PharmacologyTier 1Medical Sciences concept

MAOI-tyramine interaction (hypertensive crisis mechanism)

Core concept

MAOIs inhibit monoamine oxidase A (and B) -> dec breakdown of noradrenaline, serotonin, dopamine and dietary tyramine
Normally, gut/liver MAO-A degrades dietary tyramine before absorption ("cheese reaction" prevention)
MAOI blocks this -> tyramine absorbed intact -> displaces noradrenaline from presynaptic vesicles -> massive noradrenaline release -> hypertensive crisis

Key detail

Tyramine-rich foods: aged cheese, cured/fermented meats, tap beer, red wine, soy sauce, overripe fruit, marmite/vegemite (moderate)
Effect is indirect sympathomimetic (tyramine itself weak, acts via NA release) -- distinguishes mechanism from direct-acting pressors
Risk persists for ~2 weeks after stopping an irreversible MAOI (phenelzine, tranylcypromine) until new MAO enzyme is synthesised

Clinical relevance

Presents as sudden severe hypertension, headache, palpitations, sweating -- hypertensive emergency
Treat with short-acting agents titratable to effect (e.g. phentolamine, nitroprusside) -- avoid drugs relying on further catecholamine release
Also avoid indirect sympathomimetics (pseudoephedrine, amphetamines) and pethidine/serotonergic drugs in MAOI patients -- separate but compounding risks

Correlations

Reversible MAO-A inhibitors (moclobemide) carry much lower dietary tyramine risk -- MAO-A regenerates faster, less complete inhibition
MAOI + SSRI/SNRI/pethidine/tramadol -> serotonin syndrome, a distinct interaction from the tyramine reaction
Same indirect-sympathomimetic-displacement mechanism underlies amphetamine and ephedrine pressor effects

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