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Pharmacology > Chapter 19: Drugs for Headaches > Flashcards

Chapter 19: Drugs for Headaches Flashcards

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
Q

ergot alkaloids are a group of compounds originally isolated from a___

A

fungus that grows on grain

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26
Q

ergot alkaloids were used in the 1800’s as ___

A

anticoagulants to stop bleeding

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27
Q

ergot alkaloids act as ___

A

vasoconstrictors

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28
Q

what are 4 ergot derivatives?

A

ergotamine, LSD, bromocriptine, dihydroergotamine

29
Q

ergotamine has significant __ activity, but many additional physiologic effects due to agonist activity at several___ receptors

A

monoamine

30
Q

the hallucinogenic actions of LSD are related to stimulation of ___ in the CNS

A

serotonin receptors

31
Q

t/f bromocrpitine and dihydroergotamine are ergot derivatives that can be used clinically

A

t

32
Q

bromocriptine has a higher affinity for ____ receptors, making it useful in treatment of parkinsons

A

DA

33
Q

dihydroergotamine has a higher affinity for ____ receptors, leading to its use in migraines

A

serotonin

34
Q

what are some ADRs of ergot alkaloids?

A

nausea and hallucinations

35
Q

ergot alkaloids are contraindicated in what patients?

A

those pregnant and those with CVD (vasoconstriction)

36
Q

___ were the primary treatment for migraines from 1930’s-90’s despite their many off-target effects

A

ergot alkaloids

37
Q

the specific serotonin receptor in the cranial blood vessels is the ___ receptor

A

5-HT 1B

38
Q

t/f the 1D and 5-HT 1B serotonin receptors are very similar and are typically grouped together

A

t

39
Q

___ was the 1st triptan class drug that came to market in the early 1990’s

A

sumatriptan

40
Q

the chemical structure of sumatriptan is more closely related to ___ compared to DHE

A

serotonin

41
Q

sumatriptan is a more selective agonist for ___ and ___ receptors

A

5-HT 1B and 1D

42
Q

what is one of the most notable benefits if using sumatriptan for migraine treatment over ergots?

A

doesn’t bind to adrenergic or dopamine receptors so less ADRs

43
Q

the pathophysiology of a migraine is considered to be a __ problem

A

vascular

44
Q

agonism of ___ receptors is thought to be the primary action of triptans in migraine treatment

A

5-HT 1d/b

45
Q

what is the vascular theory of migraine?

A

vasoconstriction resolves migraine and vasodilation is likely to cause migraine

46
Q

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

A

t

47
Q

the neurogenic inflammation theory of migraines suggests a prominent role of ___ as the cause of cranial vessel dilation, inflammation, and promotion of pain signal

A

neuropeptides

48
Q

the neurogenic inflammation theory of migraines suggests that if release of ___ is blocked / reduced, the migraine pain should reduce

A

neuropeptides

49
Q

neuropeptides release along with NT in response to opening of ____ channels and AP are carried through the postsynaptic neuron

A

voltage gated ca

50
Q

1D and 1B serotonin receptors on the presynaptic neuron have what function?

A

reduces the activation of Ca channels that cause the release of Nt and neuropeptide that lwould lead to migraine pain

51
Q

what is the primary NT released in the CNS>

A

glutamate

52
Q

give 2 examples of neuropeptides that are released and cause the vasodilation and release of pro-inflammatory mediators in migraine

A

CGRP and substance P

53
Q

stimulation of 5-HT 1d/b receptors by ergots and triptans causes ___

A

inhibition of Ca channels, reducing the release of NT/ neuropeptides that would cause migraine pain

54
Q

MOA of Erenumab

A

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
Q

t/f Erenumab is a new drug, but clinical trial showed patients experience fewer migraines on this treatment

A

t

56
Q

Erenumab is given as a monthly injection, making it a ___ migraine treatment unlike the abortive therapy of triptans

A

prophylactic

57
Q

t/f CGRP has been shown t be an important mediator of migraines

A

t

58
Q

prevention of neuropeptide actions on the cranial blood vessels reduces ___, ___ and activation of ____ nerves

A

vasodilation; inflammation; trigeminal

59
Q

it is recommended that migraine abortive therapies be used less than ___ days month

A

10

60
Q

t/f there is not likely one central mechanism for a medication overuse headache

A

t

61
Q

t/f with a medication overuse headache, the patient may experience headache more often than they had b/4 treatment

A

t

62
Q

proposed mechanisms for overuse headache include alterations in the ___ pathways leading to increased excitability and increased ___ release such as CGRP

A

trigeminal nerve; neuropeptides

63
Q

if a patient needs abortive headache treatment more 10 days a month, what should their treatment be changed to?

A

preventative (prophylactic) treatment

64
Q

prophylactic strategies for migraine include reducing early phase ___, increasing levels of ___

A

vasoconstriction; serotonin (w/ antidepressants)

65
Q

give examples of drugs that can be used as migraine prophylactic agents

A

B-blockers, tricyclic anti-depressants, Ca channel blockers, botox injections, SSRIs, Erunemab

66
Q

prophylactic headache treatments are often tirade for ___ months

A

2-3

67
Q

prophylactic headache treatment is often tapered off after ___ months to determine if its still needed

A

6-12

68
Q

___ in red wines can trigger migraines in some patients

A

tannins

Pharmacology (49 decks)

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