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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)

Prostaglandins (PGE₂) — cyclopentane ring

Made from Free arachidonic acid by Cyclooxygenase (COX-1 / COX-2)

Cyclooxygenase (COX-1 / COX-2) · irreversible — Eicosanoids (COX / LOX)

Inhibited by: NSAIDs — ibuprofen, naproxen (reversible); Aspirin (irreversible acetylation); Celecoxib (COX-2 selective); Acetaminophen (mainly central)

Deficiency: NSAID-induced GI bleeding — loss of COX-1 prostaglandins that maintain gastric mucus, bicarbonate and mucosal blood flow

COX-1 is constitutive — gastric mucosa, platelets, kidney; COX-2 is induced at sites of inflammation. Blocking COX also removes the protective prostaglandins of the stomach lining, "the mechanistic basis for NSAID-induced GI bleeding" (s22).

Condition cards:NSAID-induced GI bleeding →

Becomes Gastric mucosa · pain · fever · uterine tone via PGE₂ on EP receptors

PGE₂ on EP receptors — Eicosanoids (COX / LOX)

Gastric mucus and bicarbonate, mucosal blood flow; also pain sensitisation, fever (hypothalamic set-point) and uterine tone. Misoprostol is a PGE₁ analogue given to protect the stomach during chronic NSAID use.