Chapter 19: Drugs for Headaches Flashcards

(68 cards)

1
Q

diagnosis of primary headache disorder requires consideration of if the cause is ___ or ___ based

A

physiological or anatomic

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2
Q

what are symptoms of a tension headache?

A

bilateral pressing pain/pressure around the head

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3
Q

tension headaches are often caused by __, __ and ___

A

stress; fatigue; dehydration

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4
Q

the pain caused by a tension headache is often classed as ___

A

mild to moderate

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5
Q

what are some non-pharm options for a tension headache?

A

stress-management; good sleep, proper nutrition and hydration

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6
Q

what are the symptoms of a migraine?

A

aura, nausea, photophobia/phonophobia, sensitivity to smell, worsen w/movement

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7
Q

the pain level of a migraine is ___ to ___

A

moderate to severe

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8
Q

one major difference between tension headaches and migraines is that the pain in a migraine is described as ___

A

throbbing, usually unilateral

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9
Q

what are the 2 classifications of migraine headache?

A

with aura, w/o aura

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10
Q

diagnosis of a migraine headache usually requires the presence of at least 1 ___ type symptom

A

sensory

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11
Q

___ and ___ OTC products are the most popular treatments for migraine and tension headaches

A

analgesic and anti-inflammatory

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12
Q

t/f it is important for patients to avoid headache triggers

A

t

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13
Q

what is the purpose of a headache diary?

A

helps track source/ trigger of headaches as well as the details of symptoms that can help diagnose

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14
Q

what are some common food triggers for a headache?

A

alcohol, caffeine, chocolate, aged cheese, processed foods/additives

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15
Q

what are some physiologic triggers of a headache?

A

dehydration, fatigue, stress, weather, bright lights, mestruation

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16
Q

a migraine headache is generally described as a ___ condition occurring in __ (#) phases

A

neuromuscular; 2

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17
Q

what happens in the first phase of a migraine?

A

vasoconstriction causes schema and serotonin release

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18
Q

what happens in the second phase of a migraine?

A

neuropeptides released from the trigeminal nerves cause vasodilation, inflammation and transmission of pain

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19
Q

abortive therapies for migraines often involve trying to reduce ___nerve dilation and reduce release of ___ and ___ mediators

A

cranial; pro inflammatory and pain

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20
Q

for more severe headaches that cannot resolved by NSAIDs and acetaminophen, a class of drugs called ___are used

A

triptans

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21
Q

___ are the most commonly prescribed drugs for migraine patients

A

triptans

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22
Q

before triptans, the use of ___ or ___ for migraine treatment was common, but now reserved for severe cases

A

opioids; ergot alkaloids

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23
Q

acute management of migraine with ___ is the last resort due to ADR and risk of abuse/addiction

A

opioids

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24
Q

ergot alkaloids (like DHE) can cause nausea, so they are often given with a ____ like ___

A

antiemetic like metoclopramide

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25
ergot alkaloids are a group of compounds originally isolated from a___
fungus that grows on grain
26
ergot alkaloids were used in the 1800's as ___
anticoagulants to stop bleeding
27
ergot alkaloids act as ___
vasoconstrictors
28
what are 4 ergot derivatives?
ergotamine, LSD, bromocriptine, dihydroergotamine
29
ergotamine has significant __ activity, but many additional physiologic effects due to agonist activity at several___ receptors
monoamine
30
the hallucinogenic actions of LSD are related to stimulation of ___ in the CNS
serotonin receptors
31
t/f bromocrpitine and dihydroergotamine are ergot derivatives that can be used clinically
t
32
bromocriptine has a higher affinity for ____ receptors, making it useful in treatment of parkinsons
DA
33
dihydroergotamine has a higher affinity for ____ receptors, leading to its use in migraines
serotonin
34
what are some ADRs of ergot alkaloids?
nausea and hallucinations
35
ergot alkaloids are contraindicated in what patients?
those pregnant and those with CVD (vasoconstriction)
36
___ were the primary treatment for migraines from 1930's-90's despite their many off-target effects
ergot alkaloids
37
the specific serotonin receptor in the cranial blood vessels is the ___ receptor
5-HT 1B
38
t/f the 1D and 5-HT 1B serotonin receptors are very similar and are typically grouped together
t
39
___ was the 1st triptan class drug that came to market in the early 1990's
sumatriptan
40
the chemical structure of sumatriptan is more closely related to ___ compared to DHE
serotonin
41
sumatriptan is a more selective agonist for ___ and ___ receptors
5-HT 1B and 1D
42
what is one of the most notable benefits if using sumatriptan for migraine treatment over ergots?
doesn't bind to adrenergic or dopamine receptors so less ADRs
43
the pathophysiology of a migraine is considered to be a __ problem
vascular
44
agonism of ___ receptors is thought to be the primary action of triptans in migraine treatment
5-HT 1d/b
45
what is the vascular theory of migraine?
vasoconstriction resolves migraine and vasodilation is likely to cause migraine
46
t/f despite the vascular theory, brain imaging has shown that vasodilation of the cranial nerve does not necessarily cause a migraine and migraines can occur w/o dilation of cranial nerves
t
47
the neurogenic inflammation theory of migraines suggests a prominent role of ___ as the cause of cranial vessel dilation, inflammation, and promotion of pain signal
neuropeptides
48
the neurogenic inflammation theory of migraines suggests that if release of ___ is blocked / reduced, the migraine pain should reduce
neuropeptides
49
neuropeptides release along with NT in response to opening of ____ channels and AP are carried through the postsynaptic neuron
voltage gated ca
50
1D and 1B serotonin receptors on the presynaptic neuron have what function?
reduces the activation of Ca channels that cause the release of Nt and neuropeptide that lwould lead to migraine pain
51
what is the primary NT released in the CNS>
glutamate
52
give 2 examples of neuropeptides that are released and cause the vasodilation and release of pro-inflammatory mediators in migraine
CGRP and substance P
53
stimulation of 5-HT 1d/b receptors by ergots and triptans causes ___
inhibition of Ca channels, reducing the release of NT/ neuropeptides that would cause migraine pain
54
MOA of Erenumab
monoclonal antibody that blocks the activation of the postsynaptic CGRP receptor so it cannot respond to the CGRP sent by the presynaptic neuron (blocks pain transmission)
55
t/f Erenumab is a new drug, but clinical trial showed patients experience fewer migraines on this treatment
t
56
Erenumab is given as a monthly injection, making it a ___ migraine treatment unlike the abortive therapy of triptans
prophylactic
57
t/f CGRP has been shown t be an important mediator of migraines
t
58
prevention of neuropeptide actions on the cranial blood vessels reduces ___, ___ and activation of ____ nerves
vasodilation; inflammation; trigeminal
59
it is recommended that migraine abortive therapies be used less than ___ days month
10
60
t/f there is not likely one central mechanism for a medication overuse headache
t
61
t/f with a medication overuse headache, the patient may experience headache more often than they had b/4 treatment
t
62
proposed mechanisms for overuse headache include alterations in the ___ pathways leading to increased excitability and increased ___ release such as CGRP
trigeminal nerve; neuropeptides
63
if a patient needs abortive headache treatment more 10 days a month, what should their treatment be changed to?
preventative (prophylactic) treatment
64
prophylactic strategies for migraine include reducing early phase ___, increasing levels of ___
vasoconstriction; serotonin (w/ antidepressants)
65
give examples of drugs that can be used as migraine prophylactic agents
B-blockers, tricyclic anti-depressants, Ca channel blockers, botox injections, SSRIs, Erunemab
66
prophylactic headache treatments are often tirade for ___ months
2-3
67
prophylactic headache treatment is often tapered off after ___ months to determine if its still needed
6-12
68
___ in red wines can trigger migraines in some patients
tannins