Gallbladder And Bile Ducts Flashcards
Causative agents of emphysematous cholecystitis
Anaerobes
- C Welchii/ perfringens
Aerobes
- E. coli
Complications of cholecystitis
Empyema and hydrops
Gangrene and perforation
Fistula formation and gallstone ileus
Limey and porcelain GB
What is mirizzi syndrome
Gallstone becomes impacted in the cystic duct or neck of GB causing compression of CBD resulting in CBD obstruction and jaundice
Gallstone dissolution should be limited to:
Radiolucent stones smaller than 5 mm in diameter
Dose of UDCA for gallstone dissolution
10-15 mg/kg/day
The most specific And characteristic symptom of gallstone disease
Biliary colic
Pain severe intensity 30 min to 5 h
Steady
What are the type of gallstones detected by PFA to be radioopaque
10-15% cholesterol
50% pigment stones
Material of LOW echogenic activity that forms later in most dependent portion of GB
Bile sludge
Composition of pigment stones and where conditions where you see them
Black pigment: Calcium bilirubinate Calcium and mucin glycoproteins (Chronic hemolytic states, liver cirrhosis, Gilbert's, cystic fibrosis) Brown pigment: Calcium salts of unconjugated bilirubin (Infection)
Mechanisms in the formation of lithogenic bile
- Increased biliary secretion of cholesterol
- Nucleation of cholesterol mono hydrate crystals
- Gallbladder hypomotility
Major factor controlling the evacuation of GB
Cholecystokinin
Total basal secretion of hepatic bile
500-600 ml per day
Major solute components of bile
By moles percent
Bile acids 80%
Lecithin and traces of phospholipids 16%
Unesterified cholesterol 4%
2 conditions assoc with cholesterol Stone or biliary sludge formation
Pregnancy (marked inc in cholesterol saturation of bile during 3rd trimester and sluggish GB contraction)
Rapid weight reduction through a low calorie diet
Primary bile acids
Cholic acid
Chenodeoxycholic acid
What is murphy’s sign
Subcostal palpation of RUQ produces increased pain and inspiratory arrest
Triad of acute cholecystitis
RUQ tenderness
Fever
Leukocytosis
Abnormal deposition of lipid, esp cholesteryl eaters within macrophages in the lamina propia of the GB wall
Cholesterolosis
Diffuse form of Cholesterolosis
Strawberry GB
Bilirubin levels where CBD stones should be suspected
> 5 mg/dL
If >20 mg/dL the possibility of neoplastic obstruction should be entertained
Electrolytes that are reabsorbed through the gallbladder epithelium, thereby making bile more concentrated
Cl
HCO3
Rate limiting enzyme of hepatic cholesterol synthesis
HMG CoA reductase
The most impt mechanism in the formation of stone forming bile is increased biliary secretion of cholesterol. But this is not sufficient to cause stone in itself. So what else does?
Nucleation of cholesterol monohydrate crystals. Pro nucleation - mucous glycoproteins S - heat labile proteins - immunoglobulins - pigment particles
Anyinucleation:
- apolipoproteins
- lecithin vesicles
What are the 2 abnormalities implied by a crescent layer in the most dependent portion of the gallbladder?
BILIARY SLUDGE
- Normal balance between gallbladder mucin secretion and elimination has become deranged
- Nucleation of biliary solutes has occurred
Component biliary sludge
Cholesterol
Calcium bilirubinate
Prophylactic cholecystectomy
- large stones > 3 cm
- gallstones in congenitally anomalous GB
Diagnosis patients presenting with biliary colic post operatively
Cystic duct stump syndrome
Papillary dysfunction, papillary stenosis, spasm of the sphincter of Oddi
Biliary dyskinesia
5 criteria used to define papillary stenosis
- Upper bad pain usually RUQ
- Abnormal liver tests
- Dilatation of the CBD upon Ercp exam
- Delayed drainage of contrast material from the duct
- Increased basal pressure of the sphincter of Oddi
Medical treatment dyskinesia of sphincter of Oddi
Nitrites
Anti cholinergics
Progressive inflammatory sclerosing and obliterating process affecting extrahepatic and intrahepatic ducts
Primary sclerosing cholangitis
75% assoc with IBD mostly ulcerative colitis
