Bronchiolitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Bronchiolitis is transmitted by air droplets. It is caused by [[Human respiratory syncytial virus|RSV]], which 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]]. Histopathologically, [[bronchiolitis obliterans]] shows [[intraluminal]] [[polyps]], [[inflammatory]] [[Infiltration (medical)|infiltration]], and [[macrophages]]. Constrictive bronchiolitis shows thickening of the [[airways]] and interluminal narrowing. | |||
==Pathophysiology== | ==Pathophysiology== | ||
===Transmission=== | ===Transmission=== | ||
*[[Bronchiolitis]] is not transmissible | *[[Bronchiolitis]] is not transmissible between individuals. However, when [[bronchiolitis]] is caused by [[Respiratory syncytial virus|respiratory syncytial virus (RSV)]], it may be transmitted by air droplets. | ||
*Air droplets containing [[Respiratory syncytial virus|respiratory syncytial virus (RSV)]] | *Air droplets containing [[Respiratory syncytial virus|respiratory syncytial virus (RSV)]] lead to [[infection]] of the [[Nasopharyngeal|nasopharyngeal mucosa]] and subsequent [[bronchiolitis]]. | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
[[Bronchiolitis]] is caused by a 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> | [[Bronchiolitis]] is caused by a 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]], [[Human respiratory syncytial virus|respiratory syncytial virus (RSV)]] spreads to the [[Lower respiratory tract infection|lower airway tracts]]. It spreads | *Starting from the [[nasopharyngeal]] [[mucosa]], [[Human respiratory syncytial virus|respiratory syncytial virus (RSV)]] spreads to the [[Lower respiratory tract infection|lower airway tracts]]. It spreads until it reaches the [[bronchioles]], where [[viral replication]] takes place. | ||
*The [[viral infection|respiratory syncytial virus (RSV)]] [[viral infection|infection]] induces an [[inflammatory]] response. | *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]] | *[[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 | *The [[vascular]] [[permeability]] increases, which results in [[edema]] and [[swelling]]. | ||
*This [[inflammation]] process leads to complete or partial [[obstruction]] from reduction in [[Bronchiolar epithelium|bronchiolar]] lumina. Accumulation of [[Necrosis|necrotic tissue]] | *This [[inflammation]] process leads to complete or partial [[obstruction]] from reduction in [[Bronchiolar epithelium|bronchiolar]] lumina. Accumulation of [[Necrosis|necrotic tissue]] produces a [[valve]] mechanism, leading to hyperinflation. | ||
*By this mechanism, air flow can 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 can evolve to [[atelectasis]]. In children, Kohn channels are not well developed, | *By this mechanism, air flow can 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 can evolve to [[atelectasis]]. In children, Kohn channels are not well developed, so [[atelectasis]] and hyperinflation can be greater. | ||
===Microscopic pathology=== | ===Microscopic pathology=== | ||
[[Bronchiolitis]] shows [[histopathological]] findings that differ between different types of | [[Bronchiolitis]] shows [[histopathological]] findings that differ between 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]]: | *[[Bronchiolitis obliterans]]: | ||
**Intraluminal [[polyps]] (protrusions inside the [[bronchioles]] with [[fibroblastic]] [[proliferation]]) | **Intraluminal [[polyps]] (protrusions inside the [[bronchioles]] with [[fibroblastic]] [[proliferation]]) | ||
| Line 29: | Line 29: | ||
*Constrictive bronchiolitis: | *Constrictive bronchiolitis: | ||
**[[Scar|Scars]] leading to interluminal narrowing and [[obstruction]] | **[[Scar|Scars]] leading to interluminal narrowing and [[obstruction]] | ||
**Thickening of the [[airways]] due to [[submucosal]] [[collagen]] and [[fibrosis]] | **Thickening of the [[airways]] due to [[submucosal]] [[collagen]] and [[fibrosis]] | ||
*[[Proliferative bronchiolitis]]: | *[[Proliferative bronchiolitis]]: | ||
**[[Histopathology]] shows Masson bodies (fibrotic buds extending into [[alveoli]]) | **[[Histopathology]] shows Masson bodies (fibrotic buds extending into [[alveoli]]) | ||
==References== | ==References== | ||
Revision as of 15:21, 8 August 2017
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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
Bronchiolitis is transmitted by air droplets. It is caused by 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 by air droplets.
- Air droplets containing respiratory syncytial virus (RSV) lead to infection of the nasopharyngeal mucosa and subsequent bronchiolitis.
Pathogenesis
Bronchiolitis is caused by a viral replication process and inflammation as the following:[1]
- Starting from the nasopharyngeal mucosa, respiratory syncytial virus (RSV) spreads to the lower airway tracts. It spreads until it reaches the bronchioles, where 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 inflammation process leads to complete or partial obstruction from reduction in bronchiolar lumina. Accumulation of necrotic tissue produces a valve mechanism, leading to hyperinflation.
- By this mechanism, air flow can 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 can evolve to atelectasis. In children, Kohn channels are not well developed, so atelectasis and hyperinflation can be greater.
Microscopic pathology
Bronchiolitis shows histopathological findings that differ between 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)
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.