Gallstone disease pathophysiology: Difference between revisions
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[[Image:Gallstones.jpg|thumb|200px|left|[[Gall bladder]] opened to show numerous '''gallstones'''. Their brownish to greenish color suggest they are cholesterol [[Calculus (medicine)|calculi]]. Source: Wikimedia Commons<ref>name="urlFile:Gallensteine 2006 03 28.JPG - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File:Gallensteine_2006_03_28.JPG |title=File:Gallensteine 2006 03 28.JPG - Wikimedia Commons |format= |work= |accessdate=}}</ref>]] | [[Image:Gallstones.jpg|thumb|200px|left|[[Gall bladder]] opened to show numerous '''gallstones'''. Their brownish to greenish color suggest they are cholesterol [[Calculus (medicine)|calculi]]. Source: Wikimedia Commons<ref>name="urlFile:Gallensteine 2006 03 28.JPG - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File:Gallensteine_2006_03_28.JPG |title=File:Gallensteine 2006 03 28.JPG - Wikimedia Commons |format= |work= |accessdate=}}</ref>]] | ||
It is thought that Gallstone disease is caused by bile hypersaturation, meaning that the bile becomes over saturated with a particular substance more than can be dissolved in the bile. | |||
One of the most important substances that can lead to stone formation is Cholesterol. | |||
Cholesterol is an important substance that is needed to form cell membranes and to produce steroid hormones in the body. | |||
Its quantity must be balanced internally and the only way in which the body can rid itself of it is through the bile. | |||
Occasionally, gallstones are composed of bilirubin | The process of stone formation begins with the presence of biliary sludge. | ||
This thick compound consists of glycoproteins, calcium deposits, and cholesterol crystals in the gallbladder. | |||
This precipitation is also called "crystallization". | |||
Usually there are antagonistic mechanisms in place that work to prevent cholesterol from precipitating or crystallizing in the bile. | |||
These include: pronucleating (crystallization-promoting) and antinucleating (crystallization-inhibiting) factors. | |||
Furthermore, the lack of motility in the muscular wall of the gallbladder or the excessive sphincter contraction, that prevents bile secretion may also contribute to stone formation. | |||
This causes bile to stagnate within the gallbladder. | |||
Rarely, the gallbladder may not properly fill with bile and so the bile is instead diverted from the gallbladder to the small bile duct. | |||
This exacerbates the hypomotility and accelerates stone formation. | |||
Occasionally, gallstones are composed of bilirubin and can be referred to as "pigment stones". | |||
Bilirubin is a byproduct of red blood cell breakdown. | |||
These stones are formed via two main pathways: | |||
1. An infection of the biliary tract can predispose to stone formation. | |||
2.Bile is normally recycled after its secretion back from the small bowel and to the liver. If there is increased enterohepatic cycling this may also cause the formation of a bilirubin stone. Pigment stones are seen more often in the Asian and African continents. | |||
===Associated Conditions=== | ===Associated Conditions=== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]
Overview
It has long been noted that gallbladder stone formation is associated with bile supersaturation, and this still remains the most common cause for gallstone formation.[1]
Pathophysiology
It is thought that Gallstone disease is caused by bile hypersaturation, meaning that the bile becomes over saturated with a particular substance more than can be dissolved in the bile. One of the most important substances that can lead to stone formation is Cholesterol. Cholesterol is an important substance that is needed to form cell membranes and to produce steroid hormones in the body. Its quantity must be balanced internally and the only way in which the body can rid itself of it is through the bile. The process of stone formation begins with the presence of biliary sludge. This thick compound consists of glycoproteins, calcium deposits, and cholesterol crystals in the gallbladder. This precipitation is also called "crystallization". Usually there are antagonistic mechanisms in place that work to prevent cholesterol from precipitating or crystallizing in the bile. These include: pronucleating (crystallization-promoting) and antinucleating (crystallization-inhibiting) factors. Furthermore, the lack of motility in the muscular wall of the gallbladder or the excessive sphincter contraction, that prevents bile secretion may also contribute to stone formation. This causes bile to stagnate within the gallbladder. Rarely, the gallbladder may not properly fill with bile and so the bile is instead diverted from the gallbladder to the small bile duct. This exacerbates the hypomotility and accelerates stone formation. Occasionally, gallstones are composed of bilirubin and can be referred to as "pigment stones". Bilirubin is a byproduct of red blood cell breakdown. These stones are formed via two main pathways: 1. An infection of the biliary tract can predispose to stone formation. 2.Bile is normally recycled after its secretion back from the small bowel and to the liver. If there is increased enterohepatic cycling this may also cause the formation of a bilirubin stone. Pigment stones are seen more often in the Asian and African continents.
Associated Conditions
- Diabetes mellitus type 2
- Obesity
- Pregnancy
- Gallbladder cancer
- Gallbladder polyps
- Primary sclerosing cholangitis
- Porcelain gallbladder
- Rapid weight loss
- Constipation
- Eating fewer meals
- Low intake of:
On the other hand, wine and whole grain bread may decrease the risk of gallstones.[5]
Gross Pathology
On gross pathology, multiple small stones are commonly found or less commonly a solitary stone is seen. The smaller stones represent a higher morbidity since they can easily occlude the biliary tracts.[7]
Microscopic Pathology
On microscopic histopathological analysis, variable evidences of inflammation can be noted transmurally including neutrophils, which are characteristic in gallstone disease.[8]
References
- ↑ Wang HH, Portincasa P, Wang DQ (2008). "Molecular pathophysiology and physical chemistry of cholesterol gallstones". Front. Biosci. 13: 401–23. PMID 17981556.
- ↑ name="urlFile:Gallensteine 2006 03 28.JPG - Wikimedia Commons">"File:Gallensteine 2006 03 28.JPG - Wikimedia Commons".
- ↑ Lv J, Yu C, Guo Y, Bian Z, Yang L, Chen Y, Li S, Huang Y, Fu Y, He P, Tang A, Chen J, Chen Z, Qi L, Li L (2017). "Gallstone Disease and the Risk of Type 2 Diabetes". Sci Rep. 7 (1): 15853. doi:10.1038/s41598-017-14801-2. PMID 29158491.
- ↑ R.M. Ortega (1997). "Differences in diet and food habits between patients with gallstones and controls". Journal of the American College of Nutrition. 16: 88–95. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help);|access-date=requires|url=(help) - ↑ European Journal Gastroenterology & Hepatology. 6: 585–593. 1995. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ "File:Gallensteine 2006 03 28.JPG - Wikimedia Commons".
- ↑ Ansert, Sandra (2018). Textbook of diagnostic sonography. St. Louis, MO: Elsevier. ISBN 978-0323353755.
- ↑ Fisher, M. M. (1979). Gallstones. Boston, MA: Springer US. ISBN 1461570662.
