Gb And Pancreas (1)


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Gb And Pancreas (1)

  1. 1. GALLBLADDER Fe A. Bartolome, MD, FPASMAP Department of Pathology Our Lady of Fatima University
  2. 2. Common Locations of Stones
  3. 3. BILIARY TRACT Cholelithiasis (Gallstones) Cholesterol Stones • More prevalent in: 1. Industrialized countries 2. Advancing age 20 to cholesterol 3. Caucasian women hypersecretion 4. Pregnancy & oral contraceptive use • Estrogenic influence  inc. expression of hepatic lipoprotein receptors + inc. hepatic HMG-CoA reductase activity  inc. cholesterol uptake & biosynthesis 5. Gallbladder stasis (neurogenic and hormonal)
  4. 4. BILIARY TRACT Cholelithiasis (Gallstones) Cholesterol Stones • More prevalent in: 6. Inborn error of metabolism a. Impaired bile salt secretion and synthesis b. Defects in lipoprotein receptors – hyperlipidemia syndromes 7. Obesity and rapid weight loss  increased biliary cholesterol secretion
  5. 5. BILIARY TRACT Pathogenesis: Cholesterol conc. > solubilizing Hepatocellular hypersecretion capacity of bile of cholesterol SUPERSATURATION Dec. ability of mucosa to Inc. free cholesterol penetrate detoxify by esterification GB wall Dec. responsiveness to GALLBLADDER Stasis cholecystokinin HYPOMOTILITY PROMOTE MUCUS ACCELERATED HYPERSECRETION & CHOLESTEROL CRYSTAL STONE MICROPRECIPITATION OF NUCLEATION CALCIUM SALTS
  6. 6. BILIARY TRACT Morphology: • Cholesterol monohydrate + calcium salts • Pale yellow, round to ovoid, finely granular • Pure cholesterol stones  radiolucent • If with calcium carbonate  radio-opaque • Incidental finding of cholesterolosis  accumulation of cholesterol enters within lamina propia of GB  mucosal surface with minute yellow flecks  “strawberry” gallbladder
  7. 7. Cholesterolosis Cholesterol deposits
  8. 8. BILIARY TRACT Cholesterol stones
  9. 9. BILIARY TRACT Pigment Stones • Increased incidence in: 1. Asians 2. Rural areas 3. Chronic hemolytic syndromes 4. Bacterial contamination of biliary tract 5. GI diseases – ileal disease (e.g. Crohn’s) or bypass 6. Cystic fibrosis with pancreatic insufficiency
  10. 10. BILIARY TRACT Pathogenesis: • Infection of biliary tract (E. coli, A. lumbricoides, Opistorchis sinensis)  release of microbial -glucuronidase  hydrolysis of B2  increased B1 • Intravascular hemolysis  hepatic secretion of B2  (+) deconjugation in biliary tree  increased B1
  11. 11. BILIARY TRACT Morphology: • Mixture of abnormal insoluble calcium salts of B1 + inorganic calcium salts • Two types: 1. Black pigment stones • Found in sterile GB bile • Oxidized polymers of calcium salts of B1, calcium carbonate, calcium phosphate, mucin glycoprotein and little amount of cholesterol monohydrate crystals • Rarely > 1.5 cm diameter
  12. 12. BILIARY TRACT Morphology: • Two types: 1. Black pigment stones • Present in greater number; 50% - 75% radio- opaque; crumble to touch 2. Brown stones • Found in infected intra- and extrahepatic ducts • Pure calcium salts of B1, mucin glycoprotein, substantial cholesterol fraction, calcium salts of palmitate and stearate • Laminated and soft with soap-like or greasy consistency • Radiolucent
  13. 13. BILIARY TRACT Black Pigment Stones
  14. 14. BILIARY TRACT Clinical Features of Gallstones • 70% - 80% asymptomatic • May present with biliary pain – excruciating and constant, colicky  most prominent • Complications: 1. Cholecystitis 6. Obstructive cholestasis 2. Empyema 7. Pancreatitis 3. Perforation 8. Erode into adjacent small bowel 4. Fistula formation loop  gallstone ileus 5. Cholangitis 9. Increased risk for CA
  15. 15. BILIARY TRACT CHOLECYSTITIS Acute Calculous Cholecystitis • Primary complication of gallstones • Most common reason for emergency cholecystectomy • Precipitated by obstruction of neck or cystic duct
  16. 16. BILIARY TRACT Acute Calculous Cholecystitis: Pathogenesis OBSTRUCTION Hydrolysis of luminal Production of toxic lecithins by mucosal lysolecithins phospholipases Exposure of epithelium Disruption of to direct detergent glycoprotein mucus action of bile salts layer (+) GB distention & Compromised (+) GB dysmotility inc. intraluminal mucosal blood flow pressure INFLAMMATION
  17. 17. BILIARY TRACT Acute Calculous Cholecystitis: Morphology Gross: GB enlarged and tense Bright red or blotchy; violaceous to green-black (if with necrosis, called gangrenous cholecystitis Subserosal hemorrhages Cloudy or turbid bile  fibrin, frank pus, hemorrhage • If pure pus, called empyema of gallbladder Microscopic: acute inflammation
  18. 18. Acute Cholecystitis
  19. 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.
  20. 20. BILIARY TRACT Acute Acalculous Cholecystitis • Occurs in the absence of gallstones • Seen in severely ill patients • Usually occurs in the following circumstances: 1. Post-operative state (major, non-biliary surgery) 2. Severe trauma 3. Severe burns 4. Multi-system organ failure 5. Sepsis 6. Prolonged IV hyperalimentation 7. Postpartum state
  21. 21. BILIARY TRACT Acute Acalculous Cholecystitis: Pathogenesis • Result from ischemia • Contributing factors: 1. Dehydration & multiple blood transfusion  inc. pigment load 2. Hyperalimentation & assisted ventilation  GB stasis 3. Accumulation of microcrystals of cholesterol, viscous bile and GB mucus  cystic duct obstruction without stone formation 4. Inflammation and edema of wall  compromise blood flow 5. Bacterial contamination and generation of lysolecithins
  22. 22. 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.
  23. 23. BILIARY TRACT Clinical Features of Acute Cholecystitis • Acute calculous – sudden onset • Acute acalculous – insidious onset • Symptoms include: 1. Progressive RUQ or epigastric pain 2. Mild fever 3. Anorexia 4. Tachycardia 5. Sweating 6. Nausea and vomiting
  24. 24. BILIARY TRACT Chronic Cholecystitis • Associated with cholelithiasis (90%) • Calculous or acalculous • Organisms: E. coli and Enterococci • Symptoms of chronic calculous cholecystitis similar to the acute form • Morphology: variable Subserosal fibrosis Thickened wall and opaque gray-white appearance
  25. 25. BILIARY TRACT Chronic Cholecystitis • Microscopic: Mild cases – lymphocytes, plasma cells, macrophages Severe cases – subepithelial and subserosal fibrosis with mononuclear infiltration Rokitansky-Aschoff sinuses
  26. 26. BILIARY TRACT Chronic Cholecystitis Normal gallbladder RA sinuses
  27. 27. BILIARY TRACT Chronic Cholecystitis • Other forms (rare): 1. Porcelain GB • Extensive dystrophic calcification within GB • Inc. association with GB carcinoma 2. Xanthogranulomatous cholecystitis • Shrunken, nodular and chronically inflamed GB with foci of necrosis and hemorrhage; gallstones usually present 3. Hydrops of GB • Atrophic, chronically obstructed GB containing only clear secretions
  28. 28. Xanthogranulomatous cholecystitis: fibrotic thickening of the gallbladder wall and narrowing of the gallbladder lumen.
  29. 29. BILIARY TRACT Chronic Cholecystitis: Clinical Features 1. Recurrent attacks of steady or colicky epigastric or RUQ pain 2. Nausea and vomiting 3. Intolerance for fatty foods
  30. 30. BILIARY TRACT Chronic Cholecystitis: Complications 1. Bacterial superinfection  cholangitis or sepsis 2. GB perforation and local abscess formation 3. GB rupture with peritonitis 4. Biliary enteric (cholecystenteric) fistula 5. Aggravation of pre-existing medical illness
  31. 31. BILIARY TRACT Tumors of Gallbladder 1. Adenomas • Benign epithelial  localized neoplastic growth of lining epithelium • Tubular, papillary or tubulopapillary 2. Inflammatory polyps • Sessile mucosal projections • Chronic inflammatory cells & lipid-laden macrophages 3. Adenomyosis • Hyperplasia of muscularis with intraluminal hyperplastic glands
  32. 32. BILIARY TRACT Cancer of Gallbladder • Women > males; 7th decade • (+) gallstones in 60% - 90% of cases  chronic irritation and inflammation • Majority adenocarcinoma; 5% SSCA • Two forms: 1. Infiltrative • More common; poorly-defined • Scirrhous with firm consistency • Can cause direct penetration of GB wall or fistula formation to adjacent viscera
  33. 33. BILIARY TRACT Cancer of Gallbladder 2. Exophytic • Grows into the lumen • Irregular, cauliflower mass with invasion of underlying wall • Most common site of involvement: fundus and neck; lateral wall (20%) • With centrifugal invasion of liver at time of discovery • Common site of seeding: lungs, peritoneum, GIT
  34. 34. Histologic & Molecular Sequence in the Pathogenesis of Gallbladder Carcinoma
  35. 35. Normal GB Moderately-differentiated Well-differentiated GB Carcinoma GB Carcinoma
  36. 36. BILIARY TRACT Cancer of Gallbladder • Clinical: • Indistinguishable from cholelithiasis  abdominal pain, jaundice, anorexia, nausea and vomiting • Palpable GB • Features of acute cholecystitis
  37. 37. EXTRAHEPATIC BILIARY TRACT Choledocholithiasis • Stones within the bile ducts of the biliary tree • Higher incidence in Asia  pigmented stones • Clinical: usually asymptomatic but may manifest with: 1. Obstruction 2. Pancreatitis 3. Cholangitis 4. Hepatic abscess 5. Secondary biliary cirrhosis 6. Acute calculous cholecystitis
  38. 38. EXTRAHEPATIC BILIARY TRACT Cholangitis • Bacterial infection of the bile ducts • Secondary to obstruction to bile flow due to stones • Other causes: 1. In-dwelling stents or catheters 2. Tumors 3. Acute pancreatitis 4. Benign strictures 5. Infection (viruses, fungi, parasites)
  39. 39. EXTRAHEPATIC BILIARY TRACT Cholangitis • Pathogenesis: obstruction  stasis  secondary bacterial infection  enter biliary tract via sphincter of Oddi • Organisms: enteric gram (-) aerobes (E. coli), Klebsiella, Clostridium, Bacteroides, Enterobacter, group D Streptococci • Clinical: fever and chills, abdominal pain, jaundice
  40. 40. EXTRAHEPATIC BILIARY TRACT Ascending Cholangitis • Infection of intrahepatic biliary radicals Suppurative Cholangitis • Bile ducts distended and filled with purulent bile • Most severe form  lead to sepsis
  41. 41. EXTRAHEPATIC BILIARY TRACT Biliary Atresia • Complete obstruction of lumen of extrahepatic biliary tree within the first three months of life • Pathogenesis: two forms 1. Fetal form (20% of cases) • 20 to failure of establishment of laterality of thoracic and abdominal organ development  aberrant intrauterine development of extrahepatic biliary tree • Associated with: malrotation of viscera, interrupted IVC, polysplenia, congenital heart disease
  42. 42. EXTRAHEPATIC BILIARY TRACT Biliary Atresia Pathogenesis: two forms 2. Perinatal form • More common; normally developed biliary tree destroyed following birth • Causes: a. Possible viral infection (Reovirus & Rotavirus) b. Genetic predisposition
  43. 43. EXTRAHEPATIC BILIARY TRACT Biliary Atresia Morphology: Inflammation and fibrosing stricture of hepatic or common bile ducts Periductal inflammation of intrahepatic ducts Obstruction of intrahepatic biliary tree
  44. 44. EXTRAHEPATIC BILIARY TRACT Biliary Atresia Classification: Type I – limited to CBD Type II – CBD + hepatic duct with patent proximal branches Type III – 90%; with obstruction of bile ducts at or above the porta hepatis Types I and II – surgically correctable Type III – not correctable; liver transplant
  45. 45. 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.)
  46. 46. EXTRAHEPATIC BILIARY TRACT Biliary Atresia Clinical: Female preponderance Neonatal cholestasis Normal birth weight and post-natal weight gain Initially normal stools  acholic stools Serum bilirubin = 6 – 12 mg/dL Mod. Increased aminotransferase & ALP levels
  47. 47. 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.
  48. 48. EXTRAHEPATIC BILIARY TRACT Tumors: Choledochal Cysts • Congenital dilations of CBD • Children < 10 y/o • Jaundice + symptoms of biliary colic • If with cystic dilation of intrahepatic biliary tree  Caroli disease • Predispose to: stone formation, stenosis & stricture, pancreatitis • In older patients, inc. risk of bile duct CA
  49. 49. Type I cysts represent approximately 85% of most series. They are fusiform in shape.
  50. 50. Type II cysts represents less than 2% of cases, and are often called common bile duct diverticulum.
  51. 51. Type III cysts also called choledochoceles represents approximately 2% of cases. Here the dilatation is localized to the terminal portion of the biliary tract
  52. 52. Type IV cysts represent the remaining approximately 10% of cases. Here the dilatation affects both intrahepatic and extrahepatic bile ducts
  53. 53. 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
  54. 54. 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
  55. 55. EXTRAHEPATIC BILIARY TRACT Tumors: Cancer of Extrahepatic Ducts • Insidious; painless, progressively deepening jaundice • Elderly; men > women • Risk factors: 1. Primary sclerosing cholangitis 2. Ulcerative colitis 3. Cystic liver disease (Caroli’s dse and choledochal cyst) 4. Fluke infection (Clonorchis sinensis)
  56. 56. EXTRAHEPATIC BILIARY TRACT Tumors: Klatskin Tumors • Tumors arising from the part of the CBD between the cystic duct junction and the confluence of the R and L hepatic ducts • Characteristic features: 1. Slow growth 2. Marked sclerosis 3. Rare distant metastases
  57. 57. Type I tumor Type II tumor involves the affects the main main hepatic hepatic duct duct below bifurcation the bifurcation Type III tumor Type IV involves tumors involve segmental ducts segmental beyond the ducts in both primary hepatic liver lobes duct bifurcation in one liver lobe (type IIIa: right lobe, type IIIb: left lobe)
  58. 58. Klatskin Tumor
  59. 59. 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