LFTs Flashcards

(42 cards)

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?

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
Normal urine + normal stools
pre-hepatic cause of jaundice
26
Dark urine + normal stools
hepatic cause of jaundice
27
Dark urine + pale stools
post-hepatic cause (obstructive) of jaundice
28
causes of unconjugated hyperbilirubinaemia
Haemolysis (e.g. haemolytic anaemia) Impaired hepatic uptake (drugs, congestive cardiac failure) Impaired conjugation (Gilbert’s syndrome)
29
Causes of conjugated hyperbilirubinaemia
Hepatocellular injury | Cholestasis
30
fall in albumin levels
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
albumin
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
PT
a measure of the blood’s coagulation tendency, specifically assessing the extrinsic pathway
33
increased PT
can indicate liver disease and dysfunction
34
ALT > AST
chronic liver disease
35
AST > ALT
cirrhosis and acute alcoholic hepatitis
36
acute hepatocellular damage
ALT ^^ ASP normal or ^ GGT normal or ^ bilirubin ^ or ^^
37
chronic hepatocellolar damage
ALT normal or ^ ASP normal or ^ GGT normal or ^ bilirubin normal or ^
38
cholestasis
ALT normal or ^ ASP ^^ GGT ^^ bilirubin ^^
39
common causes of acute hepatocellular injury
Poisoning (paracetamol overdose) Infection (Hepatitis A and B) Liver ischaemia
40
common causes of chronic hepatocellular injury
Alcoholic fatty liver disease Non-alcoholic fatty liver disease Chronic infection (Hepatitis B or C) Primary biliary cirrhosis
41
less common causes of chronic hepatocellular injury
alpha-1 antitrypsin deficiency Wilson’s disease Haemochromatosis
42
liver screen
``` 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 ```