Bronchiolitis pathophysiology: Difference between revisions
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Bronchiolitis}} | {{Bronchiolitis}} | ||
==Overview== | |||
The [[viral infection]] induces an [[inflammatory]] response which leads to infiltration of [[Inflamation#Celular component|inflammatory cells]] (RSV-specific lymphocytes), [[edema]] and [[necrosis]] of the [[epithelium]] in the [[bronchioles]] which is then sloughed into the lumina causing proliferation of cuboidal epithelial cells without cilia.<ref>{{Cite book | last1 = Mandell | first1 = Gerald L. | last2 = Bennett | first2 = John E. (John Eugene) | last3 = Dolin | first3 = Raphael. | title = Mandell, Douglas, and Bennett's principles and practice of infectious disease | date = 2010 | publisher = Churchill Livingstone/Elsevier | location = Philadelphia, PA | isbn = | pages = }}</ref><ref name="pmid19209271">{{cite journal| author=Wright M, Mullett CJ, Piedimonte G| title=Pharmacological management of acute bronchiolitis. | journal=Ther Clin Risk Manag | year= 2008 | volume= 4 | issue= 5 | pages= 895-903 | pmid=19209271 | doi= | pmc=PMC2621418 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19209271 }} </ref> This phenomena leads to complete or partial obstruction due to reduction of the bronchiolar lumenina and necrotic tissue accumulation, leading to hyperinflation secondary to a valve mechanism produced by the obstruction of the airway. By this mechanism, air can flow into the lungs by increased negastive pressure during inspiration but is unable to flow out of the lung as the airway's diameter is smaller during expiration.<ref>{{Cite book | last1 = Mandell | first1 = Gerald L. | last2 = Bennett | first2 = John E. (John Eugene) | last3 = Dolin | first3 = Raphael. | title = Mandell, Douglas, and Bennett's principles and practice of infectious disease | date = 2010 | publisher = Churchill Livingstone/Elsevier | location = Philadelphia, PA | isbn = | pages = }}</ref> Obstructed areas can evolve to atelectasias. In childen Kohn channels are not well developed, therefore atelectasias and hyperinfletion can be greater. | |||
Bronchiolitis is usually a self-limited infection which should be eliminated during the next 2 weeks after the infection in immunocompetent patients. However, dissemination of the virus in immunocompromised patients could remain for several months after initial infection.<ref name="pmid19209271">{{cite journal| author=Wright M, Mullett CJ, Piedimonte G| title=Pharmacological management of acute bronchiolitis. | journal=Ther Clin Risk Manag | year= 2008 | volume= 4 | issue= 5 | pages= 895-903 | pmid=19209271 | doi= | pmc=PMC2621418 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19209271 }} </ref> | |||
Some childre present recurrent episodes of wheezing after the initial RSV infection which has beed associated with the type of inflamatory response the patients presents during the initial disease. In animal and, in less dimention, human models have shown that inflamation mediated Th2 cellular response is associated with increased production of IgE and proimmflamatory mediators present in athsma patients.<ref>{{Cite book | last1 = Mandell | first1 = Gerald L. | last2 = Bennett | first2 = John E. (John Eugene) | last3 = Dolin | first3 = Raphael. | title = Mandell, Douglas, and Bennett's principles and practice of infectious disease | date = 2010 | publisher = Churchill Livingstone/Elsevier | location = Philadelphia, PA | isbn = | pages = }}</ref> | |||
==References== | ==References== | ||
Revision as of 16:38, 27 May 2014
|
Bronchiolitis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Bronchiolitis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Bronchiolitis pathophysiology |
|
Risk calculators and risk factors for Bronchiolitis pathophysiology |
Overview
The viral infection induces an inflammatory response which leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema and necrosis of the epithelium in the bronchioles which is then sloughed into the lumina causing proliferation of cuboidal epithelial cells without cilia.[1][2] This phenomena leads to complete or partial obstruction due to reduction of the bronchiolar lumenina and necrotic tissue accumulation, leading to hyperinflation secondary to a valve mechanism produced by the obstruction of the airway. By this mechanism, air can flow into the lungs by increased negastive pressure during inspiration but is unable to flow out of the lung as the airway's diameter is smaller during expiration.[3] Obstructed areas can evolve to atelectasias. In childen Kohn channels are not well developed, therefore atelectasias and hyperinfletion can be greater.
Bronchiolitis is usually a self-limited infection which should be eliminated during the next 2 weeks after the infection in immunocompetent patients. However, dissemination of the virus in immunocompromised patients could remain for several months after initial infection.[2]
Some childre present recurrent episodes of wheezing after the initial RSV infection which has beed associated with the type of inflamatory response the patients presents during the initial disease. In animal and, in less dimention, human models have shown that inflamation mediated Th2 cellular response is associated with increased production of IgE and proimmflamatory mediators present in athsma patients.[4]
References
- ↑ Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier.
- ↑ 2.0 2.1 Wright M, Mullett CJ, Piedimonte G (2008). "Pharmacological management of acute bronchiolitis". Ther Clin Risk Manag. 4 (5): 895–903. PMC 2621418. PMID 19209271.
- ↑ Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier.
- ↑ Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier.