Headache Flashcards

1
Q

Medication Overuse HA

A
  • caused by freq use of ha medications-> withdrawal symptoms (escalating use or a large amount of HA)
    offending agents:
    -Barbiturates, acetaminophen, ASA, nsaids, ergotamines

avoid by limiting to 2-3x per week for abortive therapy

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2
Q

Migraine triggers

A

increased/decreased sleep
dehydration
stress
emotional letdown
skipping meals
alcohol
meds
weather changes
smoking
strong perfumes
chocolate
caffeine
cheese
hormone changes
loud noise
physical activity

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3
Q

Goals of migraine tx

A

Primary goal: prevent, or have consistent/rapid relief with minimal AE

Other goals: minimize disability, emotional distress, enable pt to participate in ADL, manage HA w/out doc visit

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4
Q

Acute migraine tx overview

A

Mild Mod:
-Acetaminophen
-NSAIDS

Mod-Severe:
-triptans
-triptans w/ NSAIDS
-ergotamine
-calcitonin gene-related peptide receptor antagonists (CGRP)
- non-preferred: butalbital products and opioids

Adjunctive:
antiemetics
-hydroxyzine
-promethazine
-Metoclopramide
Antihistamines
Transcranial Magnetic stimulators

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5
Q

Overview of attacks

A

Prophylactic:
- BB, antidepressants, Topiramate, Verapamil, CRPG

During an acute attack:
1. Triptans
2. Dihydro-ergotamine
3. Analgesics

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6
Q

Mild to moderate migraine

A
  1. Acetaminophen
    -AE: Liver issues, unintentional overdose
  2. NSAIDS
    -AE: GI bleeding, renal impairment, cardiac issues
    AVOID IN PREGO
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7
Q

Triptans

A

Imitrex (sumatriptan) and Relpax (eletriptan)
MOA: activates SEROTONIN receptor in intracranial bv -> VC & reducing release of Pro-inflamm neuropep

1ST LINE ABORTIVE THERAPY OF MILD TO SEVERE MIGRAINES
can redose w/in 24 hrs

ae:
- htn, cardiac events, pain and pressure sensations in chest, neck, throat, jaw, dizzy, mailase

Contra:
-ischemic heart dz
-stroke
-uncontrolled htn
-MAOIs= mono amine oxidase inhibitors
-serotonin syndrome

Interactions:
1. CANNOT ADMINISTER W/IN 24 HRS OF AN ERGOTAMINE DERIVATIVE
2. CANNOT ADMINISTER W/IN 2WKS OF A MAOI

WARNINGS IN ELDERLY

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8
Q

Serotonin Syndrome

A

CAN B LETHAL
pts taking Triptan w/ Serotonin antidepressant
Triad:
1. Mental status changes
2. Autonomic instability
3. Neuromuscular abn (hyperreflexia, myoclonus)

RF: taking >1 serotonergic agent (MAOI + SSRI, SNRI, Linezolid, Antiemetic)

Causative agent:
-Tryptophan, oxitriptan, amphetamines, MDMA (ecstasy), cocaine, Mirtazapine, tramadol, dextromethorphan, SSRI, SNRI, Fentanyl, LSD, ALL MAOI, Lithium

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9
Q

Ergotamine derivatives aka Ergots

A

Ergotamine (Ergomar) and dihydroergotamine (D.H.E)
Non-selective 5-HT1 (serotonin) receptor agonists
MOA: partial agonist and/or antagonist activity against tryptaminergic, dopaminergic, and alpha-adrenergic receptors depending upon their site= contrict peripheral and cranial blood vessels -> produce depression of central vasomotor centers

AE: Extreme NVD, paresthesias, chest tightness, “ergotism”- cold, numb, painful extremities, diminished peripheral pulses and claudication

Contra:
PREGNANCY/LACTATION
RENAL AND LIVER FAILURE
CORONARY, CEREBRAL, OR PERIPHERAL VASCULAR DZ
UNCONTROLLED HTN
SEPSIS

cant use w/in 24 hrs of a Triptan B4 or after

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10
Q

Ditans - new class

A

Lasmiditan (Reyvow)
MOA: block neurogenic inflam in dura and simulation of the trigeminal nucleus caudalis

AE: dizzy, paresthesia, sedation (SPECIFIC WARNING NOT DRIVING MOTOR VEHICLE OR OPERATE HEAVY MACHINERY W/IN 8 HRS DUE TO DROWSINESS), n/v

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11
Q

Small-molecule CGRP Antagonists (“Gepants”)

A

Rimegepant (Nurtec) and Atogepant (Qulipta)
CGRP- role in trigeminovascular pain transmission and neurogenic inflam
efficacy like triptans and lasmiditan-> better tolerated

MOA: block backing CGRP receptors-> VC and decrease in neurogenic inflam

USEFUL FOR ACUTE MIGRAINE AND CHRONIC MIGRAINE PROPHYLAXIS
-Nurtec and Qulipta

only for acute tx- Ubrogepant (Ubrelvy) mod to severe migraine

AE:
Nausea- Rimegepant (Nurtec)= long half life (11 hrs)
Nausea, xerostomia, somnolence- ubrogepant (Ubrelvy) = short (5-7 hrs)

lots of interactions
avoid use in hepatic or renal impairment

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12
Q

Opioid and opioid derivatives

A

inadequate evidence to tx migraine
Probably effective: codeine + acetaminophen or tramadol + acetaminophen
Established efficacy= Butorphanol (nasal spray)

reserve use for pts w/ infrequent mod to severe HA:
-contra to conventional therapies
or
-“rescue” med after failure to conventional therapies

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13
Q

Chronic migraine prophylaxis

A
  1. Ant-calcitonin gene-related peptide (CGRP) antagonist
  2. Topiramate (Topamax)- anticonvulsant
  3. Timolol, propanolol (non-selective beta blockers)
  4. Divalproex (Depakote)

possible effectiveness:
antidepressants: amitriptyline
Anticonvulsants: valproic acid
NSAIDS
Triptans
Lisinopril
Candesartan
Verapamil

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14
Q

Calcitonin Gene-related peptide (CGRP) antagonist monoclonal ab

A

Eptinezumab (Vyepti)- infusion
Erenumab (Aimovig)- inj
Fremanezumab (Ajovy)- inj
Galcanezumab (Emgality)- inj

limitations: access and cost
no known med interactions

AE: injxn sit rxn, hypersensitivity, nasopharyngitis, constipation

cardiovasc warnings: Fremanezumab, galcanezumab

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15
Q

Adjunctive migraine therapies

A

Antiemetic: pretx b4 oral adn non-oral meds
-Metoclopramide (Reglan)
-Prochlorperazine (Compro)
-Hydroxyzine (Vistaril)
-Promethazine (Phenergan)
-Chlorpromazine, droperidol = first gen antipsychotics

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16
Q

Non pharm tx for migraine

A

ice to head
rest/sleep in a dark quiet environ
identify and avoid triggers
behavioral triggers
-relaxation
-biofeedback
-cognitive therapy

17
Q

Tension HA and cluster HA

A

Tension HA: analgesic (NSAID, acetaminophen, aspirin)-> NSAID preferred
-simple analgesic +- Caffeine
-acetaminophen, aspirin, NSAIDS (diclofenac, ibuprofen, naproxen, ketoprofen, ketorolac)

Cluster HA: Triptans + inhaled oxygen-> first line abortive therapy