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neuro 2-unit 3 (final) > Friday, 8-26-Migraines-Fitzpatrick > Flashcards

Friday, 8-26-Migraines-Fitzpatrick Flashcards

1
Q

NSAIDs and Acetaminophen are useful in treating this phase during a migraine attack:

A

Headache phase

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2
Q

What are some beta-blocking preventive agents for tx of migraine? Ca channel blockers?

A

B blockers –> propanolol, timolol

Ca channel blockers –> verapamil

Given in the Asymptomatic phase

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3
Q

In the Neurogenic inflammation theory of migraine, a wave of electrical activity and H+ and K+ passing through nerve cells stimulates the release of these neuropeptides ___ and these inflammatory mediators ___ that dilate cranial blood vessels and sensitive nerves to pain. Sensitization of nerves progresses from periphery to the brain

A

Neuropeptides=CGRP, Substance P

Inflamm mediators=NO, histamine, PG’s

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4
Q

Neurogenic inflammation is stimulated by ___

A

CGRP (neuropeptide) and NO

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5
Q

In the steps of Cortical Spreading Depression in migraines, step 1 involves brainstem dysfunction sparking a wave of excitation/depression in the cortex. Explain what happens to cerebral vasculature and the discharge from neurons:

A

Cerebral vasocontriction accompanied by H+, K+, NO discharge from neurons

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6
Q

In the steps of Cortical Spreading Depression in migraines, step 2 involves electrolytes and NO diffusing and dilating cranial arteries and depolarize perivascular trigeminal terminals. What promote the neurogenic inflammation in this stage?

A

CGRP and neuropeptides

Step 3 includes Neurogenic inflammation irritating TG nerve and transmitting migraine pain

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7
Q

These 2 key mediators interact throughout the trigeminal neurovascular system in migraines

A

CGRP and NO

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8
Q

___ used to treat CAD can provoke migraine

A

Organic nitrates (NO)

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9
Q

Cranial vessles and pre-synaptic TG nerve terminals express a distinc sub-set of 5-HT-1 receptors: Label the following:

Cranial vessels: __
Peripheral neuron: __
Central neuron: __

A

5HT-1B

5HT-1D

5HT-1B/1D

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10
Q

___ are selective serotonin 5HT-1D/1B receptor agonists

A

Triptans

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11
Q

Triptan binding to ___ receptor lowers cAMP, stimulates vasoconstriction (opposes vasodilation)

A

5HT-1B

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12
Q

Triptan binding to ___ receptor on neurons lowers cAMP and inhibits pre-synaptic release of CGRP

A

5HT-1D

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13
Q

Triptans have a high affinity for __ receptors located centrally in the region of the trigeminal nucleus caudalis in the brainstem. This modulates incoming painful sensory info from the periphery and inhibits upward transmission to the thalamus and higher brain centers where brain is perceived

A

5HT-1D

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14
Q

What is the prototypical triptan? What is it metabolized by?

A

Sumatriptan (Imitrex)

Metabolized by Monoamine Oxidase-A (it is an indoleamine)

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15
Q

These triptans have ~70% bioavailability and t1/2 of ~6 hrs

A

Almotriptan and Naratriptan

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16
Q

This triptan drug is the active metabolite

A

Zolmitriptan

17
Q

These triptans show some evidence of better tolerance, claims of better efficacy (relative to sumatriptan)

A

Rizatriptan and Eletriptan

18
Q

This triptan has a t1/2 of ~24 hrs

A

Frovatriptan

19
Q

What are pros and cons of PO triptans?

A

Pros=easy to take

Cons=ineffective if vomit

20
Q

What are pros and cons of nasal spray triptans?

A

Pros=effective with nausea/vomiting, simple, works quickly

Cons=few triptans formulated as nasal sprays

21
Q

What are pros and cons of injectable triptans?

A

Pros=works quickly

Cons=inconvenient

22
Q

Which triptans have the most delivery options?

A

Sumatriptan –> injectable subQ, nasal spray, tablets

Zolmitriptan–> tablets, orally disintegrating tablets, nasal spray

23
Q

What are some contraindications for triptan usage?

A

Contraindicated in pts with a history or suspicion of ischemic or vasospastic coronary disease or other significant CV disorder and pts with uncontrolled HTN

24
Q

Sumatriptan, rizatriptan, and zolmitriptan are contraindicated in pts taking ____

A

MAO inhibitors –> They are metabolized by MAO

25
Q

This class of drugs are still used for severe or refractory migraine. They are less specific and interact with alpha receptors, dopamine receptors, various 5-HT receptors and exhibit mixed action at different receptors - agonist, partial agonist, antagonist

A

Ergot alkaloids –> dihydroergotamine and Ergotamine and caffeine (Cafergot)

26
Q

What are some ergot alkaloids?

A

Dihydroergotamine –> sublingual, intranasal, IV, IM, SC

Ergotamine and caffeine (Cafergot) –> oral tablet, rectal suppository

27
Q

WHat should you never use a triptan with?

A

NEVER use a triptan and DHE together

28
Q

What are some side effects of ergot alkaloids?

A
  • poisons/drugs of antiquity
  • strong emetic action is a major side effect
  • vasoconstriction is worse than that seen with triptans (Saint anthonys fire)
29
Q

When should you use the following for migraine tx in pregnancy:

Aspirin: ___
Ibuprofen: __
Triptans: ___

A

Aspirin-1st, 2nd trimesters only
Ibuprofen-1st, 2nd trimesters only
Triptans-cautiously

30
Q

What migraine tx drugs are contra-indicated in pregnancy?

A

Dihydroergotamine

Other ergot alkaloids (abortion risk)

31
Q

BOTOX cleaves SNAP-25 in motor neurons, which inhibits ___ release at the motor endplate

A

Ach

32
Q

This Ca channel blocker for migraine prevention is often a 1st choice because of a good side effect profile

A

Verapamil

Normalizes vessel tone, lessens Ca-dependent vesicle fusion

33
Q

What beta blockers are FDA approved for migraine prevention?

A

Propanolol or Timolol

Anxiolytic action
Decreases sympathetic activity
Blunts cortical spreading depression
Clinically effective in 60-80% pts
Lower frequency of attacks by ~50%
34
Q

What is a contraindication for beta blocker use in migraine preventative tx?

A

Asthmatic pts

35
Q

These anti-epilepsy drugs are approved for and effective in migraine prevention in adults

A

Topirimate and valproate

36
Q

Triptans (5HT1B/1D) receptor agonists and Ergot alkaloids are useful for this phase of a migraine attack:

A

Prodrome phase

neuro 2-unit 3 (final) (15 decks)

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