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Exocrine Pancreas, Gallbladder and Liver pathology > Liver I > Flashcards

Flashcards in Liver I Deck (29):
1

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

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.

2

What is viral hepatitis? What causes it?

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

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?

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.

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?

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

5

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

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.

6

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

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.

7

What are the three clinical features of cirrhosis?

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

8

What 4 things does portal hypertension in cirrhosis lead to?

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

9

What 3 things does portal hypertension in cirrhosis lead to?

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

10

What 2 things does portal hypertension in cirrhosis lead to?

1. Hypoalbuminemia with edema
2. Coagulopathy due to decreased synthesis of clotting factors

11

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

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

12

How is coagulopathy followed in Cirrhosis?

Prothrombin time

13

How is coagulopathy followed in Cirrhosis?

Prothrombin time

14

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

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

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?

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.

16

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

Cirrhosis affecting 10-20% of alcoholics.

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?

Nonalcoholic fatty liver disease which is associated with obesity.

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?

Nonalcoholic fatty liver disease which is associated with obesity.

19

What is hemochromatosis? How does it damage the tissues?

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

20

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

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

21

What is hemochromatosis? How does it damage the tissues?

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

22

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

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

23

What causes secondary hemochromatosis?

Chronic transfusions

24

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

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

25

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

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

26

What causes secondary hemochromatosis?

Chronic transfusions

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?

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.

28

What is seen on liver biopsy in primary hemochromatosis?

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

29

What is Lipofuscin? Where is it commonly found?

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