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NMSK B Test 1 > LG 2.6 Pharmacology of Migraine Headache Medication > Flashcards

LG 2.6 Pharmacology of Migraine Headache Medication Flashcards

1
Q

What is the aura phase of a migraine?

A

Decrease in blood flow occipital lobe

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2
Q

What is the headache phase of the migraine?

A

Inflammation of meninges to trigeminal sensory nerve fibers

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3
Q

What is the main potent vasodilator of a migraine?

A

Calcitonin gene related peptide (CGRP)

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4
Q

What is the MOA of -triptans?

A

i. Vasoconstiction of painful intracranial extra cerebral vessels
ii. Inhibition of vasoactive neuropeptide
iii. Inhibition of nociceptive neurotransmission

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5
Q

What is the main use of -triptans?

A
  • Migraine pain

- Nausea, vomiting, photophobia, phonophobia

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6
Q

What is the procedure for selecting the right Triptan?

A

Triptans can be chosen via the 3 F’s:

  • Fast versus slow onset of activity; duration of action can be important for some patients
  • Formulation (oral, injection, nasal)
  • Formulary tier and availability (sumatriptan =generic)
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7
Q

What are the pharmockinetics of triptan?

A
  • oral, nasal, subcutaneous (Sumatriptan)

- rapid onset of action

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8
Q

What are the adverse effects of triptans?

A
  1. fatigue
  2. dizziness
  3. paresthesia
  4. warm sensations
  5. tightness (neck, chest, and throat)
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9
Q

What are the main contraindications of triptans?

A
  1. hepatic/renal function impairment
  2. monoamine Oxidase Inhibitor therapy
  3. hemiplegic migraine (associated with paralysis of one side of the face)
  4. basilar migraine (associated with loss of vision, double vision, loss of balance)
  5. hypersensitivity to -triptans
  6. peripheral vascular disease or uncontrolled blood pressure
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10
Q

What is the main triptan in use?

A

Sumatriptan

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11
Q

What produces Ergot alkaloids?

A

-Produced by Claviceps pururea a fungus

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12
Q

What are adverse effects of Ergot alkaloids?

A
  • Poisoning effects (hallucination)
  • vasospasm (gangrene)
  • Abortifacient (in pregnancy
  • Decreased blood flow: brain, heart, extremities
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13
Q

What is the MOA of Ergot alkaloids?

A
  1. Agonist/antagonist at α1-adrenergic, at serotonin receptors (5-HT1A and 5-HT1D )
  2. Partial or full agonist at dopamine receptors
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14
Q

What are the contraindications of Ergot alkaloids?

A
  1. peripheral vascular disease or poor circulation
  2. arteriosclerosis
  3. hypertension
  4. angina
  5. history of heart attack/ silent ischemia
  6. liver/kidney disease
  7. serious infection
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15
Q

What are the therapeutic uses of Ergotamine?

A
  1. Migraine pain

2. Effective at beginning of attack

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16
Q

What are the pharmacokinetics?

A
  1. Routes of admin: oral and suppository
  2. High first pass effect
  3. Excreted by liver
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17
Q

What do you give with Ergotamine to increase bioavailability?

A
  1. Combined with caffeine (helps bioavailability)
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18
Q

What are the adverse effects of Ergotamine?

A
  1. diarrhea
  2. nausea
  3. vomiting
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19
Q

What are the contraindications of Ergotamine?

A
  1. obstructive vascular disease

2. collagen disease

20
Q

What are the therapeutic uses of DHE?

A
  1. Intractable migraine (favored by some clinicians
21
Q

What is DHE?

A

Dihydroergotamine

22
Q

What are the pharmocokinetics of DHE?

A
  1. Routes of admin: SC, IV, IN, and oral
  2. Metabolized by liver, excretion by feces
  3. Metabolites similar to parent compound
  4. Effects last longer than expected
23
Q

What is the MOA of Beta blockers?

A

unknown.

24
Q

What is the primary therapeutic target?

A

Beta 1

25
Q

What does targeting the Beta 1 via Beta blockers cause?

A
  1. Increased heart rate
  2. Increased contractility
  3. Increased nerve conduction
26
Q

What does Beta 2 do?

A

1) Bronchodialation
2) Relaxation
3) Vasodilation

27
Q

What does Beta 3 do?

A

Relax Bladder

28
Q

What is the Beta blocker given for migraines?

A

Propranolol

29
Q

What are the pharmacokinetics of Propranolol?

A
  1. route of administration: oral
  2. hepatic first pass effect
  3. lipophilic
  4. metabolized by liver
30
Q

What are the adverse effects of Propranolol?

A
  1. bradycardia
  2. sedation
  3. vivid dreams
31
Q

What is the main drug interaction with Beta blockers?

A

-Calcium blockers i.e. verapamil

32
Q

What happens if both Beta blockers and calcium blockers are given together?

A
  1. severe hypotension
  2. bradycardia
  3. heart failure
  4. cardiac conductance abnormalities
33
Q

What are indication of migraine prevention?

A
  • Frequency greater than 2 per month
  • Duration longer than 24 hours
  • Cause major disruptions that last 3 or more days
  • Abortive therapy fails or is over used
  • Symptomatic meds are contraindicated or ineffective
  • Use of abortive meds more than 2 times a week
  • Migrane variants such as hemiplegic migraine or rare headache attacks producing profound disruption or risk of permanent neurologic injury.
34
Q

What do you do for Migraine prevention?

A
  • Start with low dose and slowly increase
  • Use 2-3 month trial period
  • Monitor with diary/calendar
  • Monitor for med overuse
  • Consider comorbidity conditions
  • Consider prevention medication combination in refractory patients.
  • Taper when headaches are controlled
35
Q

What is the therapeutic class of Prochloperazine?

A
  1. Antiemetic

2. Antipsychotic

36
Q

What is the MOA of Prochloperazine?

A

D2-antagonist in chemoreceptor trigger receptor zone”

37
Q

What is the therapeutic use of Prochloperazine?

A
  1. Associated with Migraines
    a. vomiting
    b. nausea
    c. pain
38
Q

What is the pharmacokinetics of Prochloperazine?

A

a. Route of administration: oral, rectal, IV

39
Q

What is the adverse effects of Prochloperazine?

A

a. extrapyramidal (acute dystonic effects)

b. akathisia (restlessness)

40
Q

What is given with Prochiorperazine and why?

A

Prochlorperazine often given with diphenhydramine prevents akathisia

41
Q

Which reduces pain more Prochlorperazine or Sumatriptan?

A

Prochlorperazine (I.V.) reduces pain more than Sumatriptan (subcutaneous)

42
Q

What is the MOA of Botulinum Toxin?

A

Enzymatic removal of amino acids in fusion proteins critical to the release of acetylcholine

43
Q

What does MOH stand for?

A

Medication Overuse Headache

44
Q

What causes MOH?

A

MOH caused by excessive use of headache medication

45
Q

What are some of the requirements for the diagnosis of MOH?

A
  • Regular overuse for more than 3 months of 1 or more drugs that can be taken for acute and/or symptomatic treatment of headache.
  • Ergotamine, triptans, opioids or combination analgesics on 10 or more days/months
  • Simple analgesics on 15 or more days/month
  • Any combination of acute/symptomatic drugs on 10 or more days/month without overuse of any single class alone
46
Q

What is the treatment for MOH?

A

Treatment: Detox/education

NMSK B Test 1 (27 decks)

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