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LFTs Flashcards

1
Q

why are LFTs ordered?

A
  1. to confirm clinical suspicion of potential liver injury or disease
  2. to distinguish between hepatocellular injury (hepatic jandice) and cholestasis (post-hepatic or obstructive jaundice)
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2
Q

what blood tests are used to assess liver function?

A 
alanine transaminase (ALT)
aspartate aminotransferase (AST)
alkaline phosphatase (ALP)
gamma-glutamyltransferase (GGT) 
bilirubin 
albumin 
prothrombin time (PT)
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3
Q

what is used to distinguish between hepatocellular damage and cholestasis?

A

ALT
AST
ALP
GGT

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4
Q

what is used to assess the liver’s synthetic function?

A

bilirubin
albumin
PT

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5
Q

ALT

A

3-40 iu/l

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6
Q

AST

A

3-30 iu/l

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7
Q

ALP

A

30-100 umol/l

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8
Q

GGT

A

8-60 u/l

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9
Q

bilirubin

A

3-17 umol/l

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10
Q

albumin

A

35-50 g/l

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11
Q

PT

A

10-14 s/1

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12
Q

assessing ALT and ALP

A

If the ALT is raised, decide if this is a more than a 10-fold rise (↑↑) or a less than a 10-fold rise (↑)
If the ALP is raised, decide if this is a more than a 3-fold rise (↑↑) or a less than a 3-fold rise (↑)

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13
Q

where is ALT found in high concs?

A

within hepatocytes and enters the blood following heptocellular injury

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14
Q

where is ALP concentrated?

A

in the liver, bile duct and bone tissues

often raised in liver pathology due to increased synthesis in response to cholestasis

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15
Q

A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP

A

suggests a predominantly hepatocellular injury

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16
Q

A less than 10-fold increase in ALT and a more than 3-fold increase in ALP

A

suggests cholestasis

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17
Q

is it possible to have a mixed picture involving hepatocellular injury and cholestasis?

A

yes

18
Q

raised GGT

A

suggestive of biliary epithelial damage and bile flow obstruction
can also be raised in response to alcohol and drugs such as phenytoin

19
Q

markedly raised ALP with a raised GGT

A

highly suggestive of cholestasis

20
Q

A raised ALP in the absence of a raised GGT

A

should raise your suspicion of non-hepatobiliary pathology

21
Q

causes of isolated rise in ALP

A

Bony metastases / primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy

22
Q

isolated rise in bilirubin

A

suggestive of a pre-hepatic cause of jaundice

23
Q

Causes of isolated jaundice

A

Gilbert’s syndrome (most common cause)

Haemolysis (check blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm)

24
Q

the livers main synthetic functions

A

Conjugation and elimination of bilirubin
Synthesis of albumin
Synthesis of clotting factors
Gluconeogenesis

25
Q

Normal urine + normal stools

A

pre-hepatic cause of jaundice

26
Q

Dark urine + normal stools

A

hepatic cause of jaundice

27
Q

Dark urine + pale stools

A

post-hepatic cause (obstructive) of jaundice

28
Q

causes of unconjugated hyperbilirubinaemia

A

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (drugs, congestive cardiac failure)
Impaired conjugation (Gilbert’s syndrome)

29
Q

Causes of conjugated hyperbilirubinaemia

A

Hepatocellular injury

Cholestasis

30
Q

fall in albumin levels

A

Liver disease resulting in a decreased production of albumin (e.g. cirrhosis)
Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin
Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome

31
Q

albumin

A

synthesised in the liver and helps to bind water, cations, fatty acids and bilirubin
plays a key role in maintaining the oncotic pressure of blood

32
Q

PT

A

a measure of the blood’s coagulation tendency, specifically assessing the extrinsic pathway

33
Q

increased PT

A

can indicate liver disease and dysfunction

34
Q

ALT > AST

A

chronic liver disease

35
Q

AST > ALT

A

cirrhosis and acute alcoholic hepatitis

36
Q

acute hepatocellular damage

A

ALT ^^
ASP normal or ^
GGT normal or ^
bilirubin ^ or ^^

37
Q

chronic hepatocellolar damage

A

ALT normal or ^
ASP normal or ^
GGT normal or ^
bilirubin normal or ^

38
Q

cholestasis

A

ALT normal or ^
ASP ^^
GGT ^^
bilirubin ^^

39
Q

common causes of acute hepatocellular injury

A

Poisoning (paracetamol overdose)
Infection (Hepatitis A and B)
Liver ischaemia

40
Q

common causes of chronic hepatocellular injury

A

Alcoholic fatty liver disease
Non-alcoholic fatty liver disease
Chronic infection (Hepatitis B or C)
Primary biliary cirrhosis

41
Q

less common causes of chronic hepatocellular injury

A

alpha-1 antitrypsin deficiency
Wilson’s disease
Haemochromatosis

42
Q

liver screen

A 
LFTs
Coagulation screen
Hepatitis serology (A/B/C)
Epstein-Barr Virus (EBV)
Cytomegalovirus (CMV)
Anti-mitochondrial antibody (AMA)
Anti-smooth muscle antibody (ASMA)
Anti-liver/kidney microsomal antibodies (Anti-LKM)
Anti-nuclear antibody (ANA)
p-ANCA
Immunoglobulins – IgM/IgG
Alpha-1 Antitrypsin – Alpha-1 Antitrypsin deficiency
Serum Copper – Wilson’s disease
Ceruloplasmin – Wilson’s disease
Ferritin – Haemochromatosis

GI (9 decks)

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