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.
Glycolysis
Pyruvate
Made from Phosphoenolpyruvate by Pyruvate kinase
Pyruvate kinase · irreversible — Glycolysis
Cofactors: ADP → ATP (substrate-level)
Activated by: Fructose-1,6-bisphosphate (feed-forward)
Inhibited by: ATP; Alanine; Glucagon (phosphorylation via PKA, liver isoform)
Deficiency: Pyruvate kinase deficiency — most common glycolytic enzyme defect; chronic hemolytic anemia with echinocytes (burr cells), splenomegaly, ↑ reticulocytes; heterozygotes resist P. falciparum
Second substrate-level phosphorylation. Hepatic isoform is switched off by glucagon so PEP is diverted to gluconeogenesis.
Condition cards:Pyruvate kinase (PK) deficiency →
Becomes Lactate via Lactate dehydrogenase
Lactate dehydrogenase — Glycolysis
Cofactors: NADH → NAD⁺
Anaerobic fate: regenerates NAD⁺ so GAPDH can keep running. Hypoxia, ETC poisons, or PDH failure all push pyruvate here → lactic acidosis.
Condition cards:Warburg effect (cancer aerobic glycolysis) →
Becomes Acetyl-CoA (→ TCA) via Pyruvate dehydrogenase complex
Pyruvate dehydrogenase complex — Glycolysis
Cofactors: TPP (B₁), Lipoic acid, CoA (B₅), FAD (B₂), NAD⁺ (B₃)
Aerobic fate — in the mitochondrion (see PDH & TCA). Irreversible: carbons that reach acetyl-CoA can never become glucose again.