Evaluating Liver Enzymes & Function Flashcards

1
Q

isoenzymes

A

structurally different enzymes from different genes that catalyze the same chemical reaction

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2
Q

isoforms

A

structurally different enzymes from the same gene, but different post-translational modifications, that catalyze the same chemical reaction

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3
Q

stability

A

how long the enzyme remains intact outside of the body (in the sample)

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4
Q

half life

A

how long the enzyme remains measurable in the blood after being released

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5
Q

what units are used when evaluating liver enzymes

A

IU/L or X increase above the upper limit of reference interval

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6
Q

are values lower than reference interval clinically significant for liver enzymes

A

no

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7
Q

what type of sample is used for evaluating liver enzymes

A

serum

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8
Q

what factors interfere with liver enzymes

A

color (hemolysis, lipemia, icterus)

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9
Q

causes of elevated liver enzymes

A
  1. cell injury
  2. induction of enzyme synthesis
  3. greater cell mass
  4. absorption
  5. decreased clearance
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10
Q

alanine transferase (ALT)

A

cytoplasmic enzyme (mild cell injury)

used for small animals only w/ high specificity for liver injury

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11
Q

sorbitol dehydrogenase (SDH)

A

cytoplasmic enzyme (mild cell injury)

used for large animals w/ high specificity for liver injury

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12
Q

lactate dehydrogenase

A

cytoplasmic enzyme (mild cell injury)

rarely used - low specificity for liver injury

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13
Q

aspartate aminotransferase (AST)

A

mitochondrial & cytoplasmic enzyme (severe cell injury)

used for all species

moderate specificity for liver injury - also released by muscle so check CK concurrently

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14
Q

glutamate dehydrogenase (GLDH)

A

mitochondrial & cytoplasmic enzyme (severe cell injury)

used for large animals/exotics w/ high specificity for liver injury

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15
Q

alkaline phosphatase (ALP)

A

membrane bound inducible enzyme (increased induction of enzyme synthesis)

2 isoenzymes w/ 5 isoforms

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16
Q

ALP isoenzymes & isoforms

A
  1. intestinal ALP (intestinal-ALP or corticosteroid-ALP in dogs)
  2. tissue nonspecific ALP (liver-ALP, bone-ALP, placenta-ALP)
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17
Q

causes of elevated ALP

A
  1. age: high B-ALP in young animals/neonates
  2. mechanical cholestasis: high L-ALP (dogs)
  3. drugs/hormones
  4. increased osteoblast activity
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18
Q

gamma-glutamyl transferase (GGT)

A

membrane bound inducible enzyme (increased induction of enzyme synthesis)

more sensitive than ALP in large animals

induced by cholestasis, biliary hyperplasia, drugs/hormones

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19
Q

enzymes that indicate cell injury

A

mild: ALT, SDH, LDH
severe: AST, GLDH

20
Q

enzymes that indicate increased induction

A

ALP, GGT

21
Q

pattern of cholestasis

A

increased ALP and GGT
- NOT functional cholestasis

hyperbilirubinemia/uria

possible hypercholesterolemia, coagulation, inc. serum bile acids

22
Q

pattern of feline hepatic lipidosis

A

ALP increases higher/faster than GGT

23
Q

pattern of feline hyperthyroid

A

increased ALP
normal GGT

24
Q

pattern of canine cholestatic disease

A

significantly increased ALP
increased GGT

25
Q

liver injury vs liver dysfunction

A

injury: increase in liver enzymes without clinical signs of decreased liver function

dysfunction: changes in liver values +/- clinical signs of decreased liver function

liver has large functional reserve –> can function if some hepatocytes are injured

26
Q

liver failure

A

clinical syndrome due to clinical signs that could be attributes to the loss of >75% of the liver’s functional mass

causes clinical presentation of liver dysfunction

27
Q

what is the primary waste product of the liver

A

bilirubin

28
Q

how is bilirubin metabolized

A

RBC death –> macrophage clean up –> unconjugated bilirubin binds to albumin to travel to liver –> hepatocytes conjugate bilirubin to become water soluble –> bilirubin gets excrete in urine or feces

29
Q

causes of hyperbilirubinemia

A
  1. prehepatic
  2. hepatic
  3. posthepatic
30
Q

signs of prehepatic hyperbilirubinemia

A

hemolysis:
- regenerative anemia
- normal plasma protein
- no evidence of cholestasis (ALP/GGT)

31
Q

signs of hepatic hyperbilirubinemia

A

decreased uptake, conjugation, or excretion:
- decreased functional liver mass
- functional cholestasis

functional cholestasis:
- pro-inflammatory cytokines
- inflammatory leukogram
- non-regenerative anemia
- mild/no increase in ALP/GGT

32
Q

signs of posthepatic hyperbilirubinemia

A

biliary system problems:
- marked increase in ALP/GGT
- mild hypercholesterolemia
- pancreatitis (inflammatory leukogram, increased PLI, non-septic exudate)

33
Q

how to test bile acids

A

bile acid stim test

1 sample fasting
1 sample 2 hr post prandial

should have low amount fasting and only slightly higher amount 2 hrs post prandial

34
Q

cause of increased bile acids

A
  1. decreased biliary excretion (cholestasis)
  2. decreased bile acid clearance (liver dysfunction)
35
Q

what cell is mainly responsible for detecting toxins in blood

A

Kupffer cells

36
Q

what is the main toxin that gets detoxified by hepatocytes

A

ammonia

37
Q

ammonia

A

major byproduct from protein catabolism

produced by GI microbiome

detoxified by hepatocytes to form urea & amino acids

38
Q

function of urea

A

helps the kidneys concentrate urine

39
Q

clinical signs of hyperammonemia

A

CNS toxicity –> hepatic encephalopathy

40
Q

causes of hyperammonemia

A
  1. decreased uptake due to abnormal portal blood flow
  2. decreased conversation to urea due to decreased hepatic mass
  3. increased production of ammonia from bacteria
41
Q

what 3 things does the liver synthesize (mainly)

A
  1. proteins (albumin + clotting factors)
  2. cholesterol (lipoprotein metabolism)
  3. glucose (glycogen storage and glucose production)
42
Q

CBC indicators of liver dysfunction

A
  1. anemia:
    - mild
    - normocytic/normochromic
    - poikilocytosis
  2. thrombocytopenia
    (from portal hypertension causing congestive splenomegaly –> platelet sequestration & decreased TPO production)
43
Q

coag panel indicators of liver dysfunction

A
  1. prolonged PT/PTT (dec. clotting factor production)
  2. increased D-dimers
  3. decreased fibrinogen (decreased synthesis or entering DIC)
  4. decreased antithrombin
44
Q

chemistry indicators of liver dysfunction

A
  1. increased liver enzymes (leakage and cholestatic)
  2. hyperglobulinemia (dec. clearance of GI antigens)
  3. hypoalbuminemia
45
Q

urinalysis indicators of liver dysfunction

A
  1. decreased USG (dec. urea –> less concentrated/hypotonic urine)
  2. ammonium biurate & bilirubin crystalluria
  3. bilirubinuria