Cystitis pathophysiology: Difference between revisions
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{{CMG}} {{SCC}} {{AE}} {{Maliha}} | {{CMG}} {{SCC}} {{AE}} {{Maliha}} | ||
==Overview== | ==Overview== | ||
Cystitis occurs when the normally sterile [[lower urinary tract]] ([[urethra]] and [[bladder]]) is infected by bacteria, which leads to irritation and inflammation.The pathogenesis of interstitial cystitis includes epithelial dysfunction, [[nast cell]] activation, and bladder sensory nerve up-regulation.<ref name="pmid16986036">{{cite journal| author=Sant GR| title=Etiology, pathogenesis, and diagnosis of interstitial cystitis. | journal=Rev Urol | year= 2002 | volume= 4 Suppl 1 | issue= | pages= S9-S15 | pmid=16986036 | doi= | pmc=PMC1476007 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16986036 }} </ref> | Cystitis occurs when the normally sterile [[lower urinary tract]] ([[urethra]] and [[bladder]]) is infected by bacteria, which leads to irritation and inflammation.The pathogenesis of interstitial cystitis includes epithelial dysfunction, [[nast cell]] activation, and bladder sensory nerve up-regulation.<ref name="pmid16986036">{{cite journal| author=Sant GR| title=Etiology, pathogenesis, and diagnosis of interstitial cystitis. | journal=Rev Urol | year= 2002 | volume= 4 Suppl 1 | issue= | pages= S9-S15 | pmid=16986036 | doi= | pmc=PMC1476007 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16986036 }} </ref> The urothelium acts as a barrier against damage to the [[bladder]]. The urothelium produces a mucous layer which regulates the entry of [[potassium]] in the bladder interstitium. Damage to the urothelium results in the production of cytokines which activate [[mast cell]]s in the interstitium. Mast cell activation is further triggered by the diffusion of excess [[potassium]] into the bladder interstitium.<ref name="pmid21568251">{{cite journal| author=French LM, Bhambore N| title=Interstitial cystitis/painful bladder syndrome. | journal=Am Fam Physician | year= 2011 | volume= 83 | issue= 10 | pages= 1175-81 | pmid=21568251 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21568251 }} </ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 23:26, 8 February 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Steven C. Campbell, M.D., Ph.D. Associate Editor(s)-in-Chief: Maliha Shakil, M.D. [2]
Overview
Cystitis occurs when the normally sterile lower urinary tract (urethra and bladder) is infected by bacteria, which leads to irritation and inflammation.The pathogenesis of interstitial cystitis includes epithelial dysfunction, nast cell activation, and bladder sensory nerve up-regulation.[1] The urothelium acts as a barrier against damage to the bladder. The urothelium produces a mucous layer which regulates the entry of potassium in the bladder interstitium. Damage to the urothelium results in the production of cytokines which activate mast cells in the interstitium. Mast cell activation is further triggered by the diffusion of excess potassium into the bladder interstitium.[2]
Pathophysiology
Cystitis occurs when the normally sterile lower urinary tract (urethra and bladder) is infected by bacteria and becomes irritated and inflamed. It is very common. Once bacteria enter the bladder, they are normally removed through urination. When bacteria multiply faster than they are removed by urination, infection results. Cystitis is rare in males. Females are more prone to the development of cystitis because of their relatively shorter urethra. Bacteria does not have to travel as far to enter the bladder, which is in part due to the relatively short distance between the opening of the urethra and the anus.
The pathogenesis of interstitial cystitis includes:[1]
- Epithelial dysfunction
- Mast cell activation
- Bladder sensory nerve up-regulation
The urothelium acts as a barrier against damage to the bladder. The urothelium produces a mucous layer which regulates the entry of potassium in the bladder interstitium. Damage to the urothelium results in the production of cytokines which activate mast cells in the interstitium. Mast cell activation is further triggered by the diffusion of excess potassium into the bladder interstitium.[2]
Genetics
Some genetic subtypes have been linked to the disorder:[3]
- An antiproliferative factor is secreted by the bladders of people with interstitial cystitis which inhibits bladder cell proliferation, thus possibly causing the missing bladder lining.
- PAND, at gene map locus 13q22–q32, is associated with a constellation of disorders (a "pleiotropic syndrome") including interstitial cystitis and other bladder and kidney problems, thyroid diseases, serious headaches/migraines, panic disorder, and mitral valve prolapse.
Associated Conditions
Interstitial cystitis may be associated with:[4]
References
- ↑ 1.0 1.1 Sant GR (2002). "Etiology, pathogenesis, and diagnosis of interstitial cystitis". Rev Urol. 4 Suppl 1: S9–S15. PMC 1476007. PMID 16986036.
- ↑ 2.0 2.1 French LM, Bhambore N (2011). "Interstitial cystitis/painful bladder syndrome". Am Fam Physician. 83 (10): 1175–81. PMID 21568251.
- ↑ Interstitial Cystitis. Wikipedia.https://en.wikipedia.org/wiki/Interstitial_cystitis#Genes Accessed on February 8, 2016
- ↑ Interstitial Cystitis. Wikipedia.https://en.wikipedia.org/wiki/Interstitial_cystitis#Association_with_other_conditions Accessed on February 8, 2016