Headache Flashcards

1
Q

Pain location of TTH

A

Bilateral

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2
Q

Pain location of migraine

A

Unilateral or bilateral

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3
Q

Pain quality of TTH

A

Pressing/tightening

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4
Q

Pain quality of migraine

A

Pulsating/throbbing

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5
Q

Frequency of infrequent episodic TTH

A

<1/month

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6
Q

Frequency of frequent TTH

A

1-14 days/month

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7
Q

Frequency of chronic TTH

A

> 15 days

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8
Q

Pathophysiology

A

myofascial mechanisms leading to peripheral sensitisation of nociceptors

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9
Q

Goals of TTH management

A

pain relief, prevent progression to chronic TTH

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10
Q

Acute treatment of TTH

A

Paracetamol, aspirin, NSAIDs

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11
Q

Prophylactic treatment of TTH

A

Amitriptyline

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12
Q

What is SNNOOP10 used for?

A

Secondary headache

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13
Q

S in SNNOOP10

A

Systemic symptoms including fever

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14
Q

N1 in SNNOOP10

A

Neoplasm history

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15
Q

N2 in SNNOOP10

A

Neurologic deficit/dysfunction

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16
Q

O1 in SNNOOP10

A

Onset of headache is sudden/abrupt

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17
Q

O2 in SNNOOP10

A

Older age (>50y/o)

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18
Q

P1 in SNNOOP10

A

Pattern change or recent onset of headache

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19
Q

P2 in SNNOOP10

A

Positional headache

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20
Q

P3 in SNNOOP10

A

Precipitated by sneezing, coughing, exercise

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21
Q

P4 in SNNOOP10

A

Papilledema

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22
Q

P5 in SNNOOP10

A

Progressive headache with atypical presentation

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23
Q

P6 in SNNOOP10

A

Pregnancy or puerperium

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24
Q

P7 in SNNOOP10

A

Painful eye with autonomic features

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25
P8 in SNNOOP10
Post traumatic onset of headache
26
P9 in SNNOOP10
Pathology of immune system such as HIV/immunocompromised
27
P10 in SNNOOP10
Painkiller overuse or new drug at onset of headache
28
1st phase of migraine
Prodrome (≤ 48 hours)
29
2nd phase of migraine
Aura (5-6 minutes)
30
3rd phase of migraine
Ictal (headache) (4-72 hours)
31
4th phase of migraine
Postdrome (~48 hours)
32
5th phase of migraine
Interictal
33
Pathophysiology of prodrome
Activation of hypothalamus and neuropeptides involved in homeostatic functions
34
Pathophysiology of aura
Cortical spreading depression 1. Initial wave of neuronal depolarisation - slow spreading 2. Inhibited cortical activity and reduced blood flow
35
Pathophysiology of ictal
Vasodilation of intracranial extracerebral blood vessels → activation of perivascular trigeminal nerves → release vasoctive neuropeptides → neurogenic inflammation
36
Photophobia in migraine
- Retinal and trigeminal nociceptive area converges in the thalamus which projects to the nociceptive areas of the cortex - Hypersensitised visual cortex
37
Peripheral component of trigeminovascular system
Trigeminal ganglion (located in PNS) relays trigeminovascular nociceptive input from meningeal vessels and dura mater to the CNS
38
Central component of trigeminovascular system
Trigeminocervical complex receives the peripheral trigeminovascular nociceptive pain signal from the trigeminal ganglion → relays it to the cortex via the thalamus → pain
39
How is pain experienced?
Trigeminovascular neurons are activated → relay migraine pain signal from pheripheral to the CNS
40
Criterion of migraine diagnosis
At least 5 attacks plus headache duration, characteristics, non-headache symptoms
41
(Migraine diagnosis) Headache duration
Lasts 4-72 hours
42
(Migraine diagnosis) Headache characteristics
More than 2 of the following: - Unilateral - Pulsating quality - Moderate or severe pain intensity - Aggravation by or causing voidance of routine physical activity
43
(Migraine diagnosis) Non-headache symptoms
More than 1 of the following: - N/V - Photophobia & phonophobia
44
What are the 2 classes of drugs that can result in MOH?
Opiods and barbiturates
45
When is preventive migraine treatment considered?
More than 2 headache days per week
46
Criterion for MOH
- Headache ≥15 days/month - Overuse >3months for ≥1 drug (≥10 days per month for ergot derivatives, triptans, opiods, combination analgesics, ≥15 days for nonopiods, paracetamol, NSAIDs)
47
Treatment classes for acute migraine treatment
Triptans Ergotamine derivatives Ditans Gepants NSAIDs Analgesics
48
Treatment classes for preventive migraine treatment
Anticonvulsants B-blockers Angiotensin receptor blockers Triptans cGRP mAbs
49
NSAIDs properties
Anti-inflammatory, analgesics, antipyretic, mediated by blockade of COX enzymes and subsequently inhibition of prostaglandin synthesis.
50
General MOA of triptans
5-HT1B and 5HT1D receptors agonist → decreases trigeminal neuron activity → causes: - vasoconstriction of cerebral blood vessals - inhibition of vasoactive peptide release by trigeminal neurons - inhibition of nociception
51
Which group of patients require precautions when using Triptans?
Patients with CV pathologies because of vasoconstrictor effects
52
How is cGRP relevant in migraine/headache?
CGRP (calcitonin gene-related peptide) - neuropeptides play fundamental role in neurogenic inflammation and peripheral and central sensitisation of trigeminovascular and other systems functions as vasodilator
53
MOA of Sumatriptan
1. Selectively constricts dural and meningeal vessels - Binds to vascular 5HT1B & 5HT1D receptors found predominantly on cranial blood vessels → vasoconstriction 2. Inhibits trigeminal nerve activity - Inhibits pro-inflammaotry neuropeptides released by trigeminal neurons e.g. cGRP - Reduce neurogenic inflammation
54
Indications of Sumatriptan
1. Acute relief of migraine with/without aura, and those associated with menstrual period in women 2. Acute treatment of cluster headache (SubQ)
55
Common SEs of Sumatriptan
1. Sleepy, dizzy, tired 2. Pain & tightness in throat or jaw 3. Flushing (feeling hot), tingling sensation 4. Vertigo
56
Rare but serious SEs of Sumatriptan
1. Drug allergy 2. Serotonin syndrome - Agitated, restless, other mental changes - Heavy sweating, shivering - Fast or irregular HR - Rigid or twitching muscles - N/V/D 3. Heart attack
57
Sumatriptan - elderly
Not recommended; start at lower dose
58
Sumatriptan - pregnancy
Not teratogenic, but possible increase in rate of preterm birth. Risk vs benefit.
59
Sumatriptan - breastfeeding
Excreted into breast milk (SubQ) Avoid breastfeeding for 12h after treatment
60
Sumatriptan - renal
No adjustment required
61
Sumatriptan - hepatic
Mild-moderate: 50mg max Severe: CI
62
Sumatriptan - (D) protein binding
Low
63
Sumatriptan - (M) hepatic
extensive via MAO, predominantly A isoenzyme
64
Sumatriptan - DDIs
1. MAOi - Contraindicated concurrent administration - Must not be used within 2 weeks of discontinuation of therapy with MAOIs 2. Ergotamine - Contraindicated concurrent administration - Avoid within 24 hours after taking ergotamines 3. Other Triptans - Avoid within 24 hours after sumatriptan
65
Sumatriptan - dosing
PO: 50mg, repeat dose after 2h if not better. Do not take more than four 50mg tablets a day. Limit to 9-10 days per month SubQ: Single 6mg injection, repeat at least after 1h if not feeling better. Do not use more than 2 inj per day.
66
Sumatriptan - Monitoring
- Check migraine severity (pain intensity & syndromes) is reduced. - Check BP - Migraine diary
67
MOA of Ergotamine
Ergotamine selectively binds and activates alpha-adrenergic and 5HT1B & 5HT1D receptors located on intracranial blood vessels → vasoconstriction
68
Indication of Ergotamine
Acute treatment of migraine
69
Ergotamine - CIs
- CVD - Hepatic impairment - Renal impairment
70
Ergotamine - dosing
Two 1mg ergotamine/100 mg caffeine (Cafergot) tablets, one additional every 30min Maximum 6 per day, 10 per week.
71
Ergotamine - elderly
Not recommended
72
Ergotamine - protein binding
High
73
Ergotamine - absolute F
Low
74
Ergotamine - Metabolism
Substrate of CYP3A4 - Avoid CYP3A inhibitors like macrolides (elevated concentration)
75
Ergotamine - common SEs
N/V
76
Ergotamine - rare but notable SEs
MI, vascular ischaemia
77
Why are opioids not recommended as treatment for migraine/headache?
Abusable, opioid overuse (worsening patient outcomes, MOH)
78
Criteria for initiating preventive migraine treatment
Elevated headache frequency, increased symptom severity - Attacks significantly interfere with patients' daily routine - ≥ 4 MHDs - CI or failure to acute treatment - Patient preference
79
MOA of BBs in preventive migraine treatment
Reduces blood vessel dilation
80
Gepants are _________.
Small molecules that are antagonists at CGRP receptors which bind to CGRP receptor and prevent signalling
81
MOA of anti-CGRP antibodies
Prevents CGRP from interacting with its receptors
82
MOA of anti-CGRP receptor antibodies
Bind to CGRP receptor and prevent signalling
83
Example of CGRP mAbs
Erenumab
84
When is Erenumab indicated?
Prophylaxis in adults who have at least 4 migraine days per month
85
Erenumab - dosing
SubQ: 70 to 140 mg once monthly