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Flashcards in Migraine Drugs Deck (23)
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1

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

- trigeminovascular

2

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

- calcitonin gene related peptide (CGRP)

3

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

may also induce

- vasodilation


- inflammatory response
- sensitization of trigeminal sensory neurons

4

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

role of this hormone

- serotonin


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

5

stimulation of beta 2 receptors on vascular smooth muscle causes

MOA of beta blockers

- relaxation
- vasodilation

- promote vasoconstriction
- reduce cranial blood flow

6

best beta blockers to use for preventing migraines

- propranolol

7

toxicities of beta blockers

- arrhythmias
- hypotension

8

examples of calcium channel blockers

- verapamil

9

MOA of calcium channel blockers in preventing migraine

- inhibit vascular smooth muscle contraction (which is weird because vasodilation is the problem normally)
- reduce BP

10

MOA of tricyclic SNRI anti-depressants in treating migraine

- 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

11

example of tricyclic SNRI used to treat migraines

- amitriptyline

12

toxicities of tricyclic SNRIs



what population do we not use these in?

- anti-cholinergic
- xerostoma, constipation, urinary retention, blurred vision


- not recommended in the elderly

13

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

MOA

- valproate
- topiramate

- may influence signaling pathways associated with the migraine generator

14

MOA of Erenumab


how often do you have to administer

- binds to CGRP receptor and prevents CGRP from activating it

- 4-12 weeks

15

MOA of Fremanezumab

how often do you have to administer

- binds CGRP itself and blocks binding to receptor

- 4-12 weeks

16

MOA of Galcanezumab

how often do you have to administer

- binds CGRP itself and blocks binding to receptor

- 4-12 weeks

17

toxicities of the CGRP and CGRP receptor antibodies

- injection site reaction

18

drugs for the acute treatment of migraines

- ergotamine
- triptans

19

MOA of triptans


route of administration

- serotonin 5HT-1B/D presynaptic autoreceptor agonist
- inhibit release of CGRP

- oral

20

MOA of dihydroergotamine



route of administration

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

- IV

21

toxicities of triptans

- paresthesia (tingling, numbness, itch, tactile feelings)
- transient spike in BP, myocardial ischemia and stroke secondary to vasoconstriction

22

toxicities of dihydroergotamine

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

23

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

avoid with

- triptans
- dihydroergotamine

- SSRIs, SNRIs, and MAOIs