Gallstone disease pathophysiology: Difference between revisions

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{{Gallstone disease}}
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==Overview==
==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.<ref name="pmid17981556">{{cite journal |vauthors=Wang HH, Portincasa P, Wang DQ |title=Molecular pathophysiology and physical chemistry of cholesterol gallstones |journal=Front. Biosci. |volume=13 |issue= |pages=401–23 |year=2008 |pmid=17981556 |doi= |url=}}</ref>


== Pathophysiology ==
Studies have shown that [[Gallstone disease|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 [[Metabolism|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==


[[Image:Gallstones.jpg|thumb|200px|left|[[Gall bladder]] opened to show numerous '''gallstones'''. Their brownish to greenish color suggest they are cholesterol [[Calculus (medicine)|calculi]].]]
*The most common type of gallstone is a [[cholesterol]] stone.<ref name="pmid22570746">{{cite journal |vauthors=Stinton LM, Shaffer EA |title=Epidemiology of gallbladder disease: cholelithiasis and cancer |journal=Gut Liver |volume=6 |issue=2 |pages=172–87 |year=2012 |pmid=22570746 |pmc=3343155 |doi=10.5009/gnl.2012.6.2.172 |url=}}</ref><ref name="pmid12242178">{{cite journal |vauthors=Indar AA, Beckingham IJ |title=Acute cholecystitis |journal=BMJ |volume=325 |issue=7365 |pages=639–43 |year=2002 |pmid=12242178 |pmc=1124163 |doi= |url=}}</ref><ref>{{cite book | last = McPhee | first = Stephen | title = Pathophysiology of disease : an introduction to clinical medicine | publisher = McGraw-Hill Education Medical | location = New York | year = 2014 | isbn = 0071806008 }}</ref><ref name="pmid17981556">{{cite journal |vauthors=Wang HH, Portincasa P, Wang DQ |title=Molecular pathophysiology and physical chemistry of cholesterol gallstones |journal=Front. Biosci. |volume=13 |issue= |pages=401–23 |year=2008 |pmid=17981556 |doi= |url=}}</ref><ref>{{cite journal |year=1995  |title=. |journal=European Journal Gastroenterology & Hepatology |volume=6 |pages=585-593 |accessdate= 2007-08-25}}</ref>
*When pronucleating proteins are present, such as [[mucin]], the [[bile]] becomes [[Supersaturation|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 of Oddi|sphincter]] contraction, that prevents [[bile]] secretion.
*In this way the [[bile]] stagnates within the gallbladder and promotes the formation of stones.


Progress has been made in understanding the process of gallstone formation. Researchers believe that gallstones may be caused by a combination of factors, including inherited body chemistry, [[human weight|body weight,]] gallbladder motility (movement), and perhaps diet. Additionally, people with [[erythropoietic protoporphyria]] (EPP) are at increased risk to develop gallstones.<ref>{{cite web |url=http://www.merck.com/mmhe/sec12/ch160/ch160d.html |title=Erythropoietic Protoporphyria |accessdate=2007-08-25 |work=Merck Manual}}</ref>
===Pathogenesis of Specific Stones===


Cholesterol gallstones develop when bile contains too much cholesterol and not enough bile salts. Besides a high concentration of cholesterol, two other factors seem to be important in causing gallstones. The first is how often and how well the gallbladder contracts; incomplete and infrequent emptying of the gallbladder may cause the bile to become overconcentrated and contribute to gallstone formation. The second factor is the presence of proteins in the liver and bile that either promote or inhibit cholesterol crystallization into gallstones.
*[[Cholesterol]] stones are the most common type of gallstone.
*The quantity of [[cholesterol]] is balanced within the body.
*[[Cholesterol]] is an important [[Organic Chemistry|organic]] molecule that is needed for incorporation within [[Cell membrane|cell membranes]] and to produce [[Steroid hormone|steroid hormones]] in the body.


In addition, increased levels of the hormone [[estrogen]] as a result of [[pregnancy]], [[hormone therapy]], or the use of combined (estrogen-containing) forms of [[hormonal contraception]], may increase cholesterol levels in bile and also decrease gallbladder movement, resulting in gallstone formation.
<br>
<div style="text-align: center;">'''Cholesterol Stones Formation'''<ref name="pmid22570746">{{cite journal |vauthors=Stinton LM, Shaffer EA |title=Epidemiology of gallbladder disease: cholelithiasis and cancer |journal=Gut Liver |volume=6 |issue=2 |pages=172–87 |year=2012 |pmid=22570746 |pmc=3343155 |doi=10.5009/gnl.2012.6.2.172 |url=}}</ref><ref name="pmid17547709">{{cite journal |vauthors=Marschall HU, Einarsson C |title=Gallstone disease |journal=J. Intern. Med. |volume=261 |issue=6 |pages=529–42 |year=2007 |pmid=17547709 |doi=10.1111/j.1365-2796.2007.01783.x |url=}}</ref><ref name="pmid18579815">{{cite journal |vauthors=Strasberg SM |title=Clinical practice. Acute calculous cholecystitis |journal=N. Engl. J. Med. |volume=358 |issue=26 |pages=2804–11 |year=2008 |pmid=18579815 |doi=10.1056/NEJMcp0800929 |url=}}</ref></div>
<br>
{| align="center"
|
{{Family tree/start}}
{{Family tree | | | | A01 | | | |A01=Excess [[cholesterol]] in body}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | B01 | | | |B01=The body will dispose of it by secreting it into the [[bile]]}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | C01 | | | |C01=[[Cholesterol]] [[concentration]] reaches a certain level beyond that that can be secreted into the bile}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | D01 | | | |D01=[[Biliary]] sludge starts to form}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | E01 | | | |E01=[[Biliary]] sludge is a [[Viscosity|viscous]] mixture that consists of [[mucin]] [[Glycoprotein|glycoproteins]], [[Calcium|calcium deposits]] and [[cholesterol]] crystals in the gallbladder}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | F01 | | | |F01=Over time, the sludge becomes more and more concentrated with [[cholesterol]]}}
{{Family tree | | | | |!| | | | | }}
{{Family tree | | | | G01 | | | |G01= Eventually forming gallstones}}
{{Family tree/end}}
|}
====Pigment Stones====
 
*Less commonly, gallstones can be composed of [[bilirubin]] and are sometimes referred to as "pigment stones".<ref name="pmid2022417">{{cite journal |vauthors=Trotman BW |title=Pigment gallstone disease |journal=Gastroenterol. Clin. North Am. |volume=20 |issue=1 |pages=111–26 |year=1991 |pmid=2022417 |doi= |url=}}</ref>
*[[Bilirubin]] is a byproduct of [[red blood cell]] [[Hemolysis|breakdown]] and so are usually found in patients with [[Hemoglobinopathy|hemoglobin disorders]].
*Pigment stones are formed via two main pathways:
**[[Infection]] of the [[biliary tree]] with [[bacteria]] that can release [[Hydrolysis|hydrolytic]] enzymes and form insoluble [[calcium]] salts.
**Non-bacterial, non-enzymatic hydrolysis of [[bilirubin]] conjugates such as what may happen in patients with [[Gilbert's syndrome]] and [[Hemolysis|chronic hemolysis]].
 
====Mixed Stones====


No clear relationship has been proven between diet and gallstone formation. However, low-fiber, high-cholesterol diets, and diets high in starchy foods have been suggested as contributing to gallstone formation. Other nutritional factors that may increase risk of gallstones include rapid weight loss, constipation, eating fewer meals per day, eating less fish, and low intakes of the nutrients folate, magnesium, calcium, and vitamin C.<ref>{{cite journal |author=R.M. Ortega |coauthors=M. Fernandez-Azuela, A. Encinas-Sotillos, P. Andres, and A. M. Lopez-Sobaler |year=1997 |month=February |title=Differences in diet and food habits between patients with gallstones and controls |journal=Journal of the American College of Nutrition |volume= 16 |pages=88-95 |accessdate= 2007-08-25}}</ref> On the other hand, wine and whole grain bread may decrease the risk of gallstones.<ref>{{cite journal |year=1995 |month=June |title=. |journal=European Journal Gastroenterology & Hepatology |volume=6 |pages=585-593 |accessdate= 2007-08-25}}</ref>
*There is a lack of evidence that supports a true pathology to explain how mixed stones are formed.<ref name="pmid12242178">{{cite journal |vauthors=Indar AA, Beckingham IJ |title=Acute cholecystitis |journal=BMJ |volume=325 |issue=7365 |pages=639–43 |year=2002 |pmid=12242178 |pmc=1124163 |doi= |url=}}</ref>
*However, there have been theories that include a combination of several mechanisms including supersaturation, [[infection]] and hypomotility of the [[gall bladder]].


==Associated Conditions==
==Associated Conditions==
The conditions associated with gallstone disease include:<ref name="pmid29158491">{{cite journal |vauthors=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 |title=Gallstone Disease and the Risk of Type 2 Diabetes |journal=Sci Rep |volume=7 |issue=1 |pages=15853 |year=2017 |pmid=29158491 |doi=10.1038/s41598-017-14801-2 |url=}}</ref><ref>{{cite journal |vauthors=Ortega RM, et al. |year=1997 |title=Differences in diet and food habits between patients with gallstones and controls |journal=Journal of the American College of Nutrition |volume= 16 |pages=88-95 |accessdate= 2007-08-25}}</ref>


*Diabetes Mellitus Type 2
*[[Diabetes mellitus type 2|Diabetes mellitus type 2]]
*Obesity
*[[Obesity]]
*Pregancy
*[[Pregnancy]]
*[[Gallbladder cancer]]
*[[Gallbladder]] [[Polyp|polyps]]
*[[Primary sclerosing cholangitis|Primary sclerosing cholangitis]]
*[[Porcelain gallbladder|Porcelain gallbladder]]
*Rapid [[weight loss]]
*[[Constipation]]
*Eating fewer meals
*Low intake of:
**Fish
**[[Magnesium]]
**[[Folic acid|Folate]]
**Whole grain bread
**Fiber
**[[Vitamin C]]


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
*On gross pathology, commonly multiple small stones are found and less commonly a solitary stone is seen.<ref>{{cite book | last = Ansert | first = Sandra | title = Textbook of diagnostic sonography | publisher = Elsevier | location = St. Louis, MO | year = 2018 | isbn = 978-0323353755}}</ref>
 
[[Image:Gallstone.jpg|thumb|center|500px|Cholesterol gallstones are seen. Source: commons.wikimedia.org by Noortje123 from nl, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=1805918]]


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
*On microscopic analysis, characteristic findings include:<ref>{{cite book | last = Fisher | first = M. M. | title = Gallstones | publisher = Springer US | location = Boston, MA | year = 1979 | isbn = 1461570662 }}</ref>
**Transmural thickening of the gall bladder wall
**[[Neutrophilia]]


==References==
==References==
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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

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: commons.wikimedia.org by Noortje123 from nl, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=1805918

Microscopic Pathology

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

References

  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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