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GI > LFTs > Flashcards

LFTs Flashcards

1
Q

what is jaundice

A

a clinical sign- first seen in sclera of

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2
Q

what is bilirubin a marker of

A

liver synthesis function

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3
Q

what are the liver function tests

A

bilirubin, albumin, prothrombin time, serum blood glucose

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4
Q

are ALT, ALP, GGT, AST liver function tests

A

no

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5
Q

what do ALP, ALT, AST and GGT show

A

liver damage

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6
Q

when is a rise in ALT significant

A

more than a 10 fold rise

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7
Q

when is a rise in ALP significant

A

more than a 3 fold rise

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8
Q

when is ALT raised

A

with hepatocellular injury

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9
Q

where is ALP and when is it raised

A

concentrated in the liver, bile ducts and bone. often raised in cholestasis

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10
Q

what test results show hepatocellular damage

A

more than 10x increase in ALT and less than 3x increase in ALP

raised AST

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11
Q

what test results show cholestasis

A

less than 10x increase in ALT and more than 3x increase in ALP

raised GGT

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12
Q

what is seen in a mixed pattern

A

all raised

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13
Q

what can a raised GGT mean

A

biliary epithelial damage and bile flow obstruction

can also be raised in response to alcohol and drugs

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14
Q

what does a raised ALP and GGT mean

A

cholestasis

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15
Q

what does a raised ALP and normal GGT

A

non hepatobiliary (e.g bone problem)

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16
Q

what is an isolated rise in bilirubin with no ALT or ALP increase suggestive

A

pre hepatic jaundice

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17
Q

what can cause isolated jaundice

A

gilberts syndrome, haemolysis

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18
Q

what are the livers main synthesis functions

A

conjugation and elimination of bilirubin,
synthesis of albumin,
synthesis of clotting factors, gluconeogenesis

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19
Q

what what type of jaundice is there normal coloured urine and normal stools

A

pre-hepatic (unconjugated bilirubin)

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20
Q

what what type of jaundice is there dark urine and normal stools

A

hepatic

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21
Q

what what type of jaundice is there dark urine and pale stools

A

obsructive

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22
Q

what is albumin

A

synthesised in the liver, helps to bind water, cations, fatty acids and bilirubin- maintains oncotic pressure

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23
Q

low albumin can mean

A

liver disease (cirrhosis), acute phase response to inflammation which lowers liver production, excessive loss of protein e.g nephrotic syndrome

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24
Q

what is pro thrombin time

A

measure of bloods coagulation tendency, specifically extrinsic pathway

25
Q

what can an increase PT mean

A

indicate liver disease in the absence of anticoagulants or vit K deficiency

26
Q

what test results are seen in acute hepatocellular damage

A

very increased ALT, normal/ raised ALP, normal/raised GGT, raised/very raised bilirubin

27
Q

what test results are seen in chronic hepatocellular damage

A

normal/ raised ALP, ALT, GGT, bilirubin

28
Q

what test results are seen in cholestasis

A

normal/ raised ALT, very raised ALP, GGT, bilirubin

29
Q

what are common causes of acute heatocellular damage

A

poisoning (paracetamol overdose). infection (hep A and B), liver ischaemia

30
Q

what are the common causes of chronic hepatocellular damage

A

alcoholic fatty liver disease, NAFLD, chronic infection (hep B or C), primary biliary cirrhosis

31
Q

what are the less common chronic hepatocellular injury

A

wilsons disease, alpha -1 - antitrysin deficiency, haemochromatosis (iron overload)

32
Q

what are the components of a lover screen

A

LFTs, coagulation screen, hepatitis serology (A/B/C), Epstein barr virus, cytomegalovirus, AMA, ASMA, ANA, p-ANCA, immunoglobulin, serum copper, ceruloplasmin, ferritin

33
Q

what is AMA

A

anti- mitochondrial antibody= seen in PBC (95%), autoimmunehepatitis (30%)

34
Q

what is ASMA

A

anti smooth muscle antigen= autoimmune hepaitits (70%) and PBC (50%)

35
Q

what is ANA

A

anti nuclear antibody= seen in SLE

36
Q

what is p-ANCA seen in

A

churg-struass syndrome, good pastures, UC, crohns, sclerosing cholangitis, autoimmune hep

37
Q

what is cholestasis

A

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

38
Q

what should you do in autoimmune hep

A

liver biopsy and ultrasound

39
Q

what is the treatment for autoimmune hep

A

prednisolone and azathioprine

40
Q

when is a mixed picture LFT seen

A

in ischaemia

41
Q

what drugs raised CCT

A

alcohol, rifampicin

42
Q

what do ALP, ALT and GGT not tell you about

A

the function of the liver- shows damage to the liver

43
Q

what are the serum transaminases

A

AST/ALT, alanine, asparate

44
Q

what is bilirubin transported bound to

A

albumin

45
Q

what happens to bilirubin in hepatocytes

A

undergoes conjugation

46
Q

what clotting factors does the liver synthesise

A

I, II, V, VII, IX, XII, XIII

47
Q

what is fibrinogen

A

clotting factor I

48
Q

what is prothrombin

A

II

49
Q

what does prothrombin time measure

A

time for conversion of prothrombin to thrombin- relfects synthetic function of the liver

50
Q

how does the liver affect vit k

A

decreased bile salts leads to impaired vit k absorption and deficiency

51
Q

what antibiotics can cause hepatitis

A

penicillins, beta lactams

52
Q

what can cause a increased PT time

A

prolonged jaundice, vit k malabsorption, hepatocellular dysfunction

53
Q

what tests are done for coealiac

A

tTG-IgA, HLA typing, biopsies gold standard, NAFLD +/- IDA

54
Q

what immune components indicate autoimmune hep

A

ASMA/ immunoglublins

55
Q

what suggests wilsons

A

caerulosplasmin

56
Q

what suggests haemochromatosis

A

ferritin/ staturation

57
Q

what is causes of unconjugated hyperbilirubinaemia and what are the underlying aetiologies

A

= 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)

58
Q

what does an conjugated hyperbilirubinaemia mean and what are the causes

A

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))

59
Q

what are the features of acute liver failure

A

encephalopathy, jaundice, reduced coagulability

GI (64 decks)

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