- Acute bronchitis caused by influenza virus shows an epithelial-cell desquamation in association with the presence of a lymphocytic cellular infiltrate[1].
- Chronic bronchitis On microscopic histopathological analysis there is infiltration of the airway walls with inflammatory cells, particularly CD8+ T-lymphocytes and neutrophils[2]. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airways. Further progression leads to metaplasia and fibrosis of the lower airway. The consequence of these changes is a limitation of airflow[3][4][5].
References
- ↑ 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.
- ↑ Baraldo S, Turato G, Badin C, Bazzan E, Beghé B, Zuin R, Calabrese F, Casoni G, Maestrelli P, Papi A, Fabbri LM, Saetta M (2004). "Neutrophilic infiltration within the airway smooth muscle in patients with COPD". Thorax. 59 (4): 308–12. PMC 1763819. PMID 15047950.
- ↑ Cosio MG, Saetta M, Agusti A (2009). "Immunologic aspects of chronic obstructive pulmonary disease". N. Engl. J. Med. 360 (23): 2445–54. doi:10.1056/NEJMra0804752. PMID 19494220.
- ↑ Kumar P, Clark M (2005). Clinical Medicine, 6ed. Elsevier Saunders. pp 900-901. ISBN 0702027634.
- ↑ McDonough JE, Yuan R, Suzuki M, Seyednejad N, Elliott WM, Sanchez PG, Wright AC, Gefter WB, Litzky L, Coxson HO, Paré PD, Sin DD, Pierce RA, Woods JC, McWilliams AM, Mayo JR, Lam SC, Cooper JD, Hogg JC (2011). "Small-airway obstruction and emphysema in chronic obstructive pulmonary disease". N. Engl. J. Med. 365 (17): 1567–75. doi:10.1056/NEJMoa1106955. PMC 3238466. PMID 22029978.