Major Causes of Jaundice : classified by origin
1. Pre-hepatic (TB not exceed 5 mg/dl)
1.1 Hereditary Hemolytic Processes : Hereditary spherocytosis,
G6PD deficiency, Thalassemia, Hemoglobin C disease,
Sickle cell disease
1.2 Acquired Hemolytic Processes : Hemolytic disease of the newborn,
Hemolytic transfusion reactions,
Drug-induced hemolytic anemia,
Autoimmune hemolytic anemia,
Paroxysmal noctural hemoglobinemia
1.3 Ineffective Erythropoiesis : Megaloblastic anemia, Sideroblastic anemia,
Erythroleukemia, Lead poisoning
1.4 Impaired Delivery of Bilirubin to the liver : Congestive heart failure
1.5 Sport injuries (bleeding into the tissue)  
2. Hepatic
2.1 Pre-microsomal : interfere with bilirubin uptake
Drug : rifampicm
2.2 Microsomal
Prematurity
Hepatitis : viral or drug-induced
Gilbert's syndrome
Crigler-Najjar syndrome
2.3 Post-microsomal : impaired excretion
Hepatitis
Drugs : methyltestosterone
Dubin-Johnson syndrome
2.4 Intrahepatic obstruction
Hepatitis
Cirrhosis
Infiltration : lymphoma, amyloid
Biliary atresia
Tumours
Extra-hepatic sepsis
3. Post-hepatic
Common bile duct stone
Cancer of the bile ducts, pancreas, ampulla of Vater
Bile duct stricture or stenosis
Sclerosing cholangitis
Choledochal cysts
Biliary atresia in infants
Physiological Classification of Jaundice
Unconjugated Hyperbilirubinemia Conjugated Hyperbilirubinemia
1. Production
Hemolysis : hereditary & acquired
Ineffective erythropoiesis
Rapid turnover of RBC mass


 
2. Delivery to hepatocyte
Right-side congestive heart failure
Portcaval shunt
3. Uptake across hepatocyte membrane
Competitive inhibition : Drugs
Gilbert's syndrome
Sepsis, fasting
4. Storage in Cytosol
(Protein Y and Z)
Competitive inhibition
Fever

5. Conjugation
Neonatal jaundice
Inhibition : drugs
Crigler-Najjar
Type I (complete)
Type II (partial)
Hepatocellular dysfunction
Gilbert's syndrome
1. Secretion into canaliculi
Hepatocellular disease
- Hepatitis
- Intrahepatic cholestasis
Dubin-Johnson Syndrome
Rotor Syndrome
Drugs : estradiol
2. Drainage
Extrahepatic obstruction
- Stone
- Carcinoma
- Stricture
- Atresia
Sclerosing cholangitis
Intrahepatic obstruction
- Drugs
- Granulomas
- Primary biliary cirrhosis
- Tumours
3. Septicemia, total parenteral nutrition and
certain drugs àªè¹ androgens conj bili
(äÁèÃÙé mechanism)
Inherited Disorder of Bilirubin Metabolism
Gilbert's Crigler-Najjar Dubin-Johnson Rotor
Defect :
Conjugation of bilirubin
Uptake in some cases 		Defect :
Type I : absence of
conjugating enzyme

Type II : partial defect of
conjugating enzyme

 Defect :
Hepatic excretion of bilirubin		 Defect :
Unknown
Clinicical features :
Mild, fluctuate unconjugated
hyperbilirubinemia which increases on fasting à¹×èͧ¨Ò¡ fasting ÁÕ¼ÅãËé hepatic UDP-glucuronic acid content Ŵŧ ËÃ×Í fatty acid ä»áÂè§ bilirubin ¨Ñº albumin áÅéǶ١¨Ñºà¢éÒà«ÅÅìá·¹
Normal lifespan		 Clinicical features :
Severe unconjugated hyperbilirubinemia
Early death due to kernicterus
Partial response to phototherapy
Severe unconj. hyperbilirubinemia but good response to phenobarbitone and phototherapy
Survive to adulthood		 Clinicical features :
Mild, fluctuate conjugated hyperbilirubinemia
Normal lifespan
Hepatic pigment disposition
Bilirubinuria		 Clinicical features :
Similar to Dubin-Johnson but no hepatic pigmentation
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