Evaluating Liver Enzymes & Function Flashcards

(45 cards)

1
Q

isoenzymes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

isoforms

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

stability

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

half life

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what units are used when evaluating liver enzymes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

are values lower than reference interval clinically significant for liver enzymes

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what type of sample is used for evaluating liver enzymes

A

serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what factors interfere with liver enzymes

A

color (hemolysis, lipemia, icterus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

alanine transferase (ALT)

A

cytoplasmic enzyme (mild cell injury)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

sorbitol dehydrogenase (SDH)

A

cytoplasmic enzyme (mild cell injury)

used for large animals w/ high specificity for liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lactate dehydrogenase

A

cytoplasmic enzyme (mild cell injury)

rarely used - low specificity for liver injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

glutamate dehydrogenase (GLDH)

A

mitochondrial & cytoplasmic enzyme (severe cell injury)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

alkaline phosphatase (ALP)

A

membrane bound inducible enzyme (increased induction of enzyme synthesis)

2 isoenzymes w/ 5 isoforms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

enzymes that indicate cell injury

A

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

20
Q

enzymes that indicate increased induction

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
liver injury vs liver dysfunction
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
liver failure
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
what is the primary waste product of the liver
bilirubin
28
how is bilirubin metabolized
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
causes of hyperbilirubinemia
1. prehepatic 2. hepatic 3. posthepatic
30
signs of prehepatic hyperbilirubinemia
hemolysis: - regenerative anemia - normal plasma protein - no evidence of cholestasis (ALP/GGT)
31
signs of hepatic hyperbilirubinemia
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
signs of posthepatic hyperbilirubinemia
biliary system problems: - marked increase in ALP/GGT - mild hypercholesterolemia - pancreatitis (inflammatory leukogram, increased PLI, non-septic exudate)
33
how to test bile acids
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
cause of increased bile acids
1. decreased biliary excretion (cholestasis) 2. decreased bile acid clearance (liver dysfunction)
35
what cell is mainly responsible for detecting toxins in blood
Kupffer cells
36
what is the main toxin that gets detoxified by hepatocytes
ammonia
37
ammonia
major byproduct from protein catabolism produced by GI microbiome detoxified by hepatocytes to form urea & amino acids
38
function of urea
helps the kidneys concentrate urine
39
clinical signs of hyperammonemia
CNS toxicity --> hepatic encephalopathy
40
causes of hyperammonemia
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
what 3 things does the liver synthesize (mainly)
1. proteins (albumin + clotting factors) 2. cholesterol (lipoprotein metabolism) 3. glucose (glycogen storage and glucose production)
42
CBC indicators of liver dysfunction
1. anemia: - mild - normocytic/normochromic - poikilocytosis 2. thrombocytopenia (from portal hypertension causing congestive splenomegaly --> platelet sequestration & decreased TPO production)
43
coag panel indicators of liver dysfunction
1. prolonged PT/PTT (dec. clotting factor production) 2. increased D-dimers 3. decreased fibrinogen (decreased synthesis or entering DIC) 4. decreased antithrombin
44
chemistry indicators of liver dysfunction
1. increased liver enzymes (leakage and cholestatic) 2. hyperglobulinemia (dec. clearance of GI antigens) 3. hypoalbuminemia
45
urinalysis indicators of liver dysfunction
1. decreased USG (dec. urea --> less concentrated/hypotonic urine) 2. ammonium biurate & bilirubin crystalluria 3. bilirubinuria