JAUNDICE
INTRODUCTION:
✓ Yellowish pigmentation of skin, mucous membrane and sclera resulting from an
increase in bilirubin concentration in body fluids.
✓ Scleral pigmentation due to richness of elastin – special affinity for bilirubin.
✓ Carotenaemia – yellowish pigmentation of skin by carotene but not sclera.
✓ Clinical jaundice: serum bilirubin more than 2.5 mg/dL.
✓ Latent jaundice: serum bilirubin between 1 mg/dL and 2mg/dL.
METABOLISM:
✓ 80% of the circulating bilirubin is derived from haem of haemoglobin, which in turn,
derived from senescent RBCs.
✓ 10 – 20% of bilirubin comes from myoglobin, cytochromes & other haem containing
proteins.
✓ Bilirubin is metabolised into 7 steps:
• Breakdown of RBCs: Haem is oxidised to biliverdin, which is then
reduced to bilirubin. Bilirubin being insoluble combines with albumin 1:1
ratio.
• Uptake into liver: Bilirubin combined with albumin is taken up by liver. In
hepatocytes, bilirubin binds to two cytosolic proteins, liganclin & Z-
protein, intern limiting the reflux of bilirubin back to plasma.
• Conjugation: With the help of glucuronic acid, bilirubin is converted into
conjugated bilirubin and is excreted in bile.
• Bile breakdown: Bile is broken down by gut bacteria & conjugated
bilirubin is deconjugated as urobilinogen & stercobilinogen.
• Excretion of stercobilinogen: Stercobilinogen is excreted via faces.
• Reabsorption of urobilinogen: Urobilinogen is reabsorbed from the
intestine.
• Excretion of urobilinogen: Excreted via kidney later.
CLASSIFICATION:
Classified in two ways:
• Based upon the underlying derangement of bilirubin metabolism.
✓ Predominantly unconjugated hyperbilirubinemia.
✓ Predominantly conjugated hyperbilirubinemia.
1. Predominantly unconjugated:
Overproduction: Haemolysis, ineffective erythropoiesis.
Decreased hepatic uptake: Drugs, sepsis.
Decreased conjugation: Gilbert’s syndrome, Neonatal jaundice.
INTRODUCTION:
✓ Yellowish pigmentation of skin, mucous membrane and sclera resulting from an
increase in bilirubin concentration in body fluids.
✓ Scleral pigmentation due to richness of elastin – special affinity for bilirubin.
✓ Carotenaemia – yellowish pigmentation of skin by carotene but not sclera.
✓ Clinical jaundice: serum bilirubin more than 2.5 mg/dL.
✓ Latent jaundice: serum bilirubin between 1 mg/dL and 2mg/dL.
METABOLISM:
✓ 80% of the circulating bilirubin is derived from haem of haemoglobin, which in turn,
derived from senescent RBCs.
✓ 10 – 20% of bilirubin comes from myoglobin, cytochromes & other haem containing
proteins.
✓ Bilirubin is metabolised into 7 steps:
• Breakdown of RBCs: Haem is oxidised to biliverdin, which is then
reduced to bilirubin. Bilirubin being insoluble combines with albumin 1:1
ratio.
• Uptake into liver: Bilirubin combined with albumin is taken up by liver. In
hepatocytes, bilirubin binds to two cytosolic proteins, liganclin & Z-
protein, intern limiting the reflux of bilirubin back to plasma.
• Conjugation: With the help of glucuronic acid, bilirubin is converted into
conjugated bilirubin and is excreted in bile.
• Bile breakdown: Bile is broken down by gut bacteria & conjugated
bilirubin is deconjugated as urobilinogen & stercobilinogen.
• Excretion of stercobilinogen: Stercobilinogen is excreted via faces.
• Reabsorption of urobilinogen: Urobilinogen is reabsorbed from the
intestine.
• Excretion of urobilinogen: Excreted via kidney later.
CLASSIFICATION:
Classified in two ways:
• Based upon the underlying derangement of bilirubin metabolism.
✓ Predominantly unconjugated hyperbilirubinemia.
✓ Predominantly conjugated hyperbilirubinemia.
1. Predominantly unconjugated:
Overproduction: Haemolysis, ineffective erythropoiesis.
Decreased hepatic uptake: Drugs, sepsis.
Decreased conjugation: Gilbert’s syndrome, Neonatal jaundice.
