5. BILIARY TRACT Pathogenesis: Hepatocellular hypersecretion of cholesterol Cholesterol conc. > solubilizing capacity of bile SUPERSATURATION Inc. free cholesterol penetrate GB wall Dec. ability of mucosa to detoxify by esterification Dec. responsiveness to cholecystokinin GALLBLADDER HYPOMOTILITY Stasis ACCELERATED CHOLESTEROL CRYSTAL NUCLEATION PROMOTE MUCUS HYPERSECRETION & MICROPRECIPITATION OF CALCIUM SALTS STONE
16. BILIARY TRACT Acute Calculous Cholecystitis: Pathogenesis OBSTRUCTION Hydrolysis of luminal lecithins by mucosal phospholipases Production of toxic lysolecithins Disruption of glycoprotein mucus layer Exposure of epithelium to direct detergent action of bile salts (+) GB dysmotility (+) GB distention & inc. intraluminal pressure Compromised mucosal blood flow INFLAMMATION
19. Histological section of severe acute cholecystitis showing extensive ulceration of the mucosa, haemorrhage, oedema and a dense transmural infiltrate of neutrophils and mononuclear inflammatory cells.
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23. This intraoperative photograph shows a subserosal perforation of an acute, emphysematous, acalculous cholecystitis in a 58-year-old diabetic man. He presented with features suggestive of ileus.
48. Diagram depicting types of extrahepatic biliary atresia, based on a classification established by Kasai: Type I: occlusion of common bile duct Type IIa: obliteration of common hepatic duct Type IIb: obliteration of common bile duct and hepatic and cystic ducts, with uninvolved gallbladder and cystically dilated ducts at porta hepatis Type III: obliteration of common, hepatic, and cystic ducts without anastomosable ducts at porta hepatis. (Redrawn from Desmet and Callea.)
49.
50. This 3 month old child died with extrahepatic biliary atresia, a disease in which there is inflammation with stricture of hepatic or common bile ducts. This leads to marked cholestasis with intrahepatic bile duct proliferation, fibrosis, and cirrhosis. This liver was rock hard. The dark green color comes from formalin acting on bile pigments in the liver from marked cholestasis, turning bilirubin to biliverdin.
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52. Type I cysts represent approximately 85% of most series. They are fusiform in shape.
53. Type II cysts represents less than 2% of cases, and are often called common bile duct diverticulum.
54. Type III cysts also called choledochoceles represents approximately 2% of cases. Here the dilatation is localized to the terminal portion of the biliary tract
55. Type IV cysts represent the remaining approximately 10% of cases. Here the dilatation affects both intrahepatic and extrahepatic bile ducts
56. Type V cysts are Caroli's disease .They are purely intrahepatic in nature, and the association with cancer though present is weak than the rest of the group. They are frequently associated with portal hypertension and congenital hepatic fibrosis
57. The choledochal cyst was mobilized and fixed with holding sutures. Clips are seen in the cyst, which closed the right and left hepatic ducts. Resected specimen: The gallbladder (left) and the deflated bile duct cyst were removed (right). Waidner et al. Journal of Medical Case Reports 2008 2 :5 doi:10.1186/1752-1947-2-5
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60. Type I tumor involves the main hepatic duct below the bifurcation Type II tumor affects the main hepatic duct bifurcation Type III tumor involves segmental ducts beyond the primary hepatic duct bifurcation in one liver lobe (type IIIa: right lobe, type IIIb: left lobe) Type IV tumors involve segmental ducts in both liver lobes
62. EXTRAHEPATIC BILIARY TRACT Tumors: Clinical Features Jaundice secondary to obstruction Decolorization of stools Nausea and vomiting Weight loss Hepatomegaly (50%) Palpable gallbladder (25%) Inc. serum ALP and aminotransferases Bile-stained urine