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
Studies have shown that gallstone formation is mostly due to bile supersaturation. In the United States, patients that present with gallbladder stones mostly have cholesterol stones. Cholesterol stones form when the concentration of cholesterol in the bile is much higher than the concentration of cholesterol that can be dissolved in the bile. Normally cholesterol is metabolized in the body and excess cholesterol is disposed of in the bile. There is a balance between pronucleating (crystallization-promoting) and antinucleating (crystallization-inhibiting) forces, so that gallstones don't form. When pronucleating forces take the upper hand, gallstones will form. On the other hand, moderate intake of wine and the consumption of whole grain bread may decrease the risk of developing gallstones.
Pathophysiology
The most common type of gallstone is a cholesterol stone. When pronucleating proteins are present, such as mucin, the bile becomes hypersaturated with cholesterol and cholesterol stones form. Gallstone disease can also be caused by a lack of motility in the muscular wall of the gallbladder or excessive sphincter contraction, that prevents bile secretion. In this way the bile stagnates within the gallbladder and promotes the formation of stones. [1][2][3][4][5]
Pathogenesis of Specific Stones
Cholesterol Stones Formation
| Cholesterol stones are the most common type of gallstone | |||||||||||||||||||
| Cholesterol is an important organic molecule that is needed for incorporation within cell membranes and to produce steroid hormones in the body | |||||||||||||||||||
| The quantity of cholesterol is balanced within the body | |||||||||||||||||||
| When there is excess cholesterol in the body, the body will dispose of it by secreting it into the bile | |||||||||||||||||||
| When the cholesterol concentration reaches a certain level beyond that that can be secreted into the bile, biliary sludge will start to form | |||||||||||||||||||
| Biliary sludge is a viscous mixture that consists of mucin glycoproteins, calcium deposits and cholesterol crystals in the gallbladder | |||||||||||||||||||
| Over time, this sludge becomes more and more concentrated with cholesterol and eventually stones form.[1][6][7] | |||||||||||||||||||
Pigment Stones
- Less commonly, gallstones can be composed of bilirubin and are sometimes referred to as "pigment stones".
- Bilirubin is a byproduct of red blood cell breakdown and so are usually found in patients with hemoglobin disorders.
- Pigment stones are formed via two main pathways:
- Infection of the biliary tree with bacteria that can release hydrolytic enzymes and form insoluble calcium salts.
- Nonbacterial, nonenzymatic hydrolysis of bilirubin conjugates such as what may happen in patients with Gilbert's syndrome and chronic hemolysis.[8]
Mixed Stones
There is a lack of evidence that supports a true pathology to explain how mixed stones are formed. However, there have been theories that include a combination of several mechanisms including supersaturation, infection and hypomotility of the gallbladder.[2]
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:
Gross Pathology
- On gross pathology, commonly multiple small stones are found and less commonly a solitary stone is seen.
- The smaller stones represent a higher morbidity since they can easily occlude the biliary tracts.[11]
Microscopic Pathology
- On microscopic analysis, characteristic findings include:
- Transmural thickening of the gall bladder wall
- Neutrophilia[12]
References
- ↑ 1.0 1.1 Stinton LM, Shaffer EA (2012). "Epidemiology of gallbladder disease: cholelithiasis and cancer". Gut Liver. 6 (2): 172–87. doi:10.5009/gnl.2012.6.2.172. PMC 3343155. PMID 22570746.
- ↑ 2.0 2.1 Indar AA, Beckingham IJ (2002). "Acute cholecystitis". BMJ. 325 (7365): 639–43. PMC 1124163. PMID 12242178.
- ↑ McPhee, Stephen (2014). Pathophysiology of disease : an introduction to clinical medicine. New York: McGraw-Hill Education Medical. ISBN 0071806008.
- ↑ Wang HH, Portincasa P, Wang DQ (2008). "Molecular pathophysiology and physical chemistry of cholesterol gallstones". Front. Biosci. 13: 401–23. PMID 17981556.
- ↑ European Journal Gastroenterology & Hepatology. 6: 585–593. 1995. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Marschall HU, Einarsson C (2007). "Gallstone disease". J. Intern. Med. 261 (6): 529–42. doi:10.1111/j.1365-2796.2007.01783.x. PMID 17547709.
- ↑ Strasberg SM (2008). "Clinical practice. Acute calculous cholecystitis". N. Engl. J. Med. 358 (26): 2804–11. doi:10.1056/NEJMcp0800929. PMID 18579815.
- ↑ Trotman BW (1991). "Pigment gallstone disease". Gastroenterol. Clin. North Am. 20 (1): 111–26. PMID 2022417.
- ↑ 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) - ↑ 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.