LFTs Flashcards

(59 cards)

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
what can an increase PT mean
indicate liver disease in the absence of anticoagulants or vit K deficiency
26
what test results are seen in acute hepatocellular damage
very increased ALT, normal/ raised ALP, normal/raised GGT, raised/very raised bilirubin
27
what test results are seen in chronic hepatocellular damage
normal/ raised ALP, ALT, GGT, bilirubin
28
what test results are seen in cholestasis
normal/ raised ALT, very raised ALP, GGT, bilirubin
29
what are common causes of acute heatocellular damage
poisoning (paracetamol overdose). infection (hep A and B), liver ischaemia
30
what are the common causes of chronic hepatocellular damage
alcoholic fatty liver disease, NAFLD, chronic infection (hep B or C), primary biliary cirrhosis
31
what are the less common chronic hepatocellular injury
wilsons disease, alpha -1 - antitrysin deficiency, haemochromatosis (iron overload)
32
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
33
what is AMA
anti- mitochondrial antibody= seen in PBC (95%), autoimmunehepatitis (30%)
34
what is ASMA
anti smooth muscle antigen= autoimmune hepaitits (70%) and PBC (50%)
35
what is ANA
anti nuclear antibody= seen in SLE
36
what is p-ANCA seen in
churg-struass syndrome, good pastures, UC, crohns, sclerosing cholangitis, autoimmune hep
37
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
38
what should you do in autoimmune hep
liver biopsy and ultrasound
39
what is the treatment for autoimmune hep
prednisolone and azathioprine
40
when is a mixed picture LFT seen
in ischaemia
41
what drugs raised CCT
alcohol, rifampicin
42
what do ALP, ALT and GGT not tell you about
the function of the liver- shows damage to the liver
43
what are the serum transaminases
AST/ALT, alanine, asparate
44
what is bilirubin transported bound to
albumin
45
what happens to bilirubin in hepatocytes
undergoes conjugation
46
what clotting factors does the liver synthesise
I, II, V, VII, IX, XII, XIII
47
what is fibrinogen
clotting factor I
48
what is prothrombin
II
49
what does prothrombin time measure
time for conversion of prothrombin to thrombin- relfects synthetic function of the liver
50
how does the liver affect vit k
decreased bile salts leads to impaired vit k absorption and deficiency
51
what antibiotics can cause hepatitis
penicillins, beta lactams
52
what can cause a increased PT time
prolonged jaundice, vit k malabsorption, hepatocellular dysfunction
53
what tests are done for coealiac
tTG-IgA, HLA typing, biopsies gold standard, NAFLD +/- IDA
54
what immune components indicate autoimmune hep
ASMA/ immunoglublins
55
what suggests wilsons
caerulosplasmin
56
what suggests haemochromatosis
ferritin/ staturation
57
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)
58
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))
59
what are the features of acute liver failure
encephalopathy, jaundice, reduced coagulability