A 40-year-old woman on phenelzine (an MAOI) for refractory depression eats a tyramine-rich meal (aged cheese). She develops a sudden severe headache, hypertensive crisis (BP 220/130), and diaphoresis. What is the MECHANISM of this hypertensive crisis?
- A MAO inhibition causes direct vasoconstriction through serotonin receptors
- B Tyramine directly blocks alpha-1 adrenergic receptors
- C MAO inhibition prevents tyramine metabolism in the gut/liver; absorbed tyramine displaces norepinephrine from presynaptic terminals causing a sympathomimetic surge ✓
- D MAOI causes increased renal sodium retention
Explanation
Normally, dietary tyramine is metabolized by MAO-A in the gut wall and liver before reaching systemic circulation. When MAO is inhibited by phenelzine, tyramine is absorbed intact into systemic circulation. Tyramine is an indirect sympathomimetic—it enters adrenergic neurons via the norepinephrine transporter and displaces norepinephrine from synaptic vesicles (via VMAT2), causing a massive release of catecholamines, resulting in a hypertensive crisis. Treatment is phentolamine (alpha-blocker) or nifedipine (calcium channel blocker). This 'cheese effect' is the most dangerous dietary interaction of MAOIs.
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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