LFTs Flashcards

1
Q

Why check LFTs?

A
  1. Confirm a clinical suspicion of potential liver injury / disease
  2. To distinguish between hepatic jaundice (ie hepatocellular injury) and obstructive jaundice (cholestasis)
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2
Q

What blood tests assess liver function?

A

ALT, AST, ALP, GGT (used to distinguish between hepatic and obstructive jaundice)
Bilirubin, albumin PT (used to test liver’s synthetic function)

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3
Q

What is considered a large rise for ALT and ALP?

A

ALT - moderate rise = <10-fold, large rise = >10-fold

ALP - moderate rise = <3-fold, large rise = >3-fold

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4
Q

Where is ALT usually found?

A

Found in high concentrations WITHIN hepatocytes, and enters the blood following hepatocellular injury
Therefore it is a useful marker of hepatocellular injury

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5
Q

Where is ALP usually found?

A

Concentrated in the liver, bile duct and bone tissues
Often raised in liver pathology due to increased synthesis in response to cholestasis
Therefore it is a useful indirect marker of cholestasis

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6
Q

When do you review GGT?

A

Important to review when there is a rise in ALP

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7
Q

When would GGT be raised?

A

Can be suggestive of biliary epithelial damage and bile flow obstruction
Can also be raised in response to alcohol and drugs such as phenytoin
A markedly raised ALP + raised GGT –> highly suggestive of cholestasis

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8
Q

What would an isolated rise of ALP suggest?

A

Should raise suspicion of non-hepatobiliary pathology

Increased bone breakdown can elevate ALP (eg bone mets, vit D deficiency, bone fractures)

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9
Q

What if the patient is jaundiced but ALT and ALP levels are normal?

A

Suggests a pre-hepatic cause of jaundice eg:
Gilbert’s syndrome
Haemolysis

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10
Q

What is Gilbert’s syndrome?

A

Mild genetic liver disorder
High levels of unconjugated bilirubin due low availability of UGT in the liver. Causes a ‘backlog’ in the bloodstream
Commonly causes jaundice when patients are unwell

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11
Q

What are the liver’s main synthetic functions and what are the tests that measure this?

A
  1. Conjugation and elimination of bilirubin –> serum bilirubin
  2. Synthesis of albumin –> serum albumin
  3. Synthesis of clotting factors –> PT
  4. Gluconeogenesis –> serum blood glucose
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12
Q

What is the pattern of normal/dark urine and pale/normal stools in jaundiced patients?

A

Conjugated bilirubin turns urine dark (urobilinogen)
Fat is not absorbed if bile and pancreatic lipase cannot reach the bowel due to obstruction —> turns stool pale
Normal urine + normal stools –> pre-haptic cause (aka unconjugated hyperbilirubinaemia)
Dark urine + normal stools –> hepatic cause
Dark urine + pale stools –> obstructive cause

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13
Q

What are some causes of unconjugated hyperbilirubinaemia?

A

Haemolysis eg haemolytic anaemia
Impaired hepatic uptake eg drugs, congestive heart failure
Impaired conjugation eg Gilbert’s syndrome

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14
Q

Why would albumin levels fall?

A

(helps to bind water, cations, fatty acids and bilirubin, maintains oncotic pressure of blood)
Liver disease eg cirrhosis
Inflammation
Protein-losing enteropathies, nephrotic syndrome (causing loss of albumin)

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15
Q

What is the AST/ALT ratio used for?

A

Distinguishes between likely causes of LFT derangement
ALT>AST –> chronic liver disease
AST>ALT –> cirrhosis, acute alcoholic hepatitis

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16
Q

What are some common causes of acute hepatocellular injury?

A
Poisoning (paracetamol overdose)
Acute infection (Heb A and B)
Liver ischaemia
17
Q

What are some common causes of chronic hepatocellular injury?

A
Alcoholic fatty liver disease
Non-alcoholic fatty liver disease
Chronic infection (Hep B and C)
Primary biliary cirrhosis
(Less common = a-1 antitrypsin deficiency, Wilson's disease, haemochromatosis)