HA and migraines pharm Flashcards
acute migraine drugs
serotonin agonists ergot alkaloids analgesics combo analgesics NSAIDs antiemetics
migraine prophylatics
beta blockers
CaCh blockers
antidepressents
anticonvulsants
primary HA disorders
migraine
tension
cluster
secondary HA disorders
d/t other underlying cause
infection
brain mass or swelling etc
classic migraine
30%
aura of variable duration which may involve nausea, vomiting, visual scotomas or hemianopsia, speech abnormalities
followed by sever throbbing, u/l HA lasts for hours to days
common migraine
70%
lacks aura
pathophys of migaines
trigeminal n and maybe extracranial aa involed
nn release CGRP which is an extremely powerful vasodilatation -> inflammation and edema
food triggers for migraine
alcohol caffeine/caffeine withdrawl chocolate MSG aspartame
environmental triggers of migraine
flickering lights high altitude strong smells/fumes tabacco smoke weather
Behavioral triggers of migraine
excess/insufficient sleep fatigue menstruation skipped meals strenuous activity
tension type HA (TTH)
most common type of primary HA disorder
least studied, pathophys not understood
simple analgesics and NSAIDs
amitripyline prophylaxisis
cluster HA
rare, but most severe primary HA
pain excruciating, associated with cranial autonomic symptoms
best Tx is prevention
serotonin agonists
sumatriptan
-triptan
ergot alkaloids
dihyroergotamine (DHE)
ergotamine (+/- caffeine)
combo analgesics
excedrin migraine: aspirin, acetaminophen, caffeine
antimemtics
metoclopramide
CaCh blockers
verapamil
antidepressents
antitriptyline
anticonvolssants
topiramate
synthesis of serotonin
from L-tryptophan
stored in vesicles
over 90% in in enterochromaffin cells in GI tract
in blood in platelets
metabolism of serotonin
MAO oxidizes and inactivates it
further metabolized to 5-HIAA which can be collected in 24-hr urine to evaluate serotonin synthesis
CNS actions of serotonin
mood sleep appetite temp pain BP vomiting depression, anxiety, migraine
CV effects of serotonin
contraction of vascular smooth mm, except skeletal mm and heart where is vasodilates
promotes platelet aggregation
skeletal mm effect of serotonin
contraction
triptans MOA
activates serotoninRs on presynaptic trigeminal nn -> inhibitis release of vasodialting peptides
stimulates vasoconstriction
triptan disadvantages
short half life so often must be dosed multiple times w/in course of HA
triptan use
first line acute mild-severe migraines in most people
ADRs of triptans
most are mild altered sensations dizziness mm weakness fatigue drowsiness nausea sweating neck pain if IV- injection site rxn 1-5% chest discomfort
CIs of triptans
CAD angiina ischemic heart disease uncontrolled DM DO NOT use w/in 24hrs of ergotamine MOA inhibitors
ergot alkaloids MOA
constiction of peripheral and cranial blood vessels
may also have presynaptic trigeminal nn ending effects
inhibit release of vasodilating peptides
agonists at serontonin Rs
ergot PK
absorption and rate of action improved when in combo w/caffeine
uses of PK
migraine
triptans preferred
usually preserved for prolonged attacks
ADRs of ergots
GI
prolonged vasospasm- gangrene, amputation, bowel infarction
weakness, fatigue, paresthesias, drowsiness
butalbital
can be mixed with NSAIDs
increases GABAaCh opening time -> membrane hyperpolarization
potential for abuse and tolerance
antiemetics MOA
block D2,3,4 Rsin chemoreceptor trigger zone and solitary nucleus tract
uses of antiemetics
adjuncts to Tx nausea and vomiting or migraine
has been used as monotherapy with unknown mechanism
ADRs of antiemetics
drowsiness and dizziness
extrapyramidal symptoms
betal blockers MOA
may raise migraine threshold by modulating adrenergic or serotonergic transmisison in Cx or subCx pathways
beta blocker uses
most used prophylaxis for migraines
ADRs of beta blockers
drowsiness, fatigue, sleep disturbances, vivid dreams, memory disturbance, depression
caution of beta-blockers
CHF, peripheral vascular disease, AV conduction disturbances, asthma, depression, DM
CaCh blockers MOA
inhibits Ca entry -> smooth mm relaxation
uses of CaCh blockers
migraine prophylaxis, but off label
can also be used as prophylaxis of cluster HAs
antidepressents MOA
beneficial effects independent of antidepressent activity
may result in down-regulation of central serotonin Rs, increased levels or synaptic NE, and enhances opioid R actions
antidepressent ADRs
tricyclic- sedating
GI
anticonvulsants MOA
enhance GABA mediated inhibition, modulate excitatory glutamate transisison
inhibit Na and Ca Ch activity
uses of anticonvulsants
migraine prophylaxis, particularly useful with comorbid, seizures, anxiety disorders, bipolar disorder
ADRs of anticonvulsatns
topiramate: paresthesias, fatigue, anoreia, diarrhea, weight loss, taste perversion
balporate: GI, tremor, somnolence, weight gain
mild-moderate migraine attacks
NSAIDs, if response is poor try actaminophen, aspirin, caffeine combo (excedrin)
mild-severe migraine
triptans, if unrespnsive try erogts
tension HA
simple analgesics +/- caffeine
prevention w/tricyclic antidepressent
cluster HA
oxygen, triptan, ergots
prevention w/ verapamil, lithium, prednisone, topiramate, frovatriptan
