PATHOLOGY OF HEPATOBILIARY SYSTEM AND PANCREAS Case 1: hepatitis B infection → A 30 year old nurse complained of anorexia, low grade fever, yellow sclerae, dark urine & light stools. Her serum transaminases are elevated. With the persistence of symptoms for 6 months, liver biopsy was done → Which of the following is compatible with the patient’s disease? → Signs Jaundice & serum transaminases: Means there is hepatocytic injury Light stools: Possibly obstructive jaundice → A & A1: Chronic Passive Congestion Gross (A) Smooth contour Blackish spaces: Hemorrhages?? Microscopic (A1): hepatic lobule Normally, hepatic lobule must be arranged radially, but in this slide it is in disarray Narrowing of spaces: Physiologic hyperplasia: Regeneration Dilated sinusoids: Congestion Bile in the space of disse, biliary tract & sinusoids: hepatic congestion Congestive heart failure: Right heart failure Hemorrhagic central vein necrosis Cardiac cirrhosis Bile accumulation → B & B1: Alcoholic Hepatitis Gross Yellow, enlarged (Must produce abdominal pain, which is absent in our patient) Presence of fibrosis & fatty liver Microscopic: Fatty change Fatty change: Means there is hepatic injury Cirrhosis? No: because there must be hepatocyte necrosis regeneration Fibrosis Presence of lymphocytes → C, C1, C1a, C1b: Viral Hepatitis C Lymphoid aggregates Inflammation: From central vein to portal tract distribution, involving the full thickness of the lobules C1a Diffuse presence of mononuclear Hepatocyte ballooning degeneration with central nuclei Necrosis with destruction of hepatocyte bile will escape jaundice Coagulation necrosis: acidophilia of cytoplasm, accentuated glassy homogenous appearance C1: Chronic active hepatitis: HBV Inflammation of portal region Spillage of inflammatory cells into the lobule Piecemeal necrosis → D & D1 D1 Bile pigments within space & cell Extensive bile accumulation Not the case: since the patient has obstructive jaundice, expected findings is an overflow “Bumabaha” of bile which is not present in the picture → Interpret this profile: HBsAG positive, HBeAg positive, HBeAb negative: The patient has no protection → Discuss prevention, diagnosis & outcome Possible outcome: Resolution in greater than 90% of cases, hepatocellular carcinoma, cirrhosis, hepatic failure, chronic hepatitis, fulminant hepatitis Case II
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A 55 year old bank manager was admitted because of ascites associated with difficulty of breathing. He is a known alcoholic for the past 20 years. Pertinent physical examination showed gynecomastia, distended abdomen, caput medusae & bipedal edema Signs Edema: hydrostatic pressure or oncotic pressure Gynecomastia: Estrogen Discuss the morphologic findings & correlate with portal hypertension D1: Nodular fibrosis Fibrous capsule Alcoholic hepatitis D3: Cirrhosis Fatty change Necrosis regeneration (Crowded, not linearly arranged): Hyperplasia D4: Viral hepatitis Swelling Post necrotic hepatitis E2: Hepatocellular carcinoma mitosis Atypia: pleomorphism of nucleus & cytoplasm Nuclear changes: hyperchromasia, irregularity, chromatin clumping Differentiate a primary liver malignancy from metastatic malignancy Primary Parenchymal cholangiocarcinoma: hepatocyte or biliary tracts: adenocarcinoma α feto protein: Hepatocellular carcinoma Metastatic More common Squamous cell carcinoma or adenocarcinoma (Metastasis from GI, GU) Multiple nodules Central necrosis (umbilication)
Case III: Pancreatitis → A 29 year old lawyer complained of severe abdominal pain after bouts of beer drinking in a class reunion. The pain was described to be severe, referring to the back & was slightly relieved by doubling up. Pertinent physical examination showed board like rigidity of his abdomen. Serum amylase & serum lipase were high while serum calcium was low. He was rushed to the hospital where he went into coma & expired few hours later → Signs Determine whether the patient was suffering from an acute medical abdomen (pancreatitis) or an acute surgical abdomen → Post mortem examination showed which of these processes → A & A1: Acute hemorrhagic pancreatitis High serum amylase & lipase Reflux theory: reflux of enzymes Gross Hemorrhage, inflammation Chalky white fatty necrosis Microscopic Cloudy, fatty necrosis Hemorrhage Presence of inflammatory cells: neutrophils → B & B1: Chronic Pancreatitis Fibrosis Pancreas hardens on chronic pancreatitis → C, C1, C2, C3 C: Gross Large, circular mass at the head of the pancreas C1: Adenocarcinoma Neoplastic glands replacing the normal serous glands
C2: Islet cell tumor C3: Undifferentiated carcinoma
Case IV → A 45 year old obese cook complained of severe right upper quadrant abdominal pain noted after eating fatty food in a fiesta. The persistence of the symptoms thru the night necessitated the admission to the hospital. Subsequent work up & cholecystectomy was done. Which of the following characterize her condition → Signs Exacerbated by fatty food: Fatty food will induce contraction of gallbladder which will produce pain because of inflammation Acute surgical abdomen: if it ruptures will produce peritonitis (Bile is sterile but is irritating) → A: Acute hemorrhagic Cholecystitis Hemorrhage, granular, inflammation in the mucosa → B & B1: Chronic Cholecystitis Lipid laden macrophages Cholesterol stones → C: Adenocarcinoma of the gallbladder Well differentiated Couvousier: dilated with tumor CHRABI