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Pharm > Lecture 22: Migraines > Flashcards

Lecture 22: Migraines Flashcards

1
Q

What are Migraines characterized by?

A

Recurring headaches that are moderate to severe, pulsating in nature, last from 2-72 hours

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2
Q

What is the Aura in migraines thought to be driven by?

A

Cortical spreading depression

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3
Q

What is cortical spreading depression?

A

A wave of neuronal depolarization followed by desensitization (depression) that propagates across the cortex. Vasodilation followed by Vasoconstriction

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4
Q

What causes Migraines?

A

A mix of genetic and environmental factors

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5
Q

Which sex does migraine effect more?

A

It affects women more than men

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6
Q

What is the genetic portion of migrains?

A

Familial hemiplegic migraines

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7
Q

What are Familial Hemiplegic Migraines?

A

A specific type of migraines that is driven by a genetic mutation

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8
Q

What are the additional symptoms of familial hemiplegic migraines?

A

It includes weakness of half of the body

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9
Q

What is the inheritance of Familial Hemiplegic Migraine?

A

It is autosomal dominant

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10
Q

What three genetic mutations are associated with FHM?

A
  • P/Q-type calcium channel
  • Na+/K+ ATPase
  • Na+ channel subunit
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11
Q

What do the FMH mutations do?

A

Lower the threshold for cortical spreading depression

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12
Q

What is the largest cranial nerve?

A

The Trigeminal nerve

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13
Q

What are the three branches of the Trigeminal Nerve?

A
  • Ophthalmic
  • Maxillary
  • Mandibular
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14
Q

What are the three purposes of the Trigeminal nerve?

A
  • Sense pain and temperature in the head region
  • Innervate the dura mater (membrane that surrounds the brain)
  • Controls cerebral blood vessels (trigeminovascular system)
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15
Q

What is pain in the head detected by?

A

The opthalmic branch of the trigeminal nerve innervating the dura mater and associated blood vessels

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16
Q

What are the three reasons why migraines are thought to be neurovascular?

A
  • Extracerebral vessels dilate during migraine attack
  • Cranial blood vessel stimulation provokes headache
  • Vasoconstrictor drugs alleviate pain
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17
Q

How does 5-HT affect blood vessels?

A

It causes vasoconstriction

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18
Q

What are the levels of 5-HT in people who experience migraines?

A

They have low levels of 5-HT between attacks

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19
Q

What neurotransmitter is released in the brain during migraines?

A

5-HT

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20
Q

What is the consequence of migraineurs having low levels of 5-HT between attacks?

A

Their blood vessels are already more dilated making them more susceptible to migraines

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21
Q

Why is 5-HT released during migraine attacks?

A

It is a reaction to mitigate the migraine effects

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22
Q

Where is CGRP located?

A

In the trigeminal peripheral afferents that innervate the vasculature of the dura mater

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23
Q

What happens when Trigeminal afferents are activated?

A

They can release the CGRP peptide which binds to receptors on the vasculature and leads to vasodilation

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24
Q

What does CGRP released by trigeminal afferents bind to and what does it do?

A

It binds to CGRP afferents and leads to vasodilation

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25
Q

What are the levels of CGRP in those with migraine?

A

They are elevated in those with migraines

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26
Q

What is neurogenic inflammation?

A

Activation of trigeminal nerve pain afferents causes surrounding inflammation through CGRP causing vasodilation

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27
Q

Which receptor does serotonin released during migraines bind to?

A

5-HT1D receptors

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28
Q

What does serotonin binding 5-HT1D on vasculature do during a migraine?

A

It blocks the activity of the Trigeminal nerve, so it blocks the vasodilatory effect

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29
Q

What type of receptor is a 5-HT1D coupled receptor?

A

An inhibitory G-protein receptor

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30
Q

What type of receptor is the 5HT2a receptor that LSD binds to?

A

A G-protein coupled receptor. It is Gq

30
Q

What type of receptor is the 5HT2a receptor that LSD binds to?

A

A G-protein coupled receptor. It is Gq

30
Q

What type of receptor is the 5HT2a receptor that LSD binds to?

A

A G-protein coupled receptor. It is Gq

31
Q

What are the two types of migraine treatment strategies?

A

Prophylactic and abortive strategies

32
Q

What does Prophylactic mean?

A

Treatments are taken daily to prevent attacks

33
Q

When are abortive treatments taken?

A

Once an attack occurs

34
Q

What are the Non-pharmacological Prophylactic Interventions?

A

Identify triggers

35
Q

What are the Prophylactic Pharmacological Interventions?

A
  • Beta Blockers (Propranolol)
  • Anticonvulsants (Gabapentin)
  • Antidepressants (Amitriptyline)
36
Q

What kind of drug is Propranolol?

A

A beta blocker

37
Q

What kind of drug is Gabapentin?

A

An anticonvulsant

38
Q

What kind of drug is Amitriptyline?

A

An antidepressant

39
Q

How does Beta Blockers like Propranolol affect migraines?

A

The decrease blood pressure

40
Q

How do Anticonvulsants like gabapentin affect migraines?

A

They block pain transmission

41
Q

How do Antidepressants like amitriptyline affect migraines?

A

They block SERT to inhibit serotonin reuptake which helps with vasoconstriction

42
Q

What are the non-specific analgesics that can help with migraines?

A

Aspirin, acetaminophen, NSAIDs, opioids

43
Q

What is the downside to using non-specific analgesics for migraines?

A

There is the risk of medication overuse headache

44
Q

What receptor does caffeine act at and what does it do?

A

It is an adenosine receptor antagonist

45
Q

Where are adenosine receptors located?

A

On vasculature

46
Q

What does caffeine being an antagonist at the adenosine receptors do?

A

It causes vasoconstriction

47
Q

How does Caffeine affect other analgesics?

A

It increases absorption of other analgesics

48
Q

What is an example of a migraine medication with caffeine?

A

Excedrin

49
Q

How are Ergotamine similar to LSD?

A

They are both ergot alkaloids

50
Q

Which receptors do Ergotamines act at?

A

5HT-1b/d receptors

51
Q

What does Ergotamines binding to 5HT-1b/d receptors do?

A

Inhibits neurogenic inflammation

52
Q

What kind of G-protein coupled receptors are 5HT-1b/d receptors that ergotamines bind to?

A

They are Gi because they inhibit neurogenic inflammation

53
Q

What is the issue with Ergotamines?

A

They have a low degree of receptor selectivity causing side effects like coronary vasoconstriction

54
Q

What does a low Ki mean?

A

A high binding affinity

55
Q

What does a high pKi mean?

A

High binding affinity

56
Q

Which populations should not take Ergotamines?

A

Those with any heart conditions because of its low selectivity that causes side effects

57
Q

What is the Absorption and Distribution characteristics of ergotamines?

A

It has large first pass metabolism via oral administration causing low bioavailability

58
Q

What can extend to rate and extent of absorption of Ergotamines?

A

Caffeine

59
Q

What are Ergotamines metabolized by?

A

The liver

60
Q

What are ergotamines excreted in?

A

Bile

61
Q

What is an example of a Triptan?

A

Sumatriptan

62
Q

What receptors do Triptans target and what do they do?

A

They are selective 5-HT1b/d agonists

63
Q

What are the effects of Triptans being agonists at 5-HT1b/d agonists?

A

They cause Vasoconstriction and inhibition of the trigeminal nerve

64
Q

What kind of G-protein coupled receptors are 5-HT1b/d receptors?

A

The are Gi coupled receptors

65
Q

Why are Triptans better than Ergotamines?

A

Because they avoid the side effects by being more selective

66
Q

Why is the bioavailability of Triptans better when given subcutaneously?

A

Because of first pass metabolism

67
Q

What is sumatriptan metabolized by?

A

Monoamine oxidase in the liver to indoleacetic acid and found in urine

68
Q

What does a Phase 2 clinical trial check for?

A

Efficacy

69
Q

What does Phase 1 check for?

A

Safety

70
Q

What is Rimegepant (Nurtek)?

A

A small molecule CGRP receptor antagonist

71
Q

What are CGRP antibodies?

A

Monoclonal antibodies to either CGRP receptor or CGRP itself that inhibits CGRP signalling leading to vasoconstriction

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