2017A Question 15
Outline the clinical laboratory assessment of liver function.
46.4% of candidates achieved a pass in this question.
The crucial approach to this question is to explain the physiological basis of the laboratory tests. A simple list of test names provides marks towards a pass but to reach a pass or score well a candidate had to demonstrate an understanding of the underlying physiology. As an example of a good level of explanation when discussing coagulation disturbance many candidates mentioned INR but only a few went on to explain why it was the most sensitive test for coagulation in liver failure by relating it to the half life of the factors it tests.
Common mistakes included “overviews” that could be lengthy and not relate to the question and so not add to the overall mark. Also summaries of physiological functions of the liver that were not related to tests did not accrue marks. Circular statements were another pitfall, where candidates rephrased their point as a way of explanation. Describing other forms of assessment such as imaging or signs and symptoms gained no marks. Tests of the haematological sequelae of liver failure were frequently omitted.
- Synthetic function
- Cell injury
|Alanine Aminotransferase||ALT||7-55 U/L|
|Aspartate Aminotransferase||AST||8-48 U/L|
|Alkaline Phosphatase||ALP||40-129 U/L|
|Gamma Glutamyl Transferase||GGT||8-61U/L|
|International Normalized Ratio||INR||1|
- Most abundant plasma protein
- Also negative acute phase reactant
- Maintain plasma oncotic pressure
- Binding site for ions (calcium), drugs, unconjugated bilirubin, lipid-soluble substance
- Half life 3/52 hence reduced in chronic disease
- Haem breakdown product. Normal ≤15μmol/L. Scleral icterus >50μmol/L.
- Unconjugated BR transported from RES to liver on albumin
- → BR-monoglucuronide → BR diglucuronide by UDP-GT
- ↓ Synthetic function → ↑ Unconjugated BR
- ↓ Secretion → ↑ Conjugated BR
- Liver synthesizes all coag proteins except vWF
- ↑ PT, aPTT
- ±↓ Platelet if splenomegaly
- Earliest sign of liver damage is ↑ INR, due to short half life of VII
- ↑ AST, ALT, BR
- AST and ALT are present in hepatocyte cytoplasm
- AST raised more acutely than ALT in setting of injury
AST may be more indicative of alcoholic liver disease
- ↑ ALP, GGT, BR (+/- AST, ALT)
- ALP and GGT are leaked from damaged biliary epitheliocytes
- Note significant cholestasis can cause hepatocellular injury also
- Note ALP also has a bone isomer
(Note acute alcohol → ↑ GGT)
- Plasma glucose may fall in liver failure
- Liver increases plasma glucose concentration in response to glucagon, catecholamines, corticosteroids
- Synthesises enzymes important for glycogenolysis and gluconeogenesis
- Increased in liver failure
- Leaked in centrilobular damage