ic4 + ic5 (tth, migraine) Flashcards
(34 cards)
Clinical presentation of TTH
No prodromal symptoms, aura
Bilateral
Nonpulsatile tightness
mild-moderate
What are the classifications of TTH?
What is the criteria?
Episodic infrequent: < 1 episode / month
Episodic frequent: 1-14 days / month
Chronic: ≥15 days / month
Triggers of TTH (7 points)
Stress
Holding head in one position for a long time
Alcohol
Caffeine
Cold / flu, sinus infections
Dehydration
Hunger
non pharm for TTH (5 points)
Patient education
Identify triggers via headache diary
CBT
Physical therapy
Lifestyle modification (improve sleep)
Pharmacological acute treatment for TTH (3 points)
Paracetamol (with caffeine)
Aspirin
NSAIDs (Ibuprofen, Diclofenac, Naproxen, Ketoprofen)
prophylactic treatment for TTH (3 points)
Amitriptyline (1st line, Tricyclic Antidepressants)
Mirtazapine
Venlafaxine
Requirements for medication overuse headache (3 points)
1) Headaches for ≥ 15 days / month, with pre-existing headache disorder
2) Regular overuse of medications for > 3 months eg.
Ergotamine, triptans, opioids at least 10 days / month
Paracetamol, NSAIDs at least 15 days / month
3) Headache cannot be diagnosed as something else
What are the phases of a migraine attack
Prodrome
Aura
Headache
Postdrome
Symptoms of prodrome phase
Fatigue
Cognitive difficulties
Mood changes
Food cravings
Neck pain
Yawning
symptoms of aura (2 points)
Visual aura
Speech, sensory disturbances
headache phase symptoms (3 points)
Nausea with or without vomiting
Photophobia
Phonophobia
postdrome symptoms (3 points)
Feeling weary
Difficulty concentrating
Neck stiffness
Classification of migraine
episodic VS chronic migraine
episodic: at leat 5 attacks a lifetime
Chronic: At least 15 Monthly Headache Day (MHD), out of which is 8 migraine days for 3 months
What is considered migraine without aura?
1) Headaches lasting up to 3 days when untreated / unsuccessfully treated
2) At least 2
- Unilateral location
- Pulsating
- Moderate - Severe intensity
- Aggravated or avoidance of routine physical activity
3) At least 1
- Nausea, vomiting
- Photophobia, phonophobia
What is considered migraine with aura?
1) Fully reversible aura symptoms
- Visual
- Sensory
- Speech, language
motor
2) At least 3
- Aura spreads over 5 mins
- 2 or more aura symptoms occur in succession
- Aura lasts 1hr
- Aura is unilateral
- Aura is positive
- Aura is accompanied by headache
what is the MOA of Migraines,
how do medications act on the pathway to relief headaches?
1) Vasodilation of intracranial, extracerebral (inside skull, outside brain) blood vessels
Cause 2) activation of trigeminal nerves to release vasoactive neuropeptides eg. CGRP to promote neurogenic inflammation
Cafergot and Sumatriptan acts on (1) vasodilation
Erenumab acts on (2) CGRP receptor
What is the MOA of NSAIDs?
COX 2 inhibition inhibits prostaglandin synthesis
PGI2 causes neurogenically mediated inflammation in the trigeminovascular system
MOA of Sumatriptan (3 points)
Selective vascular serotonin (1B and 1D) receptor agonist
1) Vasoconstriction of Intracranial Extracerebral BV
Does not affect cerebral blood flow (as it affects extracerebral (outside brain) blood vessels)
2) Inhibition of vasoactive peptide release by trigeminal neurons
3) Inhibit nociception neurotransmission within trigeminocervical complex
If Sumatriptan does not work, what to do?
If there is a recurrence of migraine…
Can try another triptan (even though same class)
If have recurrence of migraine within 48hrs, take another dose of triptan
DDI with sumatriptan
Concomitant MAO inhibitors
Take 2 weeks after MAOi
Concomitant Ergotamine / Ergot-type meds
Take 24hrs apart
Adverse effect associated with Sumatriptan
Side effects (3 points)
Serotonin syndrome (transient BP increase, flushing)
Dysgeusia (unpleasant taste)
LFT disturbances
Sensation of pressure on chest
MOA of cafergot
Ergotamine:
- Constrict vascular smooth muscles in intracranial extracerebral BV
- Lead to prolonged vasoconstriction by stimulating alpha adrenergic and serotonin receptors (1B and 1D receptors)
Caffeine:
- Adenosine A1, A2A, A2B receptor antagonist → vasoconstrict cerebral vasculature
- Enhance GI absorption of ergotamine by increasing solubility of ergotamine and decrease gastric PH
PK differences between cafergot and sumatriptan
Plasma protein binding:
High -> Cafergot
Low -> Sumatriptan
Sumatriptan available nasal and IV, while Cafergot available oral and rectal
DDI with Cafergot (2 points)
Vasconstrictor agents eg. ergots, sumatriptan
CYP3A4i eg. ritonavir, macrolides
Increases risk for vasospasm, leading to cerebral ischaemia