Pharm Management of Headaches Flashcards

1
Q

When would you choose to use a -triptans over an NSAID in termination of a migraine?

A

NSAIDs = first line, mild-moderate pain

use -triptans for more severe migraines or those that don’t respond to NSAIDs

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2
Q

Do you choose -triptans or ergot alkaloids first? Why?

A

-triptans bc ergot alkaloids aren’t as effective and they carry risk of vascular occlusion and gangrene

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3
Q

Vascular occlusion and gangrene are rare but major SEs for which drug?

A

ergot alkaloids

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4
Q

What 6 drugs can be used for migraine prophylaxis?

A

beta blockers, anticonvulsants, antidepressants, calcium channel blockers, NSAIDs, 5Ht2 receptor antagonists

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5
Q

Name 6 drugs for migraine abortion in order from mild–> severe pain tx.

A

NSAIDs, triptans, ergot alkaloids (ergotamine/DHE), isometheptene, tramadol

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6
Q

What are some contraindications for NSAIDs?

A
acute gastritis
peptic ulcer disease
renal insufficiency
bleeding disorders 
chronic use/prolonged periods
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7
Q

Name some non-pharm preventions for migraines.

A

avoid triggers

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8
Q

Are NSAIDs used for migraine abortion or prevention?

A

both

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9
Q

How do the triptans work?

A

they’re 5T 1b-1d agonsists (reverse vasoconstriction; prevent neuroinflammation; prevent activation of pain fibers)

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10
Q

How do the ergot alkaloids work?

A

they’re 5HT 1b-1d receoptor agonists (reverse vasoconstriction; prevent neuroinflammation; prevent activation of pain fibersreverse vasoconstriction; prevent neuroinflammation; prevent activation of pain fibers)

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11
Q

What is a problem with treating headaches with drugs?

A

you can develop analgesic overuse headaches

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12
Q

What is the first-line drug for migraine prophylaxis?

A

beta blockers (propranolol)

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13
Q

What is Spreading Cortical Depression and what does it cause?

A

a self-propagating wave of neuronal and glial depolarization that causes aura of migraine, activates trigeminal afferents, and changes the BBB permeability –> vasodilation, pain

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14
Q

This is a self-propagating wave of neuronal and glial depolarization that causes aura of migraine, activates trigeminal afferents, and changes the BBB permeability –> vasodilation, pain.

A

Spreading Cortical Depression

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15
Q

How does sensitization affect migraines?

A

causes throbbing pain, worsening of pain w/ mvmt or coughing, etc

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16
Q

How does serotonin affect migraines?

A

unsure phys for generation of migraine, but we know agonists are good tx’s

17
Q

What is Imitrex?

A

a triptan (sumatriptan)

18
Q

On which receptor does ergotamine (DHE/Migranal) act? What kind of receptor is it? What is the effect??

A

serotonin 1B (Gi/o) –> presynaptic inhibition –> prevent vasoconstriction

19
Q

On which receptor does sumatriptan (Imitrex) act? What kind of receptor is it? What is the effect??

A

serotonin 1D (Gi/o) –> decrease presynaptic release–> prevent vasoconstriction

20
Q
Which drug?
serotonin 1D (Gi/o) --> decrease presynaptic release--> prevent vasoconstriction
A

sumatriptan (Imitrex)

21
Q
Which drug?
serotonin 1B (Gi/o) --> presynaptic inhibition --> prevent vasoconstriction
A

ergotamine (DHE/Migranal)

22
Q

What is DHE?

A

an ergot alkaloid (dihydroergotamine)

23
Q

What are some rare but major SEs of the triptans?

A

coronary vasospasm, angina, MI, arrhythmia, stroke

24
Q

What causes vascular occlusion and gangrene in ergot alkaloid use?

A

alpha-1 adrenergic vasoconstriction

25
Where does Acetaminophen act on COX-2?
centrally
26
How many migraines/month are needed to classify it as chronic?
15+
27
Botox is only used on _____ migraines.
chronic
28
What is the mechanism of action of Botox?
block ACh release
29
What are some negatives to Botox tx for migraines?
it's expensive has to be administered by a pro can give HAs, neck pain, muscle weakness, ptosis category C in prego