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.
Toxin/Drug · FMK 08.4
Lead poisoning Acquired / not inherited
Defect / target: Lead inhibits ALA dehydratase (step 2, zinc-dependent) and ferrochelatase (step 8)
Mechanism: Lead displaces zinc from ALA dehydratase and inhibits ferrochelatase, so ALA accumulates upstream and protoporphyrin accumulates at the end of the pathway (zinc substitutes for the iron that cannot be inserted), producing a microcytic anemia.
↑ Accumulates: delta-Aminolevulinic acid (ALA), zinc protoporphyrin / free erythrocyte protoporphyrin, coproporphyrinogen III in urine, lead· ↓ Deficient: Heme / hemoglobin
Presentation: Pediatric patient with microcytic anemia, abdominal pain, neurotoxicity; can mimic AIP
Labs: Elevated blood lead, microcytic anemia with basophilic stippling, elevated zinc protoporphyrin, elevated urinary ALA with normal-to-mildly elevated PBG (vs AIP where both ALA and PBG are markedly elevated), elevated urinary coproporphyrin III
Treatment: Remove exposure; chelation
Two lead enzymes: ALA dehydratase and ferrochelatase. ALA up + PBG normal = lead; ALA and PBG both up = AIP
Learn the mechanism: Heme synthesis (porphyrias) →
FMK 08.4 Heme Metabolism · slide 10, 11, 30; handout