## Pathophysiology of Physiological Jaundice **Key Point:** Physiological jaundice results from a combination of increased bilirubin load and decreased hepatic clearance, NOT from hemolysis or obstruction. ### Mechanism Physiological jaundice develops due to: 1. **Increased bilirubin production** - Neonatal RBC lifespan: 70–90 days (vs. 120 days in adults) - Fetal hemoglobin (HbF) has shorter survival - Increased bilirubin load relative to adult levels 2. **Immature hepatic conjugation** - UDP-glucuronyl transferase (UGT1A1) activity is only 1–2% of adult levels at birth - Takes 2–4 weeks to reach adult levels - Results in decreased conjugation capacity 3. **Increased enterohepatic circulation** - Neonatal intestinal flora are sparse; β-glucuronidase activity is high - Unconjugated bilirubin is reabsorbed in the ileum and colon - Contributes 50–60% of the bilirubin load **High-Yield:** The combination of **immature UGT1A1** and **high enterohepatic circulation** is the hallmark of physiological jaundice. This is why early feeding and phototherapy are effective — they reduce enterohepatic circulation and enhance bilirubin clearance. ### Timing - Appears after 24 hours of life - Peaks at 3–5 days - Resolves by 1–2 weeks in term infants - Prolonged in preterm infants (up to 4 weeks) **Clinical Pearl:** Jaundice appearing in the first 24 hours is **never physiological** — investigate for hemolysis (Rh/ABO incompatibility), infection, or other pathology. [cite:Nelson Textbook of Pediatrics 21e Ch 102] 
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.