disorders of gall bladder

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diseases of the gall bladder

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  • 1. Disorders of gall bladder Dr Nor Hidayah Abu Bakar, M.D, M.Path (Anatomic Pathologist), Medical Lecturer, FPSK, UNISZA

2. Disorders of the gall bladder Disorders of the biliary tract affects significant portion of the worlds population. >95% of biliary tract disease is due to cholelithiasis (gallstone) Bile is secreted by liver and in between meals, it is stored in gall bladder 3. Learning Objectives Describe the aetiology and pathogenesis, the pathology, and the clinical manifestations of cholesterol and pigment gallstones Describe the pathology of acute and chronic cholecystitis (Rokitansky-Aschoff sinus) Describe the pathology and the clinical manifestations of gallbladder carcinoma 4. Cholelithiasis Affect 10-20% of adult population in developed countries Prevalence : certain populations are more prone than others (US, Western Europe) Clinical features: 70-80% are asymptomatic Excruciating pain localised to the right upper quadrant or epigastric region 5. 2 main types of gall stones : Cholesterol stones Pigment stones In the West, about 90% are cholesterol stones. Pigment gall stone is predominant in non- Western population associated with bacterial infection of biliary tree and parasitic infestations. 6. Cholelithiasis -cont Risk factors : Prevalence increase with age associated with metabolic syndrome and obesity. More common in women (2x) Ethnic and geographic. Cholesterol stone is more common in Native American population, related to biliary cholesterol hypersecretion. Hereditary : positive family history of stones, inborn error of metabolism associated with impaired bile salt synthesis and secretion Environmental factors : Estrogenic influence ( OCP and pregnancy) - increase expression of hepatic lipoprotein receptors stimulates HMG Co-A reductase activity enhance cholesterol uptake and synthesis excess biliary secretion of cholesterol. Clofibrate (lipid lowering agent) increase hepatic HMG Co-A reductase reduce cholesterol 7- hydroxylase activity decrease conversion of cholesterol to bile acids Obesity, rapid weight loss also increase biliary cholesterol secretion. Acquired disorders : gall bladder stasis and reduced gall bladder motility ( in pregnancy, rapid weight loss, spinal cord injury). 7. Cholesterol stone Content : Crystalline cholesterol monohydrate is predominant Pigment stone Bilirubin calcium salt is predominant Pigment stones Black pigment cirrhosis, hemolytic anemia (hemoglobinopathy, red cell disorders) Brown pigment Asian patients (infection) 8. Pathogenesis Cholesterol stone Pigment stone Pathogenesis of pigment stone: Hemolytic anemias and infections of the biliary tract increased unconjugated bilirubin in the biliary tree form precipitates : insoluble calcium bilirubinate salts. 9. Pathology Cholesterol stones : Gross : pale yellow, ovoid, firm, single to multiple with faceted surfaces Mostly radiolucent, 20% is radio opaque due to the presence of calcium carbonate content. Pigment stones: Black stone (in sterile gall bladder bile)- small size, fragile to touch, numerous, 50-70% are radioopaque Brown stone (in infected intrahepatic or extrahepatic ducts)- single to a few, soft, greasy, soaplike consistency due to presence of retained fatty acids released by bacterial phospholipases on biliary lecithins, radiolucent. Stone content : calcium salts of unconjugated bilirubin, lesser amounts of other calcium salts, mucin glycoproteins and cholesterol. 10. Summary : 11. Complications : Inflammation of gall bladder (cholecystitis) Empyema Perforation, Fistulas 12. Complications-cont Inflammation of biliary tree (cholangitis) Obstructive cholestasis Pancreatitis Erode adjacent bowel and cause intestinal obstruction (gallstone ileus) 13. Summary: 14. Summary 15. Cholecystitis Def: Inflammation of the gall bladder Can be divided into Acute cholecystitis Chronic cholecystitis Acute superimposed on chronic 16. Acute cholecystitis Can be divided into : Acute Calculous CS: 85-90% of the cases. Most common complication of gall stones and emergency cholecystectomy Acute Acalculous CS (10-15% of cases) Clinical features : progressive right upper quadrant or epigastric pain Mild fever Anorexia Tachycardia Sweating Nausea Vomiting +-hyperbilirubinemia mild to moderate leukocytosis Mild serum alkaline phosphatase 17. In acute calculous CS : previous episodes of pain May constitute acute medical emergency May also present with mild symptoms, resolved without medical intervention, attacks subsides in 7-10 days Recurrence is common Acute acalculous CS: Insidious symptoms, obscured by underlying condition precipitating the attacks Predisposing conditions : Major, non biliary surgery Severe trauma (eg: from motor vehicle crashes) Severe burns Sepsis Dehydration Gall bladder stasis and sludging Vascular compromise Bacterial contamination May complicate in gangrene and perforation (more than Calculous CS) 18. Pathogenesis of acute calculous cholecystitis stones obstruction to bile outflow inflammation of gall bladder wall due to phospholipases from the mucosa hydrolyzes biliary lecithin to lysolecithin (toxic to the mucosa) disrupt normal protective glycoprotein layer exposed the mucosal epithelium to the direct detergent action of bile salts Distended gall bladder Prostaglandin released Mucosal and mural inflammation Increase intraluminal pressure Compromise mucosal blood flow 19. Pathogenesis of Acute acalculous cholecystitis Risk factors : sepsis with hypotension and multisystem organ failure, immunosuppression, major trauma, diabetes mellitus, infections Impaired blood flow to cystic artery (end artery) compromised blood flow ischaemia of gall bladder Inflammation and edema of gall bladder wall compromising blood flow, accumulation of microcrystals of cholesterol ( biliary sludge), viscous bile, and gall bladder mucous cystic duct obstruction 20. Pathology of acute cholecystitis Gross : Enlarged, tense, edematous, red or violaceous colour (subserosal haemorrhage) Fibrinous /fibrinopurulent exudate covering the serosa +- stones obstructing the neck or cystic duct Lumen contains blood and pus (empyema) Green black necrotic Microscopic : acute inflammation in the wall mucosal ulceration. May be associated with abscess formation or gangrenous necrosis. 21. Chronic cholecystitis May be a sequelae of repeated bouts of mild to severe acute cholecystitis Associated with cholelithiasis > 90% of cases Pathogenesis : supersaturation of bile predisposes to both chronic inflammation and stone formation. 1/3 of cases : E.coli and enterococci can be isolated from the bile 22. Clinical features : recurrent attacks of epigastric or right upper quadrant pain Nausea, vomiting and intolerance to fatty foods. Pathology: Gross : smooth and glistening to dull serosa (subserosal fibrosis) thickened wall, opaque gray-white appearance Uncomplicated cases, lumen contains clear, green, mucoid bile and stones with normal mucosa 23. Microscopic : Reactive proliferation of mucosa Inflammation (lymphocytes, plasma cells, and macrophages in the mucosa and in the subserosal fibrous tissue). May be minimal. 24. Prominent outpouching of the mucosal epithelium through the wall (Rokitansky Aschoff sinuses) Marked subepithelial and subserosal fibrosis +-Superimposed acute inflammation +-Extensive calcification within the wall porcelain gall bladder increase risk of cancer 25. Xanthogranulomatous cholecystitis: massively thickened wall with shrunken, nodular, chronically inflamed with foci of necrosis and haemorrhage. Hydrops of the gall bladder : atrophic, chronically obstructed gall bladder containing only clear secretion 26. Complications of cholecystitis Bacterial superinfection with cholangitis or sepsis Gall bladder perforation and local abscess formation Gall bladder rupture with diffuse peritonitis Biliary enteric (cholecystenteric) fistula, with drainage of bile into adjacent organs, entry of air and bacteria into biliary tree and potentially gallstone-induced intestinal obstruction (ileus) Aggravating of preexisting medical illness, with cardiac, pulmonary, renal or liver decompensation Porcelain gall bladder with increased risk of cancer 27. Treatment : Cholecystectomy 28. Disorders of extrahepatic bile ducts Choledocholithiasis and cholangitis Secondary biliary cirrhosis Biliary atresia 29. Choledocholithiasis and cholangitis Choledocholithiasis = presence of stones within the biliary tree In Western nation, almost all stones derived from the gallbladder In Asia, higher incidence of primary ductal and intrahepatic, pigmented stone formation 10% are asymptomatic Sx develop secondary to Biliary obstruction Cholangitis Hepatic abscess Chronic liver disease with secondary biliary cirrhosis Acute calculous cholecystitis 30. Cholangitis = acute inflammation of the wall of bile ducts due to bacterial infection Can result from any lesions obstructing the bile flow : Choledocholithiasis Surgery involving the billiary tree Tumours Indwelling stents / catheter Acute pancreatitis Benign strictures 31. Bacteria enter the biliary tree mostly through the Sphincter of Oddi, and some through hematogenous route. Ascending cholangitis = propensity of bacteria to infect intrahepatic biliary ducts. Usual pathogens : E.coli, Klebsiella, Enterococci, Clostridium and Bacteroides. In some population, parasitic cholangitis also occur (Fasciola hepatica, schistosomiasis, Clonorchis sinensis or Opsthorchis viverrini, cryptosporidiosis) C/f bacterial cholangitis : fever, chills, abdominal pain and jaundice, suppurative cholangitis, sepsis. 32. Secondary biliary cirrhosis Prolonged obstruction of the extrahepatic biliary tree results in profound da