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Drug Action III > Migraine (MC) - Block 2 > Flashcards

Migraine (MC) - Block 2 Flashcards

1
Q

What factors affect treatment?

A

Onset: infection or nasal
DOA: Shorter DOA – might have recurrence of migraine
Presence of N/V: Nasal sprays/injectables

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2
Q

What is the difference between rescue and prophylactic?

A

Rescue: relieves existing attack
Prophylactic: prevent an attack from occurring

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3
Q

MOA of triptans?

A

Activate 5-HT1D/1B receptors on presynaptic trigeminal nerve endings -> inhibit release of vasodilating peptides

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4
Q

What is the function of 5-HT1D/1B receptors?

A

Mediate vasoconstriction

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5
Q

What is the function of 5-HT1F?

A

Inhibits trigeminal nerve activation

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6
Q

Describe the SAR of triptans?

A
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7
Q

Why was sumatriptan unable to penetrate the BBB?

A

Too hydrophilic

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8
Q

When is it best to take a triptan?

A

As soon as a patient gets a migraine attack

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9
Q

ADR of triptans?

A
  1. Altered sensations
  2. Chest discomfort (CI: CAD and angina)

ADR more severe with short half-life and faster acting

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10
Q

Triptan tablets?

A

Good absorption, slower onset, potential gastric stasis

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11
Q

ODT triptans?

A

Good absorption, may not work in all aptients, taste disturbances

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12
Q

Nasal spray triptans?

A

15 minue onset, tast disturbances

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13
Q

SC Triptans?

A

Sumatriptan only: very rapid absorption, inj site rx, expensive

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14
Q

Major interactions for triptans?

A

Major concern is serotonin syndrome
MOAI, SSRI, SNRI, ergots

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15
Q

Where is the site of action for seratonic agonists?

A

Selective 5-HT1F receptor agonist: blocks trigeminal nerve activation/inflammation
* Lacks VC action of triptans -> better CV safety than triptans

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16
Q

Types of seratonin? ADR?

A

Lasmiditan
ADR: DZ, N, parasthesias, drowsiness

17
Q

MOA for ergots?

A

Partial agonist at a-adrenoreceptor and partial agonist at 5HT2 receptors
* Vasoconstrictor
* Specific for migraine pain

18
Q

Why does ergots have poor bioavailability? How is it improved?

A

Peptide; given with caffiene to aid absorption if given PO

19
Q

ADR of ergots?

A

GI (D/N/V)
Greater degree of peripehral vasoconstriction (avoid in coronary disease)

20
Q

What drug should not be given to patient with coronary disease?

A

Ergots

21
Q

Examples of DA for N and Pain?

A

Prochlorperazine (IV/IM)
Chlorpromazine (IV/IM)
Metoclopramide (IV)

22
Q

Receptor activity of DA?

A

D2 receptors:
1. Central effect on dopaminergic neurons for migraine
2. Work at chemoreceptor trigger zone to improve nausea
3. Improves GI motility to increase medication absorption

23
Q

Function of CGRP receptor antagonist?

A

Block vasodilatory and trigeminal nerve sensitization effects of CGRP

24
Q

Examples of CGRP receptor antagonists?

A

Ubrogepant
Rimegepant
Atogepant

25
Q

Ubrogepant

ADR

A

N, fatigue, dry mouth

26
Q

Rimegepant

ADR

A

N, UTI

27
Q

What is the purpose for prophylaxise?

A
  1. Reduces frequency, severity and duration of attacks
  2. Prevent evolution of episodic headaches to chronic daily headaches
  3. Improve responsiveness to treatment of acute attacks
  4. May take 8 – 12 weeks to be effective
28
Q

Prophylaxis for migraines

A
  1. Propanalol/timolol
  2. Topiramate
  3. Amitriptyline
  4. Botox

Other agents:
1. Divalproex/Valproic acid
2. Frovatriptan (MAM)
3. Venlafaxine
4. Calcium channel blockers (verapamil) - off labe (Prevents blood vessel changes in migraine and cluster headache)
5. NSAIDs (mild acute attacks and MAMs)

29
Q

MOA of propanalol/timolol

A
  1. Vasoconstriction
  2. Anxiolytic action
  3. Decrease sympathetic activity
30
Q

Topiramate MOA?

A

Cognitive side effects/tingling sensation in figers and toes may limit use
* Weight loss + mood stabilizer

31
Q

Amitriptylline

MOA, ADR

A

MOA: Blocks reuptake of norepinephrine and/or serotonin
* Useful when migraines co-exist with tension-type headache, chronic pain conditions, disturbed sleep or depression

ADR: dry mouth, sedation, DZ, N

32
Q

Botox

MOA

A

MOA: Inhibtis release of ACh at NMJ -> inhibits striated muscle contractions
* pain relief often occurs before muscle paralysis
* Blocks peripheral nerve sensitization
* Blocks release of glutamate and SubP from nociceptive neurons

33
Q

CGRP Monoclonal Antibody Antagonists MOA?

A

Antagonize either CGRP peptide or its receptor

34
Q

TYpes of CGRP Monoclonal Antibody Antagonists?

A

Erenumab binds to CGRP receptor
Fremanezumab/galcanezumab/eptinezumab bind to CGRP + prevent binding to and activation of receptor

35
Q

CGRP Monoclonal Antibody Antagonists

ADR, Use

A

ADR: inj site rx or erythema
Use: effective, good safety/tolerability, expensive and SC

Drug Action III (23 decks)

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