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Alimentary > LFTs > Flashcards

LFTs Flashcards

1
Q

what is bilirubin derived from and what is the source of this

A

haem from Hb

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2
Q

what does haem convert to

A

biliverdin (then converted to unconjugated and conjugated bilirubin)

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3
Q

what is excreted in the bile (to the intestine)

A

bilirubin glucuronide

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4
Q

what is bilirubin glucuronide converted to by what

A

bilirubin in the intestine by B glucuronidase

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5
Q

what is bilirubin converted to in the intestine

A

urobilinogen

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6
Q

what happens to the urobilinogen

A

some is reabsorbed back into the circulation other is metabolised further to urobilinogen stercobin

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7
Q

what happens to some of the reabsorbed urobilinogen

A

some is excreted back into the bile, the rest in the urine

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8
Q

what is total bilirubin

A

conjugated and unconjugated bilirubin

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9
Q

what is direct bilirubin

A

conjugated only

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10
Q

what is indirect bilirubin

A

unconjugated. calculated by the total- direct.

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11
Q

what does raised ALT (alanine transaminase) show

A

hepatocellular damage (more specific than AST).

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12
Q

where is ALT found

A

hepatocytes and small amount in the muscle

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13
Q

what does raised AST (aspartate transamine) show

A

hepatocellular damage (less specific than ALT)

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14
Q

where is AST found

A

hepatocytes, muscle and erythrocytes

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15
Q

what does raised ALP (alkaline phosphatase) show

A

cholestasis

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16
Q

where is ALP found

A

biliary canalicular membrane of hepatocytes and biliary epithelium. also placenta, bone and intestine

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17
Q

what does GGT co localise with

A

ALP

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18
Q

what can cause a rise in GGT

A

drug induced, including alcohol

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19
Q

what is albumin

A

the main plasma protein produced by the liver

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20
Q

is albumin a good indicator of function

A

no as the liver has good synthetic function and the half life is only 20 days so would have to have a prolonged duration of injury. also negative acute phase reactant so decreases in inflammation

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21
Q

what is the best measure of function

A

prothrombin time

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22
Q

what is prothrombin time dependent on

A

vitamin K dependent coagulation factors.

23
Q

why is PT a good indicator

A

eg VII half life is 6 hours so if it is decreased and prolonged PT shows liver injury quickly

24
Q

what are the LFTs in cholestasis

A

ALP&raquo_space; ALT. bilirubin may or may not be elevated

25
Q

what are the LFTs in hepatocellular damage

A

ALT&raquo_space; ALP. bilirubin may or may not be elevated

26
Q

what can cholestatic causes of liver disease be split into

A

intra and extra hepatic

27
Q

examples of extra hepatic biliary obstruction

A

gallstones, carcinoma of head of pancreas, cholangiocarcinoma, stricture of the bile duct

28
Q

examples of intra hepatic biliary obstruction

A

cirrhosis, primary biliary cirrhosis, malignant liver disease, sepsis, drugs, primary sclerosing cholangitis

29
Q

causes of hepatocellular damage

A

infectious hepatitis (hep A,B,C,E,EBV; bacterial and protozoa); drugs/toxins (alcohol, paracetemol, statins, antibiotics); metabolic (fatty liver disease, haemachromatosis); autoimmune hep and ischaemia/infarction

30
Q

what test do you need to do if you suspect haemachromatosis

A

ferritin- do alongside CRP as ferritin is an acute phase reactant

31
Q

what liver autoantibody is tested if suspecting primary biliary cirrhosis

A

AMA (anti mitochondrial antibody)

32
Q

what liver autoantibody is tested if suspecting primary sclerosing cholangitis

A

ANCA

33
Q

what liver autoantibody is tested if suspecting chronic active hepatitis

A

anti smooth muscle antibody

34
Q

what liver autoantibody is tested if suspecting autoimmune hep

A

ANF and anti kidney microsomal antibody

35
Q

what test should be done if suspect Wilsons

A

serum copper/caeroloplasmin - both raised.

36
Q

what is Wilsons

A

inherited defect in copper metabolism

37
Q

evaluating consequences of liver disease- total protein and globulins

A

globulins can be high in inflame liver disease also high in inflam conditions, myeloma

38
Q

evaluating consequences of liver disease- platelets

A

low which shows portal hypertension

39
Q

evaluating consequences of liver disease- glucose

A

prone to hypoglycaemia because impaired function of liver- glycogenolysis and gluconeogenesis

40
Q

evaluating consequences of liver disease- lipids

A

increase cholesterol in cholestatic liver disease, increased triglycerides in fatty liver

41
Q

evaluating consequences of liver disease- urea

A

may be low in chronic liver disease

42
Q

where is the main site of urea production

A

LIVER

43
Q

evaluating consequences of liver disease- ammonia

A

may be high in liver disease and decompensated cirrhosis due to shunting of portal blood

44
Q

what are the principal signs of obstructive jaundice

A

pale stool, dark urine

45
Q

why is the stool pale (obstructive)

A

stercobilin not formed as bilirubin cant reach GIT

46
Q

why is the urine dark (obstructive)

A

as conjugated bilirubin is excreted in the urine

47
Q

urobilinogen would be negative on a urine dipstick why (obstructive jaund)

A

because it is only formed in the GIT so in obstructive jaundice it is not reaching GIT

48
Q

if bilirubin is not present in the urine what form will it be in

A

unconjugated form

49
Q

how is unconjugated bilirubin transported

A

bound to albumin but not covalently bound

50
Q

what can cause an isolated increase in serum bilirubin

A

defect in conjugation of bilirubin, or haemolysis

51
Q

what is the most common cause of hyperbilirubinaemia

A

Gilberts

52
Q

what is Gilberts syndrome

A

deficiency of UDP glucuronyl transferase which is needed for the conjugation of bilirubin thus leading to an unconjugated hyperbilirubinaemia. the same deficiency is seen in Criggler-Najjar syndrome which presents in infants and young children but it is more severe here

53
Q

what does the LFT show in acute hep

A

very high ALT and bilirubin

54
Q

which product of haem breakdown enters the enterohepatic circulation

A

urobilinogen

Alimentary (17 decks)

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