biochemical testing for liver disease Flashcards

1
Q

globulins

A

total protein - albumin

all other plasma proteins, not all made by the liver

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2
Q

liver enzymes

A

alkaline phosphatase ALP
gamma glutamyl transferase GGT
alanine aminotransferase ALT
aspartate animotransferase AST

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3
Q

the amino transferases

A

ALT, AST

if increased, implies hepatitis

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4
Q

bilirubin is a breakdown product of

A

haem

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5
Q

albumin is synthesised by

A

the liver

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6
Q

low albumin implies

A

synthetic function of the liver inhibited

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7
Q

ALP and GGT imply

A

cholestasis

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8
Q

high bilirubin implies

A

cholestasis jaundice or increased red cell turnover

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9
Q

albumin may be decreased due to

A

failure of liver synthetic function but can also be decreased by inflammation or renal losses

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10
Q

high bilirubin

A

rises if the liver fails to excrete is, but can also be increased by haemolysis

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11
Q

ALT and AST are involved in

A

amino acid metabolism

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12
Q

high AST may imply

A

non-liver related pathology

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13
Q

isolates or predominant increase in AST may indicate

A

skeletal or cardiac macula origin

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14
Q

increased AST:ALT ratio seen in

A

alcoholic hepatitis, severe liver injury, cirrhosis secondary to chronic hepatitis C infection, non-liver disease include muscle

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15
Q

increased ALT and AST is seen in

A

viral, autoimmune, alcoholic and toxic hepatitis, and non-alcoholic fatty liver disease

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16
Q

liver fibrosis

A

assessment og the presence and degree to fibrosis can be useful in patients which chronic liver disease for prognosticating and planning specific therapies top prevent progression to cirrhosis
golda standard is liver biopsy

17
Q

non-invasive tests used in place of liver biopsy for fibrosis

A

elastography for ultrasound or MRI

serum fibrosis markers

18
Q

serum fibrosis markers

A

most are reported as scores derived from algorithms incorporating several markers

19
Q

liver fibrosis markers examples

A
  • hepascore
  • APRI score
  • FIB-4
20
Q

isolated raised GGT (without raised ALP)

A

recent excessive alcohol ingestion

21
Q

cholestasis

A

jaundice and pruritus
raised ALP and GGT
mild raised ALT and AST
raised bilirubin

22
Q

biliary tree obstruction induces synthesis and release of

A

ALP and GGT

23
Q

ALP can also come from

A

bone, placenta, and other sources

24
Q

GGT can be induced by

A

alcohol and other drug ingestion

25
Q

uncongugated bilirubin

A

not water soluble, so must circulate bound to plasma proteins such as albumin

26
Q

bilirubin is congugated in the

A

liver

makes it more water soluble and it is excreted into the small intestine via bile

27
Q

what happens to the congugated bilirubin

A

is uncongugated and converted into water soluble urobilinogen in the gut
can be reabsorbed
is ultimately excretes by the kidneys as urobilin

28
Q

bilirubin if there is an abstraction to bile flow

A

conjugated bilirubin spills into the circulation instead of being excreted into the gut

29
Q

conjugated hyper bilirubinaemia

A

conjugation occurs in the liver so this implies spillage of contents from the liver, ie. biliary obstruction or hepatocellular injury

  • cholestatic liver disease
30
Q

unconjugated hyperbilirubinaemia

A

implies either haemolysis, or a defect in hepatic conjugation (ie. some inborn errors of metabolism or liver failure)

  • haemolytic disease
  • congenital defects
  • liver failure
  • drugs
  • physiological jaundice in neonates
31
Q

cholestatic liver diseases

A
  • extrahepatic - mass eg. head of pancreas, gallstones
  • intrahepatic - primary biliary cholangitis, primary sclerosing cholangitis
  • drugs
  • congenital defects (failure to excrete into bile)
32
Q

why are liver enzymes normal in advanced liver disease

A

transaminases are no longer being produced in response to damage due to liver failure to produce them

33
Q

isolated high ALP indicates

A

malignancy of bone

cholestasis less likely if GGT is normal