Learn / FMK
Every FMK condition
299 diseases, deficiencies, toxicities and drug mechanisms harvested from every FMK deck — the ones sprinkled through a single bullet as much as the ones with their own slide. Pick what you're given and what you have to name, or let it cycle; distractors come from the same category so you have to discriminate (hypoketotic vs. ketotic hypoglycemia, which GSD, which urea-cycle enzyme…). Every answer shows the whole card with the lecture and slide.
Heme · FMK 08.4
Dubin-Johnson syndrome Autosomal recessive
Defect / target: Canalicular MRP2 (MOAT) transporter for conjugated bilirubin
Mechanism: Conjugation is normal but conjugated bilirubin cannot be exported across the canalicular membrane into bile, so it refluxes into plasma; pigment accumulates in hepatocytes.
↑ Accumulates: Conjugated (direct) bilirubin; dark pigment in liver· ↓ Deficient: Biliary excretion of conjugated bilirubin
Presentation: Benign conjugated hyperbilirubinemia, grossly black/darkly pigmented liver
Labs: Conjugated hyperbilirubinemia, normal liver enzymes
Treatment: None needed
Dubin-Johnson = Dark liver; Rotor = normal liver
Learn the mechanism: Heme degradation & bilirubin (jaundice) →
FMK 08.4 Heme Metabolism · slide 21, 28; handout