LFTs

Question 1

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

Answer 1

haem from Hb

Question 2

what does haem convert to

Answer 2

biliverdin (then converted to unconjugated and conjugated bilirubin)

Question 3

what is excreted in the bile (to the intestine)

Answer 3

bilirubin glucuronide

Question 4

what is bilirubin glucuronide converted to by what

Answer 4

bilirubin in the intestine by B glucuronidase

Question 5

what is bilirubin converted to in the intestine

Answer 5

urobilinogen

Question 6

what happens to the urobilinogen

Answer 6

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

Question 7

what happens to some of the reabsorbed urobilinogen

Answer 7

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

Question 8

what is total bilirubin

Answer 8

conjugated and unconjugated bilirubin

Question 9

what is direct bilirubin

Answer 9

conjugated only

Question 10

what is indirect bilirubin

Answer 10

unconjugated. calculated by the total- direct.

Question 11

what does raised ALT (alanine transaminase) show

Answer 11

hepatocellular damage (more specific than AST).

Question 12

where is ALT found

Answer 12

hepatocytes and small amount in the muscle

Question 13

what does raised AST (aspartate transamine) show

Answer 13

hepatocellular damage (less specific than ALT)

Question 14

where is AST found

Answer 14

hepatocytes, muscle and erythrocytes

Question 15

what does raised ALP (alkaline phosphatase) show

Answer 15

cholestasis

Question 16

where is ALP found

Answer 16

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

Question 17

what does GGT co localise with

Answer 17

ALP

Question 18

what can cause a rise in GGT

Answer 18

drug induced, including alcohol

Question 19

what is albumin

Answer 19

the main plasma protein produced by the liver

Question 20

is albumin a good indicator of function

Answer 20

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

Question 21

what is the best measure of function

Answer 21

prothrombin time

Question 22

what is prothrombin time dependent on

Answer 22

vitamin K dependent coagulation factors.

Question 23

why is PT a good indicator

Answer 23

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

Question 24

what are the LFTs in cholestasis

Answer 24

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

Question 25

what are the LFTs in hepatocellular damage

Answer 25

ALT >> ALP. bilirubin may or may not be elevated

Question 26

what can cholestatic causes of liver disease be split into

Answer 26

intra and extra hepatic

Question 27

examples of extra hepatic biliary obstruction

Answer 27

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

Question 28

examples of intra hepatic biliary obstruction

Answer 28

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

Question 29

causes of hepatocellular damage

Answer 29

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

Question 30

what test do you need to do if you suspect haemachromatosis

Answer 30

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

Question 31

what liver autoantibody is tested if suspecting primary biliary cirrhosis

Answer 31

AMA (anti mitochondrial antibody)

Question 32

what liver autoantibody is tested if suspecting primary sclerosing cholangitis

Answer 32

ANCA

Question 33

what liver autoantibody is tested if suspecting chronic active hepatitis

Answer 33

anti smooth muscle antibody

Question 34

what liver autoantibody is tested if suspecting autoimmune hep

Answer 34

ANF and anti kidney microsomal antibody

Question 35

what test should be done if suspect Wilsons

Answer 35

serum copper/caeroloplasmin - both raised.

Question 36

what is Wilsons

Answer 36

inherited defect in copper metabolism

Question 37

evaluating consequences of liver disease- total protein and globulins

Answer 37

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

Question 38

evaluating consequences of liver disease- platelets

Answer 38

low which shows portal hypertension

Question 39

evaluating consequences of liver disease- glucose

Answer 39

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

Question 40

evaluating consequences of liver disease- lipids

Answer 40

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

Question 41

evaluating consequences of liver disease- urea

Answer 41

may be low in chronic liver disease

Question 42

where is the main site of urea production

Answer 42

LIVER

Question 43

evaluating consequences of liver disease- ammonia

Answer 43

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

Question 44

what are the principal signs of obstructive jaundice

Answer 44

pale stool, dark urine

Question 45

why is the stool pale (obstructive)

Answer 45

stercobilin not formed as bilirubin cant reach GIT

Question 46

why is the urine dark (obstructive)

Answer 46

as conjugated bilirubin is excreted in the urine

Question 47

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

Answer 47

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

Question 48

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

Answer 48

unconjugated form

Question 49

how is unconjugated bilirubin transported

Answer 49

bound to albumin but not covalently bound

Question 50

what can cause an isolated increase in serum bilirubin

Answer 50

defect in conjugation of bilirubin, or haemolysis

Question 51

what is the most common cause of hyperbilirubinaemia

Answer 51

Gilberts

Question 52

what is Gilberts syndrome

Answer 52

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

Question 53

what does the LFT show in acute hep

Answer 53

very high ALT and bilirubin

Question 54

which product of haem breakdown enters the enterohepatic circulation

Answer 54

urobilinogen