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
Gilbert syndrome Autosomal recessive
Defect / target: UGT1A1 promoter polymorphism (~30% activity)
Mechanism: Mildly reduced bilirubin-UDP-glucuronosyltransferase expression slows conjugation, so unconjugated bilirubin rises modestly, especially when fasting, stress or illness raises bilirubin load.
↑ Accumulates: Unconjugated (indirect) bilirubin, mildly· ↓ Deficient: Conjugated bilirubin formation (partial)
Presentation: Very common (3-7%), benign, incidental mild jaundice/scleral icterus during fasting, stress or viral illness
Labs: Mild isolated unconjugated hyperbilirubinemia, normal liver enzymes
Treatment: None needed
Gilbert, CN-I and CN-II are one enzyme (UGT1A1) on a severity spectrum
Learn the mechanism: Heme degradation & bilirubin (jaundice) →
FMK 08.4 Heme Metabolism · slide 21, 28; handout