Liver I

Question 1

What is jaundice? What is the earlies sign? What causes it?

Answer 1

Yellow discoloration of the skin. Earliest sign is scleral icterus. Due to increased serum bilirubin, usually > 2.5 mg/dL. Arises with disturbances in bilirubin metabolism.

Question 2

What is viral hepatitis? What causes it?

Answer 2

Inflammation of the liver parenchyma, usually due to hepatitis virus. Other causes include EBV and CMV

Question 3

A patient presents with fever, nausea and malaise. PE shows that he is jaundiced. His urine appears dark. Liver enzymes are elevated with ALT>AST. Symptoms have been going on for the less than 6 months. What doe she have? Which structures are affected? Which cells are affected? Does this always present with symptoms?

Answer 3

He has acute hepatitis. Inflammation involves lobules of the liver and portal tracts and is characterized by apoptosis of hepatocytes. Some cases may be asymptomatic with elevated liver enzymes.

Question 4

A patient presents with fever, nausea and malaise. PE shows that he is jaundiced. His urine appears dark. Liver enzymes are elevated with ALT>AST. Symptoms have been going on for tmore than 6 months. What doe she have? Which structures are affected? What is he at increased of?

Answer 4

He has chronic hepatitis. Inflammation involves portal tract. Risk of progression to cirrhosis.

Question 5

What is cirrhosis? What cause it? Which cells play a role, what do they do and where are they usually founf?

Answer 5

End-stage liver damage characterized by disruption of henormal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes. Fibrosis is mediated by TGF-beta from stellate cells which lie beneath the endothelial cells that line the sinusoids.

Question 6

What is cirrhosis? What cause it? Which cells play a role, what do they do and where are they usually founf?

Answer 6

End-stage liver damage characterized by disruption of the normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes. Fibrosis is mediated by TGF-beta from stellate cells which lie beneath the endothelial cells that line the sinusoids.

Question 7

What are the three clinical features of cirrhosis?

Answer 7

1. Portal hypertension
2. Decreased detoxification
3. Decreased protein synthesis

Question 8

What 4 things does portal hypertension in cirrhosis lead to?

Answer 8

1. Ascites
   2 .Congestive splenomegaly/hypersplenism
2. Portosystemic shunts (esophagela varices, hemorrhoids, caput medusae)
3. Hepatorenal syndrome

Question 9

What 3 things does portal hypertension in cirrhosis lead to?

Answer 9

1. Mental status changes, asterixis and eventual coma
2. Gynecomastia, spider angiomata and palmar erythema due to hyperestrinism
3. Jaundice

Question 10

What 2 things does portal hypertension in cirrhosis lead to?

Answer 10

1. Hypoalbuminemia with edema

2. Coagulopathy due to decreased synthesis of clotting factors

Question 11

Are the neurological issues in cirrhosis treatable? What causes them?

Answer 11

Increased serum ammonia. It is reversible since it is a metabolic process.

Question 12

How is coagulopathy followed in Cirrhosis?

Answer 12

Prothrombin time

Question 13

How is coagulopathy followed in Cirrhosis?

Answer 13

Prothrombin time

Question 14

What causes fatty liver? What does it do to the liver?

Answer 14

Alcohol consumption. Results in a heavy greasy liver and resolves with abstinence.

Question 15

A patient presents with painful hepatomegaly and elevated liver enzymes. AST>ALT. What is on the top of your differential? What usually causes this? What chemical mediates the damage? What does it look like on histology?

Answer 15

Alcoholic hepatitis which results from chemical injury to hepatocytes. Generally seen in binge drinking. Acetaldehyde (metabolite of alcohol) mediates damage. Characterized by swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments), necrosis and acute inflammation.

Question 16

What does chronic alcohol-induced liver damage lead to? How many patients does it target?

Answer 16

Cirrhosis affecting 10-20% of alcoholics.

Question 17

A patient presents with symptoms of hepatitis and cirrhosis. Liver histology shows fatty changes. He mentions that he does not drink alcohol. His liver enzymes indicate ALT>AST. What does he have and what is this associated with?

Answer 17

Nonalcoholic fatty liver disease which is associated with obesity.

Question 18

A patient presents with symptoms of hepatitis and cirrhosis. Liver histology shows fatty changes. He mentions that he does not drink alcohol. His liver enzymes indicate ALT>AST. What does he have and what is this associated with?

Answer 18

Nonalcoholic fatty liver disease which is associated with obesity.

Question 19

What is hemochromatosis? How does it damage the tissues?

Answer 19

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis). Tissue damage mediated by generation of free radicals.

Question 20

What is the inheritance pattern of primary hemochromatosis? What genes are involved? When does it present?

Answer 20

Autosomal recessive defect in iron absorption due to mutations in the HFE gene usually C282Y (cysteine replaced by tyrosine). Presents in late adulthood.

Question 21

What is hemochromatosis? How does it damage the tissues?

Answer 21

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis). Tissue damage mediated by generation of free radicals.

Question 22

What is the inheritance pattern of primary hemochromatosis? What genes are involved? When does it present?

Answer 22

Autosomal recessive defect in iron absorption due to mutations in the HFE gene usually C282Y (cysteine replaced by tyrosine). Presents in late adulthood.

Question 23

What causes secondary hemochromatosis?

Answer 23

Chronic transfusions

Question 24

What is hemochromatosis? How does it damage the tissues? What does it increase the risk of?

Answer 24

Excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis). Tissue damage mediated by generation of free radicals. Hepatocellular carcinoma

Question 25

What is the inheritance pattern of primary hemochromatosis? What genes are involved? When does it present? How is it treated?

Answer 25

Autosomal recessive defect in iron absorption due to mutations in the HFE gene usually C282Y (cysteine replaced by tyrosine). Presents in late adulthood. Phlebotomy

Question 26

What causes secondary hemochromatosis?

Answer 26

Chronic transfusions

Question 27

A patient presents with cirrhosis, secondary diabetes mellitus and bronze skin. Cardiac exam shows dilated cardiomyopahty and an arrythmia. Other finding is gonadal dysfunction. What is this indicative of? What will his ferritin, TIBC, serum iron and % saturation indicate?

Answer 27

Primary hemochromatosis with the classic triad of cirrhosis, secondary diabetes mellitus and bronze skin. Ferritin is elevated, TIBC is lowered, serum iron is elevated and % saturation is elevated.

Question 28

What is seen on liver biopsy in primary hemochromatosis?

Answer 28

Accumulation of brown pigment in hepatocytes. Prussian blue stain distinguishes iron (blue) from lipofuscin.

Question 29

What is Lipofuscin? Where is it commonly found?

Answer 29

Brown pigment in hepatocytes that is a by product from turnover of peroxidized lipids.