Exam 1: Liver Test And Hepatitis Flashcards

1
Q

What is 5NP?

A

A liver enzyme that is elevated in diseases affecting the biliary tree. 5NP can help distinguish liver as the origin

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2
Q

When GGT elevated simultaneously with ALP, what does this indicate?

A

It confirms liver origin

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3
Q

What is the first step in evaluation of a patient with elevated LFTs but no symptoms?

A

Repeat the test (fasting)

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4
Q

When is GGT useful?

A

1) when ALP is elevated, it confirms liver specificity

2) When AST/ALT is >2 it further supports alcoholic liver disease (ALD)

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5
Q

What liver tests assess liver function?

A

Bilirubin, albumin, and PT/INR

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6
Q

What labs are going to be elevated with hepatocellular damage?

A

ALT and AST

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7
Q

What labs will be elevated with a cholestatic process?

A

Total bilirubin, ALP, and GGT

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8
Q

What does elevated ALP suggest?

A

Cholestasis

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9
Q

What is fractionated bilirubin and when is its useful?

A

Fraction of total bilirubin that is direct vs indirect.

Useful when standard liver tests are normal and total bilirubin is elevated (hemolysis and Gilbert syndrome)

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10
Q

What happens to UDP glucoronyl transferase in Gilbert syndrome?

A

Activity is reduced by 30% so unconjugated bilirubin is not being conjugated and there is decreased bilirubin secretion

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11
Q

What lab findings are consistent with liver disease?

A

Elevated direct bilirubin and elevated ALT and AST

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12
Q

What lab findings are consistent with hemolysis?

A

Elevated indirect bili, anemia, normal AST and ALT

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13
Q

What lab findings are consistent with Gilbert syndrome?

A

Elevated total bili, elevated indirect bili, normal ALT and AST, no anemia

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14
Q

Do normal liver tests mean that the liver is normal?

A

NO

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15
Q

Is there a relationship between severity of liver disease and transaminase levels?

A

NO

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16
Q

Where is GGT found?

A

Hepatocytes and biliary epithelial cells

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17
Q

What herbals/vitamins can cause drug induced liver injury (DILI)?

A

Ephedra, Kava, VItamin A, and Garcinia Cambogia

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18
Q

What are the medications that can cause DILI?

A

Acetaminophen, Statins, antifungals, antibiotics, Anti TB drugs, NSAIDs, tegretol

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19
Q

What are causes other than liver injury/damage that can cause elevated LFTs?

A

Muscle injury, cholelithiasis, masses, hemodynamics disorders, celiac, hypothyroid and adrenal insufficiency

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20
Q

What labs can be elevated in muscle disorders?

A

CPK and aldolase

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21
Q

What conditions are associated with mildly elevated AST and ALT?

A

Fatty liver, EtOH, chronic viral hepatitis, and medication effects

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22
Q

What conditions are associated with AST> ALT?

A

Alcoholic hepatitis, rhabdo, cardiac, and cirrhosis

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23
Q

What is a AST: ALT ratio of >2 suggestive of?

A

Alcoholic liver disease

24
Q

What is AST/ALT ratio of less than 2 suggestive of?

A

Acute or chronic viral hepatitis, cholestatic disease, NASH, and cirrhosis

25
Q

What is NAFLD?

A

Non-alcoholic fatty liver disease with no secondary cause for fat accumulation .
No inflammation and low risk of developing significant fibrosis

26
Q

What is NASH?

A

Non alcoholic steatohepatitis, fatty liver with inflammation with hepatocyte injury and fibrosis.
-Higher risk of developing significant fibrosis, cirrhosis, liver failure, and liver cancer

27
Q

What can NASH progress to?

A

Cirrhosis

28
Q

What is the strongest predictor for NASH?

A

Metabolic syndrome

29
Q

What are the risk factors for NAFLD?

A

Abdominal obesity, DM, HLD, metabolic syndrome, and polycyclic ovarian syndrome

30
Q

How is NASH diagnosed?

A

Mildly elevated ALT and AST, fatty infiltration on imaging, negative work ups for other causes of NASH, and possibly liver biopsy

31
Q

What will a liver biopsy show in a NASH patient?

A

Steatosis, inflammation and fibrosis

32
Q

What is the management for NASH?

A

Diet and exercise, reduce EtOH, control DM and HLD, and transplant if progressed to cirrhosis

33
Q

What is hereditary hemochromatosis?

A

Autosomal recessive, most commonly due to mutations in HFE gene.
-Genetic mutation that results in increased iron absorption and iron accumulation in liver, pancreas, heart, kidneys, etc

34
Q

What can hereditary hemachromatitis do to the liver? What increases this risk?

A

May lead to fibrosis and cirrhosis.

Excessive EtOH intake and co-existing conditions increase risk

35
Q

What labs findings are seen with hereditary hemochromatosis?

A

Elevated AST and ALT

36
Q

What should you do when you have a patient with hereditary hemochromatosis with elevated transferrin saturation or elevated ferritin?

A

Refer to GI for HFE genotype analysis and further work up

37
Q

What is the treatment of hereditary hemochromatosis?

A
  • Cirrhosis prevention by avoiding vitamin C, iron supplements,EtOH, and uncooked seafood
  • Therapeutic phlebotomy
  • Hep A and B immunization
38
Q

What is Primary biliary cholangitis?

A

Immunologic attack on the intrahepatic bile ducts that eventually leads to cirrhosis and liver failure.

39
Q

What test is positive in primary biliary cholangitis?

A

Anti-mitochondrial antibodies (AMA)

40
Q

What is autoimmune hepatitis?

A

Hepatocellular inflammation presumed T-Cell mediated immune attack of liver antigens

41
Q

What is primary sclerosis cholangitis?

A

Inflammation and fibrosis of the intrahepatic and extraheptic ducts. Strong association with IBD

42
Q

Is AMA positive or negative for primary sclerosis cholangitis?

A

Negative

43
Q

What autoimmune liver diseases are predominantly in women?

A

Primary biliary cholangitis and autoimmune hepatitis

44
Q

What labs test should you order in autoimmune hepatitis?

A

Antinuclear antibodies, anti smooth muscle antibodies, liver kidney microsomal antibody, and liver cytosol

45
Q

What is alpha 1 antitrypsin deficiency?

A

Genetic disorder characterized by decreased level of normal alpha 1 antitrypsin, which protects against tissue injury

46
Q

What is Wilson’s disease?

A

A rare hereditary disorder of copper metabolism caused by an autosomal recessive defect.
-Causes impaired biliary excretion and elimination of copper from the liver

47
Q

How does Wilson’s disease cause liver damage?

A

Copper accumulates to toxic levels in the liver and copper is released into the blood stream, which accumulates in the brain, cornea, joints, kidney, heart, and pancreas

48
Q

What are the clinical findings of Wilson’s disease?

A

Predominantly hepatic, neurologic, and psychiatric (tremor, involuntary movements, dysarthria, muscle spasticity, etc)

49
Q

What is a Kayser-fleisher ring and what disease is it associated with?

A

fine pigmented granular deposits in the cornea.

Associated with Wilson’s disease

50
Q

How is Wilson’s disease diagnosed?

A

Elevated AST and ALT, ALP low, serum cerulplasmin, high urinary copper, and possible liver biopsy and genetic testing

51
Q

How is Hepatitis A spread?

A

Fecal oral route

52
Q

What labs findings are associated with hepatitis A?

A

Significantly elevated AST/ALT, elevated ALP, elevated bilirubin

53
Q

What test is diagnostic for hepatitis A?

A

Anti-HAV IgM

54
Q

How is hepatitis B spread?

A

Sexual contact, parenteral, person to person, peri-natal transmission

55
Q

Does Hepatitis A ever become chronic?

A

No