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Phar 301 > Migraine > Flashcards

Migraine Flashcards

1
Q

What are the 4 stages of migraine?

A

1) Prodromal phase (warning signs) - some patients
2) Aura: 1 in 3 patients
3) Headache (+ other symptoms)
4) Sleep

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2
Q

What is the term for Migraine with aura

A

“Classic” migraine

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3
Q

What are the 3 characteristics of a classic migraine?

A 
Less common
Two or more headaches preceded by aura
Aura symptoms:
  - blurred vision
  - flashing lights/zig-zag
  - missing area of visual field ("scotoma")
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4
Q

What are the 2 characteristics of aura symptoms?

A 
Fully reversible (within an hour)
Start at most 30 minutes before pain
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5
Q

What are the 3 characteristics of Migraine without aura?

A 
Lasts 4-72 hrs
At least two of:
  - unilateral
  - pulsating
  - moderate/severe intensity
  - aggravated by physical activity
At least one of:
  - nausea
  - vomiting 
  - photophobia
  - phonophobia
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6
Q

Migraine is more common in _____ (women / men)

A

Women

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7
Q

Why is migraine one of the most disabling disorders (*WHO)

4 symptoms

A
  • Quadriplegia
  • Psychosis
  • Dementia
  • Migraine
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8
Q

What are 3 prophylactic drugs for migraine?

A
  • Propranolol (beta blockers)
  • Valproate
  • Imipramine (Tricyclic “Antidepressants”)

These drugs are “successful” in that they prevent 50% of attacks. None is the best in terms of adverse effects (propranolol and Valproate is probably best)

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9
Q

What is the most common prophylactic drug?

A

Propranolol

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10
Q

True/False? Most Prophylactic drugs have several molecular targets

A

True

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11
Q

What are the main adverse effects of Propranolol?

A

Contraindicated where beta block causes problems

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12
Q

What are the main adverse effects of Valproate?

A

Thinning hair, fetal malformations

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13
Q

What are the main adverse effects of TCAs?

A

eg. alcohol interaction and OD risk

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14
Q

What are the main adverse effects of Topiramate?

A

Paresthesias (Tingling, pins & needles)

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15
Q

What is an abortive drug?

A

A drug used to acutely treat migraine attacks?

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16
Q

What are the 3 types of abortive drugs for migraine learned in class?

A

NSAIDs, Narcotic Analgesics, and 5-HT agonists

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17
Q

What is often given with NSAIDs when treating migraine?

A

anti-emetics

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18
Q

What is the only disadvantage of Narcotic analgesics as an abortive drug for migraine

A

Abuse

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19
Q

What are the 2 main types of 5-HT agonists for treatment of migraine?
Are they preferred over other migraine drugs? Which is used more?

A

Ergotamine, dihydroergotamine (ergot derivatives)
Triptans (____-triptan)

Triptans are more effective with fewer side effects
Mainstay for moderate-severe migraine

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20
Q

True/False? Ergot derivatives are pharmacologically richer and are more effective with fewer side effects than triptans

A

False, just richer

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21
Q

What was the prototype triptan?

A

Sumatriptan

22
Q

True/False, the preferred route of administration for sumatriptan is oral because it provides relief sooner

A

False, much slower than subcutaneous but easier

23
Q

True/False? sumatriptan is better than ergotamine, and better than ergotamine + caffeine

A

True

24
Q

Why is caffeine administered with ergotamine?

A

Caffeine increases GI absorption of ergotamine by complexing with it

25
Q

True/False? sumatriptan only works for headache symptoms

A

False, works for nausea and sensitivity to light/sound

26
Q

Adverse effects of ergot-derived drugs and triptans?

A

Both are vasoconstrictive, ergots cause mental disturbance and triptans cause myocardial ischemia (constricts coronary arteries)

27
Q

List the meninges in order of increasing proximity to the brain

A

dura mater
arachnoid
(subarachnoid space)
Pia mater

28
Q

List the evidence (3) for Wolff’s Vasodilation hypothesis

A
  • Pain pulsates like vessels
  • Vascular disease patients often suffered from headache
  • pain from:
    • stimulation of meningeal vessels
    • nitroglycerin (vasodilator)
    • angioplasty (dilating vessels)
29
Q

What is Wolff’s vasodilation hypothesis for the mechanism of a headache?

A

Some trigger ends up triggering vasodilation, and this is sensed by the NS causing pain

30
Q

What are the 5 cracks in Wolff’s vasodilation hypothesis?

A
  • vessel does not pulsate (as much as he thought)
  • vascular disease - more than vascular?
  • vasoconstriction in migraine?
  • vasodilation and pain have different pain courses
  • angioplasty dilates but also scrapes, and is usually not painful anyway
31
Q

What is the dominant hypothesis for the mechanism of action of migraine and what is the mechanism?

A

Neurogenic inflammation:

Trigger causes neurogenic inflammation, which causes vasodilation and also pain (the two are unrelated)

32
Q

How is pain produced according to the neurogenic inflammation hypothesis?

A

A trigger depolarizes the nerve terminals of the trigeminal terminal
The action potential rides up the CNS and is interpreted as pain (releases neuropeptides which cause pain)

33
Q

How is inflammation produced according to the neurogenic inflammation hypothesis?

A

A trigger depolarizes the nerve terminals of the trigeminal terminal
Neuropeptides released from this act on inflammatory cells of the immune system
IC release inflammatory mediators, which cause edema and plasma extravasation
Inflammatory mediators act on nerve terminal making them more sensitive (+ve feedback)

34
Q

What is the name of the fibers that innervate vessels?

A

C-fibres

35
Q

How can we measure inflammation in a patient?

A

CGRP (a vasodilator) can be detected in plasma

mast cells release cytokine, eicosanoids, histamine

36
Q

True/False? the sensory neurons on a rat brain’s transverse sinus are ipsilateral

A

True

37
Q

Why might inflammation cause pain?

A

Terminal ganglion cells respond to “inflammatory soup” and cause pain

38
Q

True/False? inflammatory soup can make the dura more sensitive to forces

A

True (10x)

39
Q

What are the 3 types of 5-HT receptor?

A

5-HT1
5-HT2
5-HT3

40
Q

What are 3 subtypes of 5-HT1 receptor?

A

5-HT1A
5-HT1B
5-HT1D

41
Q

Which of the 3 5-HT1 receptor subtypes are important for drugs that are abortive to migraine?

A

5-HT1B
5-HT1D
(drugs are 5-HT agonists)

42
Q

Sumatriptan binds selectively to which receptors?

A

5-HT1B

5-HT1D

43
Q

True/False? the Ki of a drug is proportional to its abortive effectiveness

A

True

44
Q

Why does “ergot” have a richer pharmacology?

A

It has high affinity for many things

45
Q

Can sumatriptan cross the blood brain barrier? Why is that important?

A

No, and that helps narrow the search for sites of action

46
Q

Neurogenically-mediated CGRP release is ________ by sumatriptan

A

Inhibited

47
Q

Pain-associated neuronal activation in spinal cord ______ by sumatriptan

A

reduced

48
Q

What causes the progression of a migraine attack (with aura)?

A

Trigger in visual cortex, depolarizes meninges which propagates depolarization to everywhere

Excess ions (K and H) stimulate nociceptors

49
Q

Does the spreading depression of a migraine correspond anatomically to the visual location of aura in humans?

A

Yes

50
Q

What causes scotoma and why doesn’t every migraineur have scotoma?

A

The persistent depolarization of visual cortex neurons inactivates them, leading to scotoma

We don’t know why only some migraineurs experience scotoma

Phar 301 (23 decks)

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