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15 Cards in this Set
- Front
- Back
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Hepatocellular indicators primary and secondary |
Primary- AST Secondary- SDH |
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Hepatobilliary indicator |
GGT |
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Functional tests primary |
Bilirubin and BUN |
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Functional tests secondary |
Bile acids, ammonia, TGL, coag factors (fibrinogen) |
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AST- hepatocellular and muscle leakage enzyme. How long will it be elevated? |
>2weeks Muscle damage shows increased CK for up to 2 days |
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SDH is elevated in increases hepatocellular injury for how long? |
3-5 days |
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What causes induction and elevation of serum GGT from the biliary epithelium? |
Cholestasis - hepatic necrosis, Viral insult, right dorsal colon displacement |
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What are the 3 groups of tests of hepatic function |
Bilirubin (direct vs indirect) Amino acid metabolism (ammonia and BUN) Protein synthesis (albumin, globulin, fibrinogen) |
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How much conjugated/direct bilirubin is abnormal? |
>30% of total |
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Amino acid metabolism- with reduce hepatic function what happens to ammonia and BUN? |
Increased ammonia (test rapidly, sample on ice) Decreased BUN (ammonia not converted to urea) |
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Protein synthesis: with reduced function- when is there a decrease in albumin? |
When there has been 80% functional loss for >3 weeks |
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Why does globulin increase then decrease with worsening hepatopathy? |
Reduced kupffer cell function > more foreign antigen. With advanced loss of function globulin production is diminished. |
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What amount of coagulation factor loss in the blood occurs before a change in clotting time is seen? |
50-70%. Decreased fibrinogen is consistent with loss of function. |
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Bile acids increase with liver damage as they’re not removed from the blood. How long does this take? |
Within 24-48h liver damage- very elevated with biliary obstruction. Not affected by fasting/eating. |
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Why are triglycerides elevated? |
Reduced uptake and clearance Impaired energy generation > mobilisation of adipose tissue |
