Migraine HA: Treatment And Prevention Flashcards Preview

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Flashcards in Migraine HA: Treatment And Prevention Deck (20)
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1
Q

What is a migraine?

A

Special form of neurovascular headache. Neural events provoke dilation of cranial blood vessels, which result in pain, further sensory and central nerve activation.

2
Q

What is the feature of a classic migraine headache?

A

Aura-> visual disturbance.

3
Q

What are the three main phase of a migraine time course?

A

1) prodrome-yawning, depression, lethargy, excitability
2) headache-mostly unilateral photophobia, photophobia, N/V
3) postdrome- exhaustion fatigue

4
Q

What are the class of drugs that are used for therapy (not prevention) of migraines and when should they be taken?

A
  • Tripatans- 5HT1B/1D receptor agonists
  • Taken at the start of the prodrome phase

-Ergot alkaloids are the older drug of choice to be given during this phase.

5
Q

What are the drugs of choice that can be used during the headache phase of a migraine?

A
  • NSAIDS

- Acetaminophen

6
Q

What are the agents that can be used for prevention of migraines?

A
  • Beta blockers
  • Tricyclic antidepressants
  • AEDs
  • Ca2+ channel blockers
7
Q

What is the etiology of a migraine?

A

-A wave of electrical activity and H+, K+ passing through nerve cells stimulates the release of neuropeptides ( CGRP, substance P) and inflammatory mediators (NO, histamine, prostaglandins) that dilate cranial blood vessels and sensitize nerves to pain.

8
Q

What is the generalized accepted events that lead to migraine formation?

A

1) Brainstem dysfunction sparks a wave of excitation/depression in cortex. This is accompanied by H+, K+, NO discharge—> cerebral vasoconstriction pushes blood into the cranial vasculature!
2) Electrolytes and NO diffuse and dilate cranial arteries and depolarize peri vascular Trigeminal terminals. This leads to CGRP and neuropeptides release–> promote neurogenic inflammation.
3) The neurogenic inflammation irritates TG nerve and transmits migraine pain.

9
Q

What commonly used CV medication can provoke migraines?

A

NO used in angina

10
Q

What subtype of 5HT receptors are located on cranial vessels, peripheral neurons, and central neurons?

A
  • Cranial vessels-> 5HT-1B
  • Peripheral vessels-> 5HT-1D
  • Central Neuron-> 5HT-1B/1D
11
Q

What is the MOA of Triptans?

A
  • Binding to 5HT1B receptor (on blood vessels) lowers cAMP and oppose the dilation.
  • Binding to 5HT-1D receptor (on nerves) lowers cAMP thus inhibiting pre-synaptic release of CGRP.
12
Q

What is the prototypical Triptan?

A
  • Sumatriptan.
  • Can be administered via nasal spray and oral tablet (poor bioavability)
  • meatabolized by MAO
13
Q

What two Triptans have longer t1/2?

A
  • Almotriptan
  • Naratriptan

T1/2 about 6 hrs

14
Q

What Triptan has an active metabolite?

A

Zolmitriptan

15
Q

What are the forms of administration of Sumatriptan?

A

-injection, nasal spray, tablets

16
Q

What are the forms of administration of Zolmitriptan?

A

-Tablets, orally disintegrating tablets, nasal spray

17
Q

When are Triptans contraindicated?

A

-Patients with ischemic heart disease, uncontrolled HTN, other CV disorders.

18
Q

What is the next mediations that can be used if Triptans do not provide relief for the patient?

A
  • Egot alkaloids.
  • Dihydroergotamine
  • Ergotamine and caffeine

These are less specific, they interact with alpha receptors, dopamine receptors, and various 5HT receptors. Act as agonists, partial agonists, and antagonists.

19
Q

What is a potential serious side effect of ergot alkaloids?

A
  • Strong emetic action

- Most severe is vasoconstriction! Can lead to dry gangrene( St. Anthony’s Fire)

20
Q

What is the Ca2+ blocker that can be used in prophylactic treatment of migraines?

A

Verapamil-> very safe and do not desentisize overtime.