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.
Lipid · FMK 03.4
Alcoholic liver disease (steatosis → hepatitis → fibrosis → cirrhosis) Acquired / not inherited
Defect / target: ↑ NADH/NAD⁺ from ADH/ALDH; CYP2E1-derived ROS
Mechanism: Excess NADH pushes DHAP → glycerol-3-P and inhibits β-oxidation (3-hydroxyacyl-CoA DH), so fatty acids are re-esterified to triglycerides and accumulate as macrovesicular steatosis; ROS from MEOS drives progression to hepatitis and cirrhosis.
↑ Accumulates: NADH, triglycerides in hepatocytes, glycerol-3-phosphate, ketone bodies· ↓ Deficient: NAD⁺, pyridoxal phosphate (ALT), B12/folate
Presentation: reversible fatty liver → alcoholic hepatitis (potentially reversible) → fibrosis (partially) → cirrhosis (irreversible)
Labs: AST > ALT (≥2:1), ↑ GGT (sensitive marker), ↑ bilirubin, ↑ INR, ↑ MCV (macrocytosis from B12/folate deficiency)
Treatment: Abstinence; supportive care
FA β-oxidation blocked + Glycerol-3-P increased → Triglycerides accumulate
Learn the mechanism: Ethanol metabolism →
FMK 03.4 Fructose, Galactose & Ethanol Metabolism · slide 17, 20, 23, 25, 26; FMK 04.4 slide 26