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
Crigler-Najjar syndrome type II Autosomal recessive
Defect / target: Partial UGT1A1 deficiency (residual activity)
Mechanism: Reduced but present bilirubin-UGT activity causes moderate unconjugated hyperbilirubinemia; residual enzyme can be induced by phenobarbital.
↑ Accumulates: Unconjugated bilirubin (moderate)· ↓ Deficient: Conjugated bilirubin (partial)
Presentation: Less severe jaundice than type I, low kernicterus risk
Labs: Moderate unconjugated hyperbilirubinemia that falls with phenobarbital
Treatment: Phenobarbital (induces residual UGT1A1)
Type II = some enzyme = phenobarbital works
Learn the mechanism: Heme degradation & bilirubin (jaundice) →
FMK 08.4 Heme Metabolism · slide 21, 28; handout