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Neuro 2 > Migraine Pharmacology > Flashcards

Migraine Pharmacology Flashcards

1
Q

How are tension HAs usually treated?

A

OTC NSAIDs by the patient

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2
Q

How are cluster HAs usually treated?

A

with nasal or SC triptans or ergots + a burst and taper steroid like prednisone

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3
Q

What is thought to initiate a migraine?

A

excitation of nociceptive nerve terminals in meningeal vessels

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4
Q

What does excitation of nociceptive nerve terminals in meningeal vessels lead to?

A

release neurotransmitters that vasodilate meningeal vessels locally and activate the trigeminal nucleus (creating the neurogenic inflammation that leads to migraine symptoms)

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5
Q

What leads to the throbbing in a migraine?

A

Dilation of meningeal blood vessels

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6
Q

What leads to N/V in a migraine?

A

activation of area postrema

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7
Q

What leads to hypersensitivity in a migraine?

A

activation of the hypothalamus

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8
Q

What leads to muscle spasm in a migraine?

A

activation of the cervical trigeminal system

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9
Q

What leads to head pain in a migraine?

A

activation of cortex and thalamus

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10
Q

What NSAIDs are used to treat mild to moderate migraine or menstrual migraine?

A

Ibuprofen
Nabumetone
Naloxone

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11
Q

Which NSAID is most likely to be overused?

A

Ibuprofen (take 4 per day)

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12
Q

What drug is useful if caffeine withdrawal is involved in HA?

A

NSAID (Acetaminophen) + Caffeine

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13
Q

What drug class is used as first line treatment for moderate to severe migraine?

A

Triptans

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14
Q

Which triptan has the fastest onset?

A

SC sumatriptan

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15
Q

Which triptans can be taken PO or nasally?

A

sumatriptan and zolmitriptan

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16
Q

What are other unique ways sumatriptan can be taken?

A

SC and patch

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17
Q

Which triptans have a longer action but slower onset?

A

Frovatriptan

Naratriptan

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18
Q

Which drug class for migraines is used in patients unresponsive to Triptans (because these are LESS effective)?

A

ergots

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19
Q

Which ergot can be given SC, IV, IM, and nasally?

A

ergotamine

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20
Q

Which ergot can be given orally or by suppository?

A

dihydroergotamine

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21
Q

What drug class should not be used (but can be used to treat allodynia) in migraines?

A

opiates

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22
Q

Which opiates are used (sometimes) to reduce the allodynia of migraine?

A

Hydrocodone
Oxycodone
Codeine

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23
Q

What should you use instead of opiates?

A

Want to use ketorolac instead (effective, not habit-forming)

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24
Q

Which drug class for migraines is contraindicated in pregnancy?

A

ergots

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25
Q

Which drug class is the mainstay of pregnancy migraines in the 1st trimester?

A

acetaminophen (avoid later in pregnancy due to patent DA, prolonged labor and delivery)

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26
Q

Which drug class can be used to treat migraines persisting into later trimesters?

A

opiates

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27
Q

Are triptans okay to take in pregnancy?

A

try to avoid

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28
Q

MOA: Thalamic GABA enhancement leads to sedative-hypnotic effects

A

Butalbital

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29
Q

When is butalbital used?

A

not really effective or important

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30
Q

MOA: Inhibit COX/ act on PGs to reduce production of inflammatory signals that would trigger MAPK upregulation & increased production of CGRP and SP

A

NSAIDs

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31
Q

MOA: Produce selective carotid (intracranial/extracranial) vasoconstriction (via 5-HT1B receptors) and presynaptic inhibiton of the trigeminovascular inflammatory responses implicated in migraine—inhibit CN V activation by vasoactive peptides and trigeminal cervical complex activation (via 5HT1D/5-HT1F receptors allowing for Ca2+ entry)

A

triptans

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32
Q

MOA: Block pre-synaptic Ca2+ receptors and open post-synaptic K+ receptors of pain fibers!

A

opiates

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33
Q

MOA: Vasoconstrictor that causes contraction of smooth muscle fibers (like those in small arteries). Central 5-HT vasoconst + peripheral α vasoconst + decreased amine reuptake

A

ergots

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34
Q

DDI: diuretics, beta blockers, ACEi’s, vasodilators, etc.

A

NSIADs

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35
Q

DDI: ETOH, porphyria and sedatives

A

butalbital

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36
Q

Triptan DDI: MAOIs

A

Sumatriptan
Zolmitriptan
Rizatriptan

37
Q

Triptan DDI: propranolol

A

Zolmitriptan
Rizatriptan
Elitriptan

38
Q

Triptan DDI: CYP3A inhibitors

A

Elitriptan

39
Q

DDI: ergots

A

triptans

40
Q

Interactions with triptans and SSRIs/SNRIs may lead to what?

A

5-HT syndrome

41
Q

DDI: beta-blockers or DA? (potentiate vasoconst action), strong CYP3A4 inhibitors (increase persistence of ergot), Triptans (24 hr rule)

A

ergots

42
Q

TOXICITY:

  • Gastric irritation chronic use
  • Additive nephrotoxicity (in the elderly)
  • Potentiation of migraine-associated nausea
A

NSAIDs

43
Q

TOXICITY:

  • Cerebral vasoconstriction
  • Postential CV interactions
A

NSAID (Acetaminophen) + caffeine

44
Q

Deficiency in what enzyme may lead to problems with the metabolism of acetaminophen?

A

G6PD

45
Q

TOXICITY:

  • Drowsiness, sedation, diminished cerebral function
  • CYP inducer and CNS/resp depressant
  • Strongly linked to analgesic overuse syndrome
A

Butalbital

46
Q

What drug class is contraindicated in heart disease, uncontrolled HTN or ischemic bowel disease due to coronary/peripheral vasospasm.?

A

triptans

47
Q

What drug class is contraindicated in vasospastic predisposing conditions (CAP, PVD, sepsis, MI, uncont. HTN?

A

Ergots

48
Q

TOXICITY:

  • CNS effects ( dizziness, drowsiness, fatigue)
  • Heaviness/tightness in chest.
A

Triptans

mostly SC sumatriptan

49
Q

TOXICITY:
paralysis of motor nerve endings in sympathetic nervous system leading to mental disorientation, convulsions, muscle cramps, and dry gangreme of limbs

A

Ergotism due to too large a dose of ergots

50
Q

TOXICITY: dependence & respiratory depression, low HR

A

Opiates

51
Q

Patients with migraine + aura on OCP are at increased risk of what?

A

Oral contraceptives increases risk of stroke (especially when person smokes, has HTN or hyperlipidemia); patients with migraine + aura also at increased risk of stroke (MULTIPLICATIVE)

52
Q

What is “analgesic overuse syndrome”?

A

Too frequent a use of anti-migraine drugs can lead to a paradoxical worsening of the clinical condition.

53
Q

A patient with analgesic overuse syndrome is a candidate for what type of treatment?

A

prophylactic migraine treatment

54
Q

How many days/month do you have to have headaches to meet criteria for analgesic overuse?

A

> 15 (and HA began or progressed in severity while taking medications + HA resolves or reverts to previous pattern within 2 months after stopping chronic drug administration)

55
Q

How many months do you have to be overusing medication to meet criteria for analgesic overuse?

A

> 3 months
o Ergots, triptans, optiods and comginations= >10 days/month
o Simple analgesics = > 15 days per month

56
Q

True or false: SHORT acting NSAIDs (least expensive) more likely to produce this than long-acting agents.

A

TRUE

57
Q

Which drugs give the highest risk for developing analgesic overuse syndrome?

A

Aspirin/acetaminophen/caffeine
Butalbital-containing combinations
Opioids

58
Q

How does analgesic overuse syndrome occur?

A

body’s adaptation to drug at the receptor—leading to changes in receptor density and transmitter synthesis.

59
Q

Incomplete initial drug treatment for migraines can lead to what?

A

Trigeminovascular system sensitization

60
Q

Trigeminovascular system sensitization leads to what?

A
  • Reduced 5-HT levels and 5-HT2 receptor upregulation
  • Cellular adaptation in an already aberrant signaling process.
  • Free radical damage in PAG
61
Q

What is the 3 faceted approach to transitioning patients away from overuse?

A

1) TRANSITION/BRIDGING:
2) BIOFEEDBACK
3) PROPHYLAXIS

62
Q

What drugs are used in transition/bridging for analgesic overuse syndrome treatment?

A
  • Control with ergotamine, prophylaxis with propranolol

- Tizanidine (antispasmotic alpha-2 agonist) + long-acting NSAID

63
Q

What drugs are used in prophylaxis for analgesic overuse syndrome treatment?

A

TCA, SSRI, beta-blockers, anti-epileptics, and NSAIDs

64
Q

List drugs used in migraine prophylaxis.

A 
Amitriptyline
Valproic Acid
Propranolol
Timolol
Topiramate
Botox
65
Q

How is botox administered to treat migraines?

A

symmetrical injection into glabellar frontalis and temporalis muscles

66
Q

What migraine prophylaxis medication is NOT FDA approved?

A

amitriptyline

67
Q

What migraine prophylaxis medication is FDA approved in children?

A

propranolol

68
Q

MOA: Na channel blocker with increased GABA activity

A

valproic acid

69
Q

MOA: Decrease reuptake of NE and 5-HT + strong anticholinergic

A

Amitriptyline

70
Q

MOA: Decreased arterial dilation and decreased NE-induced lipolysis

A

propranolol

71
Q

MOA: Blocks NA and glutamate; increased GABA activity

A

Topiramate

72
Q

MOA: possibly decrease release of mediators or decreased activation of nerves

A

Botox

73
Q

TOXICITY: Aggressiveness, weight gain, dry mouth, sedation

A

amitriptyline

74
Q

TOXICITY: Fatigue, exercise intolerance, problems with asthma, DM, AV block

A

propranolol

timolol

75
Q

TOXICITY: none (not used in episodic migriane)

A

botox

76
Q

TOXICITY: CAT X teratogen, hepatotoxic, sedation, nausea, weight gain, highly protein bound

A

valproic acid

77
Q

List the anti-emetics used in migraines.

A

Prochlorperazine
Metoclopramide
Promethazine
Chlorpromazine

78
Q

MOA: D2 block centrally; cholinergic and alpha-adrenergic blockade

A

Prochlorperazine

Chlorpromazine

79
Q

MOA: D2 blockade centrally; prokinetic by increasing Ach effects

A

Metoclopramide

80
Q

MOA: Cholinergic blockade**; H1 and weak D2 blockade

A

promethazine

81
Q

TOXICITY: Dyskinesia, Hypotension, glaucoma, urinary retention, BPH

A

Prochlorperazine

Chlorpromazine

82
Q

TOXICITY: Glaucoma, urinary retention, GPH, drowsiness, Parkinsonism

A

promethazine

83
Q

TOXICITY: Increased prolactin levels→ gynecomastia

A

metaclopramide

84
Q

What is the algorithm for migraine prophylaxis?

A
  • First line drug
  • If not successful after 2-3 months change dose
  • If not affective still, try another first line drug
  • If not affective still, combine 2 first lines
  • If not affective, try alternate
85
Q

What are externally generated signals that measure physciological process (ex. sweating, temperature, muscle tension)?

A

biofeedback

86
Q

What is the replacement of inner thoughts with salutogenic script and frame of reference?

A

cognitive behavior therapy

87
Q

What alternative therapy for migraine is associated with open mouth sores and upset stomach?

A

feverfew

88
Q

What two alternative therapies have actually been proven to reduce migraine frequency?

A

feverfew

butterbur

Neuro 2 (11 decks)

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