Cholangitis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
Cholangitis involves two main factors: bacterial increase and elevated | Cholangitis involves two main factors: bacterial increase and elevated intraductal pressure in the [[bile duct]], both which allow for [[translocation]] of [[bacteria]] or [[endotoxins]] in the [[vascular system]]. Bacterial contamination alone does not usually result in cholangitis. Increased pressure in the biliary system, from obstruction in the bile duct, widens the spaces between the cells lining the duct, which brings bacterially contaminated [[bile]] into the [[bloodstream]]. | ||
== Pathophysiology == | == Pathophysiology == | ||
Revision as of 19:29, 20 September 2016
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farwa Haideri [2]
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Overview
Cholangitis involves two main factors: bacterial increase and elevated intraductal pressure in the bile duct, both which allow for translocation of bacteria or endotoxins in the vascular system. Bacterial contamination alone does not usually result in cholangitis. Increased pressure in the biliary system, from obstruction in the bile duct, widens the spaces between the cells lining the duct, which brings bacterially contaminated bile into the bloodstream.
Pathophysiology
The onset of cholangitis involves two factors: increased bacteria in the bile duct, and elevated intraductal pressure in the bile duct that allows translocation of bacteria or endotoxins into the vascular system. Because of its anatomical characteristics, the biliary system is likely to be affected by elevated intraductal pressure. With the elevated intraductal biliary pressure, the bile ductules tend to become more permeable to the translocation of bacteria and toxins. This process results in serious infections that can be fatal, such as hepatic abscess and sepsis.[1] Functional changes in sinusoidal lining cells are often seen.[2]
Pathogenesis
Bile, produced by the liver, serves to eliminate cholesterol and bilirubin from the body, as well as emulsifying of fats to make them more soluble in water and aid in their digestion. It is formed in the liver by hepatocytes (liver cells) and excreted into the common hepatic duct. Part of the bile is stored in the gallbladder because of back pressure, and can be released at time of digestion. All bile reaches the duodenum through the common bile duct and the ampulla of Vater.[3]
The biliary tree is normally relatively free of bacteria because of certain protective mechanisms. The sphincter of Oddi acts as a mechanical barrier. The biliary system normally has low pressure and allows bile to flow freely through. This flushes bacteria, if present, into the duodenum, and does not allow establishment of an infection.[3]
Bacterial contamination alone in absence of obstruction does not usually result in cholangitis. However, increased pressure within the biliary system resulting from obstruction in the bile duct widens spaces between the cells lining the duct, bringing bacterially contaminated bile in contact with the bloodstream. Increased biliary pressure decreases production of IgA immunoglobulins in the bile. This results in bacteremia (bacteria in the blood stream) and gives rise to the systemic inflammatory response syndrome (SIRS) comprising fever (often with rigors), tachycardia, increased respiratory rate and increased white blood cell count.[4]
In ascending cholangitis, it is assumed that organisms migrate backwards up the bile duct as a result of partial obstruction and decreased function of the sphincter of Oddi.[3]
References
- ↑ Kimura Y, Takada T, Kawarada Y, Nimura Y, Hirata K, Sekimoto M, Yoshida M, Mayumi T, Wada K, Miura F, Yasuda H, Yamashita Y, Nagino M, Hirota M, Tanaka A, Tsuyuguchi T, Strasberg SM, Gadacz TR (2007). "Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines". J Hepatobiliary Pancreat Surg. 14 (1): 15–26. doi:10.1007/s00534-006-1152-y. PMC 2784509. PMID 17252293.
- ↑ Kawada, N., Takemura, Y., Minamiyama M. (1996). "Pathophysiology of acute obstructive cholangitis". Journal of Hepato-Biliary-Pancreatic Surgery. 3 (1): 4–8. doi:10.1007/BF01212771.
- ↑ 3.0 3.1 3.2 Kinney TP (2007). "Management of ascending cholangitis". Gastrointest. Endosc. Clin. N. Am. 17 (2): 289–306, vi. doi:10.1016/j.giec.2007.03.006. PMID 17556149.
- ↑ Sung JY, Costerton JW, Shaffer EA (1992). "Defense system in the biliary tract against bacterial infection". Dig. Dis. Sci. 37 (5): 689–96. PMID 1563308.