LFT / Jaundice / Gallstones Flashcards
ALT
AST
ALP
GGT
ALT: Alanine transaminase (3-40 iu/l) (skeletal muscle, cardiac, kidneys)
AST: asperate aminotransferase (3-30iu/l) also raises in liver damage but if ALT not raised, likely to be other cause. produced by liver, skeletal muscle, cardiac, brain, RBC. in alcoholic liver disease AST>ALT
ALP: alkaline phosphatase (30-100umol/l) (<120)
biliary epithelium, bone, 3rd-trimester placenta, intestine, kidney (raised in biliary obstruction)
GGT: gamma-glutamyl transferase (8-60u/l) (liver-specific not sensitive, lots of things make it raise even sneezing) *monitor in abstinence for alcohol
*can help distinguish between hepatocellular damage and cholestasis
Assessing liver funcion
Bilirubin (3-17 umol/l)
Albumin (35-50 g/l)
Prothrombin time (10-14 s/l)
Amylase- pancreas
Lipase- pancreas
ALT
A raised ALT indicated hepatocellular damage
>x10
ALT > AST chronic liver disease
AST > ALT cirrhosis and acute alcohol hepatitis
ALP
ALP is concentrated in the liver, bile duct and bone tissue
Raises if there is obstruction/cholestasis
>x3
enzyme that hydrolyses phosphotaseester
*isolated raised ALP boney metastases/sarcoma vitamin d deficiency recent bone fracture renal osteodysotrophy
GGT
Gamma Glutamyl Transferase
If there is a raise in the ALP, check the GGT
raised GGT:
bile flow obstruction
biliary epithelial damage
alcohol and drugs (phentoin)
if ALP is raised but GGT normal= bone
if ALP raised, GGT raised= cholestasis
jaundice in
- pre hepatic
- hepatic
- post hepatic
pre hepatic: normal urine and normal stools (unconjugated bilirubin
hepatic: dark urine, normal stools
post hepatic: dark urine and pale stools because the bile and pancreatic lipase cannot reach the bowel - poor absorption (pale bulky stools)
albumin
synthesised in the liver
helps bind to water
oncotic pressure
- cirrhosis= decrease in the production of albumin (ascites)
- inflammation: in high temperature, there is a decrease in the production of albumin
- loss of albumin in nephrotic syndrome
acute hepatocellular damage
- poisoning (paracetamol OD)
- infection (hepatits a/b)
- liver ischaemia
ALT very raised
ALP, GGT, bilirubin high
DILI: drug-induced liver injury
commonly- flucloxacillin, co amoxiclav
differentials if all LFT raised:
congestive heart failure obstructive jaundice pre hepatic obstruction cholangiocarcinoma head of pancreas tumor pancreatitis
interpreting LFT’s
- ALT and ALP
(ALT >AST chronic liver disease)
AST> ALT cirrhosis / acute alcohol hepatitis
AST > ALP hepatitis
ALP > AST cholestatic
high amylase- pancreas
AST normal ALT unlikely to be due to liver. - GGT
if there is a raise in ALP, chek GGT. bile flow obstruction
high ALP, high GGT= cholestasis
high ALP, normal GGT= boney metastases.
bilirubin
RBC live for 120 days
then phagocytosed by macrophages into heme and globin
globin= amino acids
heme- protophoryn
protophoryn ic converted to unconjugated bilrubin
taken to liver = conjugated by UDP. water soluable, stored in bile duct
formation: haem (RBC)
metabolism: unconjugated binds to albumin. hepatocytes conjugated bilirubin (UDP glucosyl transferase enzyme)
conjugated is transferred to bile canaliculi
in the colon - bacteria degrades conjugated bilirubin to urobilinogen and stercobilinogen
pre haptic jaundice
increased load of bilirubin
causes:
haemolysis, malaria, haemoltyic anaemia, septicaemia
Gilbert syndrome (low UGT)
Crigler Najjar (no UGT)
Dubin Johnson (deficiency in the protein which moves CB from liver to bile)
physiological jaundice of the newborn
signs:
normal urine and normal stools (unconjugated bilirubin)
if bilirubin >2.5mg/dl yellow sin
hepatic jaundice
hepatocellular jaundice (raised ALT, ALP, AST)
drugs, alcohol, viral hepatitis, autoimmune, metabolic, hereditary, viral hepatitis
high UCB and CB
signs: dark urine (CB) normal stools
viral hepatitis
autoimmune hepatitis
drugs/toxins (paracetemol OD)
alcohol
rarer- metabolic disorders hereditary haemochromatosis Wilson's disease alpha 1 antitrpsyin deficiency primary hepatoma
post hepatic jaundice
cannot excrete (conjugated) bilirubin due to an obstruction e..g gall stones, pancreatic carcinoma
bile (conjugated bilirubin) builds up, leaks between hepatocytes in the blood vessels.
obstructive- high ALP, high GGT
- extra hepatic
mechanical obstrction (gallstones)
malignancy
pancreatitis (acute/chronic)
2. intrahepatic primary biliary cirrhosis primary sclerosing cholangitis sarcoidosis pregnancy drugs/alcohol dubin johnson syndrome rotor syndrome
signs:
pale stools, dark urine (bile flow is obstructed)
pruritis (bile salts)
haemolytic jaundice
jaundice, anaemia
raised UCB
low hb, low haptoglobin, raised reticulocyte in haemolytic jaundice
ALT, ALP, GGT normal
*a type of prehepatic jaundice
