Bronchiectasis pathophysiology: Difference between revisions

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Latest revision as of 20:43, 29 July 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2], Saarah T. Alkhairy, M.D.

Overview

Bronchiectasis involves cycles of infections and inflammation that result in alveolar damage and inelastic dilated bronchi. Damage to the airway results in airflow obstruction and impaired clearance of secretions.

Pathophysiology

The following events summarize the pathophysiology of bronchiectasis:^[1]

Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions.
The dilated areas interrupt normal air pressure of the bronchial tubes, causing sputum to pool inside the dilated areas instead of being pushed upward.
The sputum contains elastase, interleukin-8, tumor necrosis factor alpha (TNF-a), and prostanoids.
The pooled sputum provides an environment favorable to the growth of infectious pathogens.
Recurrent infections are followed inflammation and infiltration of neutrophils, macrophages, and T-lymphocytes.
The more infection that the lungs experience, leads to the sustained inflammation, consequently, damage to the alveoli in the lungs.
With more injury to the lung tissue, the elasticity in the bronchial tubes is reduced and the tubes are dilated, which creates a perpetual destructive cycle

Cole's Cycle

The following events summarize Cole's cycle (Cole's "vicious cycle hypothesis"), which is the most widely known model of the development of bronchiectasis:^[2]

Two factors are required for the development of bronchiectasis:
- Persistent infection
- Host defense derangement
Impaired mucociliary clearance due to the genetic susceptibility may cause environmental insult.
Insults result in persistence of microbes in the sinobronchial tree.
The microbial infection can cause chronic inflammation, which may result in tissue damage and impaired mucociliary motility.
Inflammation ensues more infection, which in turn ensues more inflammation.

Immune Response

Bronchiectasis involves the activity of reactive oxygen species (ROS), elastases, and matrix metalloproteinases (MMPs):
- Reactive oxygen species (ROS)
  - A by product for the metabolism of oxygen
  - Increased concentration may result in cell structure damage

Elastase
- Protease that catalyzes the breaks down of elastin.
- Elastin plus collagen determine the mechanical properties of connective tissue.

Matrix metalloproteinases (MMPs)
- Responsible for the degradation of the majority of the extracellular proteins during normal tissue turn over.
- Inflammation may result in epithelial injury and mucus secretion via increased concentrations of ROS, elastase ciliotoxin, and mucus secretogogues.
- Epithelial injury and mucus hypersecretion lead to chronic bronchial infection, reduced mucociliary clearance, and plugging of the airway - which all eventually leads to airway damage and bronchiectasis.

The diagram below depicts the immune response for bronchiectasis:

Schematic representation of a vicious circle of events which occurs during chronic bronchial infection. IL: interleukin; TNF: tumour necrosis factor; LT: leukotriene; MMP: matrix metalloproteinase
European Respiratory Journal

Gross Pathology

Bronchiectasis Source:Case courtesy of Dr Yale Rosen, Radiopaedia.org, rID: 9307

References

↑ Morrissey BM (2007). "Pathogenesis of bronchiectasis". Clin Chest Med. 28 (2): 289–96. PMID 17467548.
↑ King PT (2009). "The pathophysiology of bronchiectasis". Int J Chron Obstruct Pulmon Dis. 4: 411–9. PMC 2793069. PMID 20037680.CS1 maint: PMC format (link)

Template:WH Template:WS

[1] Morrissey BM (2007). "Pathogenesis of bronchiectasis". Clin Chest Med. 28 (2): 289–96. PMID 17467548.

[pmid20037680-2] King PT (2009). "The pathophysiology of bronchiectasis". Int J Chron Obstruct Pulmon Dis. 4: 411–9. PMC 2793069. PMID 20037680.CS1 maint: PMC format (link)

[1]

[2]

@@ Line 1: / Line 1: @@
 __NOTOC__
 {{Bronchiectasis}}
-{{CMG}} {{AE}} Saarah T. Alkhairy, M.D.
+{{CMG}}; {{AE}} {{HQ}}, Saarah T. Alkhairy, M.D.
 ==Overview==
-Bronchiectasis involves bronchi that are permanently dilated, inflamed, and easily collapsible. This results in airflow obstruction and impaired clearance of secretions.
+Bronchiectasis involves cycles of [[Infection|infections]] and [[inflammation]] that result in [[Alveolus|alveolar]] damage and inelastic dilated [[Bronchus|bronchi]]. Damage to the airway results in airflow obstruction and impaired clearance of [[secretions]].
 ==Pathophysiology==
-*Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions because the dilated areas interrupt normal air pressure of the bronchial tubes, causing [[sputum]] to pool inside the dilated areas instead of being pushed upward.<ref>{{cite journal |author=Morrissey BM |title=Pathogenesis of bronchiectasis |language=English |journal=Clin Chest Med|volume=28 |issue=2 |pages=289-96 |year=2007 |pmid=17467548 |doi=}}</ref>
+The following events summarize the pathophysiology of bronchiectasis:<ref>{{cite journal |author=Morrissey BM |title=Pathogenesis of bronchiectasis |language=English |journal=Clin Chest Med|volume=28 |issue=2 |pages=289-96 |year=2007 |pmid=17467548 |doi=}}</ref>
-*The pooled [[sputum]] provides an environment conducive to the growth of infectious [[pathogen|pathogens]]. Therefore, that particular area is vulnerable to infections.
-*The more infections that the lungs experience, the more damaged the [[alveoli]] in the lung become.
-*With more damage to the lung tissue, the [[bronchial tube]]s become more inelastic and dilated. This creates a perpetual, destructive cycle within this disease.
-*The most widely known model of the development of bronchiectasis is Cole’s “vicious cycle hypothesis”. In this model, Cole proposed that an environmental insult often on a background of genetic susceptibility impaired muco-ciliary clearance resulting in persistence of microbes in the sinobronchial tree and microbial colonization. The microbial infection caused chronic inflammation resulting in tissue damage and impaired mucociliary motility. In turn this led to more infection with a cycle of progressive inflammation causing lung damage. The current view is that the two factors required for the development of this condition are persistent infection and a defect in host defense.<ref name="pmid20037680">{{cite journal| author=King PT| title=The pathophysiology of bronchiectasis. | journal=Int J Chron Obstruct Pulmon Dis | year= 2009 | volume= 4 | issue=  | pages= 411-9 | pmid=20037680 | doi= | pmc=PMC2793069 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20037680  }} </ref>
-*The biopsies indicate that the infiltrate contains [[neutrophils]], [[T lymphocytes]] and [[macrophages]]. The sputum contains [[elastase]], [[interleukin-8]], tumor necrosis factor a  (TNF-a), and prostanoids.
-==Immune Response==
+*[[Dilation]] of the [[bronchial]] walls results in airflow obstruction and impaired clearance of secretions.
-<gallery widths=200px>
+*The dilated areas interrupt normal air pressure of the [[bronchial]] tubes, causing [[sputum]] to pool inside the dilated areas instead of being pushed upward.
+*The sputum contains [[elastase]], [[interleukin-8]], [[tumor necrosis factor alpha]] ([[Tumor necrosis factor-alpha|TNF-a]]), and [[Prostanoid|prostanoids]].
+*The pooled [[sputum]] provides an environment favorable to the growth of infectious [[pathogen|pathogens]].
+*Recurrent [[Infection|infections]] are followed [[inflammation]] and infiltration of [[Neutrophil|neutrophils]], [[Macrophage|macrophages]], and [[T cell|T-lymphocytes]].
+*The more [[infections|infection]] that the [[Lung|lungs]] experience, leads to the sustained inflammation, consequently, damage to the [[alveoli]] in the [[lung|lungs]].
+*With more injury to the [[lung]] tissue, the elasticity in the [[bronchial tube]]s is reduced and the tubes are dilated, which creates a perpetual destructive cycle
+===Cole's Cycle===
+The following events summarize Cole's cycle (Cole's "vicious cycle hypothesis"), which is the most widely known model of the development of bronchiectasis:<ref name="pmid20037680">{{cite journal| author=King PT| title=The pathophysiology of bronchiectasis. | journal=Int J Chron Obstruct Pulmon Dis | year= 2009 | volume= 4 | issue=  | pages= 411-9 | pmid=20037680 | doi= | pmc=PMC2793069 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20037680  }} </ref>
+*Two factors are required for the development of bronchiectasis:
+**Persistent [[infection]]
+**Host defense derangement
+*Impaired mucociliary clearance due to the genetic susceptibility may cause environmental insult.
+*Insults result in persistence of microbes in the sinobronchial tree.
+*The microbial [[infection]] can cause chronic [[inflammation]], which may result in tissue damage and impaired [[Mucociliary clearance|mucociliary]] motility.
+*[[Inflammation]] ensues more [[infection]], which in turn ensues more [[inflammation]].
+===Immune Response===
+*Bronchiectasis involves the activity of [[reactive oxygen species]] ([[Reactive oxygen species|ROS]]), [[Elastase|elastases]], and [[Matrix metalloproteinase|matrix metalloproteinases]] ([[MMP|MMPs]]):
+**[[Reactive oxygen species]] ([[Reactive oxygen species|ROS]])
+***A by product for the metabolism of [[oxygen]]
+***Increased concentration may result in cell structure damage
+* [[Elastase]]
+** [[Protease]] that catalyzes the breaks down of [[elastin]].
+** [[Elastin]] plus [[collagen]] determine the mechanical properties of [[connective tissue]].
+* [[Matrix metalloproteinases]] ([[Matrix metalloproteinase|MMPs]])
+** Responsible for the degradation of the majority of the extracellular proteins during normal tissue turn over.
+** [[Inflammation]] may result in epithelial injury and [[mucus]] secretion via increased concentrations of [[Reactive oxygen species|ROS]], [[elastase]] ciliotoxin, and [[mucus]] secretogogues.
+** [[Epithelial]] injury and [[mucus]] hypersecretion lead to chronic [[bronchial]] infection, reduced [[mucociliary clearance]], and plugging of the [[airway]] - which all eventually leads to airway damage and bronchiectasis.
+The diagram below depicts the immune response for bronchiectasis:
+<gallery widths="200px">
 F1.large.jpg | Schematic representation of a vicious circle of events which occurs during chronic bronchial infection. IL: interleukin; TNF: tumour necrosis factor; LT: leukotriene; MMP: matrix metalloproteinase <br> [http://erj.ersjournals.com/content/31/2/396/F1.large.jpg <font size="-2">''European Respiratory Journal''</font>]
 </gallery>
+==Gross Pathology==
+[[File:Bronchiectasis-gross-pathology-1.jpg|thumb|left|369x369px|Bronchiectasis [https://radiopaedia.org/cases/bronchiectasis-gross-pathology-1 Source:Case courtesy of Dr Yale Rosen, Radiopaedia.org, rID: 9307]]]
+<br clear="left" />
 ==References==
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+{{WH}}
+{{WS}}
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