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PMCOL II > Migraine > Flashcards

Migraine Flashcards

1
Q

What are migraines

A

Primary headache disorder characterized by recurring headaches, pulsating nature, and last from 2-72 hours

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2
Q

What are the effects of migraines

A

Sensitivity to normal sensory input (light, sound, head movement)

Sometimes nausea and vomiting

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3
Q

What is a migriane aura

A

Occurs in 20% of migraines, signs of a migraine before it hits

Visual disturbance made up of flashing lights or zigzag lines across field of vision

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4
Q

Theorized mechanism behind migraine aura

A

Though to be driven by cortical spreading depression

Wave of neuronal depolarization followed by desensitization (depression, caused by hyperpolarization), that propagates across the cortex

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5
Q

How can cortical spreading depression be monitored

A

Measuring blood flow

Blood flow increase in an area means higher neuronal activity

Look for progression of excitation followed by depression
AKA high blood flow followed by low blood flow

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6
Q

What affects rate of headaches

A

Genetic contributions: Familial hemiplegic migraines (Migraines that run in the family)

Headaches also occur more in women than men specifically after puberty (hormones?)

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7
Q

What kind of inheritance is Familial Hemiplegic Migraines

A

Autosomal (one copy of gene is enough to cause disease in offspring)

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8
Q

What genetic mutations are associated with FHM?

A

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

Lowers the threshold for cortical spreading depression and makes it easier to achieve depolarization

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9
Q

What is the largest cranial nerve

A

Trigeminal nerve

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10
Q

What are the three branches of the trigeminal

A

Ophthalmic
Maxillary
Mandibular

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11
Q

What are the purposes of the trigeminal nerve

A

Sense pain and temperature in the head region
Innervate the dura mater
Control cerebral blood vessels (Trigeminovascular system)

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12
Q

Dura mater

A

Membrane that surrounds the brain

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13
Q

What causes headache pains

A

Pain caused by organs around the brain (Dura mater and trigeminal nerve)

No nociceptors on the brain so brain itself can not feel pain

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14
Q

What is the mechanism behind headaches

A

Pain in head detected by ophthalmic branch of the trigeminal nerve
Innervates the dura mater and corresponding blood vessels

Vasodilation = Migraine

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15
Q

Why are migraines considered to be a neurovascular disease

A

Extracerebral vessels dillate during migraine attack

Cranial blood vessel stimulation (causes vasodilation) provokes headache

Vasoconstrictor drugs alleviate pain

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16
Q

What is the relation between serotonin and migraines?

A

Release of 5-HT leads to vasoconstriction

Low-5HT levels in migraines between attacks

In response to a migraine 5-HT is released during an attack to counterbalance the lack of 5-HT and cause vasoconstriction to end the migraine

17
Q

CGRP

A

Calcitonin gene-related peptide is located in trigeminal peripheral afferents

It is released by afferents in response to pain and leads to vasodilation

Causes migraines
CGRP is elevated in those with migraines

18
Q

Prophylactic treatments

A

Taken daily to prevent attacks

19
Q

Abortive treatments

A

Taken once an attack occurs

20
Q

What are the two prophylactic treatment strategies against migraines

A

Non-pharmacological intervention: Identify triggers

Pharmacological interventions:
Beta-blockers (decrease blood pressure)
Anticonvulsants (Block pain transmission) Antidepressants (serotonin reuptake inhibitor, allows accumulation of serotonin)

21
Q

What the abortive treatment strategies against migraines

A

Non-specific analgesics (Asprin, acetaminophen, NSAID, opioids)

Risk of medication overuse headache
Overuse of opioids will cause greater headaches later on

22
Q

Caffeine and Migraines

A

Adenosine receptor (located on blood vessal) antagonist

Leads to vasoconstriction
Increases absorption of analgesics like acetaminophen and ergotamines
Improves migraine treatment during attack

Rebound vasodilation when caffeine wears off can trigger headaches

23
Q

Ergotasmines

A

Ergot alkaloid (LSD)

Agonists for 5HT-1b/d receptors

Inhibits neurogenic inflammation through vasoconstriction

24
Q

Issues of ergotasmines

A

Low degree of receptor selectivity, increased side effects

Coronary vasoconstriction
Patients with heart diseases should not take drug

25
Q

Pharmacokinetics of ergotamines (absorption)

A

Large first-pass metabolism, leads to low bioavailability when taken orally (<1%)
Caffeine can improve rate and extent of absorption

26
Q

Pharmacokinetics of ergotamines (Metabolism)

A

Metabolized by liver by poorly defined enzymes
Half-life 2 hours

27
Q

Pharmacokinetics of ergotamines (Excretion)

A

Excreted in bile

28
Q

Examples of a Triptans

A

Sumatriptan

29
Q

Sumatriptan

A

First line migraine therapy

Selective for 5-HT 1b/d agonist

Vasoconstriction and inhibition of trigeminal nerve

Avoids the side effects of ergotamine

30
Q

Pharmacokinetics of sumatriptan (Absorption)

A

Bioavailability is around 14% when taken orally
96% when taken subcutaneously (avoids first pass metabolism)

31
Q

Pharmacokinetics of sumatriptan (Metabolism)

A

Metabolized by monoamine oxidase in the liver, converted into indoleacetic acid
Half-life is around 2 hours

32
Q

Pharmacokinetics of sumatriptan (Excretion)

A

Cleared in the urine

33
Q

What kind of CGPR Antagonists are used?

A

Small molecule CGRP antagonists
Sits in binding pocket

Monoclonal antibodies to CGRP or CGRP receptors
Binds on to receptor and sterically inhibits binding to CGRP

34
Q

Rimegepant

A

(Nurtek)

CGRP receptor antagonists

Effective migraine treatment with less side effects
Less effect on liver aminotransferase levels (safer for long-term use)
Good bioavailability

35
Q

CGRP Antibodies

A

Monoclonal antibodies that bind to either CGRP receptors or to CGRP

Inhibits CGRP signalling leading to vasoconstriction

36
Q

Monoclonal

A

Produced antibodies that act like natural antibodies

PMCOL II (10 decks)

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