Bronchiolitis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
Bronchiolitis is caused through viral replication process and inflammation as the following:<ref name="pmid23102068">{{cite journal| author=Garibaldi BT, Illei P, Danoff SK| title=Bronchiolitis. | journal=Immunol Allergy Clin North Am | year= 2012 | volume= 32 | issue= 4 | pages= 601-19 | pmid=23102068 | doi=10.1016/j.iac.2012.08.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23102068 }} </ref> | |||
*Starting from the nasopharyngeal mucosa the RSV will spread to the lower airway tracts. It will spread till reaching the bronchioles where viral replication takes place. | |||
*Virus causes lysis to the epithelial tissue which leads to the exposure of the supepithelial tissue and nerve fibers. Hereby, cough reflex starts. | |||
*Trough this process of viral replication and necrosis of the airways epithelium, neutrophils emerge into the airways. Lymohonuclear cells after that replace the neutrophils. | |||
*The vascular permeability increases which result in edema and swelling. | |||
*The whole inflammation process leads to airway obstruction which results in clinical manifestations of the bronchiolitis as wheezing, atelectasis and lungs hyperinflation. | |||
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 name="Mandell">{{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 lumina and [[Necrosis|necrotic tissue]] accumulation producing a valve mechanism, leading to hyperinflation. By this mechanism, air can flow into the [[lungs]] by increased negative pressure during [[inspiration]] but is unable to flow out of the lung as the airway's diameter is smaller during [[expiration]].<ref name="Mandell">{{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 [[atelectasis]]. In children, Kohn channels are not well developed, therefore [[atelectasis]] and hyperinflation can be greater. | 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 name="Mandell">{{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 lumina and [[Necrosis|necrotic tissue]] accumulation producing a valve mechanism, leading to hyperinflation. By this mechanism, air can flow into the [[lungs]] by increased negative pressure during [[inspiration]] but is unable to flow out of the lung as the airway's diameter is smaller during [[expiration]].<ref name="Mandell">{{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 [[atelectasis]]. In children, Kohn channels are not well developed, therefore [[atelectasis]] and hyperinflation can be greater. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]
Overview
Pathophysiology
Transmission
- Bronchiolitis is transmitted between individuals by air droplets infected with RSV.
- This air droplets lead to infection of the nasopharyngeal mucosa.
Pathogenesis
Bronchiolitis is caused through viral replication process and inflammation as the following:[1]
- Starting from the nasopharyngeal mucosa the RSV will spread to the lower airway tracts. It will spread till reaching the bronchioles where viral replication takes place.
- Virus causes lysis to the epithelial tissue which leads to the exposure of the supepithelial tissue and nerve fibers. Hereby, cough reflex starts.
- Trough this process of viral replication and necrosis of the airways epithelium, neutrophils emerge into the airways. Lymohonuclear cells after that replace the neutrophils.
- The vascular permeability increases which result in edema and swelling.
- The whole inflammation process leads to airway obstruction which results in clinical manifestations of the bronchiolitis as wheezing, atelectasis and lungs hyperinflation.
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.[2][3] This phenomena leads to complete or partial obstruction due to reduction of the bronchiolar lumina and necrotic tissue accumulation producing a valve mechanism, leading to hyperinflation. By this mechanism, air can flow into the lungs by increased negative pressure during inspiration but is unable to flow out of the lung as the airway's diameter is smaller during expiration.[2] Obstructed areas can evolve to atelectasis. In children, Kohn channels are not well developed, therefore atelectasis and hyperinflation can be greater.
Bronchiolitis is usually a self-limited infection which should be eliminated during the next 2 weeks after infection in immunocompetent patients. However, dissemination of the virus in immunocompromised patients could remain for several months after initial infection.[3]
Some children present recurrent episodes of wheezing after the initial RSV infection which has been associated with the type of inflamatory response the patients presents during the initial disease. Animal and, in less dimension, human models have shown that inflamation mediated by Th2 cellular response is associated with increased production of IgE and proimmflamatory mediators present in asthma patients.[2]
References
- ↑ Garibaldi BT, Illei P, Danoff SK (2012). "Bronchiolitis". Immunol Allergy Clin North Am. 32 (4): 601–19. doi:10.1016/j.iac.2012.08.002. PMID 23102068.
- ↑ 2.0 2.1 2.2 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.
- ↑ 3.0 3.1 Wright M, Mullett CJ, Piedimonte G (2008). "Pharmacological management of acute bronchiolitis". Ther Clin Risk Manag. 4 (5): 895–903. PMC 2621418. PMID 19209271.