LFT's - Metabolic and Synthetic Tests Flashcards
What are the 4 main synthetic functions of the liver and what can be used to assess them - 4
What tests are used to asses the liver metabolic function? - 4
Conjugation and elimination of bilirubin
Synthesis of albumin
Synthesis of clotting factors
Gluconeogenesis
Serum bilirubin
Serum albumin
Prothrombin time (PT)
Serum blood glucose
Bilirubin
Drugs, waste products and toxins
Carbs
Lipids
Bilirubin Cycle:
In the Liver, bilirubin is ____ to make it water-soluble.
The majority of _______ bilirubin is excreted as bile acid via the bile ducts of the liver.
A portion of the ______ in the bowel is converted from ______ to _______ which is absorbed back into enterohepatic circulation.
A portion of ____ participates in the extra hepatic _____ cycle when it is reabsorbed at the _______.
The rest of the _____ is transported to the kidneys and converted to yellow urobilin, which gives urine its characteristic colour.
The _____ left in the bowel is oxidised to _______.
In the Liver bilirubin is conjugated to make it water-soluble.
The majority of Conjugated bilirubin is excreted as bile acid via the bile ducts of the Liver.
A portion of the conjugated bilirubin in the bowel is converted from conjugated bilirubin to urobilinogen which is absorbed back into enterohepatic circulation.
A portion of urobillinogen participates in the enterohepatic urobillinogen cycle when it is reabsorbed at the terminal ileum.
The rest of the urobillinogen is transported to the kidneys and converted to yellow urobilin, which gives urine its characteristic colour.
The urobillinogen left in the bowel is oxidised to stercobillin.
Bilirubin:
What is BR a breakdown product of?
Over what level is the jaundice clinically apparent?
We can differentiate between unconjugated and conjugated hyperbilirubinaemia by the patients symptoms and signs. URINE CHANGES IN:
- Unconjugated hyperbilirubinaemia
- Conjugated hyperbilirubinaemia
Hb
> 60 umol/L
It is not water-soluble when UNconjugated so can’t pass into the urine SO URINE IS NORMAL
The conjugated bilirubin builds up in the blood which turns the urine dark
Bilirubin:
Causes of unconjugated hyperbilirubinaemia:
- What are 2 causes?
- Gilbert’s syndrome is also a cause. What is it?
- What antibiotic impairs uptake of bilirubin? - R
In healthy adults conjugated bilirubin is virtually absent. Levels usually start to become increased when the liver has lost approximately ½ of its excretory capacity:
- Biliary obstruction is cause. What 3 things could cause this?
- What 2 antibiotics cause cholestasis?
- What autoimmune cholestatic diseases could cause this? - 2
Knowing this, what would reduce expiratory capacity?
Cirrhosis and hepatitis, when their is impairment in liver function.
This usually is elevated due to increased bilirubin production OR decreased hepatic uptake/conjugation:
- Haemolysis (haemolytic anaemia)
- Impaired hepatic uptake (drugs, congestive cardiac failure)
- Impaired conjugation (Gilberts syndrome)
Stones
Malignancy - Cholangiocarcinoma or pancreatic cancer
Nitrofuratoin
Penicillin - amoxicillin, flucloxacillin
PBC - intrahepatic
PSC - any level
Bilirubin - what type of cause of jaundice is it?
What does normal urine and stools suggest
What does dark urine + normal stools suggest?
What does dark urine + pale stools suggest?
Pre-hepatic cause
Hepatic cause
In hepatic jaundice, there is dysfunction of the hepatic cells. The liver loses the ability to conjugate bilirubin, but in cases where it also may become cirrhotic, it compresses the intra-hepatic portions of the biliary tree to cause a degree of obstruction.
This leads to both unconjugated and conjugated bilirubin in the blood, termed a ‘mixed picture’.
Post-hepatic cause (obstructive)
Bilirubin:
Causes of isolated jaundice:
- Gilberts syndrome - what is it?
Haemolysis is another cause - how can this be checked?
A mild liver disorder in which the liver does not properly process bilirubin
FBC
Prothrombin Time:
Why might PT be raised?
What do you need to make sure is done before measuring PT? - 1
What Vitamin deficiency should be ruled out?
What is the half life of PT?
It’s prolonged in advanced disease, so is used in scoring systems.
Liver is not producing enough clotting factors indicating liver disease and dysfunction
Anticoagulant drugs should be stopped
Vit K deficiency should be ruled out
One important thing to consider is that while a prolonged PT may indicate liver synthetic dysfunction, it can be prolonged for other reasons. In particular deficiency in fat-soluble vitamin k, which is used in the generation of factors II, VII, IX, and X, can be responsible. This is particularly true in cases of obstructive jaundice where reduced bile acid excretion impairs intestinal absorption of fat-soluble vitamins.
6 hrs so can use it to monitor disease
Albumin:
3 ways albumin levels fall:
- Why liver disease?
- Why does inflammation cause a fall?
- Where might you lose excessive amounts of albumin - 2
- Why does sepsis cause this?
Burns and IBD (inflammation) can also lead to a fall!
Decreased production (e.g. cirrhosis)
Triggers acute phase response which temporarily decreases the liver’s production of albumin
Protein-losing enteropathies
Nephrotic syndrome
Increased vascular permeability
Albumin:
The half-life of albumin is around 20 days, making it less useful as a marker of acute disease. Why could this be useful in?
What sign is seen on fingernails?
Therefore it is often more useful as a sensitive marker for chronic liver disease and has a role in prognostic scoring.
Muehrcke lines in chronic hypoalbuminemia - Leukonychia
What other test should not be forgotten as an indirect way of assessing liver function even though it presents very late?
BM
Gluconeogenesis becomes impaired very late
