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Migraine
Migraine- Pharmacology
| Question | Answer |
|---|---|
| What is the prodromal cerebral vasoconstriction phase of a migraine called? | An aura |
| Levels of this drop during the migraine prodrome attacks. | 5-HT (both plasma and platelet levels) |
| In addition to 5-HT, levels of these things also fluctuate. | Glutamate, nitric oxide, and opioid NT systems |
| The migraine starts in this part of the brain. | Occipital part of the brain, then it spreads forward. This is known as "cortical-spreading depression" |
| The aura is associated with vasoconstriction or vasodilation? | Vasoconstriction. Vasoconstriction occurs in response to a decrease in neurotransmission. |
| The trigeminal nerve participates in a positive feedback system by releasing... | nociceptive peptides (AKA substance P) that further enhance the inflammatory response/vasodilation |
| Explain the pathogenesis of a migraine. | 1) Cortical-spreading depression causes the actual trigger of the migraine |
| Aim of migraine medication | Block the receptors that are involved in releasing substance P so you can reduce the signaling causing the migraine. |
| Tricyclic antidepressants, 5-HT antagonists, B-adrenergic antagonists, MAO-Is, Ca ch blockers are all used in what type of migraine treatment? | Prophylaxis. Should be used when someone is experiencing 3-4 migraines a month or with a pregnant woman. |
| These agents cause the release of PGs and are the target of inhibition by mild analgesics. | Kinins, substance P, IL-1, IL-8 |
| Combination analgesics aim to alleviate pain associated with migraines by... | 1) PG inhibition |
| Combination analgesics are CI'd in pts with: | Glaucoma |
| MOA of mild analgesics | Irreversible inhibition of COX |
| MOA of combination analgesics | Irreversible inhibition of COX, a- & b- adrenergic antagonism, CNS depression |
| MOA of antiemetics | Inhibition of CNS vomit center stimulation |
| These two antiemetics have anti-muscarinic effects | Diphenhydramine and promethazine (both are H1-antagonists) |
| Proposed MOAs for 5-HT agonist therapy | •5-HT receptor stimulation by ergot alkaloids and sumatriptan can lead to the constriction of the intracranial arteriovenous network |
| Sumatriptan MOA | Mimics 5-HT, it is a 5-HT agonist that activates 5-HT receptors in the cerebral arteries, which causes vasoconstriction |
| Sumatriptan contraindications | Ischemic heart dz (angina pectoris, hx of MI, silent ischemia) |
| When should sumatriptan be taken for maximal effectiveness? During the aura the precedes the headache or during the actual headache? | During the actual headache |
| What is common after sumatriptan injections but less frequent after other administration routes | Brief and mild sensation of pressure in the chest or throat |
| MOA of the "other" triptans | They all have the same MOA and are better at crossing the BBB than sumatriptan |
| Slightly more effective than sumatriptan tablets but same efficacy as sumatriptan nasal spray. Like sumatriptan, this drug binds to the 5HT-1D & -1F R's on trigeminal-nerve endings and to 5-HT-1B R's on intracranial vascular-muscle cells. | Zolmotriptan |
| Comparable to sumatriptan in MOA, effectiveness, AEs, and CIs | Naratriptan |
| Slightly more effective than sumatriptan, but with more frequent dizziness and drowsiness. However, this drug produces less chest pain than sumatriptan. HA recurrence rate the same as sumatriptan ~40% | Rizatriptan |
| A combination product that is available containing imitrex and naproxen. It gives an additive effect | Treximate |
| T/F: A pt's condition will have to be considered when choosing a triptan because of their various elimination routes. | True |
| The only triptan that can be given IV | Sumatriptan |
| These two triptans come in the form of a nasal spray | Sumatriptan & zolmitriptan |
| These two triptans come in the form of orally disintegrating tables | Rizatriptan & zolmitriptan |
| T/F: All triptans come in a tablet form | True |
| Ergot Alkaloids MOA | Antagonism or partial agonism of: |
| Downfall of ergot alkaloids | Potentially severe side effects |
| This drug are useful in pts experiencing very long attacks (>48h) or as second line agents with migraines that return with triptans | Ergotamine |
| List the three ergot alkaloids | 1) Methysergide |
| This ergot alkaloid is not as effective as sumatriptan in the tx of acute attacks, but it is more effective as prophylactic tx | Methysergide |
| This drug has an affinity for H1-R's, which results in histaminic SEs (vasoconstriction and pressor effects) | Methysergide |
| Serious AE such as retroperitoneal fibrosis, pleuropulmonary fibrosis, CV disorders) have been reported | Methysergide |
| No significant psychomimetic activity reported. | Methysergide |
| Lower emetic potency than other ergot alkaloids | Dihydroergotamine |
| Lower migraine recurrence after 24 hrs than sumatriptan (a good thing!) | Dihydroergotamine. DHE has a recurrence percentage of 18% while sumatriptan has 40%. |
| This is an extremely safe drug, except that it can constrict coronary arteries, just like sumatriptan. | DHE (Dihydroergotamine) |
| DHE contraindications | definite or suspected coronary artery dz |
| Main SE of DHE | nausea |
| MOA of prophylactic agents for migraine HA tx | Largely unknown. These agents happened to reduce the incidence of migraines while the pt was taking them for a different condition. |
| These agents act at different receptors than the triptans and ergots | Serotonergic (5-HT) antagonists. Triptans and ergots act on 5-HT1. The antagonists act on different receptors. |
| MOA of B-antagonists (as prophylaxis agent) | reduce edema and reduce pressure in brain |
| These three tricyclic antidepressants are commonly prescribed as migraine prevention agents | 1) Amitriptyline |
| This group of drugs has also shown to be effective for preventative effects | GABA stimulating drugs (e.g. for seizure, i.e. Topamax, valproate) |
| These preventative agents are more as a last resort; they have been withdrawn in Europe | 5-HT antagonists |
| This drug (which I think is an ergot alkaloid) is also a 5-HT antagonist and is the oldest of the prevention agents, but is not commonly prescribed because of it's SEs (inflammatory fibrosis in retroperitoneum, lungs, and heart valves) | Methysergide |
| Untested migraine prophylactics and is preferred in children. Adults normally get potent sedative effects, but this is not normally seen in children. | Cyproheptadine |
| B-adrenergic receptor antagonists (Beta blockers): drug list | 1) Propanolol |
| B-blocker SEs | GI upset, lethargy, orthostatic hypotension |
| B-blocker contraindications | 1) asthma |
| A major anti-epileptic that have been shown to have anti-migraine effects in multiple controlled trials | Divalproex |
| Divalproex MOA | Stimulates action of GABA synthetic enzymes and inhibits the action of GABA degradative enzymes |
| This can shows a reduction in the occurrence of migraines, especially in pregnant women | Magnesium |
| Mg MOA | Mg deficiency is thoughts to make the brain more susceptible to spreading depression. Cerebral blood vessels are very sensitive to Mg. |
| Relatively safe with a wide therapeutic range. The major side effect seen in transient facial flushing with rapid IV infusion | Magnesium |
Created by:
Liza8986
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