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Flashcards in Pharm. Management of Headache Deck (9)
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1
Q

Pathophysiology of migraine

A

Current understanding suggests that a primary neuronal dysfunction leads to a sequence of intracranial and extracranial changes that account for migraine symptoms. There is strong evidence to implicate serotonin (5HT) in the pathogenesis of migraine.

2 phases:

  1. Cerebral vasoconstriction and ischemia. Serotonin release (5HT) from neurons and platelets (PERIPHERAL MECHANISMS) that acts on 5-HT2 receptors contributes to this phase.
  2. Cerebral vasodilation and pain. Trigeminal neurovascular system appears to have a central role in the second phase. Neurons in the trigeminal complex release the vasoactive peptides substance P [SP] and calcitonin gene-related peptide [CGRP] that trigger vasodilation and neuroinflammation of pial and dural vessels (sensory nerve discharge). This in turn stimulates nociceptive fibers of the trigeminal nerve that causes pain.
2
Q

Treatment of migraines

A
  1. NSAIDs and Acetaminophen
  2. If not enough, use triptans (sumatriptan)
  3. Ergot Alkaloids (Dihydroergotamine)
3
Q

Preventive therapy for migraines

A
  1. Antihypertensive agents (beta-blockers: 1st line, a channels blockers, ACE inhibitors)
  2. Antidepressants
  3. Anticonvulsants
  4. Botox
  5. Methysergide (serotonin antagonist)
  6. NSAIDs
  7. Dietary supplements (Riboflavin, butterbur, feverfew)
4
Q

Preventive therapy for tension headaches

A

SSRIs

5
Q

Abortive therapy for tension headaches

A

NSAIDs and muscle relaxants

6
Q

Adverse drug rxns with sumatriptan

A

Paresthesias, flushing, dizziness, drowsiness, chest tightness

Rarely: coronary vasospasm, angina, MI, arrhythmia, stroke, death

7
Q

Drug-drug interactions with sumatriptan

A

Additive vasoconstriction with ergot alkaloids

Increased risk of serotonin syndrome** with MAOIs - risk very much less with SNRIs-SSRIs

8
Q

Adverse drug rxns with ergot alkaloids

A

Nausea / vomiting (give w/antiemetic), diarrhea, cramps, paresthesias

Serious effects: vascular occlusion and gangrene (strict dosage limits)

Mediated via α1 adrenergic vasoconstriction

9
Q

Drug-drug interactions with ergot alkaloids

A

Severe peripheral ischemia if used with non-selective (β1-β2) beta-blockers