Learn / Metabolism
Metabolic pathways
Every FMK pathway as a clickable map. Pick one pathway to hammer it — next step, enzyme, regulator, cofactor, and the facts that get tested (NADPH and who needs it, rate-limiting steps, deficiencies) — or set it to all pathways for a mixed drill. Every answer says which enzyme and which pathway.
Heme degradation & bilirubin (jaundice)
Bilirubin–albumin (plasma)
Made from Unconjugated bilirubin (yellow, lipophilic) by Binds albumin for transport
Binds albumin for transport — Heme degradation & bilirubin (jaundice)
Inhibited by: Salicylates and sulfonamides DISPLACE bilirubin from albumin
Unconjugated ('indirect') bilirubin is lipophilic, water-insoluble, crosses the blood–brain barrier — neurotoxic — and is NOT filtered into urine (acholuric jaundice when it rises). Albumin binding is what keeps it out of the brain, so a drug that competes for that binding site raises FREE bilirubin without raising the total — sulfonamides and salicylates are therefore avoided in neonates, where the blood–brain barrier is still immature (handout).
Condition cards:Kernicterus (bilirubin encephalopathy) →Drug displacement of bilirubin from albumin (salicylates, sulfonamides) →
Becomes Hepatocyte bilirubin (ligandin) via Sinusoidal uptake (OATP) → ligandin (Y protein)
Sinusoidal uptake (OATP) → ligandin (Y protein) — Heme degradation & bilirubin (jaundice)
Deficiency: Rotor syndrome (AR) — defective hepatic storage/OATP transport: benign conjugated hyperbilirubinemia, liver NOT pigmented (vs Dubin-Johnson)
Facilitated transport across the basolateral membrane; ligandin shuttles it to the smooth ER.
Condition cards:Rotor syndrome →