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Pharmacology > Drugs for the treatment of migraine and other headaches > Flashcards

Drugs for the treatment of migraine and other headaches Flashcards

1
Q

Ergot Alkaloids and drugs that act at 5-HT receptors
(Drug names)
(2 of them)

A

1.) Ergotamine tartrate
(oral, sublingual and rectal)

2.) Dihydroergotamine
(IV, IM, SC, nasal)
dihydroergotamine mesylate nasal spray (Migranal)

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2
Q

Ergot Alkaloids and drugs that act at 5-HT receptors:
Specific 5-HT1B/1D agonists
(Drug names)
(2 of them)

A

1.) Sumatriptan- First generation
(SC, nasal spray, oral, transdermal patch)

2.) Zolmitriptan- Second Generation
(nasal or oral)

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3
Q

Dopamine Antagonists – Antiemetics (IV, IM or oral)
(Drug names)
(3 of them)

A
  1. ) Metoclopramide
  2. ) Prochlorperazine
  3. ) Chlorpromazine
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4
Q

Analgesics
(Drug names)
(3 of them)

A
  1. ) Aspirin
  2. ) Acetaminophen
  3. ) Ibuprofen
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5
Q

Miscellaneous drugs
(Drug Types and names)
(4 of them)

A

1.) Beta Blockers (e.g. propranolol, timolol, atenolol)

2.) Antidepressants-
amitriptyline

  1. ) Anticonvulsant Drugs - valproate, topiramate, gabapentin
  2. ) Botulinum toxin type A (Botox)
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6
Q

Introduction and Background to migraines and headaches. (Just read through)

A

Migraine head pain is a serious medical condition that affects a large number of adults and
children resulting in millions of work days lost in the US annually. 6-9% of men and 18-24% of women in North America suffer from migraine, with approximately 2.2% of the adult population meeting criteria for chronic migraine, it can be estimated that there are approximately 44.5 million adult migraine sufferers in the United States. Most common
age to have migraine attacks is 30 to 39. Genetics play a large role with an individual having
a 3 times greater chance of having migraines if an immediate family member is also a migraine sufferer. There is a resultant loss of 113 million workdays per year ($13 billion).
Pediatric epidemiology studies demonstrate that 6-11% of adolescents suffer migraine,
with 0.79-1.75% meeting criteria for chronic migraine.
B. Gastric motility and migraine. For unknown reasons, GI motility is slowed significantly during a migraine. As a result, the absorption and effectiveness of oral medication is greatly diminished. In addition, nausea (90% of patients) and vomiting are associated with migraine further decreasing the effectiveness of oral medication. Therefore, parenteral routes (e.g. IM, IV, nasal spray) of drug administration are preferred and may be essential for effective drug therapy.

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7
Q

Migraines are Classified by 4 Phases. What are those phases?

A
  1. ) prodrome
  2. ) aura
  3. ) headache
  4. ) postdrome
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8
Q

What are the 5 major triggers for Migraines?

A

1.) emotional stress (80%)

2.)changes in hormone
levels in women (65%)

  1. ) not eating (57%)
  2. ) weather (53%)
  3. ) sleep disturbances (50%)
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9
Q

Migraine Phases:

Prodrome

A 
≤ 60% of migraine sufferers experience prodrome characterized by the
most common symptoms: 
 -euphoria
 -depression
 -irritability
 -food cravings
 -constipation
 -neck stiffness
 -increased yawning

These appear 24 – 48 hours
before the onset of head pain.

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10
Q

Migraine Phases:

Aura

A

≤ 25% of people with migraines experience one or more neurologic
symptoms called migraine aura. Most auras are visual (e.g. “fortification spectrum”) but can be sensory, verbal or motor disturbances

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11
Q

Migraine Phases:

Headache

A

Often unilateral with a throbbing or pulsatile quality,
especially as the pain intensifies. Nausea (90%) and sometimes vomiting occur as
the intensity of the migraine increases. Photophobia and phonophobia are frequent. The pain may last 4 to 72 hours, usually resolves with sleep.

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12
Q

Migraine Phases:

Postdrome

A

During this phase some patients may feel tired/depressed or

refreshed/euphoric.

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13
Q

Menstrual migraine

A

A common migraine that coincides with the onset of menstruation; presumably due to changing hormone levels.

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14
Q

Tension type headaches (muscle contraction headaches)

A

Dull persisting, non-pulsating,
non-debilitating, bilateral pain (hatband pattern), not aggravated by physical activity, usually an absence of nausea/vomiting, and absence of aura and photophobia/phonophobia.

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15
Q

Cluster headaches

A
  • Brief episodes (< 3 hours) of excruciating unilateral pain (behind eye) that occur in clusters (closely spaced attacks) with periods of remission (months to years).
    Cluster headaches are very rare (0.07% of population), and are more common in males
    than females. Other symptoms may include: lacrimation, rhinorrhea, ptosis and miosis.
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16
Q

Proposed theories for migraine pathogenesis

4 of them

A
  1. ) “Vascular theory”
  2. ) “Spreading depression”
  3. ) Serotonergic abnormalities
  4. ) Genetic factors (e.g. abnormal P/Q calcium channels)
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17
Q

Proposed theories for migraine pathogenesis:

“Vascular theory”

A

This theory states that the aura phase of migraine is associated with intracerebral arterial vasoconstriction, and the headache phase of a migraine is associated with compensatory extracranial vasodilation.

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18
Q

Proposed theories for migraine pathogenesis:

“Spreading depression”

A

This theory states that migraine aura may result from a spreading depression in cortical electrical activity.

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19
Q

Proposed theories for migraine pathogenesis:

Serotonergic abnormalities

A

Research indicates that serotonin plays a major role
in migraine pathophysiology. Drugs that deplete serotonin from tissue stores (e.g.
reserpine, fenfluramine) can induce migraine, and intravenous injection of 5-HT
can abort spontaneous and reserpine-induced migraine. Many of the drugs used for the treatment of migraine act at the level of serotonin type 1 receptors
(See Fig 1).

20
Q

Proposed theories for migraine pathogenesis:

Genetic factors

A

An individual is 3X more

likely to have migraines if an immediate family member also has migraines

21
Q

Drugs for the abortive treatment of migraine

Read over

A

A Clinical problem with some abortive therapies is rebound headache (medication overuse headache). These rebound headaches are characterized by an increase in headache frequency and an increase in drug consumption. The abortive therapies most commonly implicated include: combination analgesics, opiates, ergotamine and the triptans. To avoid the problem of rebound headaches abortive medicines should only be used ~ 2 times a week at most. Only botulinum toxin A is effective for relieving rebound or medication overuse headaches.

22
Q

Analgesics – Effective in the treatment of mild to moderate migraine pain
(Name the 4 types)

A
  1. ) NSAIDS
  2. ) Acetaminophen
  3. ) Midrin
  4. ) Opiates
23
Q

Analgesics – Effective in the treatment of mild to moderate migraine pain:
NSAIDS

A

These drugs have been found to be effective in treating migraine. However, the relative efficacy between the different NSAIDS for treating migraine
headaches has not been clearly established. The mechanism of action of NSAIDS in migraine appears to be related to their ability to block prostaglandin synthesis, which prevents inflammation in the trigeminovascular system and lessens pain sensitization.

24
Q

Analgesics – Effective in the treatment of mild to moderate migraine pain:
Acetaminophen

A

Efficacious in treating migraine and migraine symptoms
including photophobia, phonophobia and pain. Combination of NSAID (aspirin) and acetaminophen and caffeine (Excedrin) may alleviate headache in migraine
patients.

25
Q

Analgesics – Effective in the treatment of mild to moderate migraine pain:
Midrin

A

(Isometheptene + dichloralphenazone + acetaminophen).
This drug is very effective at abortive migraine therapy and was available in the US for decades with 3 active ingredients: isometheptene (vasoconstrictor); dichloralphenazone(sedative) and acetaminophen. Midrin was introduced to the market before 1962, when the FDA first required drugs to be proven effective for the conditions they treat. Currently midrin is NOT FDA approved and requires clinical trials for full
approval.

A similar product, Prodrin (isometheptene + caffeine + acetaminophen) is currently available.

26
Q

Analgesics – Effective in the treatment of mild to moderate migraine pain:
Opiates

A

(e.g. butorphanol)
Reserved for severe infrequent headaches and ONLY
when conventional therapies are not effective or when rescue medication is needed. Nasal administration of butorphanol can provide an alternative to frequent visits to the hospital for injectable migraine therapies.

27
Q

Ergot Alkaloids and drugs that act at 5-HT receptors:

Ergotamine Tartrate – For the acute treatment of moderate to severe migraine. Second
line drug, used only after “_triptan” drug therapy fails to control migraine.
(Read Over)

A

Ergot-like compounds occur naturally in rye contaminated with the fungus claviceps purperea. Epidemics of “Ergotism” (Gangrenous mummified limbs,
spontaneous abortions) have been reported throughout history, and the condition was called holy fire and St. Anthony’s fire.

Ergotamine tartrate is available in oral, sublingual and suppository dosage forms. The half-life of ergotamine is ~2 hours, however ergotamine-induced vasoconstriction can last up to 24 hours. Caffeine is added to some ergotamine containing products to potentiate vasoconstriction, and improve intestinal absorption.

Pharmacodynamics - Ergotamine is a “dirty” drug and interacts with serotonin, dopamine, and adrenergic receptors. The effectiveness of ergotamine for migraine headache (see Figure 1) is mediated by activation of 5-HT1B receptors and vasoconstriction and may reduce neurogenic inflammation by decreasing the release of vasodilator/proinflammatory neuropeptide transmitters

28
Q

Ergot Alkaloids and drugs that act at 5-HT receptors:

Ergotamine Tartrate Toxicity, adverse reactions, and contraindications

A

Ergotamine is a powerful vasoconstrictor and is contraindicated in patients
with peripheral vascular disease. Beta-blockers may potentiate vasoconstriction caused by ergotamine.

GI upset (nausea, vomiting, anorexia) occurs in ~10% of patients due to activation of central dopamine receptors in the chemoreceptor trigger
L28- 7 zone. This side effect may require adjunct therapy with an antiemetic, e.g.
Metoclopramide (Reglan).

29
Q

Ergot Alkaloids and drugs that act at 5-HT receptors:

Dihydroergotamine- effective in the acute treatment of moderate to severe migraine.

A

A nasal spray dosage form of Dihydroergotamine, Dihydroergotamine
Mesylate (Migranal), is available.

Pharmacodynamics - The mechanism of action is similar to ergotamine tartrate (e.g. stimulation of 5HT1 receptors) and is a “dirty” drug and that
interacts with other receptors (e.g. catecholamines, serotonin, dopamine).

30
Q

Ergot Alkaloids and drugs that act at 5-HT receptors:

Dihydroergotamine Toxicity, adverse reactions, and contraindications

A

GI upset - Dihydroergotamine stimulates the chemoreceptor trigger zone and may cause vomiting/nausea.

Transient bradycardia, weakness in the legs, vasospasm (less likely than
ergotamine due to less arterial vasoconstrictor activity and more Beta-adrenergic blocking activity)

31
Q

Specific 5-HT1B/1D agonists :

Sumatriptan

A

Sumatriptan and the other triptans are the first line drugs for the acute treatment of moderate to severe migraine once OTC analgesics/NSAIDs are found to be ineffective.

32
Q

Specific 5-HT1B/1D agonists :

Sumatriptan Pharmacokinetics

A

Sumatriptan is a derivative of serotonin (5-HT).
Sumatriptan is available as a succinate salt which is administered by subcutaneous injection (thigh auto-injector), oral tablets, nasal spray or (in 2014) by transdermal
patch. Sumatriptan is metabolized by MAO-A, and the metabolites are excreted in the urine (half-life ~2 hours). The triptans may be administered four hours (or
longer) after the onset of an attack and still be effective.

33
Q

Specific 5-HT1B/1D agonists:
Sumatriptan
Pharmacodynamics

A

Sumatriptan is effective in acute migraine by causing the
constriction of inflamed/dilated intracranial arteries, and by inhibiting the release of vasodilator/proinflammatory mediators from trigeminal nerve endings (see figure 1). In addition, sumatriptan appears to relieve the nausea, vomiting, photophobia, and phonophobia associated with a migraine attack.

34
Q

Specific 5-HT1B/1D agonists:
Sumatriptan
Toxicity, adverse reactions, and contraindications

A

Cardiovascular (coronary spasm, myocardial infarction, ventricular arrhythmias) - several fatalities reported with subcutaneous sumatriptan
resulting from myocardial infarction. Also, the use of sumatriptan and another ergot-type compounds within 24 hours in contraindicated due to possible additive vasopspastic effects.

Triptan symptoms - Common with sumatriptan and newer 5HT1 agonists. Chest and throat tightness, difficulty in breathing, panic/anxiety, paresthesia, feeling of heaviness. May be caused by interaction of sumatriptan with 5HT1A receptors.

Contraindicated with use of a MAO inhibitor (e.g. Phenelzine, Isocarboxazid) within a 2 week time span after discontinuing MAO inhibitor therapy.

35
Q

Specific 5-HT1B/1D agonists: Second generation Triptans

A

Zolmitriptan

The second generation triptans have greater bioavailability versus sumatriptan. Like sumatriptan these drugs act at the peripheral components of trigeminovascular system (direct vasoconstriction, inhibiting release of vasodilator/proinflammatory mediators). However, due to greater lipid solubility, second gen triptans also act centrally to inhibit pain transmission in the trigeminal
nucleus (see Figure 1). Zolmitriptan is the only second generation triptan with nasal and oral formulations available.

36
Q

Anti-emetics

A
  1. ) Metoclopramide
  2. ) Prochlorperazine
  3. )Chlorpromazine

These dopamine antagonists are useful for the treatment of acute migraine unresponsive to a “triptan” or oral analgesics. These agents relieve headache pain and have anti-emetic activity. These drugs are typically given IV or IM. They can be used as monotherapy or as adjunctive therapy with NSAIDs or sumitriptan. If given in adjunctive therapy then oral dosing may be used.

37
Q

Drugs for prophylaxis of migraine

A
  1. ) Beta Blockers
  2. ) Antidepressants
  3. ) Anticonvulsants (anti-seizures)
  4. ) Botox A

Prophylactic migraine therapy, considered if a patient has
recurring migraines (≥ 3 per week) that don’t respond to acute therapies or if they are use acute therapies more than twice a week. These therapies need to be evaluated for 2 – 3 months before deemed ineffective. If effective, prophylactic therapy should be continued for at least 3 – 6
months, and then the patient can be examined for possible remission.

38
Q

Drugs for prophylaxis of migraine:

Beta Blockers

A

Pharmacodynamics - The mechanism of action of Beta-blockers in migraine prophylaxis is not well understood. If a patient fails to respond to a particular Beta-blocker, they may be responsive to one of the other Beta Blockers. Beta-blockers which lack partial agonist activity (intrinsic sympathomimetic activity) are the most effective in the prophylaxis of migraine (e.g. propranolol, nadolol, timolol, atenolol, metropolol).

Toxicity, adverse reactions, and contraindications:

1.) Beta-blockers may augment the vasoconstriction caused by ergotamine.

39
Q

Drugs for prophylaxis of migraine:

Antidepressants -amitriptyline

A

Mechanism of action of the tricyclic antidepressant amitriptyline in migraine prophylaxis is unknown but appears to be independent of its antidepressant action. The mechanism of action may involve down regulation of central 5-HT2 and adrenergic receptors

40
Q 
Drugs for prophylaxis of migraine:
Antiseizure Drugs (anticonvulsants)
A
  1. ) Valprolate
  2. ) Topiramate
  3. ) Gabapentin

Also proving effective in migraine prophylaxis. However, the mechanism
of action is not known.

41
Q

Drugs for prophylaxis of migraine:

Botox A

A

Widespread use of botox for wrinkles led to the observation that some patients had a beneficial effect for their migraines. In 2010, Botox
became FDA approved for the treatment of migraine headaches. The anti-migraine
mechanism of action of botox is not well understood. The anti-migraine effect may last for up to 3 months and can be useful in patients with medication rebound headaches.

42
Q

Drugs for acute/abortive treatment of other headaches:

Cluster Headache

A

1.) Oxygen inhalation - effective in ~70% of patients.

  1. ) -Ergotamine tartrate
    - Dihydroergotamine

3.) Subcutaneous Sumatriptan is also used to abort cluster headaches

43
Q

Drugs for acute/abortive treatment of other headaches:

Infrequent tension-type headaches

A
  1. ) Self-medicate with over-the-counter analgesics

2. ) Relaxation techniques

44
Q

Drugs for prophylaxis of other headaches:

Cluster headache

A

Use prophylaxis therapy only during the cluster period when headache doesn’t respond to symptomatic therapy or occur more than 2x daily.

  1. ) Ergotamine tartrate
  2. ) Prednisone – Use when patient is refractory to other medications
45
Q

Drugs for prophylaxis of other headaches:

Tension type headache

A
  1. ) Amitriptyline(Antidepressants)

2. ) Botox injection into pericranial muscles

46
Q

Migraine in Children

Read Over

A

Migraine headaches in children tend to be shorter in duration than in adults (e.g. child’s headache may last only 30 minutes while adult’s headache may last 4 – 72 hours). Also headache symptoms may be different in a child than in an adult (e.g. headache pain is in the front of the head in children and there are more G.I side effects in
children).

47
Q

Drug therapy for migraine in children

A

In addition, try to determine and eliminate migraine triggers in the child’s diet.

1.) Ibuprofen, Acetaminophen

2.) Nausea and vomiting in migraine attacks should NOT be treated with the antiemetic metoclopramide due to adverse extrapyramidal side effects in
children. The dopamine antagonist Domperidone does not penetrate very well
into the CNS, and therefore may cause less extrapyramidal side effects in children.

  1. ) Triptans
  2. ) Beta-blockers (e.g. propranolol) for prophylaxis

Pharmacology (6 decks)

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