Migraine Flashcards

1
Q

Features of a migraine

A
  • duration (4-72 hours)
  • Pulsating, more less unilateral
  • moderate to severe pain
  • impair function
  • nausea/vomiting more less photo/photophobia
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2
Q

Consistently two major issues

A
  • Vascular

- Neurogenic

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3
Q

Vascular theory on migraines

A
  • begins with vasoconstriction of cerebral vessels
  • the subsequent reduction in blood flow causes the ‘aura’
  • then there is a compensatory dilation of vessels, which leads to pain
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4
Q

Neurogenic theory on migraines

A
  • attacks precipitated by excess excitation in neocortex
  • followed by ‘cortical spreading depression’ (CSD): rapid and profound depolarization of neurons
  • this CSD leads to the aura and this triggers the pain
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5
Q

Pharmacology of migraines

A
  • dilation/inflammation of cerebral vessels
  • release of pain mediators
  • serotonin seems to play a role in both
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6
Q

Treatment of migraines

A

Triptans

Ergots

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7
Q

Sumatriptan mechanism

A

Agonist at 5HT-1B and 5HT-1D
Vasoconstrictor
Reduced release of pain transmitters

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8
Q

Sumatriptan pharmacokinetics and ROA

A
Onset varies depending on route 
Routes of administration
- Oral
- Nasal spray
- Subcutaneous
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9
Q

Triptans side effects related to vasoconstriction

A
Related to vasoconstriction 
- chest/neck discomfort 
Rare, serious:
- myocardial ischemia/infarction
- Avoid in patients with cardio-/cerebrovasscular disease
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10
Q

Triptans side effects due to serotonin

A

Nausea

Caution: serotonin syndrome

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11
Q

Ergot alkaloids example

A

Dihydroergotamine

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12
Q

Dihydroergotamine mechanism

A

Agonist at 5HT-1B, 5HT-1D, and alpha 1

  • vasoconstrictor
  • reduced release of pain mediators
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13
Q

Route of administration of ergot alkaloids

A

Injectable

Nasal Spray

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14
Q

Acute Migraine treatment

A
Anti-inflammatory: NSAIDs
Acetaminophen 
Opioids
- codeine containing products
- Butorphanol
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15
Q

Opioids in migraine

A
  • not addressing main issues, no vasoconstriction effects, no anti-inflammatory effects
  • tolerance/withdrawal/dependence
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16
Q

Butorphanol mechanism

A
  • partial agonist/mixed agonist-antagonist at opioid receptors
  • more likely to see dysphoria
  • kappa agonist
17
Q

Butorphanol route of administration

A

Nasal spray

- definite potential for dependence

18
Q

Medication overuse headache

A
Frequent headaches (>15/month)
- Can occur with any drugs for migraine: some drugs are higher risk than others
19
Q

MOH mechanism

A
  • unknown
  • effects of chronic drug use for headache: changes in neurotransmitter levels, decreases threshold for developing a subsequent headaches
20
Q

MOH management

A
  • discontinue headache medication

- switch to prophylaxis

21
Q

Migraine prophylaxis

A
Reuptake inhibitors (tricyclic antidepressants)
Na+ channel blockers (Valproic Acid) 
Calcium alpha 2 delta channel blockers (Gabapentin)
22
Q

Pain mechanism

A
  • Increase number of Na+ channels
  • Facilitates propagation of action potentials (noxious stimuli no longer necessary
  • Calcium channel opens
  • prompts release of pain mediators
23
Q

Beta blockers for migraine

A

Propranolol

24
Q

Beta blockers mechanism

A

Inhibit SNS activity - may modulate hyperexcitability

Some beta blockers may also modulate 5HT: off target effects

25
Q

Calcium channel blocker for migraines

A

Verapamil