Pharm management of HA Flashcards by A B

Tension HA

Abortive treatment

NSAIDs +/- acetaminophen
Add caffeine if unresponsive

can add muscle relaxants

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Tension HA

Prophylaxis

Amitryptiline (TCA)
SNRIs
SSRIs
Anticonvulsants

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Migraine

Abortive treamtent

1) triptan
2) ergots = ergotamine or DHE
3) NSAIDs
4) Tramadol
5) isometheptene

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Migraine

Prophylaxis

1) Antihypertensives (beta blocker or CCB)
2) anticonvulsants (topiramate and valproate)
3) antidepressants (amitryptiline)
4) NSAIDs
5) 5-HT2 receptor antagonists (methysergide)

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Cluster HA

abortive treatment

1) ergots (DHE and ergotamine)
2) glucocorticoids (interrupt chain)
3) lidocaine
4) oxygen
5) triptans (sumatriptan)

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Cluster HA

Prophylaxis

1) lithium
2) methysergide
3) verapamil (CCB)

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Current model of migraine HA

1) neuropetpide trigger cascade of neuroinflamm
2) Phase 1 = 5HT release from neurons and platelets periph on to vessels causes vasoconstriction and ischemia
3) Phase 2 = cerebral vasodilation and pain regul by trigeminal neurovasc system

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how do agonists of serotonin reduce pain in migraine

via release of pain inducing neuropeptides (CGRP)

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5-HT1A
Location

Physiology

CNS

decr camp

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5-HT1A

effects

1) neuronal inhib
2) sleep
3) anxiety

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5-HT1A
agonists
antago

agonist= buspirone

antag = ergotamine

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5-HT1B
Location

Physiology

CNS, blood vessel

decr camp

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5-HT1B

effects

1) presynap inhib

2) pulm vasoconstriction

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5-HT1B

agonists

ergotamine

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5-HT1D
location

physiology

CNS, blood vessel

decr camp

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5-HT1D

effects

cerebral vasoconstriction

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5-HT1D
agonist

antagonist

sumatriptan

ergotamine

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5-HT2A
location

physiology

CNS

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5-HT2A

effects

1) behavior effects
2) contraction
3) aggregation

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5-HT2A
agonist
antago

LSD

methysergide

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5-HT2C
location

physiology

CNS

incr IP3/DAG

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5-HT2C

effects

CSF secretion

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5-HT2C

antagonist

methysergide

NSAIDs

Mechanism of action

COX1/2 inhibitors

interrupts inflamm mediator release caused by CGRP

NSAIDs administration duration

most OTC = oral indomethacin = suppository 4-6 hrs to 8-12 hrs

NSAIDs | uses

sufficient for mild to moderate migrates without nausea or diability used for short term prevention

NSAIDs | side effects

1) avoid in gastritis, peptic ulcers 2) affects platelet aggreg so avoid in bleeding disorders 3) avoid in renal insufficiency tylenol = liver tox

NSAIDs | DDI

incr bleeding risk with antiplatelets or anticoags

Triptans | mechanism of action

5HT1B and 1D agonists 1) cerebral vasoconstriction 2) inhib release of neuropeptides causing vasodilation, inflamm 3) inhib trigeminal pain fibers

Triptans | administration

1) oral mainly, nasal, subq 2) sumatriptan = poor CNS distrib short half life

Triptans | uses

first line for moderate-severe migraines decr dilution-induced HA

Triptans | side effects

paresthesias, flushing, drowsiness, dizzy, chest tightness (worst with sumi) rarely coronary vasospasm *ASSOC WITH DHE, MI, angina, arrhythmia, stroke, death (avoid with HTN and heart dz)

Triptans | DDI

additive constriction with ergot incr risk of 5-HT syndrome with MAOIs (less with SNRI, SSRI)

Ergots | mechanism

5-HT1B and 1D | same as triptans

Ergots | administration

dihydroergotamine = oral, sublingal, rectal, incr abs with caffeine DHE = intranasal and parenteral

Ergots | uses

less effective than triptans but also used in migraines

ergots | side effects

n/v (give with anti-emetics) diarrhea, cramps, paresthesia serious = vascular occlusion, gangrene via alpha 1 vasoconstriction

ergots | ddi

severe peripheral ischemia if used with beta blockers additive constriction with triptans avoid with CYP3A4 inhib = vaosspasm

when should you consider prophylaxis

1) severe, long last >12 hrs, frequent- more than 4 or disabling

prophylaxis beta blockers propranolol timolol causes side effect

first line for migraine prophylaxis antihypertensive causes fatigue, exercise intolerance, depression, ortho hypotension

prophylaxis beta blockers propranolol timolol contraindicated in

asthma diabetes conduction disturbances

prophylaxis CCB verapamil

third line for migraine prophylaxis | tolerance develops

prophylaxis CCB verapamil contraindiction

don't use with beta blocker= heart block

prophylaxis ACEI/ARB lisinopril candesartan

2nd or 3rd line

TCA amitryptiline side effect

incr monoamine transmission, second line sedation, dry mouth, tachy, weight gain, urinary retention

anticonvulsants topiramate side effect

effect similar to propranolol | side effect = paresthesias, weight loss, taste perversion, fatigue

pathophys of migraine

1) trigeminal neurovasc dysfunction 2) trigem neurovasc activ 3) release of vasoactive peptides 4) neuroinflamm and vasodilation of pial and dural vessels 5) pain

phase 1 of migraines

cerebral vasoconstriction and ischemia cortical spreading depression (decr CBF from vasoconstrict --> aura) activate trigem nerve afferents

phase 2 of migraines

cerebral vasodilation | trigeminal neurons release vasocactive peptides (substance P, CGRP) = vasodilation and neuroinflamm

role of sensitization

1) throbbing pain 2) worsening pain with coughing-bending-sudden head movements 3) hyperalgesia 4) allodynia

abortive treatment of migraine with n/v

SC sumatriptan | IV metoclopramide + diphenhydramine

abortive treatment of migraine with intractable HA

IV DHE

severe side effect of triptans, ergots esp DHE

vasoconstriction and vasooclusion but more common in ergots and DHE due to alpha1 blockage

frontal lobe lesion causes urinary __

urgency

spinal cord lesions above S2-S4 spinal cord lesions of S2-S4 or injury to periph nerves innerv bladder

spastic bladder (think UMN) --> reflux up ureters flaccid bladder (think LMN) --> overflow incontinence