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]


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.


Pathogenesis of Specific Stones

Cholesterol Stones Formation[1][6][7]

Excess cholesterol in body
The body will dispose of it by secreting it into the bile
Cholesterol concentration reaches a certain level beyond that that can be secreted into the bile
Biliary sludge starts to form
Biliary sludge is a viscous mixture that consists of mucin glycoproteins, calcium deposits and cholesterol crystals in the gallbladder
Over time, the sludge becomes more and more concentrated with cholesterol
Eventually forming gallstones

Pigment Stones

Mixed Stones

  • There is a lack of evidence that supports a true pathology to explain how mixed stones are formed.[2]
  • However, there have been theories that include a combination of several mechanisms including supersaturation, infection and hypomotility of the gall bladder.

Associated Conditions

The conditions associated with gallstone disease include:[9][10]

Gross Pathology

  • On gross pathology, commonly multiple small stones are found and less commonly a solitary stone is seen.[11]
Cholesterol gallstones are seen. Source: by Noortje123 from nl, CC BY-SA 3.0,

Microscopic Pathology

  • On microscopic analysis, characteristic findings include:[12]


  1. 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. 2.0 2.1 Indar AA, Beckingham IJ (2002). "Acute cholecystitis". BMJ. 325 (7365): 639–43. PMC 1124163. PMID 12242178.
  3. McPhee, Stephen (2014). Pathophysiology of disease : an introduction to clinical medicine. New York: McGraw-Hill Education Medical. ISBN 0071806008.
  4. Wang HH, Portincasa P, Wang DQ (2008). "Molecular pathophysiology and physical chemistry of cholesterol gallstones". Front. Biosci. 13: 401–23. PMID 17981556.
  5. European Journal Gastroenterology & Hepatology. 6: 585–593. 1995. |access-date= requires |url= (help)
  6. 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.
  7. Strasberg SM (2008). "Clinical practice. Acute calculous cholecystitis". N. Engl. J. Med. 358 (26): 2804–11. doi:10.1056/NEJMcp0800929. PMID 18579815.
  8. Trotman BW (1991). "Pigment gallstone disease". Gastroenterol. Clin. North Am. 20 (1): 111–26. PMID 2022417.
  9. 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.
  10. Ortega RM, et al. (1997). "Differences in diet and food habits between patients with gallstones and controls". Journal of the American College of Nutrition. 16: 88–95. |access-date= requires |url= (help)
  11. Ansert, Sandra (2018). Textbook of diagnostic sonography. St. Louis, MO: Elsevier. ISBN 978-0323353755.
  12. Fisher, M. M. (1979). Gallstones. Boston, MA: Springer US. ISBN 1461570662.

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