Path 18S882-9

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95% biliary tract disease is attributable to

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cholelithiasis (gallstones); 10-20% adult population in dvlped countries; >80% silent

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bile secreted by liver per day

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as much as 1 L

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adult gallbladder capacity

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50 mL

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2 main types of gallstones

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cholesterol stones (90% in West) and pigment stones

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cholesterol stone components

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more than 50% crystalline cholesterol monohydrate

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pigement stone components

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predominately bilirubin calcium salts

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when do pigment stones tend to arise

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setting of bacterial infections of biliary tree and parasitic infections

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estrogenic influence and gallstones

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increases expression of hepatic lipoprotein receptors and stimulates hepatic HMG-CoA reductase activity=enhances both cholesterol uptake and biosynthesis; important in pregnancy and oral contraceptive use

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Clofibrate

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lower blood cholesterol-increases hepatic HMG-CoA reductase and decreases conversion of cholesterol to bile acids by reducing cholesterol 7-a-hydroxylase activity

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D19H variant and gallstones

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absorb less, but synthesize more cholesterol (HMG-CoA inhibitors may decrease gallstone formation in these ppl)

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when does cholesterol nucleate into solid cholesterol monohydrate crystals

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cholesterol concentrations exceed solubilizing capacity of bile

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4 simultaneous conditions for cholesterol gallstone formation

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1) bile supersaturated with cholesterol 2) hypomotility of gallbladder 3) cholesterol nucleation accelerated 4) hypersecretion of mucus in gallbladder traps nucleated cells leading to aggregation

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biliary tract infections assocaited with pigment stones

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E. coli, Ascaris lumbricoides, or liver fluke O. sinensis

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Pure cholesterol stone morphology

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pale yellow round to ovoid, finely granular, hard external surface; transection reveals glistening radiating crystalline palisade

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what else can be incuded into a cholesterol stone

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calcium carbonate, phosphate, and bilirubin; may be lamellated and gray-white to black

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Pigment gallstones that are black

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in sterile gallbladder; contain oxidized polymers of calcium salts of unconjugated bilirubin, cmall amounts of calcium carbonate, calcium phosphate, and mucin glycoprotein (some cholesterol monohydrate crystals)

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pigment gallstones that are brown

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in infected intrahepatic or extrahepatic ducts; pure calcium salts of unconjugated bilirubin, mucin glycoprotein, substantial cholesterol fraction, and calcium salts of pamitate and stearate

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black stones size and consistency

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rarely >1.5 cm and in great number; may crumble to touch; contour spiculated and molded; 50-75% radioopaque

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brown stones size and consistency

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laminated and soft and may have soaplike or greasy consistency; radiolucent

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cholangitis

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inflammation (bacterial infection) of the biliary tree

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gallstone ileus or Bouveret's syndrome

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large gallstone erodes directly into an adjacent loop of small bowel, generating intestinal obstruction

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acute calculous cholecystitis

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acute inflammation of gallbladder precipitated 90% by obstruction of neck or cystic duct; chemical irritation and inflammation of obstructed gallbladder

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action of mucosal phospholipases in acute calculous cholecystitis

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hydrolyzes luminal lecithins to toxic lysolecithins-normally protected glycoprotein mucus layer disrupted, exposing mucosal epithelium to direct detergent action of bile salts

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what is acute acalculous cholecystitis thought to result from

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ischemia; cystic artery has no collateral circulation

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risk factors for acute acalculous cholecystitis

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1) sepsis with hypotension and multisystem organ failure 2) immunosuppression 3) major trauma and burns 4) diabetes mellitus 5) infections

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morphology of acute cholecystitis

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enlarged and tense; bright red or blotchy, violaceous to green-black discoloration

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galbladder lumen in acute cholecystitis

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one or more stones, filled with cloudy or turbid bile that may contain large amount of fibrin, pus, and hemorrhage

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empyema of the gallbladder

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contained exudate is virtually pure pus

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what can cause acute 'emphysematous' cholecystitis

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invasion of gas-forming organisms like clostridia and coliforms in acute cholecystitis

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attack of acute cholecystitis presentation

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progressive right upper quadrant/epigastric pain; frequently mild fever, anorexia, tachycardia, sweating, nausea, and vomiting; most free of jaundice; mild/moderate leukocytosis with mild elevations in serum ALP values

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attack duration without intervention in acute cholecystitis

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subsides in 7-10 days and frequently within 24 hours; 25% get more severe and need intervention

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Rokitansky-Aschoff sinuses

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outpouchings of the mucosal epithelium through the wall

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porcelain gallbladder

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extensive dystrophic calcification within gallbladder wall-markedly increased incidence of assocaited cancer

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Xanthogranulomatous cholecystitis

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rare condition in which gallbladder has massively thickened wall, shunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage

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hydrops of the gallbladder

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atrophic, chronically obstructed gallbladder may contain only clear secretions

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choledocholithiasis

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presence of stones within the bile ducts of the biliary tree; usually associated with biliary tree infections (pigmented stones)

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choledocholithiasis symptoms

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obstruction, pancreatitis, cholangitis, hepatic abscess, secondary biliary cirrhosis, acute calculous cholecystitis

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where do bacteria most likely enter biliary tract and what bacteria infect

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sphincter of Oddi; usually enteric gram-neg aerobes like E. coli, Klebsiella, Interococcus, or Enterobacter (Clostridium and Bacteroides cause mixed infection)

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Cholangitis presentation

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fever, chills, abdominal pain, jaundice

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major contributor to neonatal cholestasis

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biliary atresia-complete/partial obstruction of lumen of extrahepatic biliary tree within first 3 months of life

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fetal vs perinatal biliary atresia occurance

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20% fetal, rest perinatal

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morphology of biliary atresia

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inflammation and fibrosing stricture, periductulat inflammation or intrahepatic bile ducts, and progressive destruction of intrahepatic biliary tree

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what occurs when biliary atresia is unrecognized or uncorrected

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cirrhosis develops within 3-6 months of birth

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Type I, II, and II biliary atresia

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I=limited to common bile duct; II=hepatic bile ducts eith patent proximal branches; III=obstruction of bile ducts at or above porta hepatis (90% patients with biliary atresia-not correctable)

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stools in infants with biliary atresia

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initially normal than acholic as disease evolves

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Choledochal cysts

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congenital dilations of the common bile duct; usually presents b4 10 with nonspecific symptoms (jaundice and/or recurrent abdominal pain); increased risk of stones, etc

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adenomyosis of gallbladder

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hyperplasia of muscle layer, containing intramural hyperplastic glands

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most common malignancy of the extrahepatic biliary tract

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carcinoma of the gallbladder

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2 growth patterns of gallbladder carcinomas

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infiltrating and exophytic (most adenocarcinomas)

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infiltrating carcinoma pattern

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more common; poorly defined area of diffuse thickening and induration of gallbladder wall that may cover several square cm or entire gallbladder; deep ulceration can occur causing fistulas; firm consistency

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exophytic pattern

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lumen as irregular, cauliflower mass that invades underlying wall