Master Sumatriptan with Picmonic for Medicine

Sumatriptan is a quick-acting medication and exhibits a short half-life, which is roughly 2 hours.

This drug binds to 5-HT1B/1D autoreceptors which inhibit the firing of serotonin neurons and cause a reduction in the synthesis and release of serotonin upon activation. After sumatriptan binds to these receptors, adenylate cyclase activity is inhibited via regulatory G-proteins, intracellular calcium is increased, and other intracellular events are affected. This results in vasoconstriction and inhibition of trigeminal nerve firing.

Triptans cause adenylate cyclase activity inhibition via regulatory G-proteins. This increases intracellular calcium, and affects other intracellular events, leading to inhibition of sensory nociceptive (trigeminal) nerve firing.

As this drug inhibits adenylate cyclase activity via regulatory G-proteins (through 5-HT autoreceptor activity), intracellular Ca2+ increases. This causes vasoconstriction and reduces vascular dilation.

This drug is indicated to treat acute migraine headache attacks.

Sumatriptan is efficacious in treating cluster headaches. This drug has been shown to abort cluster headaches within 15 minutes of administration in 96% of patients.

When sumatriptan is used in combination with other drugs that have 5-HT agonist function (e.g., tricyclic antidepressants as migraine prophylaxis), there is an increased risk of serotonin syndrome.

Mild paresthesias including tingling and numbness are reported in up to 14% of patients who use sumatriptan.

Rarely, sumatriptan can lead to coronary vasospasm in patients, and thus should be used with caution in cardiac patients.

Sumatriptan is contraindicated in patients with Prinzmetal's angina due to vasospastic side effects.

Sumatriptan is associated with a general cardiac risk and is contraindicated in patients with severe coronary artery disease (CAD).