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

Gall bladder opened to show numerous gallstones. Their brownish to greenish color suggest they are cholesterol calculi. Source: Wikimedia Commons[2]

Pathogenesis[edit | edit source] The exact pathogenesis of [disease name] is not fully understood. OR

It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3]. [Pathogen name] is usually transmitted via the [transmission route] route to the human host. Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell. [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells]. The progression to [disease name] usually involves the [molecular pathway]. The pathophysiology of [disease/malignancy] depends on the histological subtype. Genetics[edit | edit source] [Disease name] is transmitted in [mode of genetic transmission] pattern. Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3]. The development of [disease name] is the result of multiple genetic mutations.



Associated Conditions

On the other hand, wine and whole grain bread may decrease the risk of gallstones.[5]

Gross Pathology

Gall bladder opened to show numerous gallstones. Source: Wikimedia Commons[6]



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

[[Image:path89-05.jpg|thumb|200px|right|Gall bladder shows cholecystitis with cholelithiasis. Source: Duke University [8]


On microscopic histopathological analysis, variable evidences of inflammation can be noted transmurally including neutrophils, which are characteristic in gallstone disease.[9]

References

  1. Wang HH, Portincasa P, Wang DQ (2008). "Molecular pathophysiology and physical chemistry of cholesterol gallstones". Front. Biosci. 13: 401–23. PMID 17981556.
  2. name="urlFile:Gallensteine 2006 03 28.JPG - Wikimedia Commons">"File:Gallensteine 2006 03 28.JPG - Wikimedia Commons".
  3. 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.
  4. 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)
  5. European Journal Gastroenterology & Hepatology. 6: 585–593. 1995. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  6. "File:Gallensteine 2006 03 28.JPG - Wikimedia Commons".
  7. Ansert, Sandra (2018). Textbook of diagnostic sonography. St. Louis, MO: Elsevier. ISBN 978-0323353755.
  8. "web.duke.edu".
  9. Fisher, M. M. (1979). Gallstones. Boston, MA: Springer US. ISBN 1461570662.

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