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
Q

Where does Acetaminophen act on COX-2?

A

centrally

26
Q

How many migraines/month are needed to classify it as chronic?

A

15+

27
Q

Botox is only used on _____ migraines.

A

chronic

28
Q

What is the mechanism of action of Botox?

A

block ACh release

29
Q

What are some negatives to Botox tx for migraines?

A

it’s expensive
has to be administered by a pro
can give HAs, neck pain, muscle weakness, ptosis
category C in prego