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MS2 Unit 3 > Pharm: Headache (not done yet) > Flashcards

Pharm: Headache (not done yet) Flashcards

1
Q

What are the 4 phases of migraine?

A

Prodrome
Aura
Headache
Resolution

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2
Q

Gender differences in migraines

A

Before puberty, slightly more common in boys

After puberty 3:1 ratio of women:men.

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3
Q

What is the prodrome of a migraine?

A
  • occurs in 20% of migraineurs
  • hours to days before onset of migraine
  • psychological, neurologic, constitutional, or autonomic features
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4
Q

What is the aura of a migraine?

A
  • a complex of focal neurological symptoms that precedes, accompanies, or follows the headache
  • most are 5-20 min and usually less than 60
  • may occur w/o headache
  • MC is visual, followed by parasthesias
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5
Q

What is the headache part of a migraine?

A
  • unilateral, throbbing, moderate-severe
  • aggravated by physical activity and relieved by rest
  • most often starts between 5 AM- noon
  • 4-72 hours
  • a/w anorexia, nausea, vomiting, osmo/photo/phonophobia
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6
Q

What is the resolution of a migraine?

A
  • headache wanes, person is tired, washed out and irritable

- may have impaired concentration, scalp tenderness, or mood changes

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7
Q

Pathophys of migraine baseline

A

migraine has a strong familial association

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8
Q

Pathyophys of migraine prodrome

A

sx suggest hypothalamic role, but we don’t rly know

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9
Q

Pathophys of aura

A
  • a/w reduction of cerebral blood flow that moves across that cortex at a rate of 2-3 mm/min
  • not a primary vascular event b/c it’s not due to vasoconstriction and it doesn’t respect cerebral vascular territories
  • actually the result of neuronal dysfunction called CORTICAL SPREADING DEPRESSION
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10
Q

Pathophys of migraine headache

A
  • activation of trigeminovascular system (trigem nucleus and sensory nerve fibers from opthalmic division of trigem nerve)
  • these fibers release vasodilating and permeability-promoting peptides (substance P, calcitonin gene-related peptide) from perivascular nerve endings
  • peptides promote sterile inflammation –> pain
  • cascade mediated by presynaptic 5HT1B-D receptors
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11
Q

Pathophys of migraine treatment

A
  • 5HT1 is a family of inhibitory G protein linked receptors
  • Triptans are 5HT1-B agonists which cause vasoconstriction of intracranial extracerebral blood vessels and block inflammation
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12
Q

Acute/abortive pharmacologic tx for migraine

A
  • Used after attack has already begun

- Can be specific for migraine or nonspecific (effective for migraine as well as other nonheadache pain)

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13
Q

Analgesics for migraine

A
  • some NSAIDS and analgesic better than placebo for mild-moderate migraine: aspirin, acetaminophen, naproxen, indomethacin, piroxicam, diclofenac, ibuprofen
  • combo of acetaminophen, aspirin, + caffeine effective for moderate migraine
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14
Q

Barbiturates for migraine

A
  • sometimes prescribed, but never been shown to be effective in RPC studies
  • side effects: drowziness, dizziness, risk of overuse and withdrawal
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15
Q

Opioids for migraine

A
  • several available for migraine: codeine, meperidine, oxycodone, hydromorphone, morphine, methadone, butorphanol
  • oral, parenteral, or nasal form
  • widely prescribed but high risk for overuse and development of chronic daily headaches
  • should not be used more than 2 days a week
  • good for situations when other meds are contraindicated
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16
Q

Steroids for migraine

A
  • various forms available
  • not known how they work
  • used for brief periods of time in prolonged headache state
17
Q

Ergotamine and DHE for migraine

A
  • ergot: a-adrenergic and serotenergic agonist
  • DHE: weaker arterial vasoconstrictor, less emetic and less effect on uterus
  • both act by reducing cell activity in the trigeminovascular system (5HT1b-d agonist)
  • DHE IV used for status migrainosus, a severe and intractable headache-state lasting over 72h
18
Q

Triptans

A
  • premier migraine abortive meds
  • 5HT1b-d agonists that penetrate CNS, causing vasoconstriction of extracerebral intracranial vessels + inactivation of the trigeminovascular system
  • also reduce photo/phonophobia, nausea + vom
19
Q

Preventive migraine tx

A
  • Recommended for people with more than 3 severe headaches/month, more than 2 mild-moderate headaches/week, inability to use effective symptomatic therapy, overuse of acute meds, pt preference
20
Q

Antidepressants for migraine

A
  • TCAS: amitriptyline, nortriptyline, protriptyline

- SSRIS: fluoxetine, paroxetine, sertraline for coexistent depression and chronic daily headache

21
Q

Antihypertensives

A
  • Beta blockers and calcium channel blockers
  • Propanalol MC, nadolol + atenolol longer half lives, timolol
  • side effects: drowsy, depression, low libido, hypotension, memory probs. contraindicated in asthma, DM, CHF, Reynauds
  • Verapamil best for pts with prolonged aura or complicated migraines
22
Q

Anti-epileptic drugs for migraine

A
  • divalproex sodium ER: side effects - sedation, hair loss, weight gain, tremor, change in cognition, hepatotoxicity, blood dyscrasias, pancreatitis
  • Topiramate: side effects - changes in cognition, paresthesias, weight loss, kidney stones, acute closed angle glaucoma, decreased serum bicarb
23
Q

Botox for migraine

A
  • FDA approved for chronic migraine (migraine >15 days/month for more than 3 months in the absence of medication overuse)
  • 155 units of botox given q12weeks in 31 fixed-site fixed-dose (up to 40 more units at doc’s discretion)
  • Adverse effects: distant spread of toxin, dysphagia, dysarthria, dyspnea
  • Side effects: injection site pain, headache post injection, neck weakness, ptosis
24
Q

Tension type headache

A
  • MC primary headache syndrome
  • Episodic vs. chronic
  • No prodrome or aura, pain is dull, achey, non-pulsatile, pressure-like, bilateral, usually mild-moderate in severity, may have neck discomfort
  • photo/phonophobia and nausa may be present but mild
  • poor sleep is a trigger
25
Q

Pathophys of TTH

A
  • initial belief was that sustained muscle contraction of pericranial muscles as a consequence of stress caused TTH –> this is not true
  • no association w/ depression/anxiety
  • some NTs are diff than controls, but we don’t know the significance
26
Q

Acute tx of TTH

A
  • Analgesics alone or in combo w/ caffeine, codeine, or anxiolytics –> can cause overuse headache
  • Naproxen, ketorolac, indomethacin most effective NSAIDS
  • Combos w/ caffeine, butalbital sometimes effective
  • Muscle relaxants NOT effective
27
Q

Chronic tx of TTH

A
  • used if more than 2 headaches/week for 4+ hours and severity might lead to disability or med overuse
  • TCAs followed by SSRIS
  • maybe muscle relaxants, Botox
28
Q

Cluster headache

A
  • annual rhythm, occur at same time of day, usually after falling asleep
  • male:female ratio is 4:1, age of onset 27-31
  • familial complonent
  • leonine facies
  • many are smokers, alcohol and altitude are triggers
  • SEVERE unilateral pain, pt is restless, a/w ipsilateral lacrimation, nasal congestion, rhinorrhea, facial sweating, miosis, ptosis, eyelid edema, conjunctival injection
29
Q

Episodic cluster headache vs chronic cluster headache

A

Episodic: periods lasting 7 days-1 year separated by pain free periods lasting 1 month

Chronic: more than 1 year without remission or remission less than 1 month

30
Q

Pathophys of cluster headache

A
  • who knows
  • location implies involvement of opthalmic division of trigem
  • sympathetic dysfunction and parasympathetic overaction
  • annual rhythm and daily occurrence suggest hypothalamic source
31
Q

Acute tx for cluster headache

A
  • Oxygen (tx of choice)
  • triptans
  • DHE
  • anesthetics
32
Q

Chronic tx for cluster headache

A
  • short term preventatives: corticosteroids, daily ergotamine
  • long term: verapamil, topiramate, divalproex sodium, lithium

MS2 Unit 3 (21 decks)

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