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3 major etiologies of hepatocellular carcinoma

Viral infection with hep B or C
Chronic alcoholism
Food contaminants (aflotoxin)

Cirrhosis is not required for dx but seems to be a major contributor

1

What is the marker for HCC?

alpha-fetoprotein (AFP)

2

Hemtemesis, palpable spleen, esophageal varices, portal hypertension, no abnormalities on liver biopsy. Dx?

Portal vein thrombosis. (Long-term alcohol would show cirrhosis on biopsy)

3

Crigler-naijar syndrome

Autosomal recessive absence of liver conjugation enzymes. Causes unconjugated hyperbilirubinemia. UCB cannot be excreted, so builds up in tissues like the brain, causes bilirubin encephalopathy.

4

Kernicterus

Bilirubin encephalopathy, potentially fatal condition with severe jaundice and neurological impairment. UCB builds up in basal ganglia

5

Dubin-Johnson syndrome

Autosomal recessive absence of biliary transport protein, defective liver excretion. Causes conjugated bilirubinemia, benign except for black liver.

6

Rotor syndrome

Like Dubin-Johnson but milder: defect of biliary transport protein, defective liver excretion. Causes conjugated bilirubinemia, benign and NO black liver

7

Lab tests that assess liver function

prothrombin time, bilirubin, albumin, cholesterol

8

Lab tests that assess structural/cellular integrity of liver

Transaminases (AST, ALT)

9

Lab tests that assess biliary tract

Alkaline phosphatase (nonspecific, found in lots of tissues), gamma glutamyl transferase (more specific)

10

Elevated alkaline phosphatase: what is next thing to check?

gamma glutamyl transpeptidase

11

What is acute cholecystitis? Main cause?

Acute inflammation of gallbladder, initiated by obstruction of gallbladder neck or cystic duct. This is the major complication of cholelithiasis

12

Gilbert syndrome

Mild familial decrease in UDG conjugation enzyme. Only clinical sign is jaundice in times of stress: fasting, fever, hemolysis, fatigue, exertion.

13

Treatment of acetominophen overdose, mechanism

N-acetyl cysteine, binds toxic metabolite and provides sulfhydryl groups to sulfonate and metabolize

14

Antidote in iron poisoning

Deferoxamine

15

"Serum sickness", malaise, fever, skin rash, pruritis, lymphadenopathy, joint pain. Followed by anorexia, jaundice, RUQ pain.

Acute viral Hep B

16

Acute viral hepatitis labs

Significant elevations in ALT and AST (ALT>AST), rise in bilirubin and alk phos

17

What tests do you need to do for pt on statins

LFTs

18

Most common malignant hepatic lesion

Metastasis

19

Black pigment stones

Gallstones seen in chronic extravascular hemolysis. Usually small, spiculated, crumbly, and radioopque. Form when UCB precipitates as calcium bilirubinate.

20

Significant risk factor for cholesterol stones, black pigment stones, brown pigment stones

Cholesterol: Obesity, Crohn, CF, age, estrogen, drugs
Black: hemolysis
Brown: infection

21

Mechanism of damage in hepatic steatosis

Increased activity of dehydrogenase enzymes --> increased NADH --> decreased fatty acid oxidation.

22

Possible outcomes of hep B infection

- Acute hepatitis with complete resolution (95%)
- Chronic hepatitis (with or without cirrhosis)
- Fulminant hepatitis with massive liver necrosis

23

HIDA scan

Nadionuclide scan, used for dx of acute cholecystitis. If you don't see gall bladder on the scan, the cystic duct is obstructed and it is a positive test result.

24

Gross and histo findings in Dubin-Johnson syndrome

Gross: black liver
Histo: normal, may see dense pigment with epinephrine metabolites within lysosomes

25

Middle aged woman, insidious onset, pruritis, fatigue, hepatosplenomegaly, jaundice, steatorrhea, portal htn osteopenia. Elevated alk phos and cholesterol. Serum anti mitochondrial antibodies. Maybe associated with autoimmune disease

Primary biliary cirrhosis

26

Primary biliary cirrhosis pathophys

Autoimmune destruction of intrahepatic bile ducts and cholestatis.

27

Primary biliary cirrhosis: associations

Sjogren syndrome, CREST, Raynaud's, RA, celiac, thyroid disease

28

Hepatitis B: risk of hepatocellular carcinoma?

Increased. Virus integrates DNA into host genome

29

Main mechanism of excess copper removal (healthy)

In liver, incorporated into ceruloplasmin. Some goes into plasma (most of circulating copper), some is excreted via bile, stool.