Bronchiolitis pathophysiology: Difference between revisions
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{{Bronchiolitis}} | {{Bronchiolitis}} | ||
{{CMG}}; {{AE}} {{Alonso}} | {{CMG}}; {{AE}} {{Alonso}}, {{AEL}} | ||
==Overview== | ==Overview== | ||
Bronchiolitis is transmitted via air droplets. It is caused by [[respiratory syncytial virus]] ([[Human respiratory syncytial virus|RSV]]), which [[Infect|infects]] the [[nasopharyngeal]] [[mucosa]]. After the [[infection]], the [[virus]] spreads to the [[Lower respiratory tract|lower airway tracts]] until it reaches the [[bronchioles]], where [[viral replication]] takes place. The viral [[infection]] induces [[inflammation]], which leads to [[edema]] and [[necrosis]] of the [[bronchioles|bronchiolar]] [[epithelium]]. [[Cough reflex]] occurs due to exposure of the subepithelial [[tissue]] and [[nerve fibers]]. [[Vascular]] [[permeability]] increases, leading to [[edema]] and [[swelling]]. [[Histopathological|Histopathologically]], [[bronchiolitis obliterans]] shows [[intraluminal]] [[polyps]], [[inflammatory]] [[Infiltration (medical)|infiltration]], and [[macrophages]]. Constrictive bronchiolitis shows thickening of the [[airways]] and [[Lumen|interluminal]] narrowing. | |||
==Pathophysiology== | |||
===Transmission=== | |||
*[[Bronchiolitis]] is not transmissible between individuals. However, when [[bronchiolitis]] is caused by [[Respiratory syncytial virus|respiratory syncytial virus (RSV)]], it may be transmitted via air droplets. | |||
*Air droplets containing [[Respiratory syncytial virus|respiratory syncytial virus (RSV)]] lead to [[infection]] of the [[Nasopharyngeal|nasopharyngeal mucosa]] and subsequent [[bronchiolitis]]. | |||
===Pathogenesis=== | |||
[[Bronchiolitis]] is caused by [[viral replication]] and [[inflammation]] as follows:<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]], [[Human respiratory syncytial virus|respiratory syncytial virus (RSV)]] spreads to the [[Lower respiratory tract|lower respiratory tracts]]. After reaching the [[bronchioles]], [[viral replication]] takes place. | |||
*The [[viral infection|respiratory syncytial virus (RSV)]] [[viral infection|infection]] induces an [[inflammatory]] response. This leads to [[Infiltration (medical)|infiltration]] of [[Inflamation#Celular component|inflammatory cells]] ([[RSV]]-specific [[lymphocytes]]), [[edema]], and [[necrosis]] of the [[epithelium]] in the [[bronchioles]]. The [[epithelium]] is then sloughed into the [[Luminal|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> | |||
*[[Virus|Respiratory syncytial virus (RSV)]] causes [[lysis]] of the [[epithelial]] [[tissue]], which leads to the exposure of the subepithelial [[tissue]] and [[nerve fibers]], inducing a [[cough reflex]]. | |||
*The [[vascular]] [[permeability]] increases, which results in [[edema]] and [[swelling]]. | |||
*This [[inflammatory]] process leads to complete or partial [[obstruction]] due to reduction in [[Bronchiolar epithelium|bronchiolar]] lumina. Accumulation of [[Necrosis|necrotic tissue]] produces a [[valve]] mechanism, leading to hyperinflation of the [[lungs]]. | |||
*By this mechanism, air flow may increase 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 may evolve into areas of [[atelectasis]]. | |||
*In children, Kohn channels are not well developed, so [[atelectasis]] and hyperinflation may be more severe. | |||
== Associated conditions == | |||
* There are no associated conditions with bronchiolitis. | |||
== | == Gross pathology == | ||
* There are no specific findings in the gross pathology of bronchiolitis. | |||
==Microscopic pathology== | |||
[[Bronchiolitis]] shows [[histopathological]] findings which vary according to different types of [[bronchiolitis]].<ref name="pmid16088569">{{cite journal| author=Couture C, Colby TV| title=Histopathology of bronchiolar disorders. | journal=Semin Respir Crit Care Med | year= 2003 | volume= 24 | issue= 5 | pages= 489-98 | pmid=16088569 | doi=10.1055/s-2004-815600 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16088569 }} </ref> | |||
*[[Bronchiolitis obliterans]]: | |||
**Intraluminal [[polyps]] (protrusions inside the [[bronchioles]] with [[fibroblastic]] [[proliferation]]) | |||
**[[Inflammatory]] [[Infiltration (medical)|infiltration]] | |||
**[[Pneumocytes|Type two pneumocytes]] lining the [[alveoli]] | |||
**[[Macrophages]] | |||
*Constrictive bronchiolitis: | |||
**[[Scar|Scars]] leading to interluminal narrowing and [[obstruction]] | |||
**Thickening of the [[airways]] due to [[submucosal]] [[collagen]] and [[fibrosis]] | |||
*[[Proliferative bronchiolitis]]: | |||
**[[Histopathology]] shows Masson bodies ([[Fibrosis|fibrotic]] buds extending into [[alveoli]]) | |||
[[Image:Acute bronchiolitis (8519105494).jpg|500px|thumb|center|Acute inflammatory exudate causing occlusion of the lumen of the bronchiole. Source: Yale Rosen - Acute bronchiolitis, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31127127 ]] | |||
==References== | ==References== | ||
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[[Category:Pediatrics]] | [[Category:Pediatrics]] | ||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Infectious disease]] | |||
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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], Ahmed Elsaiey, MBBCH [3]
Overview
Bronchiolitis is transmitted via air droplets. It is caused by respiratory syncytial virus (RSV), which infects the nasopharyngeal mucosa. After the infection, the virus spreads to the lower airway tracts until it reaches the bronchioles, where viral replication takes place. The viral infection induces inflammation, which leads to edema and necrosis of the bronchiolar epithelium. Cough reflex occurs due to exposure of the subepithelial tissue and nerve fibers. Vascular permeability increases, leading to edema and swelling. Histopathologically, bronchiolitis obliterans shows intraluminal polyps, inflammatory infiltration, and macrophages. Constrictive bronchiolitis shows thickening of the airways and interluminal narrowing.
Pathophysiology
Transmission
- Bronchiolitis is not transmissible between individuals. However, when bronchiolitis is caused by respiratory syncytial virus (RSV), it may be transmitted via air droplets.
- Air droplets containing respiratory syncytial virus (RSV) lead to infection of the nasopharyngeal mucosa and subsequent bronchiolitis.
Pathogenesis
Bronchiolitis is caused by viral replication and inflammation as follows:[1]
- Starting from the nasopharyngeal mucosa, respiratory syncytial virus (RSV) spreads to the lower respiratory tracts. After reaching the bronchioles, viral replication takes place.
- The respiratory syncytial virus (RSV) infection induces an inflammatory response. This leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema, and necrosis of the epithelium in the bronchioles. The epithelium is then sloughed into the lumina, causing proliferation of cuboidal epithelial cells without cilia.[2]
- Respiratory syncytial virus (RSV) causes lysis of the epithelial tissue, which leads to the exposure of the subepithelial tissue and nerve fibers, inducing a cough reflex.
- The vascular permeability increases, which results in edema and swelling.
- This inflammatory process leads to complete or partial obstruction due to reduction in bronchiolar lumina. Accumulation of necrotic tissue produces a valve mechanism, leading to hyperinflation of the lungs.
- By this mechanism, air flow may increase 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 may evolve into areas of atelectasis.
- In children, Kohn channels are not well developed, so atelectasis and hyperinflation may be more severe.
Associated conditions
- There are no associated conditions with bronchiolitis.
Gross pathology
- There are no specific findings in the gross pathology of bronchiolitis.
Microscopic pathology
Bronchiolitis shows histopathological findings which vary according to different types of bronchiolitis.[3]
- Bronchiolitis obliterans:
- Intraluminal polyps (protrusions inside the bronchioles with fibroblastic proliferation)
- Inflammatory infiltration
- Type two pneumocytes lining the alveoli
- Macrophages
- Constrictive bronchiolitis:
- Scars leading to interluminal narrowing and obstruction
- Thickening of the airways due to submucosal collagen and fibrosis
- Proliferative bronchiolitis:
- Histopathology shows Masson bodies (fibrotic buds extending into alveoli)
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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 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.
- ↑ Couture C, Colby TV (2003). "Histopathology of bronchiolar disorders". Semin Respir Crit Care Med. 24 (5): 489–98. doi:10.1055/s-2004-815600. PMID 16088569.