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IDT Fall > Headache Therapy > Flashcards

Headache Therapy Flashcards

1
Q

describe a sinus HA

A

pain usually behind forehead and/or cheekbones

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2
Q

describe a cluster HA

A

pain in and around one eye

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3
Q

describe a tension HA

A

pain like a band squeezing the head

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4
Q

describe a migraine HA

A

pain, nausea and visual changes

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5
Q

what are classified as primary HAs?

A

tension-type, migraine, and cluster

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6
Q

secondary HA disorders are defined as?

A

HAs which occur as a result of another health problem

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7
Q

what is the most common primary HA type?

A

tension-type

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8
Q

what is the other name for a tension-type HA?

A

ordinary or muscle-tension HA

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9
Q

what are the triggers for tension-type HAs?

A

stress, anger, fatigue

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10
Q

what type of HA describes mild-moderate, bilateral pain with a pressing/tightening feeling?
a. Cluster
b. Tension
c. Migraine
d. Sinus

A

b

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11
Q

what are non-pharm treatments for tension HA?

A

palpation of pericranial nerves or cervical muscles
stress management

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12
Q

how to treat tension HA if treatment failure with OTCs?

A

high dose NSAIDs
combo analgesics with butalbital or codeine

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13
Q

Migraines are characterized by pain plus one or both of what 2 symptoms?

A

nausea/and or vomiting
photophobia and phonophobia (sensitivity to sound)

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14
Q

women are more common to experience what type of HA? what hormone is a trigger?

A

migraines
estrogen

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15
Q

which two types of HAs are considered vascular HAs?

A

migraine and cluster

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16
Q

how are migraines characterized?

A

unilateral pain that’s pulsing, aggravated by physical stimul

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17
Q

what are the two types of migraines?

A

common migraine (without aura) and classic migraine (with aura)

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18
Q

what are visual symptoms of aura?

A

flickering, spots, vision loss, flashing lights

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19
Q

what are sensory symptoms of aura?

A

numbness, tingling/pins and needles

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20
Q

*auras can cause speech disturbances

A

.

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21
Q

Imaging reveals aura is characterized by transient wave of activity in the ______ _____ followed by long-lasting ________

A

cerebral cortex, suppression

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22
Q

cortical spreading of depression:
transient wave of ________ _______ activity in cerebral cortex followed by ________ and longer-lasting ________ in blood flow

A

depolarization excitation, repolarization, decrease

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23
Q

*trigeminal neuron is activated by aura

A

.

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24
Q

what are the four phases in order of time of occurrence of a migraine attack?

A
  1. prodrome premonitory
  2. Aura
  3. pain and associated symptoms
  4. postdrome
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25
Q

what is the job of the trigeminal nerve?

A

sends info about pain to brain stem

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26
Q

where in the brain is pain perceived?

A

thalamus and cerebral cortex

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27
Q

how do we treat trigeminal neuralgia?

A

with carbamazepine or oxcarbazepine

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28
Q

depolarization of trigeminal nerve causes release of CGRP which causes?

A

vasodilation

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29
Q

what are the 3 subunits of CGRP Rs?

A

calcitonin-like receptor
receptor activity-modifying protein
receptor component protein

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30
Q

tissue damage and the source of pain during a migraine is the ______ vasculature at the level of the _______

A

cerebral, meninges

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31
Q

what does vasodilation of blood vessels in brain do?

A

initiates a neurogenic inflammatory response

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32
Q

how do intracranial blood vessels utilize serotonin?

A

it is used to cause vasoconstriction

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33
Q

CGRP is co-expressed with which type of serotonin Rs?

A

5-HT1

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34
Q

the trigeminal nerve is an example of a ______________ nerve that expresses presynaptic serotonin Rs

A

non-serotonergic

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35
Q

what drug class is sumatriptan?

A

5-HT 1B/1D agonist

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36
Q

T/F sumatriptan can be used prophylactically for migraines

A

false

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37
Q

what is sumatriptans mechanism of action?

A

inhibits release of neuropeptides and causes vasoconstriction

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38
Q

serotonin’s affinity for which 5-HT receptors increases the risk of side effects contraindicated in patients with ischemic heart disease?

A

5-HT 1B

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39
Q

second generation triptan drugs usually have ________ oral bioavailability and ________ half-life than sumatriptan

A

higher
longer

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40
Q

which triptan would be best if you are looking for one with a long half-life?

A

Frovatriptan

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41
Q

what is the name of the first CNS penetrating 5-HT 1F agonist?

A

lasmiditan

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42
Q

side effects from sumatriptan are most common via which route of administration?

A

subQ

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43
Q

what formulations is sumatriptan available as?

A

injection
nasal spray
oral

44
Q

patients should not use triptans if they have what risk factors?

A

cardiovasc disease, risk of stroke, hypertension

45
Q

are triptans safe in pregnancy?

A

inconclusive

46
Q

triptans should not be co-administered with?
why?

A

another triptan
an ergot derivative
SSRIs, SNRIS, and MAO inhibitors
increased risk of serotonin syndrome

47
Q

what drug class are Ubrogepant, Rigmegepant, Atogepant, and Zavegepant?

A

CGRP antagonist

48
Q

T/F CGRP antagonists can be used prophylcatically

A

True

49
Q

what does it mean to say Rigemegepant (Nurtec ODT) has duel efficacy?

A

its used as needed with onset of migraine and taken every other day to prevent migraines

50
Q

Ergotamine and dihydroergotamine have affinity for _______ and _____ receptors, and their affinity for ______ receptors explains a direct ______ effect

A

dopamine, alpha, dopamine, emetic

51
Q

why do ergot alkaloids have increased risk of drug-induced side effects?

A

they have low receptor selectivity

52
Q

Ergot alkaloids, triptans, lasmiditan, and CGRP antagonists are effective for vascular HA and cluster HA, but not for what?

A

tension-type HA or facial pain

53
Q

what is in fiorinal?

A

aspirin, butalbital and caffeine

54
Q

what is in fiorinal with codeine?

A

aspirin, butalbital, caffeine and codeine

55
Q

what is in fioricet?

A

acetaminophen, butalbital and caffeine

56
Q

what is in fioricet with codeine?

A

acetaminophen, butalbital, caffeine and codeine

57
Q

what is in midrin?

A

acetaminophen, isometheptene, and dichloralphenazine

58
Q

what is in excedrin migraine?

A

acetaminophen, aspirin, and caffeine

59
Q

what substance would exacerbate a rebound headache?

A

caffeine

60
Q

what are the symptoms of a complex (atypical) migraine?

A

aphasia, slurred speech, limb weakness, touch sensations

61
Q

what migraine medications should not be used to treat complex migraines? why?

A

triptans and ergot alkaloids
don’t want vasoconstriction

62
Q

what is a good treatment for complex migraines?

A

combo analgesics such as fioricet

63
Q

what type of migraine is considered a channelopathy?

A

hemiplegic migraine

64
Q

what are the symptoms of a hemiplegic migraine?

A

aura occurs as temporary unilateral weakness, usually before pain but can persist after

65
Q

familial hemiplegic migraine sufferers have a mutation in the alpha subunit of the voltage-gated ________ calcium channel

A

P/Q-type

66
Q

what migraine medications should not be used to treat hemiplegic migraines?

A

triptans and ergot alkaloids

67
Q

what drugs can patients use to control nausea and vomiting caused by HAs?

A

metoclopramide
prochlorperazine
chlorpromazine

68
Q

what is the common steroidal anti-inflamm drug used for migraines?

A

dexamethasone

69
Q

beta blockers (metoprolol, propranolol…) are considered what type of migraine treatment?

A

prophylactic

70
Q

antidepressants (SNRIs, amitriptyline) are considered what type of migraine treatment?

A

prophylactic

71
Q

how do we determine if a pt is experiencing rebound HAs who have preexisting HA condition?

A

if they have a HA 15 or more days per month

72
Q

when are rebound HAs the most painful?

A

in morning/upon waking

73
Q

describe the process of how a migraine occurs

A

cortical spreading depression (aura): glutamate excitation in cerebral cortex followed by k+ repolarization and long-lasting decrease in blood flow
trigeminal nerve is activated to cause pain and nausea, photophobia, or phonophobia
TGN dumps vasoactive peptides like CGRP and causes vessel dilation

74
Q

what is the relationship between triptans mechanism and the trigeminal nerve?

A

triptans target pre-synaptic serotonin receptors to modulate signals to the trigeminal nerve. the nerve is not directly affected by serotonin

75
Q

T/F photophobia or phonophobia can occur, but not at the same time

A

true

76
Q

how long can butalbital combos be used consecutively?

A

5 days

77
Q

T/F tension type HAs are vascular

A

false

78
Q

T/F cluster HAs are vascular

A

true

79
Q

what is the main indicator of a cluster HA?

A

sudden stabbing of one eye

80
Q

what are acute treatments of cluster HAs?

A

oxygen mask
triptans (non-oral)
intranasal lidocaine (if non-responsive to other treatments)

81
Q

what drugs can be used to prevent cluster HAs?

A

verapamil
lithium

82
Q

why do we not give triptans orally for cluster HAs or pts feeling nausea from HA?

A

they will vomit the drug up

83
Q

where does pain and inflammation from a migraine occur specifically in the brain?

A

in the meninges (not the brain itself)

84
Q

T/F migraines are vascular

A

true

85
Q

what are the signs/symptoms of the prodrome premonitory phase of a migraine?

A

fatigue, irritability, cravings, mood changes, muscle tension

86
Q

when should a patient use preventative therapy for their migraine?

A

right before they know the aura is coming

87
Q

how long does the aura last before the pain starts with a migraine?

A

about 60 minutes

88
Q

when should abortive therapy for migraine be used?

A

after patient begins to experience aura symptoms

89
Q

what is the mechanism of NSAIDs?

A

they decrease prostaglandin inflammation

90
Q

what drug class is lasmiditan?

A

selective 5-HT1F agonist

91
Q

how do preventative treatments help with migraines?

A

they reduce severity and frequency of migraines, but do not prevent them

92
Q

when should preventative treatments be prescribed on top of abortive treatments?

A

for pts having more than 15 migraines per month

93
Q

Ergot drugs should not be administered _______, should not be mixed with _______ and should always be combined with _______ due to nausea

A

orally
MAOIs
antiemetics

94
Q

T/F triptans all have equal efficacy

A

true

95
Q

Gepants do/do not have renal dose adjustment, do/do not have repeat dosing, and are considered ______ line

A

do have renal dose adjustment. do not repeat dose. third line

96
Q

Do gepants cause vasoconstriction?

A

no

97
Q

do triptans cause vasoconstriction?

A

yes

98
Q

do ditans cause vasoconstriction?

A

no

99
Q

which triptans have more routes of administration than just oral?

A

sumatriptan, zolmitriptan, and rizatriptan

100
Q

name the antiemetic drugs

A

metoclopramide
chlorpromazine
prochlorpromazine

101
Q

why should metoclopramide be given with diphenhydramine?

A

it is a dopamine antagonist which increases risks of EPS

102
Q

what drug is given IV to reduce brain swelling in severe attacks?

A

dexamethasone

103
Q

what drug classes are used for preventative therapy?

A

beta blockers
antidepressants
anticonvulsants
CGRP MAB
botox

104
Q

what is the CGRP MAB drug name we use for preventative therapy and what differentiates it from other preventative drugs?

A

remegepant, it also can be used as abortive therapy

105
Q

which of the triptans are the only 2 with long duration? the other triptans have what length of duration?

A

naratriptan and frovatriptan
rest have short duration

106
Q

which triptan has the longest half-life?

A

frovatriptan

107
Q

which of the triptans have the shortest time for onset?

A

sumatriptan
eletriptan
zolmitriptan
rizatriptan

IDT Fall (29 decks)

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