Bronchiectasis pathophysiology: Difference between revisions
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*The more infections that the lungs experience, the more damaged the [[alveoli]] in the lung become. | *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. | *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. | ||
===Cole's Cycle<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>=== | |||
*Also known as Cole's "vicious cycle hypothesis" | |||
*The most widely known model of the development of bronchiectasis | |||
*Impaired muco-ciliary clearance due to genetic susceptibility causes environmental insult | |||
*Results in persistence of microbes in the sinobronchial tree and microbial colonization | |||
*The microbial infection causes chronic inflammation | |||
*This results in tissue damage and impaired mucociliary motility | |||
*This leads to more infection with a cycle of inflammation causing lung damage | |||
*Two factors required for the development of this condition are persistent infection and a defect in host defense | |||
*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. | *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== | ===Immune Response=== | ||
<gallery widths=200px> | <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>] | 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> | </gallery> | ||
**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 | |||
==References== | ==References== | ||
Revision as of 12:45, 29 June 2015
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Bronchiectasis Microchapters |
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Bronchiectasis pathophysiology On the Web |
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American Roentgen Ray Society Images of Bronchiectasis pathophysiology |
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Risk calculators and risk factors for Bronchiectasis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: 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.
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.[1]
- The pooled sputum provides an environment conducive to the growth of infectious 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 tubes become more inelastic and dilated. This creates a perpetual, destructive cycle within this disease.
Cole's Cycle[2]
- Also known as Cole's "vicious cycle hypothesis"
- The most widely known model of the development of bronchiectasis
- Impaired muco-ciliary clearance due to genetic susceptibility causes environmental insult
- Results in persistence of microbes in the sinobronchial tree and microbial colonization
- The microbial infection causes chronic inflammation
- This results in tissue damage and impaired mucociliary motility
- This leads to more infection with a cycle of inflammation causing lung damage
- Two factors required for the development of this condition are persistent infection and a defect in host defense
- 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
-
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
- 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