Liver Function Tests Flashcards
What is the current weekly recommended alcohol allowance for men and women? Why has it been lowered?
14 units per week, lowered because of newly learned link between alcohol consumption and cancer (not just between alcohol consumption and liver damage)
What is cholestasis and how does it present?
Blockage/reduction in bile flow, results in dark urine (lots of urobilinogen excreted) and pale stool (can’t excrete stercobilinogen)
What does an increased number of spider naevi above the nipple line indicate?
Alcoholic liver disease
Why is the liver a common site of metastasis?
Lots of blood flow here, so often metastases travel via blood and end up here
What do raised ALT and AST indicate?
Hepatocellular damage
What do raised ALP and GGT indicate?
Obstruction
Where does bilirubin come from?
Produced from the breakdown of RBCs
What are the products of the breakdown of RBCs and what happens to each of them?
Iron (re-used), globin (re-used), biliverdin (reduced to bilirubin)
What is biliverdin formed from? What is it reduced to?
Biliverdin (green) is formed from haem. It is reduced to form bilirubin.
Name three conditions which increase bilirubin levels
Cholestasis (biliary obstruction), hepatocellular damage, haemolysis
What is ‘conjugated bilirubin’? Where is bilirubin conjugated?
Bilirubin with glucuronic acid (bilirubin glucuronate), conjugated in the liver
What is the solubility of conjugated and unconjugated bilirubin?
Conjugated bilirubin is soluble in water, unconjugated bilirubin is insoluble
Why is it important that conjugated bilirubin is water soluble?
So it can be excreted into the duodenum as bile
Why does liver damage increase bilirubin levels? What condition does this lead to?
Liver damage means that bilirubin can’t be conjugated with glucuronic acid, so it can’t be excreted (because insoluble) so builds up- Leads to jaundice
Where is soluble bilirubin excreted? In what forms is bilirubin excreted in urine and stool?
. Excreted from liver through bile duct into duodenum
. Stercobilin in stools, urobilin in urine
Some bilirubin enters enterohepatic recycling. What does this involve?
Bilirubin/bile salts/urobilinogen are send back to the liver to be re-used, so lots of new bile salts don’t have to be synthesised from scratch
How do pale stools indicate liver dysfunction?
. Liver not working so can’t conjugate bilirubin
. Bilirubin glucuronate not converted to stercobilin, which normally colours stool brown
What does dark stool indicate with regards to the liver?
Shows too much bilirubin in blood, likely from cholestasis (bile duct blocked so bilirubin can’t be excreted into duodenum, builds up), hepatocellular damage (unconjugated bilirubin can’t be excreted, builds up), haemolysis (RBCs broken down to produce excess bilirubin)
What is the half-life of albumin? Why is this significant when using albumin as a marker for liver damage?
16-24 days- Quite long half-life, so low albumin is a marker of long term liver damage (liver normally synthesised albumin and clotting factors)
How can low albumin contribute to ascites?
Low albumin causes a decrease in oncotic pressure in the blood, so fluid leaks from interstitial spaces into the peritoneal cavity instead
How come low levels of clotting factors can show acute/chronic liver damage, whereas low albumin indicates long term/chronic damage?
Clotting factors have a short half life, so can’t really differentiate acute/chronic damage. Albumin has a longer half life, so low albumin indicates more chronic long-term damage
Why does jaundice present with pruritus?
Excess bilirubin is toxic, which presents as itching of the skin
What is prehepatic jaundice? What is it often caused by? (Give 2)
. Unconjugated bilirubin produced faster than liver can conjugate it for excretion, so there’s a backlog build up of bilirubin in the blood
. Often caused by haemolytic anaemias e.g. spherocytosis (Lots of RBCs broken down produces excess bilirubin) or Gilbert’s syndrome (reduced levels of UDP-glucuronosyl transferase, which normally conjugates bilirubin)
What is hepatocellular jaundice? How is this usually detected? What symptoms often present?
. Hepatocellular damage so can’t conjugate bilirubin to bilirubin glucuronate, so there’s reduced excretion of bilirubin (=build up in blood)
. Detected by elevated ALT and AST (transaminases) in blood
. Normal/pale stools (stercobilin not excreted due to lack of soluble bilirubin)
What is the physiology behind pale stools?
If there’s a lack of bilirubin glucuronate (soluble bilirubin), it means less stercobilin can be produced to colour stool brown
What can you prescribe to relieve symptoms jaundice, pruritus, and nausea? What does this drug do?
. Cholestyramine
. Binds to bile (and thus bilirubin/bile salts) and prevents them being recycled and reabsorbed, causing bilirubin to be excreted
. Reduces toxic levels of bilirubin to relieve symptoms
How can liver cirrhosis lead to ascites?
Liver cirrhosis can cause decrease in BP, so lots of aldosterone is produced to counteract this (secondary hyperaldosteronism). This causes sodium retention, which can then draw fluid into the abdominal cavity (=ascites)
How can liver dysfunction lead to encephalopathy? How would you treat this?
Gut flora produce many nitrous products (e.g. ammonia) which are normally cleared by the liver but can be toxic in higher amounts
Prescribe neomycin, metronidazole, and lactulose
Why is gastric bleeding of particular concern in those with liver disease?
Damaged liver doesn’t produce sufficient clotting factors to deal with a gastric bleed, so could be excessive gastric bleeding
How can you decrease the risk of bleeding oesophageal varices?
Prescribe beta-blockers to decrease BP
What is the main test for liver fibrosis?
Fibroscan (Transient Elastography, TE)
