Obstructive jaundice

Question 1

What is jaundice?

clinically

Answer 1

Yellowing of the skin, usually visible when the bilirubin level reaches 50 micromol/L, with the upper limit of normal being 25 micromol/L

Question 2

How is jaundice classified?

Answer 2

• Pre-hepatic
• Hepatocellular (Hepatic)
• Obstructive/cholestatic (Post-hepatic)

Question 4

Describe the bilirubin metablism

(not an objective)

Answer 4

• When r.b.c reach the end of their life (120 days), they are destroyed in the reticuloendothelial system of the spleen
• The haem is converted to biliverdin and then to bilirubin (insoluble/indirect bilirubin), which is bound by albumin in the plasma
• Bilirubin can then be taken up by hepatocytes as it is protein bound, and it is conjugated by glucuronyl transferase to bilirubin glucuronide (solube/direct bilirubin)
• This soluble bilirubin is excreted in the bile into the bowel lumen, where it is transformed by bacteria to urobilinogen
• Most urobilinogen is excreted in the stools to give it the dark colour (aka stercobilinogen)
• A small amount of urobilinogn is reabsorbed from the intestine into the portal venous tributaries and passes back to the liver, wheremost of it is excreted once more into the gut
• Some of this reabsorbed urobilinogen reaches the systemic circulation, and this is excreted by the kidney into the urine
• When the urobilinogen in the urine is exposed to air, it is oxidized to urobilin to give urine a dark colour

Question 5

What cause pre-hepatic jaundice?

Answer 5

• Occurs secondary to increased erytrocyte (RBC) breakdown
  
  • Haemolytic anamias (sickle cell, G6PD deficiency, pyruvate, kinase deficiency, hereditary spherocytosis)
  • Malaria
  • Thalassaemias
• The bilirubn has not yet been processed by the liver, thus is mainly unconjugated in the blood

Question 6

How is cholestatic (obstructive) jaundice classified? (what is it?)

Give the causes for each

Answer 6

Intra hepatic obstruction:

• Obstruction of the hepatic bile canniliculi (failure of bile secretion)
• Can occur secondary to multiple different causes:
  
  • Hepatitis
  • Cirrhosis
  • Neoplasm
  • Drugs
  • Pregancy

Extra hepatic obstruction:

• Obstruction of the hepatic ducts, or biliary tree
• Causes within lumen:
  
  • Gallstones
• Causes within the wall:
  
  • Cholangiocarcinoma
  • Primary sclerosing cholangitis
  • Congenital atresia of the common bile duct
• External causes:
  
  • Pancreatitis
  • Tumour of pancreatic head

Question 7

Why does cholestatic jaundice occur? (Give an overview)

Answer 7

• There is an obstruction to bile outflow from the liver, leading to ‘cholestasis’

Question 8

What are the clinical features of obstructive jaundice?

Why do they occur?

Answer 8

• Jaundice of skin and sclera - high bilirubin
• Pruritus (itching) - bilirubin deposition
• Dark urine
  
  • As the bilirubin has been processed by the liver, it is mainly conjugated in the blood, and thus can also enter the urine giving dark urine
• Pale stools
  
  • The bilirubin cannot enter the GI tract and thus is not excreted in faeces, giving pale stools
• Steatorrhoea
  
  • reduced fat soluble vitamin absorption

Question 9

What investigations would you do for a patient presenting with obstruction jaundice?

(laboratory and radiological)

Answer 9

Urine and stools investigation:

• Very little bile can enter the gut, thus stercobilinogen low, giving pale stools
• As the bilirubin is conjugated in the blood, urinary bilirubin is present, giving dark urine

​Bloods:

• FBC, reticulocytes, LFTs, U&Es, clotting, glucose, bilirubin levels
  
  • Transaminases most raised in intrahepatic jaundice
  • ALP most raised in extrahepatic cholestasis
  • Glucose may be low in liver failure, or raised in pancreatic disease

Imaging:

• Ultrasound
  
  • Will show dilated duct system to confirm obstruction
  • Gallstones within the gall bladder can be demonstrated accurately
• MRCP
  
  • Gives non-invasive high resolution imaging of the biliary tress