LFTs Flashcards
what is jaundice
a clinical sign- first seen in sclera of
what is bilirubin a marker of
liver synthesis function
what are the liver function tests
bilirubin, albumin, prothrombin time, serum blood glucose
are ALT, ALP, GGT, AST liver function tests
no
what do ALP, ALT, AST and GGT show
liver damage
when is a rise in ALT significant
more than a 10 fold rise
when is a rise in ALP significant
more than a 3 fold rise
when is ALT raised
with hepatocellular injury
where is ALP and when is it raised
concentrated in the liver, bile ducts and bone. often raised in cholestasis
what test results show hepatocellular damage
more than 10x increase in ALT and less than 3x increase in ALP
raised AST
what test results show cholestasis
less than 10x increase in ALT and more than 3x increase in ALP
raised GGT
what is seen in a mixed pattern
all raised
what can a raised GGT mean
biliary epithelial damage and bile flow obstruction
can also be raised in response to alcohol and drugs
what does a raised ALP and GGT mean
cholestasis
what does a raised ALP and normal GGT
non hepatobiliary (e.g bone problem)
what is an isolated rise in bilirubin with no ALT or ALP increase suggestive
pre hepatic jaundice
what can cause isolated jaundice
gilberts syndrome, haemolysis
what are the livers main synthesis functions
conjugation and elimination of bilirubin,
synthesis of albumin,
synthesis of clotting factors, gluconeogenesis
what what type of jaundice is there normal coloured urine and normal stools
pre-hepatic (unconjugated bilirubin)
what what type of jaundice is there dark urine and normal stools
hepatic
what what type of jaundice is there dark urine and pale stools
obsructive
what is albumin
synthesised in the liver, helps to bind water, cations, fatty acids and bilirubin- maintains oncotic pressure
low albumin can mean
liver disease (cirrhosis), acute phase response to inflammation which lowers liver production, excessive loss of protein e.g nephrotic syndrome
what is pro thrombin time
measure of bloods coagulation tendency, specifically extrinsic pathway
what can an increase PT mean
indicate liver disease in the absence of anticoagulants or vit K deficiency
what test results are seen in acute hepatocellular damage
very increased ALT, normal/ raised ALP, normal/raised GGT, raised/very raised bilirubin
what test results are seen in chronic hepatocellular damage
normal/ raised ALP, ALT, GGT, bilirubin
what test results are seen in cholestasis
normal/ raised ALT, very raised ALP, GGT, bilirubin
what are common causes of acute heatocellular damage
poisoning (paracetamol overdose). infection (hep A and B), liver ischaemia
what are the common causes of chronic hepatocellular damage
alcoholic fatty liver disease, NAFLD, chronic infection (hep B or C), primary biliary cirrhosis
what are the less common chronic hepatocellular injury
wilsons disease, alpha -1 - antitrysin deficiency, haemochromatosis (iron overload)
what are the components of a lover screen
LFTs, coagulation screen, hepatitis serology (A/B/C), Epstein barr virus, cytomegalovirus, AMA, ASMA, ANA, p-ANCA, immunoglobulin, serum copper, ceruloplasmin, ferritin
what is AMA
anti- mitochondrial antibody= seen in PBC (95%), autoimmunehepatitis (30%)
what is ASMA
anti smooth muscle antigen= autoimmune hepaitits (70%) and PBC (50%)
what is ANA
anti nuclear antibody= seen in SLE
what is p-ANCA seen in
churg-struass syndrome, good pastures, UC, crohns, sclerosing cholangitis, autoimmune hep
what is cholestasis
a decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts. Blockage of biliary system causing jaundice and increase in ALP and GGT
what should you do in autoimmune hep
liver biopsy and ultrasound
what is the treatment for autoimmune hep
prednisolone and azathioprine
when is a mixed picture LFT seen
in ischaemia
what drugs raised CCT
alcohol, rifampicin
what do ALP, ALT and GGT not tell you about
the function of the liver- shows damage to the liver
what are the serum transaminases
AST/ALT, alanine, asparate
what is bilirubin transported bound to
albumin
what happens to bilirubin in hepatocytes
undergoes conjugation
what clotting factors does the liver synthesise
I, II, V, VII, IX, XII, XIII
what is fibrinogen
clotting factor I
what is prothrombin
II
what does prothrombin time measure
time for conversion of prothrombin to thrombin- relfects synthetic function of the liver
how does the liver affect vit k
decreased bile salts leads to impaired vit k absorption and deficiency
what antibiotics can cause hepatitis
penicillins, beta lactams
what can cause a increased PT time
prolonged jaundice, vit k malabsorption, hepatocellular dysfunction
what tests are done for coealiac
tTG-IgA, HLA typing, biopsies gold standard, NAFLD +/- IDA
what immune components indicate autoimmune hep
ASMA/ immunoglublins
what suggests wilsons
caerulosplasmin
what suggests haemochromatosis
ferritin/ staturation
what is causes of unconjugated hyperbilirubinaemia and what are the underlying aetiologies
= increased production, extra/intravascular haemolysis, impaired uptake (heart failure, portosystemic shunts, drugs; rifampicin, probenecid), impaired conjugation (congenital- gilberts/ CN type II)(hyperthyroidism)(advanced liver disease)
what does an conjugated hyperbilirubinaemia mean and what are the causes
extrahepatic cholestasis (biliary obstruction; cholelithiasis, PSC, cholangiocarcinoma, HoP mass, acute/ chronic pancreasitis), intrahepatic cholestasis (sepsis, hypoperfusion states, cirrhosis, infiltrative diseases, TPN (total parentral nutrition), acute hepatitis, drugs (steroids, herbs, rifampicin))
what are the features of acute liver failure
encephalopathy, jaundice, reduced coagulability
