Gallstone disease pathophysiology
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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
Researchers believe that gallstones may be caused by a combination of factors, including:
- Inherited body chemistry
- Body weight
- Gallbladder motility
- Diet
- Erythropoietic protoporphyria[3]
Cholesterol gallstones develop when bile contains too much cholesterol and not enough bile salts. The following factors also play a role:
- Gallbladder contraction
- Incomplete and infrequent emptying concentrates bile
- Presence of proteins in the liver and bile causing either promotion or inhibition of cholesterol crystallization into gallstones
- Increased levels of the estrogen hormone may increase cholesterol levels in bile and also decrease gallbladder movement
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.[6]
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".
- ↑ "Erythropoietic Protoporphyria". Merck Manual. Retrieved 2007-08-25.
- ↑ 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) - ↑ 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.
