Migraine Treatment Flashcards

1
Q

describe migraine headache

A

unilateral, gradual onset, moderate intensity, patients wants quiet, dark room, last 4-72 hours and associated with n/v, photo/phonophobia

increased risk of stroke in aura migraine with OCs

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2
Q

describe tension headache

A

bilateral, pressure/tightness, waxes & wanes, pt may be active or may rest, variable duration

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3
Q

describe cluster headache

A

unilateral & behind/around one ye, quick onset, deep excruciating pain, patient remains active, .5-3 hr duration, associated with lacrimation, sinusitis, horners, sensitive to EtOH

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4
Q

NSAIDs for treatment of headaches

A

nabumetone, ibuprofen, naproxen

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5
Q

moa of NSAIDs

A

cox inhibition and dec sysnthesis of pro-inflammatory mediators

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6
Q

AE of NSAIDs

A

∙ gastric irritation with chronic use
∙ additive nephrotoxicity (especially elderly)
∙ fluid retention, HTN, edema, CHF
∙ potentiation of migraine-assoc nausea

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7
Q

pregnancy category for NSAIDs

A

Category C – but avoid later in pregnancy due to effects on PDA & prolonging L&D

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8
Q

order nsaids from shortest duration to longest duration

A

ibuprofen (4x/d) - naproxen (2x/d)- nabumetone (1x/d)

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9
Q

DDI of NSAIDs

A

attenuate diuretics, b-blockers, ACE inhibitors, vasodilators, central alpha-2 agonists, peripheral alpha-1 & ARBs

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10
Q

caution in NSAID combos

A

G6PD deficiency

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11
Q

triptans for HAs

A

eletriptan, sumatriptan (-triptans)

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12
Q

CI of triptans

A

CI: heart disease, uncontrolled HTN, ischemic bowel disease, <24 hrs after ergot tx

beware of serotonin syndrome with SSRIs/SNRIs

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13
Q

Triptans DDI with MAOIs

A

sumatriptan

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14
Q

triptans DDI with propanolol

A

elitriptan

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15
Q

triptans DDI with CYP3A4 inhibitors

A

elitriptan

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16
Q

which triptans have short onset, short duration

A

elitriptan and sumatriptan

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17
Q

which triptans are given for quick action against severe headache

A

sumatriptan (can be given nasal spray, suma can be given SC)

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18
Q

MOA of triptans

A

selective carotid vasoconstriction (via 5-HT1B receptors) and presynaptic inhibition of trigeminovascular inflammatory responses in migraine (via 5-HT1D/5-HT1F receptors)

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19
Q

what effects do triptans have on 5-HT(1B) agonist

A
  1. Selective intracranial/extracerebral vasoconstriction
  2. Inhibition of trigeminal nerve activation by vasoactive peptides
  3. Inhibition of trigeminal cervical complex activation
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20
Q

AE of triptans

A

∙ Most prominent in sumatriptan
∙ CNS (drowsiness, dizziness, fatigue)
∙ heaviness & tightness of chest
∙ Coronary & peripheral artery vasospasm

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21
Q

ergots for headaches

A

ergotamine, dihydroergotamine

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22
Q

moa of ergots

A

complex agonist effects multiple receptors, central (5-HT) + peripheral (a) vasoconstriction + ↓amine reuptake

23
Q

moderate dose action of ergots

A

contraction of smooth muscle fibers

24
Q

large dose action of ergots

A

paralyzes motor nerve endings of sympathetic nervous system

25
Q

AE of ergots

A

St. Anthony’s Fire) = mental disorientation, convulsions, muscle cramps, dry gangrene of extremities

26
Q

CI of ergots

A

vasospastic predisposing conditions = peripheral vascular disease or CAD, sepsis, MI, uncontrolled HTN

27
Q

pregnancy category of ergots

A

X, no breastfeeding either

28
Q

DDI of ergots

A

∙ b-blocker/DA = potent vasoconstrictor
∙ CYP3A4 inhibitor =↑ ergot persistence
∙ Triptans = 24 hour rule

29
Q

metabolism and elimination of ergots

A

hepatic metabolism and renal excretion

30
Q

opiates used for migraines

A

hydrocodone, oxycodone, codeine

31
Q

AE of opiates

A

dependence, respiratory depression, bradycardia, histamine release, QT prolongation, constipation, N/V

32
Q

antiemetics

A

prochlorperazine, chlorpromazine, promethazine, metoclopramide

33
Q

moa of prochlorperazine chlropromazine

A

D2 blockade centrally & also cholinergic & alpha-adrenergic blockade

34
Q

moa of promethazine

A

cholinergic blockade & also H1 & weak D2 blockade

35
Q

moa of metoclopramide

A

D2 blockade centrally & also prokinetic by ↑Ach effects

36
Q

AE of prochlorperazine and chlorpromazine

A

dyskinesia, hypotension, glaucoma, urinary retention, BPH

37
Q

AE of promethazie

A

glaucoma, urinary retention, BPH, drowsiness, Parkinson like syndromes

38
Q

AE of metoclopramide

A

↑prolactin levels & gynecomastia

39
Q

headache prophylaxis

A

amitryptiline, valproic acid, propanolol, timolol, topiramate

40
Q

MOA amitriptyline

A

↓reuptake of NE and 5-HT & strong anticholinergic action

41
Q

MOA valproic acid

A

Na channel blocker, ↑GABA activity

42
Q

MOA propanolol & timolol

A

↓arterial dilation, ↓NE induced lipolysis

43
Q

Moa of topiramate

A

↓Blocks Na & glutamate, ↑GABA activity

44
Q

AE of amitryptiline

A

aggressiveness, ↑weight, dry mouth, sedation

45
Q

AE of valproic acid

A

hepatotoxic, sedation, nausea, ↑weight

Category X

46
Q

AE of propanolol and timolol

A

fatigue, exercise intolerance, problems with asthma, diabetes, AV block

47
Q

AE of topiramate

A

parasthesias, fatigue, nausea, narrow therapeutic range

48
Q

which headache prophylactic rx is highly protein bound

A

valproic acid

49
Q

which is the only rx FDA approved for HA prophylaxis tx of children

A

propanolol

50
Q

botulinum toxin MOA

A

↓release of mediators or ↓muscle activation of nerves

51
Q

4 criteria for analgesic overuse syndrome

A
  1. HA for > 15 days & fulfill 3 & 4
  2. regular rx overuse >3 months
  3. HA began or progressed in severity w/ rx
  4. HA resolves or reverts in <2 months after stopping Rx
52
Q

Mechanism of analgesic overuse syndrome

A

related to adaptation to drug at receptor, leading to changes in receptor density & transmitter synthesis

53
Q

which drugs are high risk for overuse syndrome

A

aspirin/acetaminophen/caffeine, butalbital-containing combinations, opioids

54
Q

prophylaxis for analgesic overuse syndrome

A

TCAs, SSRIs, BBs, AEDs