Migraine Drugs Flashcards

1
Q

the signals created by the migraine generator are carried by the _________ system

A
  • trigeminovascular
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2
Q

signals from the migraine generator induce the release of ______ from trigeminal sensory neurons in the dura mater and subarachnoid space

A
  • calcitonin gene related peptide (CGRP)
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3
Q

CGRP binds to its cognate receptor on vascular smooth muscle and causes __________

may also induce

A
  • vasodilation
  • inflammatory response
  • sensitization of trigeminal sensory neurons
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4
Q

data also show that the level of ______ in the brain decreases during migraines

role of this hormone

A
  • serotonin
  • induces vasoconstriction through 5HT-2A receptor
  • blocks release of CGPR by agonizing the presynaptic 5HT-1B/D receptors on vascular smooth muscle
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5
Q

stimulation of beta 2 receptors on vascular smooth muscle causes

MOA of beta blockers

A
  • relaxation
  • vasodilation
  • promote vasoconstriction
  • reduce cranial blood flow
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6
Q

best beta blockers to use for preventing migraines

A
  • propranolol
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7
Q

toxicities of beta blockers

A
  • arrhythmias

- hypotension

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8
Q

examples of calcium channel blockers

A
  • verapamil
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9
Q

MOA of calcium channel blockers in preventing migraine

A
  • inhibit vascular smooth muscle contraction (which is weird because vasodilation is the problem normally)
  • reduce BP
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10
Q

MOA of tricyclic SNRI anti-depressants in treating migraine

A
  • increase synaptic concentrations of serotonin and NE
  • promote serotonin-induced vasoconstriction in cranial arteries
  • reduce likelihood that stress acts as a trigger for migraine attack
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11
Q

example of tricyclic SNRI used to treat migraines

A
  • amitriptyline
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12
Q

toxicities of tricyclic SNRIs

what population do we not use these in?

A
  • anti-cholinergic
  • xerostoma, constipation, urinary retention, blurred vision
  • not recommended in the elderly
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13
Q

the anti-seizure drugs ____ and ____ are first-line drugs in the prevention of migraines

MOA

A
  • valproate
  • topiramate
  • may influence signaling pathways associated with the migraine generator
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14
Q

MOA of Erenumab

how often do you have to administer

A
  • binds to CGRP receptor and prevents CGRP from activating it
  • 4-12 weeks
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15
Q

MOA of Fremanezumab

how often do you have to administer

A
  • binds CGRP itself and blocks binding to receptor

- 4-12 weeks

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16
Q

MOA of Galcanezumab

how often do you have to administer

A
  • binds CGRP itself and blocks binding to receptor

- 4-12 weeks

17
Q

toxicities of the CGRP and CGRP receptor antibodies

A
  • injection site reaction
18
Q

drugs for the acute treatment of migraines

A
  • ergotamine

- triptans

19
Q

MOA of triptans

route of administration

A
  • serotonin 5HT-1B/D presynaptic autoreceptor agonist
  • inhibit release of CGRP
  • oral
20
Q

MOA of dihydroergotamine

route of administration

A
  • serotonin 5HT-1B/D presynaptic autoreceptor agonist
  • alpha 1 stimulator to induce vasoconstriction and reduce local blood flow
  • IV
21
Q

toxicities of triptans

A
  • paresthesia (tingling, numbness, itch, tactile feelings)

- transient spike in BP, myocardial ischemia and stroke secondary to vasoconstriction

22
Q

toxicities of dihydroergotamine

A
  • induce uterine smooth muscle contraction (pregnancy category X)
  • transient spike in BP, myocardial ischemia and stroke secondary to vasoconstriction
23
Q

which migraine drugs do you also have to be careful with because of serotonin syndrome

avoid with

A
  • triptans
  • dihydroergotamine
  • SSRIs, SNRIs, and MAOIs