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103 Cards in this Set
- Front
- Back
which HA
bilateral band like pressure dental, cervical, visual corrections |
tension HA
|
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which HA:
unilateral behind eye 15 min - 3 hrs 0.5% of population |
cluster
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which HA?
pulsating pain periorbital ice-pick like pai unilateral hours to days 10-20% of population |
migraine
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primary HA
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tension
cluster migraine |
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secondary ha due to:
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organic causes:
hemorrhage infection stroke tumor |
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which ha is bilateral
|
tension
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which ha is behind eye?
periorbitial |
cluster: behind eye
migraine: periorbital |
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which has ice-pick like pain
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migraine
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some triggers of migraines
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stress
anxiety hormonal lack of sleep chocolate red wine MSG cheese |
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migraines possibly due to ----- ----- overactive
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somatosensory cortex
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what's thicker w/ migraines
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somatosensory cortex
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how long do migraines last
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hours to days
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what % of the pop has migraines
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10-20%
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migraines:
disorder of the ---- blood vessels |
cranial
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migraine involve --- and/or ---
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5HT
NE |
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migraines may involve -----, ---, nad histamine sensitivities
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glutamate
NO histamine |
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majory excitable transmitter in the brain
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glutamate
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migrain involve ---- nerve sensory afferents
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trigeminal (5)
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in migraines initially there's --- then later ---- of bl vessels
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contraction
dilation |
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phases of migraine
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premonitory
aura ha postdrome |
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when can a migraine pt have the premonitory phase
|
hrs to days
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what type of premonitory
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psych
sensory autonomic |
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aura include
|
visual
sensory motory language disturbances |
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migraine ha can last for
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4-72 hrs
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what's accompanied by ha
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photophobia
phonophobia sensory stimulation |
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postdrome can last up to
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24 hrs
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how do postdrome feel
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euphoric
depressed irritable |
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vascular theory --- followed by ----
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vasoconstriction
vasodilation |
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spreading depresison theory
spreading wave of neuronal depolarization results in changes in --- --- and activates vascular responses, --- implicated |
blood flow
glutamate |
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neurogenic model
neuronal --- w/ subsequent -- changes |
dysfunction
vascular |
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neurogenic model:
there's a release of vasoactive ------ |
neuropeptides
|
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vasoactive neuropeptides include
|
sub p
calcitonin gene related peptide neurokin A |
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neuropeptides can cause vaso----, plasma -----, --- cell degranulation, --- inflammation
|
vasodilation
plasma extravasation mast cell degranulation neurogenic |
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ascending projections of ==== nerve activate --- pain centers
|
trigeminal
thalamic |
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in the neurogenic model --- nerve activated
|
facial (7)
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what can cause the aura
|
cortical spreading depression
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ineffective oral analgesics for acute tx include
|
asa
nsaids apap |
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route of ketorolac
|
IM
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what does ketorolac decrease
|
pain
nausea photophobia |
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t/f
antiemetics just tx nausea associated w/ ha |
t
|
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antiemetic agents
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cholorpromazine
metoclopromide promethazine |
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ergots cause vaso----
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constriction
|
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route of ergotamine tartrate
|
oral
suppository |
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route of dihyroergotamine
|
nasal spray
|
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ergots work by activating ------ receptors on vessels
|
5HT 1D/1B
|
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ergots activated ---- 5HT 1D/1B receptors to decrease release in peptides causing pain, vasodilation, and inflammation
|
presynatpic
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5HT 1B presynaptic inhibit --- ---- ----
|
vasoactive peptides release
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5HT 1Dalpha decrease --- and ---- ----
|
locomotion
neurogenic inflammation |
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5HT 1DB cause -----
|
vasoconstriction
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activation of 5HT 1D/1B receptors prevent activation of --- ----
|
trigeminal nerves
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side effects of ergots
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nausea
muscle weakness pain |
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CI of ergots
|
vascular/coronary disease
hypertension pregnancy impaired renal and hepatic fx |
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why is ergot CI in pregnancy
|
decrease bl flow to fetus
|
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why are ergots CI in vascular/coronary disease
|
too much vasoconstriction
|
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route of sumatriptan
|
NS
SC oral |
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bioavailabilty of sumtriptan oral
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15%
|
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route of zolmitriptan
|
oral
nasal spray |
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naratriptan has a long ---
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t 1/2
bioavailable: 70% |
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which triptan has the highest bioavailabity
|
naratriptan
almotriptan |
|
low triptan bioavailability
|
sumatriptan
|
|
triptans are 5HT --- ---- receptors agonists
|
5HT 1D/1B
|
|
MOA of triptans
activate 5HT 1D/1B receptors and . . . |
vasoconstrict
prevent activation of trigeminal nerves |
|
moa of triptans will also
activate presynaptic 5HT 1D/1B receptors and decrease |
release of peptide causing pain, vasodilation, and inflammation
|
|
why's there a 40% recurrence w/ triptans
|
due to short t1/2
give ones w/ longer t 1/2: naratriptan and frovotriptan |
|
triptan w/ difference in men and women bioavailability
|
frovotriptan
|
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why might a pt experience cp w/ triptans
|
due to vaso constriction of bl vessels
|
|
triptans might cause:
--- aka lack of strenght/fatigue nausea somolence dizziness --- aka tingling or weird sensation in hands/fingers |
asthenia
parathesia |
|
triptans CI w/
|
coronary artery disease
MI angina MAOI and w/in 24 hrs of ergots |
|
t/f
triptans more effective if given w/ ergot |
f
don't give w/in 24 hrs due to over vasoconstriction |
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what other med should be held for 24 hrs w/ triptans/ergots
|
methysergide. ..
5HT 2A/2C receptor antagonist. .. . prophylactic use med |
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why avoid MAOI w/ triptans
|
cuz they metabolize 5HT, so MAOI will prolong 5HT
|
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opiaties are limited to --- or ---- HA
|
severe
intractable |
|
t/f
opiates deal w/ cause and not pain |
f
deal w/ pain and not cause |
|
opiates are often combined w/ --- or ---
|
ASA
APAP |
|
what has opiate like acitvity
|
tramadol
|
|
tramadol has mixed --- -------, inhibits ---, ---
|
u-agonist
NE 5HT |
|
why should you limit frequency of any tx to 2 day/week
|
to prevent rebound HA
|
|
migraines that occur more than -- a month needs prophylaxis
|
2-3
|
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migraines prophylaxis for attacks that last more than ---hrs and are ----
|
48
severe |
|
migraine prophylaxis if --- tx provides little relief
|
acute
|
|
t/f
bb are used for acute relief |
f
prophylaxis |
|
which bb work best
|
lack of ISA
increase activity |
|
how might bb work w/ migraine
|
block vasodilation
decrease 5HT release platelets |
|
bb decrease -- and --- of migraines
|
severity
frequency |
|
tricyclics used in migraines prophylaxis
|
amitriptyline
nortriptyline protriptyline |
|
t/f
ssri's may worsen migraines |
t
|
|
ssri's sued in migraine prophylaxis
|
fluoxetine
paroxetine |
|
ssri's effect --- and -- reuptake sites
|
NE
5HT |
|
t/f
anticonvulsants can also be used for prophylaxis ha |
t
topiramate valproate/divalproex gabapentin |
|
what does topiramate block
|
Na
Ca channels GABAa AMPA Kainate receptors |
|
topiramate inhibits spreading ----
|
depression
|
|
topiramate decrease ---- activation
|
trigeminal
|
|
ae of topiramate
|
paresthesia
fatigue cns depression decrease appetite |
|
how does valproate/divalproex work against migraines
|
effect early wave spreading depression
|
|
gabapentin decrease --- and --
|
Ca
glutamate |
|
gabapentin can cause --- and ----
|
drowsiness
dizziness |
|
methylsergide inhibits plasma --- and ---
|
extravasation
inflammation |
|
botulism works best w/ this ha
|
tension
|
|
ARB that used as prophylaxis for migraine
|
candesartan
|
|
ACEI that's used as prophylaxis for migraine
|
Lisinopril
|
|
CCB can decrease ---
it has minimal effect on ----- more effective against ---- |
frequency
severity aura |
|
CCB used for migraine prophylaxis
|
verapamil
|
|
--- more effective in cluster HA
|
lithium
|