Week 9 - Chapter 30 Headache Drugs Flashcards

1
Q

Aura

A

sensory disturbances, usually visual but can also be hearing etc.

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2
Q

Calcitonin-Gene-Related Peptide (CGRP)

A

compound that is to promote migraine

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3
Q

Cluster Headache

A

occur in a series or “cluster” of attacks. Each attack lasts 15 minutes to 2 hours and is characterized by severe, throbbing, unilateral pain in the orbital-temporal area (ie, near the eye). A typical cluster consists of one or two such attacks every day for 2 to 3 months.

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4
Q

Ergot Alkaloid

A

cause vasoconstriction. Accordingly, if one triptan is combined with another or with an ergot alkaloid, excessive and prolonged vasospasm could result. Accordingly, suma­triptan should not be used within 24 hours of an ergot derivative or another triptan.

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5
Q

Ergotism

A

Acute or chronic overdose of Ergotamine can cause serious toxicity known as this.

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6
Q

Medication Overuse Headache

A

People who take headache medicine every day often develop medication overuse headaches (MOHs). A MOH is a chronic headache that develops in response to frequent use of headache medicines and that resolves days to weeks after the overused drug is withdrawn. The stage for MOH is set when headache drugs are taken too often, especially if the dosage is high. Discontinuing the medication brings on the MOH, which causes the patient to resume taking medicine—setting up a repeating cycle of MOH, followed by medication use and discontinuation, followed by another MOH, and so on. One reason the cycle gets established is that patients don’t realize that the drugs they’re taking to treat headache can, if taken too often, become the cause of headache. Failing to recognize MOH for what it is, patients take more and more medicine to make their headaches go away, but only succeed in making MOH worse.

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7
Q

Menstrually Associated Migraine

A

migraine that routinely occurs within 2 days of the onset of menses. An important trigger is the decline in estrogen levels that precedes menstruation. For many women, menstrually associated migraine can be prevented by taking estrogen supplements, which compensate for the premenstrual estrogen drop. Topical preparations—estrogen gel and estrogen patches work well.

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8
Q

Migraine Headache

A

characterized by throbbing head pain of moderate to severe intensity that may be unilateral (60%) or bilateral (40%). Most patients also experience nausea and vomiting, along with neck pain and sensitivity to light and sound. Physical activity intensifies the pain. During a prolonged attack, patients develop hyperalgesia (augmented responses to painful stimuli) and allodynia (painful responses to normally innocuous stimuli). Migraines usually develop in the morning after arising. Pain increases gradually and lasts 4 to 72 hours (median duration 24 hours). On average, attacks occur 1.5 times a month. Precipitating factors include anxiety, fatigue, stress, menstruation, alcohol, weather changes, and tyramine-containing foods.

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9
Q

Serotonin 1B1D Receptor Agonists

A

Compound that suppresses migraines

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10
Q

Tension-Type Headache

A

(formerly called muscle-contraction headaches) are the most common headache type. These headaches are characterized by 314moderate, nonthrobbing pain, usually located in a “headband” distribution. Headache is often associated with scalp tingling and a sense of tightness or pressure in the head and neck. Precipitating factors include eye strain, aggravation, frustration, and life’s daily stresses. Depressive symptoms (sleep disturbances, including early and frequent awakening) are often present. Tension headaches may be episodic or chronic. By definition, chronic tension-type headaches occur 15 or more days per month for at least 6 months.

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11
Q

Aspirin

A

Aspirin, acetaminophen, naproxen, diclofenac, and other aspirin-like analgesics can provide adequate relief of mild to moderate migraine attacks. In fact, when combined with 307metoclopramide (to enhance absorption), aspirin may work as well as sumatriptan, a highly effective antimigraine drug. Moreover, the combination of aspirin plus metoclopramide costs less than sumatriptan and causes fewer adverse effects.
Acetaminophen should be used only in combination with other drugs, not alone. One effective combination, marketed as Excedrin Migraine, consists of acetaminophen, aspirin, and caffeine.

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12
Q

Sumatriptan - Mechanism of Action

A

an analog of 5-HT, causes selective activation of 5-HT1B and 5-HT1D receptors (5-HT1B/1D receptors). The drug has no affinity for 5-HT2 or 5-HT3 receptors, nor does it bind to adrenergic, dopaminergic, muscarinic, or histaminergic receptors. Binding to 5-HT1B/1D receptors on intracranial blood vessels causes vasoconstriction. Binding to 5-HT1B/1D receptors on sensory nerves of the trigeminal vascular system suppresses release of CGRT, a compound that promotes release of inflammatory neuropeptides. As a result, sumatriptan reduces release of inflammatory neuropeptides, and thereby diminishes perivascular inflammation. Both actions—vasoconstriction and decreased perivascular inflammation—help relieve migraine pain.

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13
Q

Sumatriptan - Use

A

abort an ongoing migraine attack

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14
Q

Sumatriptan - Category

A

first triptan available

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15
Q

Sumatriptan - Adverse Effects

A

generally well tolerated. Most side effects are transient and mild. Coronary vasospasm is the biggest concern.

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16
Q

Ergotamine - Use

A

second-line drug for stopping an ongoing migraine attack in patients who have not responded to a triptan

17
Q

Ergotamine - Adverse Effects

A

generally well tolerated. Can stimulate the chemoreceptor trigger zone, causing nausea and vomiting in about 10% of patients, thereby augmenting nausea and vomiting caused by the migraine itself. Concurrent treatment with metoclopramide or a phenothiazine antiemetic (eg, prochlorperazine) can help reduce these responses. Other common side effects include weakness in the legs, myalgia, numbness and tingling in the fingers and toes, angina-like pain, and tachycardia or bradycardia.

18
Q

Ergotamine - Category

A

Ergot Alkaloids

19
Q

Ergotamine - Mechanism of Action

A

alter transmission at serotonergic, dopaminergic, and alpha-adrenergic junctions. Current evidence suggests that antimigraine effects are related to agonist activity at subtypes of serotonin receptors, specifically 5-HT1B and 5-HT1D receptors. Additional evidence indicates that ergotamine can block inflammation associated with the trigeminal vascular system, perhaps by 311suppressing release of CGRP. Relief may also be related to vascular effects. In cranial arteries, ergotamine acts directly to promote constriction and reduce the amplitude of pulsations. In addition, the drug can affect blood flow by depressing the vasomotor center.