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Neonatal jaundice
Metabolic pathway of bilirubin with pathologies relating to unconjugated hyperbilirubinemia. 1. ABO incompatibility, Rhesus incompatibility, shorter RBC lifespan in neonates, bruising during delivery; 2. induced by inflammatory mediators associated with comorbidities of prematurity (e.g., respiratory distress syndrome, infection); 3. dissociation increased by acidosis, ketosis, renal failure; 4. permeable blood-brain barrier in term neonates and premature babies; 5. mutation in UGT1A1 gene results in Gilbert syndrome or Crigler-Najjar syndrome I and II; 6. unconjugated bilirubin load increased by decreased gut motility
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Neonatal jaundice
Detail of liver lobule and its functions, highlighting pathologies that cause conjugated hyperbilirubinemia. Pathologies include: 1. portal vein thrombosis; 2. choledochal cyst; 3. infection (sepsis, E coli urinary tract infection, hepatitis A or B, toxoplasmosis, cytomegalovirus, syphilis, herpes), metabolic (Rotor syndrome, galactosemia, tyrosinemia, alpha-1 antitrypsin deficiency, hypothyroidism, cystic fibrosis, Zellweger syndrome), drugs, idiopathic neonatal hepatitis, total parenteral nutrition, neonatal hemochromatosis, shock/hypoxia/ischemia; 4. bile duct paucity, biliary atresia, Alagille syndrome, idiopathic neonatal cholestasis, progressive familial intrahepatic cholestasis, inspissated bile syndrome; 5. MRP2 (also known as ABCC2) gene mutations on the canalicular membrane of hepatocytes result in Dubin-Johnson syndrome, absence of OATP1B1 and OATP1B3 at the sinusoidal membrane of hepatocytes result in Rotor syndrome
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