Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PR3153 > IC4 Migraine > Flashcards

IC4 Migraine Flashcards

1
Q

Explain the pathophysiology of headache & migraine

A
  • Vasodilation of intracranial extracerebral blood vessels (meningeal blood vessels)
  • Results in the activation of the perivascular trigeminal nerves that release vasoactive neuropeptides → promote neurogenic inflammation
  • Central pain transmission may also activate other brainstem nuclei, resulting in associated symptoms (nausea, vomiting, photophobia & phonophobia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is an important mediator of migraine headache that we can leverage on for anti-migraine treatment?

A
  • Serotonin
  • Agonists of vascular & neuronal 5-HT1 receptor subtypes can cause vasoconstriction of meningeal blood vessels → inhibit release of vasoactive neuropeptide & pain signal transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the anti-migraine medications

A

Cafergot
Sumatriptan
Erenumab
Paracetamol
NSAIDS

Bolded = For moderate / severe migraines refractive to NSAIDS or paracetamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

🥓 Which anti-migraine medications are for acute treatment, & which are for prophylaxis?

A

Acute
Cafergot
Sumatriptan

Prophylaxis
Erenumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

🥓 What is Cafergot? Describe its MOA

A
  • A combination med containing caffeine ☕ & ergotamine 🍞
  • Stimulates alpha-adrenergic & 5-HT receptors (esp 5-HT1B & 5-HT1D receptors) to exert a tonic action on vascular smooth muscles in the external carotid network → vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the indication of Cafergot?

A

Acute treatment of migraine (given at first symptom of attack)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the PK profile of Cafergot (administration routes, absorption, plasma protein binding, bioavailability)

A
  • Oral & rectal
  • Rapidly absorbed (maximum plasma concentrations reached in 1.5 to 2h)
  • High plasma protein binding
  • Low absolute bioavailability of 2-5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

🥓 What class of drugs should Cafergot not be used concomitantly with?

A
  • Cafergot inhibits liver CYP3A
  • So it should NOT be used with other CYP3A inhibitors like macrolide antibiotics (will suppress hepatic enzymes too much)
  • Or it can lead to elevated exposure to ergot toxicity (vasospasm & tissue ischaemia)
  • It should also NOT be used with other vasoconstrictor agents including ergot alkaloids, Sumatriptan & other 5HT1 agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the common side effects of Cafergot?

A

Nausea & vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the rare side effects of Cafergot?

A
  • Hypersentivity
  • Myocardial infarct
  • Ergotism (vascular ischaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the MOA of Sumatriptan?

A
  • Selective vascular serotonin (5-HT1D) receptor agonist
  • Selectively constricts the carotid arterial circulation, but does not alter cerebral blood flow (as it acts on intracranial, extracerebral vessels, ie meningeal area)
  • Inhibits trigeminal nerve activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the indication of Sumatriptan?

A

Acute treatment of migraine with or without aura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the PK profile of Sumatriptan (administration routes, absorption, plasma protein binding)

A
  • Oral, nasal, IV
  • Rapidly absorbed
  • Low plasma protein binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is Sumatriptan eliminated?
State the contraindications for its use

A

Eliminated primarily by oxidative metabolism mediated by monoamine oxidase A (MAO)

Contraindications
1. Known hypersensitivity to triptans
2. Concurrent administration with MAO inhibitors
3. Myocardial infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the common side effects of Sumatriptan?

A
  • Dysgeusia (unpleasant taste)
  • Transient BP increase
  • Flushing
  • Sensation of cold, pressure, tightness

Transient BP increase & flushing side effects are like Serotonin syndrome!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a rare side effect of Sumatriptan?

A

Minor disturbances in liver function tests

17
Q

Which receptors do Cafergot & Sumatriptan act on?

A

Cafergot
5-HT1B & 5-HT1D

Sumatriptan
5-HT1D

18
Q

What is the MOA of Erenumab?

A
  • Erenumab is a monoclonal antibody that inhibits/blocks Calcitonin-related Gene product (CGRP)
  • CGRP is a vasodilator & a nociceptive neuropeptide (causes pain) at the trigeminal ganglion
  • Its levels are known to increase with migraine & can trigger migraine-like headaches when given IV
19
Q

What is the indication of Erenumab?

A

Migraine prophylaxis in adults who have ≥ 4 migraine days per month

20
Q

Describe the PK profile of Erenumab (administration routes, duration before clinical benefits observed, linearity of kinetics)

A
  • Given as monthly SC injection
  • Clinical benefit typically within 3 months
  • Linear kinetics at therapeutic doses (as CGRP receptor binding is saturated)
21
Q

What are the side effects of Erenumab?

A
  • Hypersensitivity
  • Injection site reactions
  • Pruritus
  • Constipation

PR3153 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions