Interpreting liver chemistries Flashcards

1
Q

Liver chemistry abnormalities indicating hepatocellular damage

A

AST and ALT

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2
Q

Liver chemistry abnormalities indicating cholestasis, impaired conjugation or biliary obstruction

A

bilirubin

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3
Q

liver chemistry abnormalities indicating cholestasis, infiltrative disease, or biliary obstruction

A

alkaline phosphatase

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4
Q

liver chemistry abnormalities indicating synthetic dysfunction

A

albumin, prothrombin time

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5
Q

What does PT (prothrombin time) assess?

A

extrinsic clotting pathway

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6
Q

prolonged PT

A

significant hepatocellular dysfunction, vitamin K deficiency

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7
Q

role of AST/ALT aminotransferases

A

catalyze transfer of amino acid groups to form hepatic metabolites

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8
Q

organs expressing AST

A

liver, heart, muscle, blood

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9
Q

organs expressing ALT

A

liver only

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10
Q

AST:ALT ratio > 2

A

suggests alcoholic liver disease.

preferential alcohol-induced injury to mitochondria enriched in AST

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11
Q

Causes of severe ( > 15x normal) AST and ALT elevations

A

acute viral hepatitis, meds/toxins, ischemic hepatitis, autoimmune hepatitis, Wilson’s disease, acute Budd-Chiari syndrome, thrombosis

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12
Q

alkaline phosphatase role

A

hydrolase –> removes phosphate groups from nucleotides, proteins and alkaloids

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13
Q

causes of alk phos elevation

A

cholestatic/infiltrative diseases of liver, obstruction of biliary system, bone disease, pregnancy, chronic renal failure

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14
Q

What lab is used to differentiate hepatobiliary vs nonhepatobiliary etiology for rise in alk phos?

A

5’ nucleotidase and

GGT: not present in bone. elevated in alcohol consumption and almost all types of liver disease

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15
Q

infiltrating liver diseases –> high alk phos

A

sarcoidosis, tuberculosis, fungal infection, amyloid, lymphoma, metastasis, HCC

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16
Q

process of bilirubin conjugation

A

unconjugated bilirubin in the sinusoids –> uptake to hepatocytes via oatp –> conjugation –> ATP pump of conjugated bilirubin into bile canaliculus

17
Q

mechanism of hemolytic jaundice

A

high levels of unconjugated bilirubin in the blood –> overwhelmed oatp –> unconjugated bilirubin cannot be completely taken up by hepatocytes –> rise in indirect bilirubin levels

18
Q

mechanism of biliary obstruction jaundice

A

conjugated bilirubin cannot exit canaliculus/duct –> shunt to blood –> rise in serum direct bilirubin levels

19
Q

Gilbert’s disease

A

stress-related hyperbilirubinemia (rise in indirect bilirubin)

20
Q

Crigler-Najjar syndrome

A

Autosomal recessive

Type 1 = absence of UDP-GT –> severe jaundice, neuro impairment

21
Q

Dubin-Johnson syndrome

A

defective secretion of conjugated bilirubin (mutated MRP2 in ATP binding region) –> elevated conjugated bilirubin

benign

22
Q

mechanism of bilirubin elevation in cirrhosis

A

increased fibrosis –> decreased unconjugated bilirubin into the hepatocytes –> rise in indirect bilirubin

increased hemolysis in severe liver disease