Cystitis pathophysiology: Difference between revisions
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===Interstitial Cystitis=== | ===Interstitial Cystitis=== | ||
The pathogenesis of | The pathogenesis of Interstitial Cystitis also known as Bladder Pain Syndrome, includes:<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><ref name="pmid27976711">{{cite journal| author=Kind T, Cho E, Park TD, Deng N, Liu Z, Lee T et al.| title=Interstitial Cystitis-Associated Urinary Metabolites Identified by Mass-Spectrometry Based Metabolomics Analysis. | journal=Sci Rep | year= 2016 | volume= 6 | issue= | pages= 39227 | pmid=27976711 | doi=10.1038/srep39227 | pmc=5156939 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27976711 }} </ref><ref name="pmid22233286">{{cite journal| author=Friedlander JI, Shorter B, Moldwin RM| title=Diet and its role in interstitial cystitis/bladder pain syndrome (IC/BPS) and comorbid conditions. | journal=BJU Int | year= 2012 | volume= 109 | issue= 11 | pages= 1584-91 | pmid=22233286 | doi=10.1111/j.1464-410X.2011.10860.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22233286 }} </ref><ref name="pmid16946082">{{cite journal| author=Winnard KP, Dmitrieva N, Berkley KJ| title=Cross-organ interactions between reproductive, gastrointestinal, and urinary tracts: modulation by estrous stage and involvement of the hypogastric nerve. | journal=Am J Physiol Regul Integr Comp Physiol | year= 2006 | volume= 291 | issue= 6 | pages= R1592-601 | pmid=16946082 | doi=10.1152/ajpregu.00455.2006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16946082 }} </ref> | ||
*Epithelial dysfunction | |||
*Epithelial dysfunction | |||
*[[Mast cell]] activation | *[[Mast cell]] activation | ||
*Bladder sensory nerve up-regulation | *Bladder sensory nerve up-regulation | ||
*Organ Cross Talk | |||
Certain foods have been associated with causing the interstitial cystitis some of these include: | |||
*Spicy foods | |||
*Citrus Fruit | |||
*Tomatoes | |||
*Carbonated and Alcoholic drinks | |||
*Coffee or tea | |||
*Vitamin C | |||
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> | 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> | ||
Revision as of 21:08, 6 January 2017
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Cystitis pathophysiology On the Web | |
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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 either infected by bacteria or rarely a fungus, which leads to irritation and inflammation or from trauma, chemicals or foreign bodies. 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 any structural or functional pathology. In women, vaginal colonization of the uropathogens leads to the development of a urinary tract infection. 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. [1][2]
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. Complicated cystitis is usually a result of an abnormality in the structure or function of the urinary tract. This abnormality can result from various causes like foreign bodies e.g kidney stones, urinary catheters or other draining devices, structural defects, renal failure, pregnancy or immunosuppression. Any process leading to the obstruction leads to over distension and so bacterial growth is facilitated by the residual urine. Stasis of urine flow allows entry of pathogens into the urinary tract and also hinders the natural preventive mechanism by which urine flushes away the pathogens and prevents colonisation in the urinary tract.[1][5][6][7]
Recurrent Cystitis
Recurrent inflammation of the bladder that is usually due to an infection, needs intensive investigation. Immunodeficiency, contraceptive device, sexual intercourse or a structural or a genetic defect can be a reason of the recurrent infections of the urinary bladder. The most common pathogen involved in recurrent infections resulting in inflammation of the bladder is E.coli.[8][9][10][11]
Interstitial Cystitis
The pathogenesis of Interstitial Cystitis also known as Bladder Pain Syndrome, includes:[12][13][14][15]
- Epithelial dysfunction
- Mast cell activation
- Bladder sensory nerve up-regulation
- Organ Cross Talk
Certain foods have been associated with causing the interstitial cystitis some of these include:
- Spicy foods
- Citrus Fruit
- Tomatoes
- Carbonated and Alcoholic drinks
- Coffee or tea
- Vitamin C
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.[16]
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.[17][18]
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.
- ↑ Pallett A, Hand K (2010). "Complicated urinary tract infections: practical solutions for the treatment of multiresistant Gram-negative bacteria". J Antimicrob Chemother. 65 Suppl 3: iii25–33. doi:10.1093/jac/dkq298. PMID 20876625.
- ↑ Nicolle LE (2001). "A practical guide to antimicrobial management of complicated urinary tract infection". Drugs Aging. 18 (4): 243–54. PMID 11341472.
- ↑ Lichtenberger P, Hooton TM (2008). "Complicated urinary tract infections". Curr Infect Dis Rep. 10 (6): 499–504. PMID 18945392.
- ↑ Franco AV (2005). "Recurrent urinary tract infections". Best Pract Res Clin Obstet Gynaecol. 19 (6): 861–73. doi:10.1016/j.bpobgyn.2005.08.003. PMID 16298166.
- ↑ Wada K, Uehara S, Ishii A, Sadahira T, Yamamoto M, Mitsuhata R; et al. (2016). "A Phase II Clinical Trial Evaluating the Preventive Effectiveness of Lactobacillus Vaginal Suppositories in Patients with Recurrent Cystitis". Acta Med Okayama. 70 (4): 299–302. PMID 27549677.
- ↑ Holland SM, Gallin JI (1998). "Evaluation of the patient with recurrent bacterial infections". Annu Rev Med. 49: 185–99. doi:10.1146/annurev.med.49.1.185. PMID 9509258.
- ↑ Arbiser JL (1995). "Genetic immunodeficiencies: cutaneous manifestations and recent progress". J Am Acad Dermatol. 33 (1): 82–9. PMID 7601952.
- ↑ Sant GR (2002). "Etiology, pathogenesis, and diagnosis of interstitial cystitis". Rev Urol. 4 Suppl 1: S9–S15. PMC 1476007. PMID 16986036.
- ↑ Kind T, Cho E, Park TD, Deng N, Liu Z, Lee T; et al. (2016). "Interstitial Cystitis-Associated Urinary Metabolites Identified by Mass-Spectrometry Based Metabolomics Analysis". Sci Rep. 6: 39227. doi:10.1038/srep39227. PMC 5156939. PMID 27976711.
- ↑ Friedlander JI, Shorter B, Moldwin RM (2012). "Diet and its role in interstitial cystitis/bladder pain syndrome (IC/BPS) and comorbid conditions". BJU Int. 109 (11): 1584–91. doi:10.1111/j.1464-410X.2011.10860.x. PMID 22233286.
- ↑ Winnard KP, Dmitrieva N, Berkley KJ (2006). "Cross-organ interactions between reproductive, gastrointestinal, and urinary tracts: modulation by estrous stage and involvement of the hypogastric nerve". Am J Physiol Regul Integr Comp Physiol. 291 (6): R1592–601. doi:10.1152/ajpregu.00455.2006. PMID 16946082.
- ↑ 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.