Bronchitis pathophysiology: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{CMG}} | {{CMG}}{{AE}}{{MehdiP}} | ||
{{Bronchitis}} | {{Bronchitis}} | ||
==Overview== | ==Overview== | ||
[[ | [[Bronchitis]] is the inflammatory response of the bronchial epithelium to infections or irritants. The pathophysiological finding seen with acute bronchitis include: thickening, hyperemia and edema of the bronchial mucosa. When process becomes chronic, decreases in the bronchial mucociliary function leads to airway clogging by debris which causes copious mucus secretion that causes the characteristic cough of bronchitis. | ||
==Pathophysiology== | ==Pathophysiology== | ||
* [[Acute bronchitis]] | * '''[[Acute bronchitis]]:''' | ||
:Inflammatory response of the bronchial epithelium to infections or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa. | |||
: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:''' | |||
: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. | |||
:[[Microscope|Microscopically]] there is [[Infiltration (medical)|infiltration]] of the airway walls with [[Inflammation|inflammatory]] cells, particularly [[neutrophils]]. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to [[metaplasia]] (abnormal change in the tissue) and [[fibrosis]] (further thickening and scarring) 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== | ||
Revision as of 15:04, 14 September 2016
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
|
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, hyperemia and edema of the bronchial mucosa. When process becomes chronic, decreases in the bronchial mucociliary function leads to airway clogging by debris which causes copious mucus secretion that causes the characteristic cough of bronchitis.
Pathophysiology
- Inflammatory response of the bronchial epithelium to infections or irritants that involve the medium and large size airways results in thickening of the bronchial and tracheal mucosa.
- Bronchitis caused by influenza virus shows an epithelial-cell desquamation in association with the presence of a lymphocytic cellular infiltrate[1].
- 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.
- Microscopically there is infiltration of the airway walls with inflammatory cells, particularly neutrophils. Inflammation is followed by scarring and remodeling that thickens the walls resulting in narrowing of the small airway. Further progression leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening and scarring) of the lower airway. The consequence of these changes is a limitation of airflow[2][3][4].
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.
- ↑ 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.