HA and migraines pharm Flashcards by laura gibbons

acute migraine drugs

serotonin agonists
ergot alkaloids
analgesics
combo analgesics
NSAIDs
antiemetics

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migraine prophylatics

beta blockers
CaCh blockers
antidepressents
anticonvulsants

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primary HA disorders

migraine
tension
cluster

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secondary HA disorders

d/t other underlying cause
infection
brain mass or swelling etc

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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

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common migraine

70%

lacks aura

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pathophys of migaines

trigeminal n and maybe extracranial aa involed

nn release CGRP which is an extremely powerful vasodilatation -> inflammation and edema

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food triggers for migraine

alcohol
caffeine/caffeine withdrawl
chocolate
MSG
aspartame

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environmental triggers of migraine

flickering lights
high altitude
strong smells/fumes
tabacco smoke
weather

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Behavioral triggers of migraine

excess/insufficient sleep
fatigue
menstruation
skipped meals
strenuous activity

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tension type HA (TTH)

most common type of primary HA disorder
least studied, pathophys not understood
simple analgesics and NSAIDs
amitripyline prophylaxisis

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cluster HA

rare, but most severe primary HA
pain excruciating, associated with cranial autonomic symptoms
best Tx is prevention

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serotonin agonists

sumatriptan

-triptan

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ergot alkaloids

dihyroergotamine (DHE)

ergotamine (+/- caffeine)

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combo analgesics

excedrin migraine: aspirin, acetaminophen, caffeine

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antimemtics

metoclopramide

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CaCh blockers

verapamil

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antidepressents

antitriptyline

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anticonvolssants

topiramate

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synthesis of serotonin

from L-tryptophan
stored in vesicles
over 90% in in enterochromaffin cells in GI tract
in blood in platelets

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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