Acute cholecystitis pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
Acute calculous cholecystitis is usually caused by the mechanical obstruction of the [[gallbladder]] due to [[gallstones]]. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. [[Gallstones]] are the most common cause of physical obstruction of the [[gallbladder]] usually at the neck or in the cystic duct. Cholesterol gallstones are the most common type of gallstones. The obstruction causes an increased pressure as the [[gallbladder]] mucosa continues to produce [[mucus]]. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis. Mechanical obstruction of the gallbladder as a result of [[Polyp|polyps]], [[Gallbladder cancer|malignancy]], an infestation of the gallbladder with [[parasites]], foreign bodies, and [[trauma]] may also lead to the acute cholecystitis. Acute cholecystitis is more common in siblings and first degree relatives of affected persons. Lith gene is involved in the pathogenesis of cholecystitis. Mutations in the hepatic cholesterol transporter [[ABCG8]] also predispose an individual to the develop gallstones. Acute cholecystitis is associated with [[diabetes]], [[insulin resistance]], [[cardiovascular diseases]], [[non-alcoholic fatty liver disease]] (NAFLD) and [[Gastrointestinal cancer|gastrointestinal malignancies]]. Microscopic histopathology shows [[Edema|edematous]] and [[hemorrhagic]] [[Gallbladder wall thickening|gallbladder wall]], mucosal [[necrosis]] with [[neutrophil]] infiltration. Bile infiltration of the gallbladder wall and bile and [[leucocyte]] margination of blood vessels are specific findings for acalculous cholecystitis.
 
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].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==


===Pathogenesis===
===Pathogenesis===
The pathogenesis of acute cholecystitis involves the following:<ref name="pmid5442405">{{cite journal |vauthors=Foard DE, Haber AH |title=Physiologically normal senescence in seedlings grown without cell division after massive gamma-irradiation of seeds |journal=Radiat. Res. |volume=42 |issue=2 |pages=372–80 |year=1970 |pmid=5442405 |doi= |url=}}</ref><ref name="pmid29083717">{{cite journal |vauthors=Jones MW, Ferguson T |title=Gallbladder, Cholecystitis, Acalculous |journal= |volume= |issue= |pages= |year= |pmid=29083717 |doi= |url=https://www.ncbi.nlm.nih.gov/books/NBK459182/#article-17050.s1}}</ref>
[[Inflammation]] of the [[gallbladder]] is termed as cholecystitis. Acute calculous cholecystitis is usually caused by the mechanical obstruction due to [[gallstones]]. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. The pathogenesis of acute cholecystitis involves the following:<ref name="pmid5442405">{{cite journal |vauthors=Foard DE, Haber AH |title=Physiologically normal senescence in seedlings grown without cell division after massive gamma-irradiation of seeds |journal=Radiat. Res. |volume=42 |issue=2 |pages=372–80 |year=1970 |pmid=5442405 |doi= |url=}}</ref><ref name="pmid29083717">{{cite journal |vauthors=Jones MW, Ferguson T |title=Gallbladder, Cholecystitis, Acalculous |journal= |volume= |issue= |pages= |year= |pmid=29083717 |doi= |url=https://www.ncbi.nlm.nih.gov/books/NBK459182/#article-17050.s1}}</ref><ref name="pmid24679431">{{cite journal |vauthors=Knab LM, Boller AM, Mahvi DM |title=Cholecystitis |journal=Surg. Clin. North Am. |volume=94 |issue=2 |pages=455–70 |year=2014 |pmid=24679431 |doi=10.1016/j.suc.2014.01.005 |url=}}</ref><ref name="pmid22872303">{{cite journal |vauthors=Yokoe M, Takada T, Strasberg SM, Solomkin JS, Mayumi T, Gomi H, Pitt HA, Gouma DJ, Garden OJ, Büchler MW, Kiriyama S, Kimura Y, Tsuyuguchi T, Itoi T, Yoshida M, Miura F, Yamashita Y, Okamoto K, Gabata T, Hata J, Higuchi R, Windsor JA, Bornman PC, Fan ST, Singh H, de Santibanes E, Kusachi S, Murata A, Chen XP, Jagannath P, Lee S, Padbury R, Chen MF |title=New diagnostic criteria and severity assessment of acute cholecystitis in revised Tokyo Guidelines |journal=J Hepatobiliary Pancreat Sci |volume=19 |issue=5 |pages=578–85 |year=2012 |pmid=22872303 |pmc=3429769 |doi=10.1007/s00534-012-0548-0 |url=}}</ref><ref name="pmid23340953">{{cite journal |vauthors=Yokoe M, Takada T, Strasberg SM, Solomkin JS, Mayumi T, Gomi H, Pitt HA, Garden OJ, Kiriyama S, Hata J, Gabata T, Yoshida M, Miura F, Okamoto K, Tsuyuguchi T, Itoi T, Yamashita Y, Dervenis C, Chan AC, Lau WY, Supe AN, Belli G, Hilvano SC, Liau KH, Kim MH, Kim SW, Ker CG |title=TG13 diagnostic criteria and severity grading of acute cholecystitis (with videos) |journal=J Hepatobiliary Pancreat Sci |volume=20 |issue=1 |pages=35–46 |year=2013 |pmid=23340953 |doi=10.1007/s00534-012-0568-9 |url=}}</ref><ref name="pmid20478482">{{cite journal |vauthors=Wang HH, Portincasa P, Afdhal NH, Wang DQ |title=Lith genes and genetic analysis of cholesterol gallstone formation |journal=Gastroenterol. Clin. North Am. |volume=39 |issue=2 |pages=185–207, vii–viii |year=2010 |pmid=20478482 |doi=10.1016/j.gtc.2010.02.007 |url=}}</ref><ref name="pmid27317033">{{cite journal |vauthors=Loozen CS, Oor JE, van Ramshorst B, van Santvoort HC, Boerma D |title=Conservative treatment of acute cholecystitis: a systematic review and pooled analysis |journal=Surg Endosc |volume=31 |issue=2 |pages=504–515 |year=2017 |pmid=27317033 |doi=10.1007/s00464-016-5011-x |url=}}</ref><ref name="pmid27133241">{{cite journal |vauthors=Avegno J, Carlisle M |title=Evaluating the Patient with Right Upper Quadrant Abdominal Pain |journal=Emerg. Med. Clin. North Am. |volume=34 |issue=2 |pages=211–28 |year=2016 |pmid=27133241 |doi=10.1016/j.emc.2015.12.011 |url=}}</ref><ref name="pmid27121416">{{cite journal |vauthors=Lammert F, Gurusamy K, Ko CW, Miquel JF, Méndez-Sánchez N, Portincasa P, van Erpecum KJ, van Laarhoven CJ, Wang DQ |title=Gallstones |journal=Nat Rev Dis Primers |volume=2 |issue= |pages=16024 |year=2016 |pmid=27121416 |doi=10.1038/nrdp.2016.24 |url=}}</ref><ref name="pmid17252293">{{cite journal |vauthors=Kimura Y, Takada T, Kawarada Y, Nimura Y, Hirata K, Sekimoto M, Yoshida M, Mayumi T, Wada K, Miura F, Yasuda H, Yamashita Y, Nagino M, Hirota M, Tanaka A, Tsuyuguchi T, Strasberg SM, Gadacz TR |title=Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines |journal=J Hepatobiliary Pancreat Surg |volume=14 |issue=1 |pages=15–26 |year=2007 |pmid=17252293 |pmc=2784509 |doi=10.1007/s00534-006-1152-y |url=}}</ref><ref name="urlAcute cholecystitis | The BMJ">{{cite web |url=http://www.bmj.com/content/325/7365/639 |title=Acute cholecystitis &#124; The BMJ |format= |work= |accessdate=}}</ref>
*Inflammation of the gallbladder is termed as cholecystitis. Acute calculous cholecystitis is usually caused by the mechanical obstruction due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis.
*'''Obstruction of the gallbladder:'''
**'''Obstruction of the gallbladder:'''
**[[Gallstones]] are the most common cause of physical obstruction of the gallbladder usually at the [[Neck of gallbladder|neck]] or in the [[cystic duct]]. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce [[mucus]]. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis.
***Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis.
***There are two major types of gallstones:
****There are two major types of gallstones:
****<u>Cholesterol gallstones:</u>
*****<u>Cholesterol gallstones:</u>
*****Cholesterol [[gallstones]] are the most predominant form of the [[Gallstone|gallstones]]. They account for approximately 80% of the total [[gallstones]].
******Cholesterol gallstones are the most predominant form of the gallstones. They account for approximately 80% of the total gallstones.
*****The formation of gallstones is dependant on the following factors:
******The formation of gallstones is dependant on the following factors:
******Cholesterol supersaturation in the bile
*******Cholesterol supersaturation in the bile
******Crystal nucleation
*******Crystal nucleation
******Gallbladder dysmotility
*******Gallbladder dysmotility
******Gallbladder absorption  
*******Gallbladder absorption  
****<u>Pigmented gallstones:</u>
*****<u>Pigmented gallstones:</u>
*****There are two types of pigmented gallstones.
******There are two types of pigmented gallstones.
******Black stones
*******Black stones
*******Black stones consist of calcium bilirubinate and mucin [[glycoproteins]].
********Black stones consist of calcium bilirubinate and mucin glycoproteins.
*******Black stones are predominantly associated with [[Hemolysis|hemolytic conditions]] or [[cirrhosis]] (as a result of increased levels of [[unconjugated bilirubin]]).
********Black stones are predominantly associated with hemolytic conditions or cirrhosis (as a result of increased levels of unconjugated bilirubin).
*******These stones are usually located in the gallbladder.
********These stones are usually located in the gallbladder.
******Brown stones
*******Brown stones
*******Brown stones are usually associated with bacterial infection.  
********Brown stones are usually associated with bacterial infection.  
*******Brown stones are usually located elsewhere in the [[biliary tree]] as opposed to the [[gallbladder]].
********Brown stones are usually located elsewhere in the biliary tree as opposed to the gallbladder.
**Mechanical obstruction of the gallbladder as a result of [[Polyp|polyps]], [[Gallbladder cancer|malignancy]], an infestation of the gallbladder with [[parasites]], foreign bodies, and [[trauma]] may also lead to the acute cholecystitis.
***Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis.
*'''Gallbladder stasis:'''
**'''Gallbladder stasis:'''
**[[Gallbladder]] stasis is usually due to the lack of gallbladder stimulation and [[contractility]].
***Gallbladder stasis is usually due to the lack of gallbladder stimulation and contractility.
** This leads to concentration of the bile salts with a build-up of pressure within the organ. An increased intraluminal pressure results in [[ischemia]] and [[necrosis]] of the [[gallbladder]].
*** This leads to concentration of the bile salts with a build-up of pressure within the organ. An increased intraluminal pressure results in ischemia and necrosis of the gallbladder.
** The [[gallbladder]] stasis also facilitates the proliferation of the bacteria such as ''[[Escherichia coli]], [[Klebsiella]], [[Bacteroides]], [[Proteus]], [[Pseudomonas]], and [[Enterococcus faecalis]]''. This can also cause an inflammatory reaction in the [[gallbladder]].
*** The gallbladder stasis also facilitates the proliferation of the bacterias such as ''Escherichia coli, Klebsiella, Bacteroides, Proteus, Pseudomonas, and Enterococcus faecalis''. This can also cause an inflammatory reaction in the gallbladder.


==Genetics==
==Genetics==
*Acute cholecystitis is more common in siblings and first degree relatives of affected persons.<ref name="urlAn Increased Familial Frequency of Gallstones - Gastroenterology">{{cite web |url=http://www.gastrojournal.org/article/S0016-5085(83)80118-8/abstract |title=An Increased Familial Frequency of Gallstones - Gastroenterology |format= |work= |accessdate=}}</ref><ref name="pmid6517051">{{cite journal |vauthors=Weiss KM, Ferrell RE, Hanis CL, Styne PN |title=Genetics and epidemiology of gallbladder disease in New World native peoples |journal=Am. J. Hum. Genet. |volume=36 |issue=6 |pages=1259–78 |year=1984 |pmid=6517051 |pmc=1684666 |doi= |url=}}</ref>
*Acute cholecystitis is more common in siblings and first degree relatives of affected persons.<ref name="urlAn Increased Familial Frequency of Gallstones - Gastroenterology">{{cite web |url=http://www.gastrojournal.org/article/S0016-5085(83)80118-8/abstract |title=An Increased Familial Frequency of Gallstones - Gastroenterology |format= |work= |accessdate=}}</ref><ref name="pmid6517051">{{cite journal |vauthors=Weiss KM, Ferrell RE, Hanis CL, Styne PN |title=Genetics and epidemiology of gallbladder disease in New World native peoples |journal=Am. J. Hum. Genet. |volume=36 |issue=6 |pages=1259–78 |year=1984 |pmid=6517051 |pmc=1684666 |doi= |url=}}</ref>
*Lith gene is involved in the pathogenesis of cholecystitis.<ref name="pmid20478482">{{cite journal |vauthors=Wang HH, Portincasa P, Afdhal NH, Wang DQ |title=Lith genes and genetic analysis of cholesterol gallstone formation |journal=Gastroenterol. Clin. North Am. |volume=39 |issue=2 |pages=185–207, vii–viii |year=2010 |pmid=20478482 |doi=10.1016/j.gtc.2010.02.007 |url=}}</ref>
*Lith gene is involved in the pathogenesis of cholecystitis.<ref name="pmid20478482">{{cite journal |vauthors=Wang HH, Portincasa P, Afdhal NH, Wang DQ |title=Lith genes and genetic analysis of cholesterol gallstone formation |journal=Gastroenterol. Clin. North Am. |volume=39 |issue=2 |pages=185–207, vii–viii |year=2010 |pmid=20478482 |doi=10.1016/j.gtc.2010.02.007 |url=}}</ref>
*Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones.<ref name="pmid27121416">{{cite journal |vauthors=Lammert F, Gurusamy K, Ko CW, Miquel JF, Méndez-Sánchez N, Portincasa P, van Erpecum KJ, van Laarhoven CJ, Wang DQ |title=Gallstones |journal=Nat Rev Dis Primers |volume=2 |issue= |pages=16024 |year=2016 |pmid=27121416 |doi=10.1038/nrdp.2016.24 |url=}}</ref>
*Mutations in the hepatic cholesterol transporter [[ABCG8]] also predispose an individual to the develop gallstones.<ref name="pmid27121416">{{cite journal |vauthors=Lammert F, Gurusamy K, Ko CW, Miquel JF, Méndez-Sánchez N, Portincasa P, van Erpecum KJ, van Laarhoven CJ, Wang DQ |title=Gallstones |journal=Nat Rev Dis Primers |volume=2 |issue= |pages=16024 |year=2016 |pmid=27121416 |doi=10.1038/nrdp.2016.24 |url=}}</ref>


==Associated Conditions==
==Associated Conditions==
The following conditions are associated with acute cholecystitis:<ref name="pmid27508070">{{cite journal |vauthors=Tiderington E, Lee SP, Ko CW |title=Gallstones: new insights into an old story |journal=F1000Res |volume=5 |issue= |pages= |year=2016 |pmid=27508070 |pmc=4962289 |doi=10.12688/f1000research.8874.1 |url=}}</ref>
The following conditions are associated with acute cholecystitis:<ref name="pmid27508070">{{cite journal |vauthors=Tiderington E, Lee SP, Ko CW |title=Gallstones: new insights into an old story |journal=F1000Res |volume=5 |issue= |pages= |year=2016 |pmid=27508070 |pmc=4962289 |doi=10.12688/f1000research.8874.1 |url=}}</ref>
*Diabetes
*[[Diabetes]]
*Insulin resistance
*[[Insulin resistance]]
*Cardiovascular diseases
*[[Cardiovascular diseases]]
*Non-alcoholic fatty liver disease (NAFLD)
*[[Non-alcoholic fatty liver disease]] (NAFLD)
*Gastrointestinal malignancies
*[[Gastrointestinal cancer|Gastrointestinal malignancies]]:
**Gastric cancer
**[[Gastric cancer]]
**Hepatocellular carcinoma
**[[Hepatocellular carcinoma]]
**Cholangiocarcinoma
**[[Cholangiocarcinoma]]
**Pancreatic cancer
**[[Pancreatic cancer]]
**Cancer of the ampulla of Vater
**Cancer of the [[ampulla of Vater]]


==Gross Pathology==
==Gross Pathology==
*On gross pathology, acute cholecystitis has the following features:<ref name="pmid16241996">{{cite journal |vauthors=Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V, Syrjälä H, Karttunen TJ |title=Histopathology of acute acalculous cholecystitis in critically ill patients |journal=Histopathology |volume=47 |issue=5 |pages=485–92 |year=2005 |pmid=16241996 |doi=10.1111/j.1365-2559.2005.02238.x |url=}}</ref><ref name="pmid14719768">{{cite journal |vauthors=Owen CC, Bilhartz LE |title=Gallbladder polyps, cholesterolosis, adenomyomatosis, and acute acalculous cholecystitis |journal=Semin. Gastrointest. Dis. |volume=14 |issue=4 |pages=178–88 |year=2003 |pmid=14719768 |doi= |url=}}</ref><ref name="pmid14627341">{{cite journal |vauthors=McChesney JA, Northup PG, Bickston SJ |title=Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology |journal=Dig. Dis. Sci. |volume=48 |issue=10 |pages=1960–7 |year=2003 |pmid=14627341 |doi= |url=}}</ref><ref name="pmid20818819">{{cite journal |vauthors=Huang SM, Yao CC, Pan H, Hsiao KM, Yu JK, Lai TJ, Huang SD |title=Pathophysiological significance of gallbladder volume changes in gallstone diseases |journal=World J. Gastroenterol. |volume=16 |issue=34 |pages=4341–7 |year=2010 |pmid=20818819 |pmc=2937116 |doi= |url=}}</ref><ref name="pmid29083717">{{cite journal |vauthors=Jones MW, Ferguson T |title=Gallbladder, Cholecystitis, Acalculous |journal= |volume= |issue= |pages= |year= |pmid=29083717 |doi= |url=https://www.ncbi.nlm.nih.gov/books/NBK459182/#article-17050.s1}}</ref>
*On gross pathology, acute cholecystitis has the following features:<ref name="pmid16241996">{{cite journal |vauthors=Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V, Syrjälä H, Karttunen TJ |title=Histopathology of acute acalculous cholecystitis in critically ill patients |journal=Histopathology |volume=47 |issue=5 |pages=485–92 |year=2005 |pmid=16241996 |doi=10.1111/j.1365-2559.2005.02238.x |url=}}</ref><ref name="pmid14719768">{{cite journal |vauthors=Owen CC, Bilhartz LE |title=Gallbladder polyps, cholesterolosis, adenomyomatosis, and acute acalculous cholecystitis |journal=Semin. Gastrointest. Dis. |volume=14 |issue=4 |pages=178–88 |year=2003 |pmid=14719768 |doi= |url=}}</ref><ref name="pmid14627341">{{cite journal |vauthors=McChesney JA, Northup PG, Bickston SJ |title=Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology |journal=Dig. Dis. Sci. |volume=48 |issue=10 |pages=1960–7 |year=2003 |pmid=14627341 |doi= |url=}}</ref><ref name="pmid20818819">{{cite journal |vauthors=Huang SM, Yao CC, Pan H, Hsiao KM, Yu JK, Lai TJ, Huang SD |title=Pathophysiological significance of gallbladder volume changes in gallstone diseases |journal=World J. Gastroenterol. |volume=16 |issue=34 |pages=4341–7 |year=2010 |pmid=20818819 |pmc=2937116 |doi= |url=}}</ref><ref name="pmid29083717">{{cite journal |vauthors=Jones MW, Ferguson T |title=Gallbladder, Cholecystitis, Acalculous |journal= |volume= |issue= |pages= |year= |pmid=29083717 |doi= |url=https://www.ncbi.nlm.nih.gov/books/NBK459182/#article-17050.s1}}</ref>
**Enlarged/distended gallbladder
**Enlarged/distended [[gallbladder]]
**Serosal or mucosal exudates
**Serosal or mucosal exudates
**Thickened wall with hemorrhage and edema  
**[[Gallbladder wall thickening|Thickened wall]] with [[hemorrhage]] and [[edema]]
**Ulcers, pus, bile, and gallstones
**[[Ulcer|Ulcers]], [[pus]], [[bile]], and [[gallstones]]
**Rokitansky-Aschoff sinuses
***Rokitansky-Aschoff sinuses are entrapped epithelial crypts, pseudodiverticula, or pockets in the wall of the gallbladder


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, acute cholecystitis has the following features:<ref name="pmid14719768">{{cite journal |vauthors=Owen CC, Bilhartz LE |title=Gallbladder polyps, cholesterolosis, adenomyomatosis, and acute acalculous cholecystitis |journal=Semin. Gastrointest. Dis. |volume=14 |issue=4 |pages=178–88 |year=2003 |pmid=14719768 |doi= |url=}}</ref><ref name="pmid14627341">{{cite journal |vauthors=McChesney JA, Northup PG, Bickston SJ |title=Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology |journal=Dig. Dis. Sci. |volume=48 |issue=10 |pages=1960–7 |year=2003 |pmid=14627341 |doi= |url=}}</ref><ref name="pmid21574105">{{cite journal |vauthors=Kasprzak A, Malkowski W, Biczysko W, Seraszek A, Sterzyńska K, Zabel M |title=Histological alterations of gallbladder mucosa and selected clinical data in young patients with symptomatic gallstones |journal=Pol J Pathol |volume=62 |issue=1 |pages=41–9 |year=2011 |pmid=21574105 |doi= |url=}}</ref><ref name="pmid26602767">{{cite journal |vauthors=Yaylak F, Deger A, Bayhan Z, Kocak C, Zeren S, Kocak FE, Ekici MF, Algın MC |title=Histopathological gallbladder morphometric measurements in geriatric patients with symptomatic chronic cholecystitis |journal=Ir J Med Sci |volume=185 |issue=4 |pages=871–876 |year=2016 |pmid=26602767 |doi=10.1007/s11845-015-1385-3 |url=}}</ref>
*On microscopic histopathological analysis, acute cholecystitis has the following features:<ref name="pmid14719768">{{cite journal |vauthors=Owen CC, Bilhartz LE |title=Gallbladder polyps, cholesterolosis, adenomyomatosis, and acute acalculous cholecystitis |journal=Semin. Gastrointest. Dis. |volume=14 |issue=4 |pages=178–88 |year=2003 |pmid=14719768 |doi= |url=}}</ref><ref name="pmid14627341">{{cite journal |vauthors=McChesney JA, Northup PG, Bickston SJ |title=Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology |journal=Dig. Dis. Sci. |volume=48 |issue=10 |pages=1960–7 |year=2003 |pmid=14627341 |doi= |url=}}</ref><ref name="pmid21574105">{{cite journal |vauthors=Kasprzak A, Malkowski W, Biczysko W, Seraszek A, Sterzyńska K, Zabel M |title=Histological alterations of gallbladder mucosa and selected clinical data in young patients with symptomatic gallstones |journal=Pol J Pathol |volume=62 |issue=1 |pages=41–9 |year=2011 |pmid=21574105 |doi= |url=}}</ref><ref name="pmid26602767">{{cite journal |vauthors=Yaylak F, Deger A, Bayhan Z, Kocak C, Zeren S, Kocak FE, Ekici MF, Algın MC |title=Histopathological gallbladder morphometric measurements in geriatric patients with symptomatic chronic cholecystitis |journal=Ir J Med Sci |volume=185 |issue=4 |pages=871–876 |year=2016 |pmid=26602767 |doi=10.1007/s11845-015-1385-3 |url=}}</ref>
**Edematous and hemorrhagic gallbladder wall
**[[Edema|Edematous]] and [[hemorrhagic]] gallbladder wall
**Mucosal necrosis with neutrophil infiltration
**Mucosal [[necrosis]] with [[neutrophil]] infiltration
**Eosinophilic infiltration of the gallblader mucosa
**[[Eosinophilic]] infiltration of the [[gallbladder]] mucosa
*Specific microscopic features of acalculous cholecystitis:<ref name="pmid16241996">{{cite journal |vauthors=Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V, Syrjälä H, Karttunen TJ |title=Histopathology of acute acalculous cholecystitis in critically ill patients |journal=Histopathology |volume=47 |issue=5 |pages=485–92 |year=2005 |pmid=16241996 |doi=10.1111/j.1365-2559.2005.02238.x |url=}}</ref>
*Specific microscopic features of acalculous cholecystitis:<ref name="pmid16241996">{{cite journal |vauthors=Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V, Syrjälä H, Karttunen TJ |title=Histopathology of acute acalculous cholecystitis in critically ill patients |journal=Histopathology |volume=47 |issue=5 |pages=485–92 |year=2005 |pmid=16241996 |doi=10.1111/j.1365-2559.2005.02238.x |url=}}</ref>
**Bile infiltration of gall bladder wall
**[[Bile]] infiltration of [[Gallbladder|gallbladde]]<nowiki/>r wall
**Bile infiltration and leucocyte margination of blood vessels
**[[Bile]] infiltration and [[leucocyte]] margination of blood vessels
**Lymphatic dilation
**[[Lymphatic]] dilation
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
|background: "#FFFFFF;" |[[File:Acute cholecystitis -- low mag.jpg|400px|thumb|center|Histological image of acute cholecystitis; Low magnification. <small> By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30991393 Source:<ref name="urlAcute cholecystitis - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/Acute_cholecystitis |title=Acute cholecystitis - Libre Pathology |format= |work= |accessdate=}}</ref>]]
|
|background: "#FFFFFF;" |[[File:Acute cholecystitis - a -- intermed mag.jpg|400px|thumb|center|Histological image of acute cholecystitis; Intermediate magnification. <small> By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30991393 Source:<ref name="urlAcute cholecystitis - Libre Pathology">{{cite web |url=https://librepathology.org/wiki/Acute_cholecystitis |title=Acute cholecystitis - Libre Pathology |format= |work= |accessdate=}}</ref>]]
<br clear="left" />
|}


==References==
==References==
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Latest revision as of 15:11, 8 January 2018

Acute cholecystitis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Overview

Acute calculous cholecystitis is usually caused by the mechanical obstruction of the gallbladder due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. Cholesterol gallstones are the most common type of gallstones. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis. Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis. Acute cholecystitis is more common in siblings and first degree relatives of affected persons. Lith gene is involved in the pathogenesis of cholecystitis. Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones. Acute cholecystitis is associated with diabetes, insulin resistance, cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and gastrointestinal malignancies. Microscopic histopathology shows edematous and hemorrhagic gallbladder wall, mucosal necrosis with neutrophil infiltration. Bile infiltration of the gallbladder wall and bile and leucocyte margination of blood vessels are specific findings for acalculous cholecystitis.

Pathophysiology

Pathogenesis

Inflammation of the gallbladder is termed as cholecystitis. Acute calculous cholecystitis is usually caused by the mechanical obstruction due to gallstones. Acute acalculous cholecystitis is caused predominantly by the gallbladder stasis. The pathogenesis of acute cholecystitis involves the following:[1][2][3][4][5][6][7][8][9][10][11]

  • Obstruction of the gallbladder:
    • Gallstones are the most common cause of physical obstruction of the gallbladder usually at the neck or in the cystic duct. The obstruction causes an increased pressure as the gallbladder mucosa continues to produce mucus. This raised pressure may cause the venous congestion which is followed by the arterial congestion. Eventually, the raised pressure and stasis leads to the gallbladder ischemia and necrosis.
      • There are two major types of gallstones:
        • Cholesterol gallstones:
          • Cholesterol gallstones are the most predominant form of the gallstones. They account for approximately 80% of the total gallstones.
          • The formation of gallstones is dependant on the following factors:
            • Cholesterol supersaturation in the bile
            • Crystal nucleation
            • Gallbladder dysmotility
            • Gallbladder absorption
        • Pigmented gallstones:
          • There are two types of pigmented gallstones.
            • Black stones
            • Brown stones
              • Brown stones are usually associated with bacterial infection.
              • Brown stones are usually located elsewhere in the biliary tree as opposed to the gallbladder.
    • Mechanical obstruction of the gallbladder as a result of polyps, malignancy, an infestation of the gallbladder with parasites, foreign bodies, and trauma may also lead to the acute cholecystitis.
  • Gallbladder stasis:

Genetics

  • Acute cholecystitis is more common in siblings and first degree relatives of affected persons.[12][13]
  • Lith gene is involved in the pathogenesis of cholecystitis.[6]
  • Mutations in the hepatic cholesterol transporter ABCG8 also predispose an individual to the develop gallstones.[9]

Associated Conditions

The following conditions are associated with acute cholecystitis:[14]

Gross Pathology

Microscopic Pathology

Histological image of acute cholecystitis; Low magnification. By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30991393 Source:[21]
Histological image of acute cholecystitis; Intermediate magnification. By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=30991393 Source:[21]


References

  1. ↑ Foard DE, Haber AH (1970). "Physiologically normal senescence in seedlings grown without cell division after massive gamma-irradiation of seeds". Radiat. Res. 42 (2): 372–80. PMID 5442405.
  2. ↑ 2.0 2.1 Jones MW, Ferguson T. "Gallbladder, Cholecystitis, Acalculous". PMID 29083717.
  3. ↑ Knab LM, Boller AM, Mahvi DM (2014). "Cholecystitis". Surg. Clin. North Am. 94 (2): 455–70. doi:10.1016/j.suc.2014.01.005. PMID 24679431.
  4. ↑ Yokoe M, Takada T, Strasberg SM, Solomkin JS, Mayumi T, Gomi H, Pitt HA, Gouma DJ, Garden OJ, Büchler MW, Kiriyama S, Kimura Y, Tsuyuguchi T, Itoi T, Yoshida M, Miura F, Yamashita Y, Okamoto K, Gabata T, Hata J, Higuchi R, Windsor JA, Bornman PC, Fan ST, Singh H, de Santibanes E, Kusachi S, Murata A, Chen XP, Jagannath P, Lee S, Padbury R, Chen MF (2012). "New diagnostic criteria and severity assessment of acute cholecystitis in revised Tokyo Guidelines". J Hepatobiliary Pancreat Sci. 19 (5): 578–85. doi:10.1007/s00534-012-0548-0. PMC 3429769. PMID 22872303.
  5. ↑ Yokoe M, Takada T, Strasberg SM, Solomkin JS, Mayumi T, Gomi H, Pitt HA, Garden OJ, Kiriyama S, Hata J, Gabata T, Yoshida M, Miura F, Okamoto K, Tsuyuguchi T, Itoi T, Yamashita Y, Dervenis C, Chan AC, Lau WY, Supe AN, Belli G, Hilvano SC, Liau KH, Kim MH, Kim SW, Ker CG (2013). "TG13 diagnostic criteria and severity grading of acute cholecystitis (with videos)". J Hepatobiliary Pancreat Sci. 20 (1): 35–46. doi:10.1007/s00534-012-0568-9. PMID 23340953.
  6. ↑ 6.0 6.1 Wang HH, Portincasa P, Afdhal NH, Wang DQ (2010). "Lith genes and genetic analysis of cholesterol gallstone formation". Gastroenterol. Clin. North Am. 39 (2): 185–207, vii–viii. doi:10.1016/j.gtc.2010.02.007. PMID 20478482.
  7. ↑ Loozen CS, Oor JE, van Ramshorst B, van Santvoort HC, Boerma D (2017). "Conservative treatment of acute cholecystitis: a systematic review and pooled analysis". Surg Endosc. 31 (2): 504–515. doi:10.1007/s00464-016-5011-x. PMID 27317033.
  8. ↑ Avegno J, Carlisle M (2016). "Evaluating the Patient with Right Upper Quadrant Abdominal Pain". Emerg. Med. Clin. North Am. 34 (2): 211–28. doi:10.1016/j.emc.2015.12.011. PMID 27133241.
  9. ↑ 9.0 9.1 Lammert F, Gurusamy K, Ko CW, Miquel JF, Méndez-Sánchez N, Portincasa P, van Erpecum KJ, van Laarhoven CJ, Wang DQ (2016). "Gallstones". Nat Rev Dis Primers. 2: 16024. doi:10.1038/nrdp.2016.24. PMID 27121416.
  10. ↑ Kimura Y, Takada T, Kawarada Y, Nimura Y, Hirata K, Sekimoto M, Yoshida M, Mayumi T, Wada K, Miura F, Yasuda H, Yamashita Y, Nagino M, Hirota M, Tanaka A, Tsuyuguchi T, Strasberg SM, Gadacz TR (2007). "Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines". J Hepatobiliary Pancreat Surg. 14 (1): 15–26. doi:10.1007/s00534-006-1152-y. PMC 2784509. PMID 17252293.
  11. ↑ "Acute cholecystitis | The BMJ".
  12. ↑ "An Increased Familial Frequency of Gallstones - Gastroenterology".
  13. ↑ Weiss KM, Ferrell RE, Hanis CL, Styne PN (1984). "Genetics and epidemiology of gallbladder disease in New World native peoples". Am. J. Hum. Genet. 36 (6): 1259–78. PMC 1684666. PMID 6517051.
  14. ↑ Tiderington E, Lee SP, Ko CW (2016). "Gallstones: new insights into an old story". F1000Res. 5. doi:10.12688/f1000research.8874.1. PMC 4962289. PMID 27508070.
  15. ↑ 15.0 15.1 Laurila JJ, Ala-Kokko TI, Laurila PA, Saarnio J, Koivukangas V, Syrjälä H, Karttunen TJ (2005). "Histopathology of acute acalculous cholecystitis in critically ill patients". Histopathology. 47 (5): 485–92. doi:10.1111/j.1365-2559.2005.02238.x. PMID 16241996.
  16. ↑ 16.0 16.1 Owen CC, Bilhartz LE (2003). "Gallbladder polyps, cholesterolosis, adenomyomatosis, and acute acalculous cholecystitis". Semin. Gastrointest. Dis. 14 (4): 178–88. PMID 14719768.
  17. ↑ 17.0 17.1 McChesney JA, Northup PG, Bickston SJ (2003). "Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology". Dig. Dis. Sci. 48 (10): 1960–7. PMID 14627341.
  18. ↑ Huang SM, Yao CC, Pan H, Hsiao KM, Yu JK, Lai TJ, Huang SD (2010). "Pathophysiological significance of gallbladder volume changes in gallstone diseases". World J. Gastroenterol. 16 (34): 4341–7. PMC 2937116. PMID 20818819.
  19. ↑ Kasprzak A, Malkowski W, Biczysko W, Seraszek A, Sterzyńska K, Zabel M (2011). "Histological alterations of gallbladder mucosa and selected clinical data in young patients with symptomatic gallstones". Pol J Pathol. 62 (1): 41–9. PMID 21574105.
  20. ↑ Yaylak F, Deger A, Bayhan Z, Kocak C, Zeren S, Kocak FE, Ekici MF, Algın MC (2016). "Histopathological gallbladder morphometric measurements in geriatric patients with symptomatic chronic cholecystitis". Ir J Med Sci. 185 (4): 871–876. doi:10.1007/s11845-015-1385-3. PMID 26602767.
  21. ↑ 21.0 21.1 "Acute cholecystitis - Libre Pathology".

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