Bronchiectasis pathophysiology: Difference between revisions
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*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. | ||
*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 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]]. | |||
===Classification=== | |||
There are three types of bronchiectasis, varying by level of severity. Fusiform (cylindrical) bronchiectasis (the most common type) | There are three types of bronchiectasis, varying by level of severity. | ||
*Fusiform (cylindrical) bronchiectasis also known as follicular bronchiectasis (the most common type) - mildly inflamed [[bronchi]] that fail to taper distally.<ref>{{cite journal |author=Mysliwiec, V, Pina, JS |title=Bronchiectasis: the 'other' obstructive lung disease |language=English |journal=POSTGRADUATE MEDICINE |volume=106 |issue=1 |pages=252-63 |year=1999 |pmid= |doi=}}</ref> | |||
*Varicose bronchiectasis - the bronchial walls appear beaded because areas of dilation are mixed with areas of constriction.<ref>{{cite journal |author=Mysliwiec, V, Pina, JS |title=Bronchiectasis: the 'other' obstructive lung disease |language=English |journal=POSTGRADUATE MEDICINE |volume=106 |issue=1 |pages=252-63 |year=1999 |pmid= |doi=}}</ref> | |||
*Saccular (cystic) bronchiectasis - characterized by severe, irreversible ballooning of the bronchi peripherally, with or without air-fluid levels.<ref>{{cite journal |author=Mysliwiec, V, Pina, JS |title=Bronchiectasis: the 'other' obstructive lung disease |language=English |journal=POSTGRADUATE MEDICINE |volume=106 |issue=1 |pages=252-63 |year=1999 |pmid= |doi=}}</ref> | |||
==References== | ==References== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.
- 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.[2]
- 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.
Classification
There are three types of bronchiectasis, varying by level of severity.
- Fusiform (cylindrical) bronchiectasis also known as follicular bronchiectasis (the most common type) - mildly inflamed bronchi that fail to taper distally.[3]
- Varicose bronchiectasis - the bronchial walls appear beaded because areas of dilation are mixed with areas of constriction.[4]
- Saccular (cystic) bronchiectasis - characterized by severe, irreversible ballooning of the bronchi peripherally, with or without air-fluid levels.[5]
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.
- ↑ Mysliwiec, V, Pina, JS (1999). "Bronchiectasis: the 'other' obstructive lung disease". POSTGRADUATE MEDICINE. 106 (1): 252–63.
- ↑ Mysliwiec, V, Pina, JS (1999). "Bronchiectasis: the 'other' obstructive lung disease". POSTGRADUATE MEDICINE. 106 (1): 252–63.
- ↑ Mysliwiec, V, Pina, JS (1999). "Bronchiectasis: the 'other' obstructive lung disease". POSTGRADUATE MEDICINE. 106 (1): 252–63.