Liver

Question 1

Jaundice

Answer 1

yellowing of skin, scleral icterus from increased serum bilirubin

1. Extravascular hemolysis or Ineffective erythropoiesis
2. Physiologic jaundice of the newborn
3. Gilbert syndrome
4. Crigler-Najjar syndrome
5. Dubin-Johnson syndrome
6. Biliary tract obstruction (obstructive jaundice)
7. Viral hepatitis

Question 2

Viral Hepatitis

Answer 2

inflammation of liver parenchyma from hepatitis virus

• acute: jaundice, dark urine, fever, malaise, neusa, ALT; inflammation of lobules and portal tracts characterized by apoptosis of hepatocytes
• chronic: hepatitis symptoms that last more than 6 months; inflammation of portal tracts and can progress to cirrhosis

Hep A (travelers) and Hep E (water/seafood): fecal-oral, acute, IgM means active, IgG is protective; HEV in pregnancy= fulminant (failure with necrosis)

Hep B: parenteral

Hep C: parenteral, chronic in most, decreased RNA indicates recovery

Hep D: dependent on HBV for infection (superinfection is more severe than coinfection)

Question 3

Cirrhosis

Answer 3

stellate cells–> TGF-B–> bands of fibrosis and regenerative nodules of hepatocytes

*portal HTN (ascites, shunts), decreased detoxification (high estrogen levels), decreased protein synthesis (decreased clotting factors)

Question 4

Alcohol-Related Liver Disease

Answer 4

damage to hepatic parenchyma causing fatty liver or alcoholic hepatitis (chemical injury)

-acetaldehyde causes damage (swelling, Mallory bodies, necrosis, acute inflammation) presenting with painful hepatomegaly and AST

Question 5

Nonalcoholic Fatty Liver Disease

Answer 5

fatty change, hepatitis and/or cirrhosis what develops without exposure to alcohol but is associated with obesity causing higher ALT

Question 6

Hemochromatosis

Answer 6

iron in tissues (hemosiderosis) and organ damage (hemochromatosis) due to defect in iron absorption (HFE-C282Y gene mutation) or chronic transfusions

• presentation: cirrhosis, secondary DM, bronze skin
• brown pigment in hepatocytes (blue with Prussian stain)

Question 7

Wilson Disease

Answer 7

ATP7B gene defect in ATP-mediated hepatocyte copper transport (lack of copper transport into bile and lack of copper incorporation into ceruloplasmin) causing buildup and tissue damage

-presents in childhood with: cirrhosis, neurologic manifestations, and Kayser-Fleischer rings in the corna

Question 8

Primary Biliary Cirrhosis

Answer 8

autoimmune granulomatous destruction of intrahepatic bile ducts with antimitochondrial antibodies presenting with features of obstructive jaundice

*late complication: cirrhosis

Question 9

Primary Sclerosing Cholangitis

Answer 9

inflammation and fibrosis of intrahepatic and extrahepatic bile ducts (periductal fibrosis with onion skin appearance leading to beaded appearance on imaging) presenting with obstructive jaundice and cirrhosis

-associated with ulcerative colitis and p-ANCA is positive

Question 10

Reye Syndrome

Answer 10

fulminant liver failure and encephalopathy related to mitochondrial damage of hepatocytes presenting with hypoglycemia, elevated liver enzymes and N/V

Question 11

Hepatic Adenoma

Answer 11

benign tumor of hepatocytes associated with OCs which can rupture causing intraperitoneal bleeding

*tumors are subscapsular and grow with exposure to estrogen

Question 12

Hepatocellular Carcinoma

Answer 12

malignant tumor of hepatocytes with increased risk for Budd Chiari syndrome (liver infarction from hepatic vein obstruction causing painful hepatosplenomegaly and ascites); detected by a-fetoprotein

-risk factors: chronic hepatitis, cirrhosis, aflatoxins from Aspergillus

Question 13

Metastasis to Liver

Answer 13

more common that primary tumors (from colon, pancreas, lung and breast) causing multiple nodules and hepatomegaly with nodular free edge of the liver