Obstructive Jaundice

Question 1

How to differentiate between Obstructive and non-obstructive Jaundice via blood tests?

Answer 1

• In obstructive jaundice, ALP and GGT levels will be significantly elevated
• In non-obstructive jaundice ALP and GGT levels may be only mildly elevated or normal

Question 2

What is the normal bilirubin? when does Jaundice becomes apparent on the patient’s skin colour?

Answer 2

Normal bilirubin level: <21 umol/L.

Apparent jaundice —> 35 umol/L

Question 3

How does high bilirubin (jaundice) affect coagulation studies?

Answer 3

increased prothrombin time or INR

Question 3

Why is the coagulation profile deranged in jaundiced patient?

Answer 3

• Liver synthesizes most of the clotting factors.
• Severe liver damage and billiary obstruction can result in decreased absorption of vitamin K which is required to activate factors 2, 7, 9, and 10.

Question 4

In what form does bilirubin circulate within the plasma?

Answer 4

As free bilirubin and conjugated to glucuronic acid

Question 5

How would you correct these coagulation abnormalities in pts with obstructive jaundice/liver damage?

Answer 5

• IV Vit. K.
• Fresh frozen plasma.
• Prothrombin complex concentrates.
• Consult haematologist.

Question 6

What are ALT & AST? when do they increase?

Answer 6

• Enzymes present in hepatocytes and their increase is suggestive for liver damage
• Usually ALT > AST

Question 7

What is ALP? When does it increase?

Answer 7

• Enzyme located in the epithelium of bile canaliculi, bone and placental tissue
• Increases in cholestasis to a far greater extent than ALT, AST

Question 8

You’re asked to see a 45 -year-old female patient complaining of 2-day history of epigastric pain, nausea, vomiting, diarrhea. She has dark urine. O/E she is jaundiced and has mild epigastric tenderness. Labs: significantly Increasesd ALT, AST, ALP, GGT. Urobilinogen undetectable in urine.

How would you investigate this patient?

Answer 8

• Blood tests: measure liver function
• US : check for Dilatation of intra- or extrahepatic bile ducts
• Endoscopic retrograde cholangiopancreatography (ERCP): examine the bile ducts and potentially remove any obstructions
• Liver biopsy: evaluate the extent of liver damage and rule out other potential causes of jaundice

Question 9

If you find a CBD stone on US, what to do?

Answer 9

ERCP and endoscopic sphincterotomy

Question 9

What would be your diagnosis if the patient had fever, pain, chills?

Answer 9

Ascending cholangitis.

Question 10

How can you Manage ascending cholangitis?

Answer 10

• IV fluids, antibiotics and to relieve the obstruction
• Sepsis 6 if in septic Shock

Question 11

Causes of Jaundice

Answer 11

• Pre-hepatic
  
  • Haemolytic anaemia sickle cell
  • Gibert’s syndrome
  • Transfusion reaction
• Hepatic
  
  • Alcohol liver disease
  • hepatitis
  • Primary billary cirrhosis
  • Hepatocellular carcinoma
• Post-hepatic
  
  • Gall stones
  • Primary sclerosing cholangitis
  • Pancreatic cancer

Question 11

Classification of obstructive Jaundice

Answer 11

1. Intrahepatic obstructive jaundice: This occurs when there is an obstruction within the liver, such as in the small bile ducts. Causes of intrahepatic obstructive jaundice include primary biliary cirrhosis and certain medications.
2. Extrahepatic obstructive jaundice: This occurs when there is an obstruction outside the liver, such as in the common bile duct. Causes of extrahepatic obstructive jaundice include gallstones and pancreatic cancer.

Question 11

Bile - Function?

Answer 11

• Emulsification of fat into micelles thus provides a greatly increased surface area for the action of the enzyme pancreaticlipase
• Bile salt anions form micelles around lipid droplets, with hydrophobic sides facing the fat and hydrophilic sides facing outwards. The negatively charged hydrophilic sides prevent fat droplets from re-aggregating into larger particles.

Question 12

Bile - Constituents?

Answer 12

• Water, Cholesterol, Lecithin (a phospholipid)
• Bile pigments, salts, acids
• Small amounts of copper and other excreted metals.

Question 13

Bile - conjugation?

Answer 13

conjugates with glucuronic acid by the enzyme glucuronyl transferase

Question 14

What is urobilinogen? How is it formed?

Answer 14

It is a byproduct of bilirubin metabolism formed in the intestine by gut flora.

Question 14

Bile - metabolism?

Answer 14

• Conjugated bilirubin → bile →small intestine.
  
  • most of it resorbed in the terminal ileum → enterohepatic circulation → back to liver & GB
  • Some not absorbed → the colon, colonic bacteria disconjugate → colourless urobilinogen
    
    • Most of it oxidized → stercobilin, (characteristic brown stool colour)
    • 10% of the urobilinogen →enterohepatic circulation → the bile
      
      • some processed by the kidneys → the urine yellow

Question 15

What are the advantages of enterohepatic circulation?

Answer 15

Allows high rate of secretion and low rate of production from the liver.

Question 15

What is the enterohepatic circulation?

Answer 15

Reabsorption of bile salts from the terminal ileum and returning them back to the liver (95%).

Question 16

How much bile is secreted in 24 hours?

Answer 16

500-1000 ml/day.

Question 17

Complications of reduction of bile salts in small intestine?

Answer 17

• Steatorrhea due to malabsorption of fat
• Poor absorption of fat-soluble vitamins (ADEK)

Question 18

Full explanation of the metabolism and circulation of bile

Answer 18

• Conjugated bilirubin goes into the bile and thus out into the small intestine. Though most bile acid is resorbed in the terminal ileum to participate in enterohepatic circulation, conjugated bilirubin is not absorbed and instead passes into the colon
• There, colonic bacteria disconjugate and metabolize the bilirubin into colorless urobilinogen, which can be oxidized to form stercobilin, these give stool its characteristic brown color
• 10% of the urobilinogen is reabsorbed into the enterohepatic circulation to be re-excreted in the bile: some of this is instead processed by the kidneys, coloring the urine yellow.
• It is a byproduct of bilirubin metabolism formed in the intestine by gut flora.
• Some are excreted in the feces after oxidation (stercobilinogen) and some are reabsorbed into the portal circulation again.
• Some of the reabsorbed urobilinogen is again excreted by the liver but small amounts enter the systemic circulation.