migraine headache treatment Flashcards

1
Q

how would you treat cluster headaches?

A

nasal or subq triptans or ergots + “burst & taper” steroid, like prednisone

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2
Q

how do you treat mild-moderate or menstrual migraines?

A

non-narcotics analgesics (NSAIDs)

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3
Q

how do you treat moderate-severe migraines?

A

short acting triptan

  • oral or faster acting nasal spray
  • naratriptan & frovatriptan (longer action but slower onset)
  • Subq sumatriptan is most effective & fastest onset
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4
Q

which triptan is the most effective and fastest onset drug to treat migraines?

A

Subq sumatriptan

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5
Q

what are the 5 drugs that are used for prophylactic treatment of migraines?

A
topiramate
valproate
propanolol
timolol
metoprolol
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6
Q

what can happen with too frequent use of anti-migraine drugs?

A

this can lead to a paradoxical worsening of the migraines (analgesic overuse syndrome)

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7
Q

how do you try to fix the problem of analgesic overuse syndrome in migraine therapy?

A

start transition program

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8
Q

how are the NSAIDs effective drugs for treating migraines?

A

block PG production, and so reduce the production of inflamm. signals that trigger MAPK upregulation & the increased neuronal production of CGRP & substance P for release from nerve endings

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9
Q

how are triptans effective agents in treating migraines?

A

produce selective carotid vasoconstriction (via 5-HT1B receptors) & presynaptic inhibition of trigeminovascular inflamm. responses implicated in migraine (via 5-HT1D/5-HT1F receptors)

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10
Q

when is the best time to take NSAIDs for treating migraines?

A

SOONER

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11
Q

what are some of the adverse effects of NSAIDs in the elderly?

A

additive nephrotoxicity

  • fluid retention, HTN, edema
  • potentiation of migraine-associated nausea
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12
Q

name the NSAIDs that are commonly used to treat migraines?

A
Ibuprofen
Ketoprofen
Fenoprofen
Nabumetone
Naproxen
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13
Q

which type of NSAIDs are less likely to cause problems with analgesic overuse?

A

long acting NSAIDs

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14
Q

why are NSAIDs contraindicated in late pregnancy?

A
  1. effects upon patency of ductus arteriosus

2. prolonging labor and delivery

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15
Q

what kind of metabolic deficiency may be important with chronic doses of acetaminophen?

A

G6PD deficiency

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16
Q

which drug represents a class of drugs that are strongly linked to analgesic overuse syndrome?

A

butalbital-barbiturate

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17
Q

what are the adverse effects of barbituates?

A

CYP inducers & CNS/resp. depressant

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18
Q

barbituates are contraindicated with what other substances and conditions?

A

porphyria, ethanol, sedative contraindications

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19
Q

MOA of triptans?

A
  • selective intracranial/extracerebral vasoconstriction
  • inhibition of trigeminal nerve activation by vasoactive peptides
  • inibition of trigeminal cervical complex activation
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20
Q

the triptans are agonists at which 2 serotonin receptors in the CNS?

A

5-HT1B & 5-HT1D

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21
Q

which 2 triptans are available as nasal sprays which speed up the onset of action?

A

sumatriptan

zolmitriptan

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22
Q

which triptan can be administered subq, which provides the quickest onset of drug action and is considered the most effective drug and delivery route?

A

sumatriptan

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23
Q

which two triptans both produce a more durable effect but at the expense of a longer onset time?

A

naratriptan

frovatriptan

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24
Q

adverse effects are most prominent with which triptan?

A

sumatriptan Subq

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25
Q

what are the adverse effects of triptans?

A

Side Effects may limit utility:
-CNS effects, like dizziness, drowsiness & fatigue may reflect aspects of migraine remaining after successful pain relief
-heaviness of tightness of chest
May cause coronary and peripheral vasospasm

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26
Q

triptans are contraindicated in what conditions?

A

heart dz, uncontrolled HTN, or ischemic bowel dz (use w/ caution w/ other vascular risk factors like DM)

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27
Q

triptans are contraindicated how long following ergot or triptan treatment?

A

<24 hrs

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28
Q

which triptans are affected with MAO inhibitors that prevent the breakdown?

A

Riza-, Suma-, Zolmitriptan

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29
Q

which beta blocker increases the serum levels of Eli-, Riza-, & Zolmitriptan?

A

propanolol

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30
Q

which triptan has interactions with CYP3A inhibitors that would result in an increase in the serum drug level?

A

Eletriptan

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31
Q

using SSRIs or SNRIs with triptans may precipitate what adverse effect?

A

SEROTONIN SYNDROME

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32
Q

what are the two ergots?

A

ergotamine

dihydroergotamine

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33
Q

what are the clinical symptoms/signs of acute and chronic ergotism?

A

characterized by mental disorientation, convulsions, muscle cramps, & dry gangrene of the extremities

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34
Q

what effect does ergotamine have in moderate doses?

A

causes contraction of smooth muscle fibers

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35
Q

which antimigraine drug has also been used to promote uterine contraction in childbirth?

A

ergotamine

36
Q

what effect does ergotamine have in large doses?

A

paralyzes motor nerve endings of sympathetic nervous system

37
Q

how can people get ergotism?

A

by eating contamina`ted baked goods

38
Q

what pregnancy category are the ergots?

A

category x (also contraindicated in lactation)

39
Q

which class of drugs has complex agonist effects on multiple receptors for example central (5-HT) + peripheral (alpha) vasoconstriction & decreased amine reuptake?

A

ergots

40
Q

ergots are contraindicated w/ vasospastic predisposing conditions such as what?

A

peripheral vascular or CAD, sepsis, MI, uncontrolled HTN

41
Q

what is the consequence of ergots interacting with beta blockers and dopamine?

A

potentiate vasoconstrictive action

42
Q

what is the consequence of ergots interacting with strong CYP3A4 inhibitors?

A

increased ergot persistence

43
Q

what is the consequence of triptans interacting with the ergots?

A

24 HOUR RULE

44
Q

migraines are a common problem in which trimester of pregnancy?

A

1st trimester (when fetus is at greatest risk of toxicity)

45
Q

what is the mainstay treatment for migraines in 1st trimester of pregnancy?

A

acetaminophen

46
Q

what class of drugs can be added to treat migraines in pregnancy if the condition persists into later trimesters?

A

opioids

47
Q

__________are contraindicated in treating migraines in pregnancy and other classes should be used ONLY when unavoidable

A

ergots

48
Q

what may be the indication for using ergots to treat migraines?

A

can be appropriate in pts who are unresponsive to triptan therapy

49
Q

what are the most frequently used drugs to treat menstrual migraine?

A

NSAIDs

50
Q

when should you start taking NSAIDs to treat menstrual migraines?

A

2-3 days before menstrual period starts and continue until the period ends

51
Q

for severe menstrual migraines or when taking oral contraceptivese, begin NSAID on ______ day of cycle and continue through the second day of the next cycle

A

19

52
Q

the combo of what two risk factors produces a multiplicative increase in risk of ischemic stroke?

A
  1. low dose combo of oral contraceptives

2. migraine with aura

53
Q

combo oral contraceptives are ok to treat what kind of migraines?

A

migraines w/o aura

54
Q

triptans are ineffective for treating what kind of migraines?

A

migraines that produce allodynia

55
Q

if you didn’t want to give narcotics to a pt suffering from migraines with allodynia, what could you give them instead?

A

Keratolac

56
Q

name the 3 antiemetic drugs used to treat vomiting in migraines that work via D2 blockade centrally?

A

metoclopramide
Prochlorperazine
Chlorpromazine

57
Q

explain the MOA of the antiemetic effect of promethazine?

A

cholinergic blockade, H1 & Weak D2 blockade

58
Q

name the drug: prokinetic by increasing ACh effects and has AEs of increasing prolactin levels leading to gynecomastia, used to treat emesis in migraines

A

metoclopramide

59
Q

name the 2 drugs that block D2 receptors centrally and have other effects including cholinergic + alpha-adrenergic blockade, used to treat emesis in migraines

A

prochlorperazine

Chlorpromazine

60
Q

what are the AEs of prochlorperazine and chlorpromazine?

A

dyskinesia, hypotension, glaucoma, urinary retention, BPH

61
Q

when would prophylactic treatment migraine be a good idea?

A
  1. recurrent migraine, interfering with daily routine despite acute treatment
  2. contraindication to or troublesome side effects from acute meds
  3. overuse of acute meds
  4. hemiplegic migraine; risk of neurologic injury
62
Q

which 4 classes of drugs are used for prophylactic treatment of migraines?

A

antiepileptic drugs, antidepressant drugs, beta-blockers, Ca2+ blockers

63
Q

what are the 1st line prophylactic treatments for migraines?

A

amitriptyline
Divalproex or Valproic acid
Propanolol or timolol
Topiramate

64
Q

if 2-3 months of prophylactic treatment of migraines still doesn’t work, what do you do next?

A

combine 2 first line agents

65
Q

MOA of amitriptyline

A

decrease reuptake of NE & serotonin + strong anticholinergic action

66
Q

what are the AEs of amitriptyline?

A

aggressiveness, increase weight, dry mouth sedation

67
Q

MOA of divalproex & valproic acid

A

Na+ channel blocker, increases GABA activity

68
Q

what are the adverse effects of divalproex & valproic acid?

A

Cat. X, hepatotoxic, sedation, nausea, increase weight, highly protein bound

69
Q

what is the MOA of propanolol & timolol in prophylactic migraine treatment?

A

decreased arterial dilation

decreased NE-induced lipolysis

70
Q

what are the AEs of propanolol & timolol in prophylactic migraine treatment?

A
fatigue
exercise intolerance
asthma probz
DM
AV block
71
Q

MOA for topiramate

A

blocks Na & glutamate, increases GABA activity

72
Q

what are the AEs of topiramate?

A

paresthesias
fatigue
nausea
narrow therapeutic range

73
Q

what is the only drug that has proven to be effective for migraine prophylaxis in children?

A

propanolol

74
Q

how is botox administered to treat migraines prophylactically?

A

symmetrical injection into glabellar frontalis & temporalis muscles

75
Q

botox injection is not recommended for what kind of migraines?

A

episodic migraines

76
Q

what are the 4 analgesic overuse syndrome criteria?

A
  1. headaches for > 15 days/month that also fulfill criteria #3 & #4
  2. regular med overuse > 3 months
  3. headaches began or progressed in severity while taking meds
  4. headache resolves or reverts to previous pattern w/i 2 months after discontinuing chronic drug administration
77
Q

what is the mechanism behind analgesic overuse syndrome?

A

cellular adaptation in teh already aberrant signaling processes

78
Q

trigeminovascular system sensitization is due to what?

A

incomplete initial drug treatment

79
Q

which 3 categories of drugs have a high risk for developing analgesic overuse syndrome?

A
  1. aspirin/acetaminophen/caffeine
  2. butalbital-containing combos
  3. opioids
80
Q

which 3 types of drugs have a low risk for developing analgesic overuse syndrome?

A
  1. long acting NSAIDs
  2. Tramadol
  3. Dihydroergotamine
81
Q

which types of drugs have a moderate risk of development of analgesic overuse syndrome?

A

triptans

short acting NSAIDs

82
Q

what is the 3 faceted approach to treating analgesic overuse syndrome?

A
  1. transition or bridging program: control w/ ergotamine, prophylaxis w/ propanolol
  2. biofeedback
  3. prophylaxis: TCA, SSRI, beta-bockers, antiepileptics, NSAIDs
83
Q

the american academy of neurology supports what 3 techniques of mind-body therapy to reduce migraine incidence?

A
  1. biofeedback
  2. cognitive behavior therapy
  3. relaxation training
84
Q

which two alternative therapies has clinical evidence to show symptomatic relief of headache?

A

riboflavin

coenzyme Q10

85
Q

which two alternative therapies have demonstrated an ability to reduce the frequency of migraine attacks?

A

feverfew & butterbur

86
Q

which alternative therapy med used to treat migraines has an inssue with pyrrolizidine alkaloids?

A

butterbur (look for products that are alkaloid-free)

87
Q

what three alternative migraine therapies are not to be used in pregnancy?

A

feverfew, butterbur, riboflavin