MCQ Hepatobiliary Bile duct pathology

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  1. Incidence of bile duct injury?
    • During open cholecystectomy - 0.1–0.2%Q
    • During laparoscopic cholecystectomy - 0.3–0.85%Q
  2. Stewart-Way classification of laparoscopic bile duct injury?
    • I - CBD mistaken for cystic duct but recognized; cholangiogram incision of cystic duct extended into CBD
    • II - Lateral damage to common hepatic duct from cautery or clips placed on duct; associated bleeding, poor visibility
    • III - CBD mistaken for cystic duct, not recognized; CBD, CHD, RHD, LHD transected or resected
    • IV - RHD mistaken for cystic duct, RHA mistaken for cystic artery, RHD and RHA transected; lateral damage to the RHD from cautery or clips placed on ducts
  3. Bismuth Classification of Bile Duct Strictures?
    • Type 1 - Low common hepatic duct stricture; hepatic duct stump >2cmQ
    • Type 2 - Mid common hepatic duct stump < 2 cmQ
    • Type 3 - High stricture (hilar), no hepatic duct stump; confluence intactQ
    • Type 4 - Destruction of the hilar confluence; right and left hepatic ducts separatedQ
    • Type 5 - Involvement of aberrant right sectoral hepatic duct alone with or without a concomitant hepatic duct strictureQ
  4. Shortcomings in Bismuths classification?
    • It did not stipulate the length of the stricture
    • It did not take into account the presence of biliary leaks, which are more common after laparoscopic cholecystectomy.
    • This, latter fact has been incorporated in Strasberg’s classification.
  5. Strasberg Classification of Laparoscopic Biliary Injuries
    • Type A - • Bile leaks from minor ducts still in continuity with the CBDQ, Includes leakage from cystic duct stump and from a subvesical duct of LuschkaQ
    • Type B • Occlusion of a part of the biliary tree, almost always an aberrant right sectoral ductQ
    • Type C • Transection without ligation of an aberrant right sectoral ductQ
    • Type D • A lateral injury to an extrahepatic ductQ
    • Type E • Includes biliary strictures, divided into E1 to E5 as classified by Bismuth
  6. MC causes of biliary leaks (Strasberg) seen after laparoscopic cholecystectomyQ?
    Type A
  7. A small amount of biliary drainage following cholecystectomy resolves within how many days?
    1 or 2 daysQ
  8. What is Hepp-Couinaud approach to bile duct reconstruction?
    Dissection of the hilar plate to expose the left hepatic duct and allow for a side-to-side anastomosis of the left hepatic duct to the Roux-en-Y jejunal limb.
  9. Modified Milwaukee classification is used for?
    Biliary Sphincter of Oddi dysfunctionQ
  10. USG finding of Sphinchter of Oddi dysfunction?
    • Dilated CBD (>12 mm diameter) or increase in CBD diameter in response to CCK is a typical ultrasound findingQ
    • Endoscopic manometry is considered gold standard Q for diagnosis
  11. Treatment of choice for sphincher of oddi dysfunction?
    Transduodenal sphincteroplasty with transampullary septectomyQ
  12. What is Vanishing Bile Duct Syndrome?
    Decreased number of bile ducts seen in liver biopsy specimensQ
  13. What are the Causes of Vanishing Bile Duct Syndrome?
    • • Chronic rejectionQ after liver transplantation
    • • Graft-versus-host diseaseQ after BM transplantation
    • • SarcoidosisQ
    • • Drugs: ChlorpromazineQ
    • • IdiopathicQ
  14. Clinical course in untreated biliary atresia?
    Biliary cirrhosis, portal hypertension, and death by 2 years of ageQ.
  15. Associated malformations in biliary atresia?
    Polysplenia, malrotation, preduodenal portal vein, and intrahepatic vena cavaQ
  16. USG finding in biliary atresia?
    • GB is shrunken and CBD is not visibleQ.
    • Triangle cord signQ
    • Gallbladder ghost triadQ - gallbladder is short (<1.9 cm) and irregular and lacks an echogenic inner lining
  17. Treatment of biliary atresia?
    • Kasai hepatoportoenterostomyQ
    • Liver transplantation - who develop progressive hepatic fibrosis with resultant portal hypertension and progressive cholestasisQ
  18. Postoperative Management of biliary atresia?
    Ursodeoxycholic acid (facilitate bile flow) + Methylprednisolone (anti-inflammatory agent) + TMP-SMX (antimicrobial prophylaxis)Q
  19. MC post-operative complicationQ in biliary atresia?
  20. Major factors in successful outcome after Portoentreostomy?
    • • Age in days at diagnosis and initial surgery (30–60 days)Q
    • • Length of time jaundice was present before surgeryQ
    • • Successful and persistent bile flow postoperativelyQ
    • • Size and nature of the microscopic ducts (>150 μm)Q
    • • Degree and extent of fibrotic changes in the liverQ
    • • Need for phototherapy as a neonateQ
    • • Technical aspects of the portoenterostomy and anastomosisQ
    • • Presence of bile in hepatic lobular zone
  21. What is Primary Sclerosing Cholangitis?
    Cholestatic liver disease characterized by fibrotic strictures involving the intrahepatic and extrahepatic biliary treeQ in the absence of a known precipitating cause.
  22. Diseases Associated with Primary sclerosing cholangitis?
    • • Chronic ulcerative colitisQ
    • • Crohn's diseaseQ
    • Riedel's thyroiditisQ
    • SarcoidosisQ
  23. Diseases in which Smoking is protective?
    UC and PSCQ
  24. Histologic finding in PSC?
    “Onion skin appearance”Q
  25. How to differentiate PSC from PBC?
    • Involvement of large intrahepatic and extrahepatic ductQ distinguishes PSC from PBC.
    • Absence of the smallest intrahepatic ducts leading to a reduction in the branching of the biliary tree (give rise to pruned-tree appearanceQ on direct cholangiography).
  26. Earliest finding in PSC?
    Asymptomatic elevation of GGTQ
  27. Gold standard for diagnosis of PSC?
  28. ERCP finding of PSC?
    • • Multifocal stricturing and beadingQ throughout the biliary tree
    • • Beaded or pruned tree appearanceQ
    • • PseudodiverticulaQ (tiny diverticulum like outpouchings) of the extrahepatic bile ducts are nearly pathognomonic of PSC, seen in one fourth of the cases.
    • • The hepatic duct bifurcation is the most severely stricturedQ segment of the biliary tree
  29. Treatment of PSC?
    • High dose UDCAQ (25–30 mg/kg/day).
    • Recurrent biliary sepsis: antibiotics and surveillance
    • Biliary strictures: Dilated or stented
    • Liver transplantation - PSC and end-stage liver diseaseQ
    • Cholestyramine, Phenobarbital, Ursodeoxycholic acid are approved for the treatment of pruritusQ
  30. Sex predilection in PSC and PBC?
    • PSC and Cholangiocarcinoma is more common in malesQ.
    • PBC is more common in femalesQ.
    • Colectomy has no effect on the course of PSCQ.
  31. What is Primary Biliary Cirrhosis?
    Autoimmune etiology, leading to progressive destruction of intrahepatic bile ductsQ
  32. Pathology of primary biliary cirrhosis?
    • Florid duct lesion is characterized by lymphocytic or granulomatous bile duct infiltrationQ.
    • In the setting of positive AMA, the florid duct lesion is essentially diagnosticQ.
  33. Commonest and earliest symptomQ in PBC?
  34. Treatment of PBC?
    • Cholestyramine is mainstay of treatment of pruritusQ.
    • Ursodeoxycholic acid - associated with significant delay to time of transplantationQ.
    • Transplantation - intolerable lethargy or intractable pruritusQ
  35. Etiopathogenesis of recurrent pyogenic cholangitis?
    • • Infection is caused by bacterial contamination, usually biliary pathogens, and biliary parasites, such as Clonorchis sinensis, Opisthorchis viverrini, and Ascaris lumbricoidesQ.
    • • Partial obstruction of biliary tree caused by biliary sludge and dead bacterial cell bodies, which form brown pigment stonesQ
  36. Treatment of recurrent pyogenic cholangitis?
    Roux-en-Y hepaticojejunostomyQ with a subcutaneous afferent limb (Hudson loopQ) to provide access to the biliary tree for stone extractionsQ
Card Set:
MCQ Hepatobiliary Bile duct pathology
2017-09-13 04:22:04
Bile duct

Bile duct pathology
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