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PMCOL 200 > Migraine > Flashcards

Migraine Flashcards

1
Q

what is the leading cause of disability worldwide in those under 50?

A

migraine

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2
Q

what is a migraine?

A

primary headache disorder characterized by recurring moderate to severe, pulsating headaches that can last from 2-72 hours

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3
Q

t/f: migraines can cause a sensitivity to light, sound, and head movements

A

true, any normal sensory input

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4
Q

t/f: migraines won’t cause nausea or vomiting

A

false

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5
Q

what is migraine aura?

A

visual disturbances such as flashing lights or zigzag lines that precede a migraine (~20%)

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6
Q

what is thought to drive migraine aura?

A

cortical spreading depression

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7
Q

what is cortical spreading depression?

A

wave of neuronal depolarization followed by period of desensitization/depression (ref. period) that propagates across cortex

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8
Q

what are 2 factors that can incr migraine risk?

A

genetic and enviro

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9
Q

do migraines affect women or men more?

A

women

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10
Q

in women, when does migraine incidence incr?

A

after puberty (hormones?)

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11
Q

what type of migraine has genetic contribution?

A

familial hemiplegic migraines (FHM)

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12
Q

what are FHMs?

A

migraines that include weakness in half the body

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13
Q

what kind of inheritance does FHM exhibit?

A

autosomal dominance (haplosufficient)

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14
Q

what are 3 known genetic mutations associated w/ FHM?

A

P/Q-type Ca channels, Na/K ATPases, Na channel subunit

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15
Q

how do mutations affect the threshold for cortical spreading depression?

A

decr threshold (incr risk)

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16
Q

what is the trigeminal system?

A

sensory/motor innervation of the face and skull

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17
Q

what is the largest cranial nerve?

A

trigeminal nerve

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18
Q

what are the 3 branches of peripheral trigeminal processes?

A

ophthalmic (top), maxillary (middle), mandibular (bottom)

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19
Q

what are 3 purposes of the trigeminal system?

A

sense pain/temp in head region, innervate dura mater, control cerebral blood vessels

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20
Q

what is the dura mater?

A

membrane that surrounds the brain

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21
Q

what is the system that controls cerebral blood vessels?

A

trigeminovascular system

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22
Q

what branch of the trigeminal nerve detects pain in the head?

A

ophthalmic (top 1/3) innervating dura mater and blood vessels

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23
Q

what kind of disease are migraines thought to be?

A

neurovascular

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24
Q

what are 3 observations of migraines?

A
  1. extracerebral vessels dilate during migraine
  2. cranial blood vessel stimulation provokes headache
  3. vasoconstrictor drugs alleviate pain
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25
Q

release of what NT leads to vasoconstriction?

A

5-HT

26
Q

when are 5-HT levels low vs high in migraineurs?

A

low: btwn migraines
high: during migraine

27
Q

what 5-HT receptor in particular is associated w/ vasoconstriction for migraines?

A

5-HT 1D

28
Q

incr of what molecule is associated w/ migraines?

A

calcitonin gene-related peptide (CGRP)

29
Q

where is CGRP located?

A

in trigeminal peripheral afferents (on nociceptors)

30
Q

what is CGRP released in response to?

A

pain (from afferents)

31
Q

what do high levels of CGRP cause? (2)

A

vasodilation and migraine

32
Q

what are the 2 treatment strategies for migraines?

A

prophylactic and abortive

33
Q

whats the difference btwn prophylactic vs abortive migraine strategies?

A

prophylactic: taken daily to prevent migraines
abortive: taken when an attack occurs

34
Q

what are non-pharmacological prophylactic migraine interventions?

A

identify and reduce triggers (diet, exercise, sleep, caffeine, alcohol, stress)

35
Q

what are 3 pharmacological prophylactic migraine interventions?

A

beta-blockers (propranolol-decr BP), anticonvulsants (gabapentin-decr pain transmission), antidepressants (amitriptyline-SSRI)

36
Q

what are 4 examples of abortive migraine drugs?

A

aspirin, acetaminophen, NSAIDs, opioids (non-specific analgesics)

37
Q

what is the risk of taking non-specific analgesics for chronic migraines?

A

medication overuse headache (make headache worse)

38
Q

what is caffeine?

A

adenosine receptor antagonist

39
Q

what does caffeine binding to adenosine receptors cause?

A

vasoconstriction (antagonism)

40
Q

what is an additional benefit of caffeine for migraines?

A

incr absorption of some analgesics (acetaminophen, ergotamines) which improves migraine treatment during attack (improve rate/extent of absorption)

41
Q

what is an adverse effect of using caffeine for migraines?

A

can trigger headaches or rebound headaches/withdrawal

42
Q

what were the 1st specific anti-migraine agents (1926) but aren’t 1st line therapy anymore?

A

ergotamines (ergot alkaloid - like LSD)

43
Q

what are ergotamines/ergot alkaloids?

A

5HT-1b/d agonists

44
Q

what does ergotamines/ergot alkaloids binding to 5HT-1b/d Rs cause?

A

vasoconstriction that inhibits neurogenic inflammation (blocks migraine)

45
Q

what is the issue with ergotamines/ergot alkaloids for migraines?

A

low receptor selectivity which incr risk of side effects (like LSD)

46
Q

ergotamines/ergot alkaloids having low receptor selectivity can cause what?

A

can bind to a-adrenergic Rs and produce coronary vasoconstriction (ischemic changes/anginal pain in coronary artery diseased ppl)

47
Q

what are 4 contraindications of using ergotamines/ergot alkaloids for migraines?

A

peripheral vascular disease, coronary heart disease, uncontrolled hypertension, stroke

48
Q

what is the absorption/distribution of ergotamines? (2)

A

large first-pass metabolism (oral), low bioavailability (<1%)

49
Q

what is the metabolism and half-life of ergotamines?

A

metabolized by poorly-defined liver enzymes, half-life is 2hrs

50
Q

where are ergotamines excreted?

A

bile

51
Q

what is the first-line migraine therapy? ex?

A

triptans, sumatriptan

52
Q

what are triptans?

A

selective 5HT-1b/d agonists (~ergotamines)

53
Q

what are 2 effects/mechanisms of triptans?

A

vasoconstriction and inhibition of trigeminal nerve (5HT-1b/d Rs on blood vessels and peripheral pain neurons)

54
Q

do triptans have similar side effects to ergotamines? why?

A

no, avoid ergotamine side effects bcse are more selective (decr a-adrenergic binding)

55
Q

what is the bioavailability (absorption/distribution) of sumatriptan when taken orally vs subcutaneously?

A

14% when oral, 96% subcutaneously

56
Q

what metabolizes sumatriptan and its half-life?

A

monoamine oxidase (also 5-HT), half-life is 2hrs

57
Q

where is sumatriptan excreted?

A

urine

58
Q

what do CGRP antagonists do?

A

prevents CGRP binding during a migraine causing vasodilation (CGRP released from trigeminal pain afferents)

59
Q

what are 2 forms of CGRP antagonists?

A

small-molecule CGRP antagonists or monoclonal antibodies for CGRP/CGRP receptors

60
Q

what are the 6 stages of clinical drug trials?

A

preclinical (research), phase 1 (safety), phase 2 (efficacy), phase 3 (detect side effects), FDA review, phase 4

61
Q

why is 5-HT low btwn migraines and high during migraines if it leads to vasoconstriction?

A

btwn: low levels account for susceptibility to migraine (decr vasoconstrictors)
during: released as a rxn to vasodilation

PMCOL 200 (27 decks)

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