2-migraine Flashcards
what drives aura
cortical spreading depression
what is cortical spreading depression
wave of depolarization followed by desensitization (depression) that propagates across the cortex
what are familial hemiplegic migraines
migraines that include weakness in half of the body
what is the inheritence of familial hemiplegic migraines
autosomal dominance
what are the mutated genes associated with familial hemiplegic migraines
P/Q type Ca channel
NaK ATPase
Na channel subunit
(maintain hyperexcitability of neuron)
what are the reasons that familial hemiplegic migraines happen
lowered threshold for cortical spreading depression
what is the trigeminal nerve special for
the largest cranial nerve
what does the trigeminal system do
sense pain in face and head, including vasculature and dura matter
what are the three branches of the trigeminal system
ophthalmic, maxillary, mandibular
where is pain in the head detected and by who
in the dura mater and blood vessels, ophthalmic branch
what does 5HT do to blood vessels
vasoconstriction
what are the 5HT levels of migraineurs between attacks
low
what happens to 5HT during attacks
released
where is CGRP located
in trigeminal peripheral afferents
what does CGRP release cause
vasodilation (in response to pain)
what are the CGRP levels in migraineurs
high
what does prophylatic treatment mean
preventative, taken daily
what are some pharmacological prophylatic interventions for migraine
beta blockers (decrease bp), anticonvulsants(block pain transmission), antidepressants(increase serotonin)
why can caffeine be good for migraine
it leads to vasocontriction
where does caffeine bind to
caffeine is an adenosine receptor antagonist
how else does caffeine help headaches (because vaso-)
increases absorption of some analgesics
-constriction
what receptors do ergotamines bind to and what does it cause
5HT-1b 5HT-1d
inhibit neurogenic inflammation
but low specificity, more side effects
what do ergotamines do to coronary vessels
vasoconstrict
what are bad things that can happen to people with coronary artery disease taking ergotamines
can change blood flow and anginal pain
also bad for other vessel and heart diseases
what is the absorption and distribution of ergotamines
large first pass metabolism, low bioavailability
what is the half life and metabolism of ergotamines
in liver by poorly defined enzymes, 2 hour half life
how is ergotamines excreted
in bile
where do triptans bind
5-HTb/d agonists
what are the mechanisms of triptans
vasoconstriction and inhibition of trigeminal nerve
why are triptans better than ergotamines
avoids the side effects (Cardiac!)
what is sumatriptan bioavailability and half life
14% oral
96% subcutaneously
2 hours
how is sumatriptan metabolized
by monoamine oxidase in liver into indoleacetic acid
how is sumatriptan excreted
urine
how do CGRP antagonists work
antibodies or to receptor
block inflammation, vasodilation and pain
what is olcegepant and its story
good at treating migraine, poor bioavailability
abandoned phase 2 trials
what is the half life and metabolism of ergotamines
in liver by poorly defined enzymes, 2 hour half life
how is ergotamines excreted
in bile
where do triptans bind
5-HTb/d agonists
what are the mechanisms of triptans
vasoconstriction and inhibition of trigeminal nerve
why are triptans better than ergotamines
avoids the side effects (Cardiac!)
what is sumatriptan bioavailability and half life
14% oral
96% subcutaneously
2 hours
how is sumatriptan metabolized
by monoamine oxidase in liver into indoleacetic acid
how is sumatriptan excreted
urine
how do CGRP antagonists work
antibodies or to receptor
block inflammation, vasodilation and pain
what is telcagepant and its story
good at treating migraine, but daily it was bad for liver (aminotranferase elevated)
abandoned phase 3 trials
what is rimegepant and its story
very effective migraine treatment, less effect on liver
