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35 Cards in this Set
- Front
- Back
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Vasoconstriction
Due to release of serotonin from CNS and platelets Aura associated with hypoperfusion of bra |
prodromal phase
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Derived from kininogens via enzymatic action of kallikrein.
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Kinins
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activate phospholipase; inhibitors glucocorticoids (lipocortin) and NSAIDs
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Bradykinin and Kallidin
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(also called peptidyl dipeptidase) metabolizes Bradykinin and kallidin (inactive metabolite)
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Kininase II
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inhibits kininase II
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ACE inhibitors
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Serotonin synthesized in ....
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Brain and enterochromaffin cells
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...........only store 5HT, release it on aggregation.
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Platelets
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......metabolizes 5HT
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MAO
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a urinary metabolite; elevated in cancer of enterochromaffin cells; variable levels in migraine
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5 hydroxyindoleacetic acids
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Vascular action for 5HT is.....
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vasoconstriction
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Headache phase has a Longer duration , low serotonin levels, vasodilation of cerebral vessels and release of neuropeptides that produce pain and inflammation (CGRP, neurokinin, VIP, bradykinin, etc.)
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second phase
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Beta Blockers
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Propranolol (preferred) or timolol; can’t use in asthmatics
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TCAs
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Amitryptilline, side effects of dry mouth, urine retention & wt. gain
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Anticonvulsants
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Topiramate and valproate, advantage for patients with epilepsy; can’t use valproate in pregnancy (teratogen)
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Calcium Channel Blockers
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(nifedipine & verapamil)
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Beta blockers
TCAs Anticonvulsants Calcium Channel Blockers |
Prophylactic Drugs
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5-HT1 agonists which mediate cerebral vasoconstriction
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Ergots and Triptans
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function as presynaptic autoreceptors
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5HT1
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activation of 5HT1D results in....
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inhibition of neuron and decline in inflammatory peptides
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cerebral vasoconstriction via adenosine antagonist
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caffiene and acetominaphen
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NSAIDS (ibuprofen, ketorolac, aspiring, naproxen)
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non-specific agents
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use for moderate to severe migraine; given iv (unique for NSAIDs) or oral (Can’t use
more than 5 days due to PG inhibition) |
Ketorolac
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5-HT1 agonists, mediate cerebral vasoconstriction & inhibit pain inducing peptides
only used for abortive puropses no prophylaxis |
Ergots and Triptans
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5-HT1A,1B,1D and 5-HT2, α-adrenergic and dopaminerigc receptor agonists; less specific than
Triptans causes more side effects esp. nausea and peripheral vasoconstriction |
Ergot alkaloids
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abortive given sublingually
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Ergotamine
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Abortive, inhaled or injected
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Dihydroergotamine
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Concurrent use of ....... and fluoxetine will induce ergot toxicity due to inhibition of P450 metabolism by
Fluoxetine (FYI for Step 1) |
ergots
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Pregnancy
PVD Ischemic CAD Triptan usage |
contraindications for Ergots
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5-HT1B/D agonists; NO interaction with other 5-HT receptors, adrenergic or dopaminergic receptors
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Triptans
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Adverse effects are drowsiness, fatigue, dizziness
-Avoid concurrent use with SSRI agents as excess 5-HT accumulation may induce serotonin syndrome |
Triptans
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(excess
serotonin muscle twitching, hyperthermia, agitation, Nasea, Vomiting , Diarrhea |
serotonin syndrome
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-Use of an ergot within 24 hrs
-Peripheral vascular disease -Ischemic heart disease |
Contraindications for Triptan use
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-Administered Subcutaneous, oral or nasal spray
-Half-life 2 hrs is Metabolized by MAO -Sulfonamide allergy history may be sensitive to this drug -Use of MAO inhibitors (FYI for Step 1) |
Sumatriptan
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– Administered oral
– Half-life is 6 hrs; Metabolized by P450; Must lower dose in renal dysfunction |
Naratriptan
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-Available as quick dissolving tablet (sbulingual)
-Faster onset and less nausea than sumatriptan -Half-life 2 hrs; Metabolism via MAO -Use of MAO inhibitors (FYI for Step 1) |
Rizatriptan
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