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Pharmacology II Exam 1 > Migraines > Flashcards

Migraines Flashcards

1
Q

What is the first and rate limiting step in serotonin synthesis?

A

Tryptophan is converted to 5-hydroxytryptophan by tryptophan hydroxylase

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2
Q

What is the 2nd reaction in serotonin synthesis?

A

5-hydroxytryptophan is converted to 5-hydroxytryptamine by L-aromatic amino acid decarboxylase

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3
Q

What is the function of SERT?

A

It is a high affinity presynaptic serotonin transporter than terminates the action of serotonin via reuptake

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4
Q

5-HT is actively transported into storage vesicles by ___ (inhibited by ___).

A

VMAT-2, reserpine

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5
Q

T/F: One of serotonin’s functions is vasodilation.

A

False (vasoconstriction)

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6
Q

T/F: One of serotonin’s functions is pain.

A

true

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7
Q

When is the prodromal phase of migraine headaches?

A

24-48 hours prior to headache onset

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8
Q

Phase of migraine headache just prior to and/or concurrent with headache phase; last about an hour

A

Aural

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9
Q 
Which of the following is NOT associated with migraine headaches?
A. Slowed GI motility
B. Hypertension and sweating
C. Light and/or sound sensitivity
D. Nausea and vomiting
A

b

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10
Q

What is the cortical spreading depression of leao?

A

Self-propagating wave of neuronal and glial depolarization that spreads across the cortex

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11
Q

What 3 things is the cortical spreading depression thought to cause?

A

Auras, activated afferent trigeminal nerve pathways (pain), and altered cerebral vascular tone and permeability

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12
Q

The cortical spreading depression of leao is thought to activate the trigeminovascular system —> release of substance P, __, ___ —> vasodilation & plasma extravasation of cranial blood vessels

A

The cortical spreading depression of leao is thought to activate the trigeminovascular system —> release of substance P, calcitonin gene-related peptide (CGRP), neurokinin A —> vasodilation & plasma extravasation of cranial blood vessels

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13
Q

Although the role of 5-HT in migraine pathogenesis is unknown, what 2 actions might it do?

A

Inhibit activation of trigeminal pain pathways and regulate cerebral vascular tone (vasoconstrictor)

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14
Q

What serotonin subtypes are considered the most important targets for the acute treatment of migraines?

A

5-HT1b, 5-HT1d

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15
Q

(Serotonin subtype) autoreceptor - activation produces selective vasoconstriction of cranial blood vessels

A

5-HT1b

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16
Q

Where is 5-HT1d found? What does its stimulation do?

A

Trigeminal afferents; reduces activity of these pain pathways

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17
Q

Stimulation of trigeminal afferents by 5-HT1d reduces the activity of these pain pathways and reduces the release of what substance?

A

CGRP (calcitonin gene-related peptide)

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18
Q

T/F: Dopamine agonists can relieve migraine symptoms and improve GI motility.

A

False (antagonists)

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19
Q

Which is more effective in treating migraines: smaller, repetitive doses or large single doses (both more effective when given early)

A

Large single doses

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20
Q

For mild migraine attacks, what general treatment is recommended?

A

Analgesic/combination preparations +/- antiemetic

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21
Q

For moderate migraine attacks, what general treatment is recommended?

A

PO migraine-specific drugs (triptans, ergots) + antiemetics

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22
Q

For severe/emergent attacks, what general treatment is recommended?

A

Non-oral forms of migraine-specific drugs + antiemetics

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23
Q

T/F: All migraine medications have the potential for causing rebound migraines if used too frequently.

A

True

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24
Q

What 3 drug types have the highest risk for rebound migraines?

A

Opioids, barbiturates, ASA/APAP/caffeine combos

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25
Q

What 2 drug types have lower and the lowest risk for rebound migraines (respectively)?

A

Triptans, NSAIDs (are lowest)

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26
Q

Risk for rebound migraines is minimized by using drugs for less than ___ and maximizing prophylactic therapies for patients with frequent migraines.

A

10 days per month

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27
Q

List the mild analgesic combinations that can be used for mild/infrequent migraines with or without aura

A

Aspirin, APAP, ibuprofen OR naproxen) +/- caffeine

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28
Q

List the 2 most common side effects of NSAIDs/acetaminophen

A

Dyspepsia, GI irritation

29
Q

Used as a last resort in patients who do not respond to other therapies

A

Barbiturates and opioids (butalbital, butorphanol)

30
Q

Uses: last resort migraine therapy, tension or muscle contraction headaches

A

Barbiturates (butalbital)

31
Q

Side effects of butalbital (3

A

CNS depression, dependence, overdose risk (schedule III)

32
Q

MOA butorphanol

A

Kappa receptor agonist

33
Q

Used as a nasal spray for patients with severe nausea, CIV

A

Butorphanol

34
Q

ADEs: CNS depression, dependence, hypotension, withdrawal can aggravate migraines, may decrease response to triptans

A

Butorphanol

35
Q

What would you use as an adjunct for treating migraine headaches with nausea and vomiting?

A

Dopamine receptor antagonists (metoclopramide, prochlorperazine)

36
Q

Parenteral forms of these drugs can be used as monotherapy for migraine pain. Although, they are normally used as adjuncts for NA/vomiting symptoms.

A

Dopamine receptor antagonists (metoclopramide, prochlorperazine)

37
Q

MOA of metoclopramide

A

M3 agonist, mixed 5HT3 antagonist/5HT4 agonist in upper GI tract increases gastric emptying; D2 antagonist antiemetic effect

38
Q

ADEs: fatigue, restlessness, extrapyramidal symptoms & tardive dyskinesia, depression, HTN, arrhythmias

A

Metoclopramide

39
Q

Metoclopramide BBW

A

(Big beautiful women heh heh heh) extrapyramidal symptoms, tardive dyskinesia

40
Q

1st generation antipsychotic also used as an antiemetic

A

Prochlorperazine (antiemetic D2 effect)

41
Q 
Which of the following's long term use for psychosis is associated with serious side effects?
A. Prochlorperazine 
B. Sumatriptan
C. Dihydroergotamine
D. Butalbital
42
Q

MOA: 5-HT1 selective agonist for 1B/1D subtypes

A

Sumatriptan (migraine-specific)

43
Q

Therapeutic effects of sumatriptan (5-HT1 agonist for 1B/1D)

A

Cerebrovascular vasoconstriction, blocks release of CGRP, relieves pain, reduces nausea/vomiting, increases GI motility

44
Q

Sumatriptan administration

A

PO or non-oral (SQ, nasal spray, TD)

45
Q

Onset of action & half-life of sumatriptan

46
Q

Used for short-term (1 week) prophylaxis of menstrual migraine; started 2 days before menstruation

A

Frovatriptan

47
Q

What other headache type can sumatriptan treat? (Not a trick question, so don’t say menstrual migraines for frovatriptan)

A

Cluster headaches

48
Q

Frovatriptan time to onset & half-life

A

3 hours; 26 hours

49
Q

Which of the following is NOT a limitation of triptans?
A. Not effective in migraine with aura until after aura is over & headache has started
B. They have significantly different efficacy, so hard to pick an agent to initiate or switch to
C. Short half-lives (2 hour) mean DOA is often shorter than duration of migraine
D. Do not work consistently for all patients
E. All of the above (meaning, none of these are limitations)

A

B (roughly equal efficacy; if one doesn’t work, try another)

50
Q

CNS side effects of sumatriptan:

A

Dizziness, weakness, drowsiness

51
Q

CV side effects of sumatriptan:

A

Coronary artery vasospasm (angina), HTN, peripheral vascular ischemia, stroke

52
Q

Should not be given IV (HA med)

A

sumatriptan

53
Q

Contraindicated in patients with CV disease & taking MAOIs (HA med)

A

Sumatriptan (serotonin syndrome with MAOIs)

54
Q 
MOA: #1 non-specific agonist, partial agonist, & antagonist effects on 5-HT1
#2 action at alpha-adrenergic and dopaminergic receptors
A

Dihydroergotamine (ergot alkaloids)

55
Q

How does dihydroergotamine produce cerebral vasoconstriction?

A

Non-selective 5-HT1 receptor agonist and partial agonist at alpha-1 receptors

56
Q

Describe the use of ergot alkaloids (dihydroergotamine) in relation to triptans.

A

Alternative, but rarely DOC due to side effects and uncertain efficacy

57
Q

Boxed warning of dihydroergotamine

A

Ergotism - intense vasoconstriction leading to coronary vasospasm and cerebral & peripheral vascular ischemia (gangrene)

58
Q

Risk of ergotism is especially high in patients taking ___.

A

CYP3A4 inhibitors

59
Q

ADEs: nausea/vomiting

Retroperitoneal/pleural and cardiac valvular fibrosis with long-term use

A

Dihydroergotamine

60
Q

Contraindicated in CVD and pregnancy (X)

A

Dihydroergotamine

61
Q

5 indications for migraine prophylaxis:

A
  • Episodic migraines become more frequent (>4/month)
  • chronic migraine (>15/month for at least 3 months)
  • episodic migraines cause significant disability
  • cannot tolerate acute treatment drugs, menstrual cycle-related
62
Q

MOA of prophylaxis agents

A

Unclear; may alter cerebral pain sensitization pathways

63
Q

First-line agents for migraine prophylaxis

A

Beta blockers

64
Q

How long does propranolol take to show results in migraine prophylaxis?

A

Several weeks

65
Q

Off-label antidepressant used for migraine prophylaxis, but with limited use due to anticholinergic side effects

A

Amitriptyline (TCA, also venlafaxine)

66
Q

Anti-seizure drug FDA-approved for migraine prophylaxis

A

Valproic acid (Depakote, also topiramate)

67
Q

Effective in migraine prophylaxis but contraindicated in females of childbearing age (teratogen)

A

Valproic acid (Depakote)

68
Q

Describe the use of botulinum toxin for the prophylaxis of migraines (what type of migraines? Off label?)

A

FDA-approved 2nd line for chronic migraines - NOT effective for episodic migraines

Pharmacology II Exam 1 (9 decks)

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