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
Gallstones are hard, pebble-like structures that obstruct the cystic duct. The formation of gallstones is often preceded by the presence of biliary sludge, a viscous mixture of glycoproteins, calcium deposits, and cholesterol crystals in the gallbladder or biliary ducts.5 In the U.S., most gallstones consist largely of bile supersaturated with cholesterol.1,2 This hypersaturation, which results from the cholesterol concentration being greater than its solubility percentage, is caused primarily by hypersecretion of cholesterol due to altered hepatic cholesterol metabolism.1,3 A distorted balance between pronucleating (crystallization-promoting) and antinucleating (crystallization-inhibiting) proteins in the bile also can accelerate crystallization of cholesterol in the bile.1-3,5 Mucin, a glycoprotein mixture secreted by biliary epithelial cells, has been documented as a pronucleating protein. It is the decreased degradation of mucin by lysosomal enzymes that is believed to promote the formation of cholesterol crystals.3
Loss of gallbladder muscular-wall motility and excessive sphincteric contraction also are involved in gallstone formation.1 This hypomotility leads to prolonged bile stasis (delayed gallbladder emptying), along with decreased reservoir function.3,5 The lack of bile flow causes an accumulation of bile and an increased predisposition for stone formation. Ineffective filling and a higher proportion of hepatic bile diverted from the gallbladder to the small bile duct can occur as a result of hypomotility.1,5
Occasionally, gallstones are composed of bilirubin, a chemical that is produced as a result of the standard breakdown of RBCs. Infection of the biliary tract and increased enterohepatic cycling of bilirubin are the suggested causes of bilirubin stone formation. Bilirubin stones, often referred to as pigment stones, are seen primarily in patients with infections of the biliary tract or chronic hemolytic diseases (or damaged RBCs).1,3,6 Pigment stones are more frequent in Asia and Africa.3,6
The pathogenesis of cholecystitis most commonly involves the impaction of gallstones in the bladder neck, Hartmann’s pouch, or the cystic duct; gallstones are not always present in cholecystitis, however.5 Pressure on the gallbladder increases, the organ becomes enlarged, the walls thicken, the blood supply decreases, and an exudate may form.2,5 Cholecystitis can be either acute or chronic, with repeated episodes of acute inflammation potentially leading to chronic cholecystitis. The gallbladder can become infected by various microorganisms, including those that are gas forming. An inflamed gallbladder can undergo necrosis and gangrene and, if left untreated, may progress to symptomatic sepsis.1,2,5 Failure to properly treat cholecystitis may result in perforation of the gallbladder, a rare but life-threatening phenomenon.2,5,7 Cholecystitis also can lead to gallstone pancreatitis if stones dislodge down to the sphincter of Oddi and are not cleared, thus blocking the pancreatic duct.1
It is thought that Gallstone disease is caused by bile hypersaturation.
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.
