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Biliary tract disease - gallstones and cholecystitis
Terms in this set (42)
Risk factors for cholesterol gallstones
- increased age, female gender, metabolic syndrome/obesity. oral contraceptives, hereditary mutation in ATP binding cassette (ABC) transporters for biliary lipids.
conditions for gallstone formation
1. bile must be supersaturated with cholesterol
2. hypomotility of gallbladder promotes nucleation
3. cholesterol nucleation in bile is accelerated
4. hypersecretion of mucus in gallbladder traps nucleated crystals.
complex mixture of abnormal insoluble calcium salts of unconjugated bilirubin along with inorganic calcium salts.
associated with hemolytic syndromes, ileal dysfunction, abcterial contamination of biliary tree.
Biliary tract infections
microbial beta-glucoronidases hydrolize bilirubin glucoronides -- leading to increased pigment stone formation. E. coli, ascaris lumbricoides, liver fluke O. sinensis.
pure cholesterol stones
pale yellow round to ovoid and have finely granular hard external surface. radiolucent. if sufficient calcium carbonate is present they will be opaque.
- glistening radiating crystalline palisade. coloration icreases with calcium carbonate, phosphates and bilirubin.
classified as black and brown. black are in sterile bile, 50-75% radioopaque. brown are in infected intrahepatic or extrahepatic ducts, radiolucent. black stones contain oxidized polymers of calcium salts of unconjugated bilirubin.
clinical presentation of gallstones
asymptomatic for a lifetime. convert to symptomatic forms at 1-4% per year.
biliary pain - spasmodic RUQ pain from obstruction of biliary tree
complications of gallstones
inflammation with empyema, perforation, fistulas, inflammation of biliary tree and obstructive cholestasis or pancreatitis. increased risk for carcinoma of gallbladder.
which is more dangerous: small gallstones or large gallstones?
small gallstones. "gravel" - produce obstruction.
"gallstone ileus" - when a large gallstone erodes directly into an adjacent loop of small bowel generating intestinal obstruction.
inflammation of gallbladder precipitated 90% of the time by obstruction of the neck or cystic duct by gallstone.
cholecystitis without gallstones. occurs in severely ill patients accounting for 10% of cholecystitis cases. .
pathogenesis of acalculous cholecystitis
- chemical irritation of obstructed gallbladder
- mucosal phospholipases hydrolyze lecithin to toxic lysolecithin -- disrupted mucus layer = no protection.
- detergent action of bile salts on GB lumen --> GB dysmotility
- distension and increased intraluminal GB pressure compromises blood flow to mucosa.--> ischemia.
when edema of GB wall in acalculous cholecystitis compromises blood flow, accumulation of microcrystals, vixcous bile and mucus -- cause cystic duct obstruction.
risk factors for acalculous cholecystitis
1. sepsis with hypotension and organ failure
3. major trauma and burns.
4. diabetes mellitus
morphology of acute cholecystitis
enlarged tense GB -- bright red or blotchy with violaceous green-black discoloration. mild cases: wall thickened, edematous and hyperemic.
- subserosal hemorrhage, fibrin deposition.
- absent macroscopic stones in acalculous form.
- obstructing stones usually in neck of GB or cystic duct.
emyema of gallbladder
when exudate in lumen of inflammed gallbadder is virtually pure pus.
severe cases where organ is necrotic, green-black. invasion of gas forming organisms (clostridia and coliforms) cause emphysematous cholecystitis
clinical presentation of acute cholecystitis
- progressive RUQ pain/epigastric pain
- mild fever, anorexia, tachycardia, sweating, nausea, vomiting
(most pts free of jaundice)
- hyperbilirubinemia -- indicates obstruction of common bile duct.
clinical sx of acute acalculous cholecsytitis
more insidious onset -- obscured by underlying conditions precipitating the attacks. higher proportion of pts have no sx.
incidence of gangrene and perforation much higher in acalculous cholecystitis
bacterial causes of acute cholecystitis
primary infections of salmonella typhi and staphylococci
repeated bouts of mild to severe acute cholecystitis. assocaited with cholelithiasis in more than 90% of cases. similar symptoms and histology with calculous vs. acalculous forms.
- E. coli and enterococci cultured from bile in 1/3 of cases.
morphology of chronic cholecystitis
variable, sometimes minimal.
- dense fibrous adhesions as sequelae of preexisting acute inflammation.
- wall thickening. opaque gray-white appearance.
- luemin with clear green-yellow mucoid bile and usually stones.
- infiltrate of lymphocytes, plasma cells and macrophages in mucosa and subserosal fibrous tissue.
chronic cholecystitis-- reactive proliferation of GB mucosa and fusion of mucosal folds -- giving riske to burided crypts of epithelium -- outpouchings of epithelium throug the wall may be quite prominent. implies acute exacerbation of alread injuted GB.
extensive dystrophic calcificaiton within GB. markedly increased incidence of cancer.
rare condition where GB has massively thickened wall, is shrunken, nodular and chronically inflamed with foci of necrosis and hemorrhagie.
hydrops of gallbaldder
atrophic chronically obstructed gallbladder that contains only clear secretions.
complications of chronic cholecystitis
- bacterial superinmfection with cholangitis or sepsis
- GB perforation and local abscess formation
- GB rupture with peritonitis
- biliary enteric fistual with bile drainage into adjacent oragns -- air and bacteria enter into biliary tree.
- aggravation of preexisting medical illness with cardiac, pulmonary, renal or liver decompensatiaon.
- porcelaoid gallbladder wth icnreased risk of cancer.
presence of stones within bile ducts of the biliary tree as opposed to cholelithiasis -- in the gallbladder. stones are usually pigmented and associated with bilairy tract infections.
complications of choledocholithiasis
obstruction, pancreatitis, cholangitis, hepatic abscess, secondary biliary cirrhosis and acute calculous cholecystitis.
bacterial infection of the bile ducts. any lesion that creases bile flow obstruction (choledocholithiasis or stricture, tumor, parasite...) bacteria enter throug sphincter of oddi
infection of intrahepatic biliary radicles starting at sphincter of oddi. gram neg anaerobes: E. coli, klebsiella, interococcus, enterobacter. clostridium and bacteroides with mixed infection.
clinical presentation of cholangitis
fever, chills, abdominal pain and jaundice (inflammatio of wall of bile ducts with entry of neutrophils into lumen).
- sepsis dominates clinical picture.
1/3 of neonatal cholestasis. complete or partial obstruction of the lumen of extrahepatic biliary tree within the first 3 months of life.
- progressive infalmmation and fibrosis of intrahepatic and extrahepatic ducts.
- mcc of death from liver dz in early childhood.
- accounts for 50-60% of children referred for liver transplant
fetal form biliary atresia
20% of cases. associated with othe ranomalies (malrotation of abdominal viscera, interrupted IVC, polysplenia etc.)
- aberrant intrauterine development of extrahepatic biliary tree.
Perinatal form biliary atresia
presumed normally developed biliary tree is destroyed after birth. maybe viral infection or autoimmune destruction. ex/ reovirus, rotavirus, CMV.
Type 1 biliary atresia
when the disease is limited to the common bile duct.
type II biliary atresia
when disease invovles the heaptic bile ducts with patent proximal branches.
type III biliary atresia
disease that involves obstruction of bile ducts at or above the porta hepatis. noncorrectable with surgery.
surgical procedure to correct bilary atresia -- cures type I and type II disease.
clinical presentation of biliary atresia
neonatal cholestasis. initially normal stools to acholic stools as dz evolves.
- serum bilirubin starts out with 6-12, only mod elevated aminotransferase, alkaline phosphatase.
congenital dilations of common bile duct. most often in kids before age 10. sx of jaundice, recurrent abd pain typical of biliary colic.
- predipose to stone formation, stricture, stenosis, pancreastitis. increased bile duct carcinoma in adults.
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