migraine headache treatment

Question 1

NSAID moa in migraines

Answer 1

COX inhibition reduces the production of PGs, thereby reducing the production of inflammatory signals that would trigger MAPK upregulation and the increased neuronal production of CGRP and substance P for release from nerve endings

Question 2

triptans moa in headaches

Answer 2

produce selective carotid vasoconstriction via 5-HT1B receptors and presynaptic inhibition of the trigeminovascular inflammatory responses implicated in migraines via 5-HT1D/1F receptors

Question 3

NSAID adverse effects

Answer 3

gastric irritation with chronic use,
additive nephrotoxicity, especially in elderly - leads to fluid retention, HTN, edema, and rarely CHF
potentiation of migraine-associated nausea

Question 4

NSAID drug interactions

Answer 4

attenuate diuretics, beta-blockers, ACE inhibitors, vasodilators, central alpha-2 agonists, peripheral alpha-1 antagonists and ARBs

Question 5

longest acting NSAIDs

Answer 5

vabumetone

Question 6

shortest acting NSAIDs

Answer 6

ibuprofen and fenoprofen

Question 7

butalbital moa

Answer 7

sedative-hypnotic effects via thalamic GABA enhancement; used in combination with aspirin or acetaminophen and caffeine

Question 8

butalbital adverse effects

Answer 8

drowsiness, sedation, diminished cerebral function; strongly linked to analgesic overuse syndrome; CNS/respiratory depression

Question 9

butalbital contraindications

Answer 9

porphyria, ethanol, and sedatives

Question 10

caffeine adverse effects

Answer 10

cerebral vasoconstriction and potential CV interactions

Question 11

triptans (drugs)

Answer 11

almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan

Question 12

triptan moa

Answer 12

specific agonism of 1B and 1D serotonin receptors in the CNS - selective intracranial/extracranial vasoconstriction, inhibition of trigeminal nerve activation by vasoactive peptides, inhibition of trigeminal cervical complex activation (decrease release of substance P and CGRP)

Question 13

triptans with fastest onset of action

Answer 13

sumatriptan (nasal spray and SC) and zolmitriptan (nasal spray)

Question 14

triptans with longest half lives and longest onsets

Answer 14

frovatriptan and naratriptan

Question 15

triptan side effects

Answer 15

CNS - dizziness, drowsiness, fatigue
CV - heaviness/tightness of chest
coronary and peripheral vasospasm - contraindicated in heart disease, uncontrolled HTN or ischemic bowel disease
use with SSRIs or SNRIs may precipitate serotonin syndrome

Question 16

triptans that interact with MAOIs

Answer 16

rizatriptan, sumatriptan, and zolmatriptan

Question 17

triptans that increase serum propranolol levels

Answer 17

eletriptan, rizatriptan, zolmatriptan

Question 18

triptans that are cyp 3A4 inhibitors

Answer 18

eletriptan

Question 19

ergotism

Answer 19

caused by excessive intake of ergots; results in mental disorientation, convulsions, muscle cramps, and dry gangrene of extremities

Question 20

ergot alkaloid moa

Answer 20

agonist effects on multiple receptors: central 5-HT, peripheral alpha vasoconstriction + decreased amine reuptake; causes contraction of smooth muscle fibers in moderate doses

Question 21

ergot drugs

Answer 21

dihydroergotamine and ergotamine

Question 22

ergot interactions

Answer 22

triptans - vasoconstriction

Question 23

ergot contraindications

Answer 23

vasospastic predisposing conditions, peripheral vascular or CAD, sepsis, MI, uncontrolled HTN; pregnancy and breast feeding

Question 24

migraines in pregnancy treatment

Answer 24

acetaminophen is 1st line; opoids if persistence into later trimesters

Question 25

1st line for menstrual migraines

Answer 25

NSAIDs | if without aura - COCs may be useful

Question 26

allodynia producing migraines

Answer 26

IM ketorolac

Question 27

metoclopromide moa

Answer 27

D2 blockade centrally; pro-kinetic by increasing ACh effects | used for antiemesis

Question 28

chlorperazine and prochlorperazine moa

Answer 28

D2 blockade centrally; cholinergic and alpha-adrenergic blockade used for antiemesis

Question 29

promethazine moa

Answer 29

cholinergic blockade; H1 and weak D2 blockade | used for antiemesis

Question 30

promethazine adverse effects

Answer 30

glaucoma, urinary retention, BPH, drowsiness, parkinson-like symptoms

Question 31

chlorpromazine and prochlorperazine adverse effects

Answer 31

dyskinesia, hypotension, glaucoma, urinary retention, and BPH

Question 32

metoclopramide adverse effects

Answer 32

increased prolactin levels --> gynecomastia

Question 33

amitriptyline moa

Answer 33

decreased reuptake of NE and serotonin and strong anticholinergic action

Question 34

amitriptyline adverse effects

Answer 34

aggressiveness, increased weight, dry mouth, sedation

Question 35

divalproex and valproic acid moa

Answer 35

Na channel blocker; increased GABA activity

Question 36

divalproex and valproic acid adverse effects

Answer 36

hepatotoxicity, sedation, nausea, weight gain, highly protein bound; category X

Question 37

propranolol and timolol moa

Answer 37

beta-blockers - decreased arterial dilation and NE-induced lipolysis

Question 38

propranolol and timolol adverse effects

Answer 38

fatigue, exercise intolerance, problems with asthma, diabetes, AV block

Question 39

topiramate moa

Answer 39

blocks Na and glutamate, increasing GABA activity

Question 40

topiramate AEs

Answer 40

paresthesias, fatigue, nausea, narrow therapeutic range

Question 41

low risk of analgesic overuse syndrome

Answer 41

long-acting NSAIDs, tramadol, dihydroergotamine

Question 42

high risk of analgesic overuse syndrome

Answer 42

aspirin/acetominophen/caffeine, butalbital-containing combinations, opoids

Question 43

migraine prophylaxis in children

Answer 43

propranolol

Question 44

bad news in G6PD deficiency

Answer 44

acetaminophen

Question 45

triptan with worse AEs

Answer 45

SC sumatriptan