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 04.1
NSAID-induced GI bleeding Acquired / not inherited
Defect / target: Cyclooxygenase (COX-1/COX-2) inhibited by NSAIDs (e.g., ibuprofen)
Mechanism: NSAIDs block COX-derived prostaglandins and thromboxanes, including the protective gastric-mucosal prostaglandins, so the stomach lining erodes and bleeds.
· ↓ Deficient: Protective gastric prostaglandins (PGE2), thromboxane A2
Presentation: GI bleeding, gastric ulceration (the 71-year-old on ibuprofen case)
COX pathway = prostaglandins/thromboxanes (NSAID-sensitive); LOX pathway = leukotrienes/lipoxins (unaffected)
Learn the mechanism: Eicosanoids (COX / LOX) →
FMK 04.1 Lipid Structure & Function · slide 22, 23