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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.

Pathway

Eicosanoids (COX / LOX) · Membrane phospholipid → cytosol; local hormones acting on GPCRs near where they are made. Enzymes sit beside the arrows, ★ = rate-limiting, ⊕/⊖ = activators/inhibitors (toggle), −ATP +NADH = what the step spends and makes (toggle ⚡), dashed = allosteric signal, shaded bands = compartment. Drag to pan.

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Eicosanoids (COX / LOX)

Thromboxane A₂ — oxane ring

Made from Free arachidonic acid by Cyclooxygenase (COX-1, platelets)

Cyclooxygenase (COX-1, platelets) — Eicosanoids (COX / LOX)

Inhibited by: Aspirin (irreversible — platelets cannot resynthesise COX)

Thromboxane A₂ "promotes platelet aggregation and vasoconstriction" (s21). Platelets have no nucleus, so aspirin's irreversible acetylation lasts the platelet's ~7–10-day life — the basis of low-dose aspirin for cardiovascular prophylaxis.

Condition cards:Aspirin (irreversible COX suicide inhibition / toxicity) →

Becomes Platelet aggregation · vasoconstriction via TXA₂ on TP receptors

TXA₂ on TP receptors — Eicosanoids (COX / LOX)

Platelet aggregation and vasoconstriction — opposed by endothelial prostacyclin (PGI₂).