Cystitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Cystitis occurs when the normally sterile [[lower urinary tract]] ([[urethra]] and [[bladder]]) is infected by bacteria, which leads to irritation and [[inflammation]]. Females are more prone to the development of cystitis because of their relatively shorter and straighter [[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 complicated cystitis include obstruction and stasis of urine flow. Normal flow of urine washes away the pathogens and clears the tract. Obstruction leads to overdistension and bacterial growth is facilitated by the residual urine. Stasis of urine flow allows entry of pathogens into the urinary tract.<ref name="pmid10969044">{{cite journal| author=Hooton TM| title=Pathogenesis of urinary tract infections: an update. | journal=J Antimicrob Chemother | year= 2000 | volume= 46 Suppl A | issue= | pages= 1-7 | pmid=10969044 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10969044 }} </ref> | Cystitis occurs when the normally sterile [[lower urinary tract]] ([[urethra]] and [[bladder]]) is infected by bacteria, which leads to irritation and [[inflammation]]. It may also result from trauma, chemicals, foreign body along with pathogens that are usually bacterial but can less commonly be fungal as well. Females are more prone to the development of cystitis because of their relatively shorter and straighter [[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 complicated cystitis include obstruction and stasis of urine flow. Normal flow of urine washes away the pathogens and clears the tract. Obstruction leads to overdistension and bacterial growth is facilitated by the residual urine. Stasis of urine flow allows entry of pathogens into the urinary tract.<ref name="pmid10969044">{{cite journal| author=Hooton TM| title=Pathogenesis of urinary tract infections: an update. | journal=J Antimicrob Chemother | year= 2000 | volume= 46 Suppl A | issue= | pages= 1-7 | pmid=10969044 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10969044 }} </ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
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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. It may also result from trauma, chemicals, foreign body along with pathogens that are usually bacterial but can less commonly be fungal as well. Females are more prone to the development of cystitis because of their relatively shorter and straighter 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 complicated cystitis include obstruction and stasis of urine flow. Normal flow of urine washes away the pathogens and clears the tract. Obstruction leads to overdistension and bacterial growth is facilitated by the residual urine. Stasis of urine flow allows entry of pathogens into the urinary tract.[1]
Pathophysiology
Acute uncomplicated cystitis
Acute Uncomplicated Cystitis is an inflammation of the urinary bladder that occurs in the absence of nay structural or functional pathology.[2]In women, vaginal colonization of the uropathogens leads to the development of a urinary tract infection.[1] Cystitis occurs when the normally sterile lower urinary tract (urethra and bladder) are infected by bacteria and become irritated and inflamed. 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 but when occurs, is predominantly found in homosexual or uncircumscribed individuals. 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.[3][4]
Complicated cystitis
The pathogenesis of complicated cystitis include obstruction and stasis of urine flow. Obstruction leads to overdistension and bacterial growth is facilitated by the residual urine. Stasis of urine flow allows entry of pathogens into the urinary tract.[1]
Interstitial Cystitis
The pathogenesis of interstitial cystitis includes:[5]
- 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.[6]
Cystitis cystica
Chronic irritation from infection, calculi or even tumors results in metaplasia of the urothelium, which proliferates into buds, which grow down into the connective tissue beneath the epithelium in the lamina propria. In the case of cystitis cystica, the buds then differentiate into cystic deposits.[7][8]
References
- ↑ 1.0 1.1 1.2 Hooton TM (2000). "Pathogenesis of urinary tract infections: an update". J Antimicrob Chemother. 46 Suppl A: 1–7. PMID 10969044.
- ↑ Nicolle LE (2008). "Uncomplicated urinary tract infection in adults including uncomplicated pyelonephritis". Urol Clin North Am. 35 (1): 1–12, v. doi:10.1016/j.ucl.2007.09.004. PMID 18061019.
- ↑ Russell DB, Roth NJ (2001). "Urinary tract infections in men in a primary care population". Aust Fam Physician. 30 (2): 177–9. PMID 11280121.
- ↑ Platt R, Polk BF, Murdock B, Rosner B (1986). "Risk factors for nosocomial urinary tract infection". Am J Epidemiol. 124 (6): 977–85. PMID 3776980.
- ↑ Sant GR (2002). "Etiology, pathogenesis, and diagnosis of interstitial cystitis". Rev Urol. 4 Suppl 1: S9–S15. PMC 1476007. PMID 16986036.
- ↑ French LM, Bhambore N (2011). "Interstitial cystitis/painful bladder syndrome". Am Fam Physician. 83 (10): 1175–81. PMID 21568251.
- ↑ Cystitis Cystica. Radiopaedia 2016. http://radiopaedia.org/articles/cystitis-cystica. Accessed on February 9, 2016
- ↑ Halder P, Mandal KC, Mukherjee S (2016). "Prolapsing cystitis cystica causing bladder outlet obstruction: An unusual complication". Indian J Urol. 32 (4): 329–330. doi:10.4103/0970-1591.189718. PMC 5054670. PMID 27843222.