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54 CNS > Headache > Flashcards

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
Q

P8 in SNNOOP10

A

Post traumatic onset of headache

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26
Q

P9 in SNNOOP10

A

Pathology of immune system such as HIV/immunocompromised

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27
Q

P10 in SNNOOP10

A

Painkiller overuse or new drug at onset of headache

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28
Q

1st phase of migraine

A

Prodrome (≤ 48 hours)

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29
Q

2nd phase of migraine

A

Aura (5-6 minutes)

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30
Q

3rd phase of migraine

A

Ictal (headache) (4-72 hours)

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31
Q

4th phase of migraine

A

Postdrome (~48 hours)

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32
Q

5th phase of migraine

A

Interictal

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33
Q

Pathophysiology of prodrome

A

Activation of hypothalamus and neuropeptides involved in homeostatic functions

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34
Q

Pathophysiology of aura

A

Cortical spreading depression
1. Initial wave of neuronal depolarisation - slow spreading
2. Inhibited cortical activity and reduced blood flow

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35
Q

Pathophysiology of ictal

A

Vasodilation of intracranial extracerebral blood vessels → activation of perivascular trigeminal nerves → release vasoctive neuropeptides → neurogenic inflammation

36
Q

Photophobia in migraine

A
  • Retinal and trigeminal nociceptive area converges in the thalamus which projects to the nociceptive areas of the cortex
  • Hypersensitised visual cortex
37
Q

Peripheral component of trigeminovascular system

A

Trigeminal ganglion (located in PNS) relays trigeminovascular nociceptive input from meningeal vessels and dura mater to the CNS

38
Q

Central component of trigeminovascular system

A

Trigeminocervical complex receives the peripheral trigeminovascular nociceptive pain signal from the trigeminal ganglion → relays it to the cortex via the thalamus → pain

39
Q

How is pain experienced?

A

Trigeminovascular neurons are activated → relay migraine pain signal from pheripheral to the CNS

40
Q

Criterion of migraine diagnosis

A

At least 5 attacks plus headache duration, characteristics, non-headache symptoms

41
Q

(Migraine diagnosis) Headache duration

A

Lasts 4-72 hours

42
Q

(Migraine diagnosis) Headache characteristics

A

More than 2 of the following:
- Unilateral
- Pulsating quality
- Moderate or severe pain intensity
- Aggravation by or causing voidance of routine physical activity

43
Q

(Migraine diagnosis) Non-headache symptoms

A

More than 1 of the following:
- N/V
- Photophobia & phonophobia

44
Q

What are the 2 classes of drugs that can result in MOH?

A

Opiods and barbiturates

45
Q

When is preventive migraine treatment considered?

A

More than 2 headache days per week

46
Q

Criterion for MOH

A
  • 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
Q

Treatment classes for acute migraine treatment

A

Triptans
Ergotamine derivatives
Ditans
Gepants
NSAIDs
Analgesics

48
Q

Treatment classes for preventive migraine treatment

A

Anticonvulsants
B-blockers
Angiotensin receptor blockers
Triptans
cGRP mAbs

49
Q

NSAIDs properties

A

Anti-inflammatory, analgesics, antipyretic, mediated by blockade of COX enzymes and subsequently inhibition of prostaglandin synthesis.

50
Q

General MOA of triptans

A

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
Q

Which group of patients require precautions when using Triptans?

A

Patients with CV pathologies because of vasoconstrictor effects

52
Q

How is cGRP relevant in migraine/headache?

A

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
Q

MOA of Sumatriptan

A
  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
Q

Indications of Sumatriptan

A
  1. Acute relief of migraine with/without aura, and those associated with menstrual period in women
  2. Acute treatment of cluster headache (SubQ)
55
Q

Common SEs of Sumatriptan

A
  1. Sleepy, dizzy, tired
  2. Pain & tightness in throat or jaw
  3. Flushing (feeling hot), tingling sensation
  4. Vertigo
56
Q

Rare but serious SEs of Sumatriptan

A
  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
Q

Sumatriptan - elderly

A

Not recommended; start at lower dose

58
Q

Sumatriptan - pregnancy

A

Not teratogenic, but possible increase in rate of preterm birth. Risk vs benefit.

59
Q

Sumatriptan - breastfeeding

A

Excreted into breast milk (SubQ)
Avoid breastfeeding for 12h after treatment

60
Q

Sumatriptan - renal

A

No adjustment required

61
Q

Sumatriptan - hepatic

A

Mild-moderate: 50mg max
Severe: CI

62
Q

Sumatriptan - (D) protein binding

A

Low

63
Q

Sumatriptan - (M) hepatic

A

extensive via MAO, predominantly A isoenzyme

64
Q

Sumatriptan - DDIs

A
  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
Q

Sumatriptan - dosing

A

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
Q

Sumatriptan - Monitoring

A
  • Check migraine severity (pain intensity & syndromes) is reduced.
  • Check BP
  • Migraine diary
67
Q

MOA of Ergotamine

A

Ergotamine selectively binds and activates alpha-adrenergic and 5HT1B & 5HT1D receptors located on intracranial blood vessels → vasoconstriction

68
Q

Indication of Ergotamine

A

Acute treatment of migraine

69
Q

Ergotamine - CIs

A
  • CVD
  • Hepatic impairment
  • Renal impairment
70
Q

Ergotamine - dosing

A

Two 1mg ergotamine/100 mg caffeine (Cafergot) tablets, one additional every 30min
Maximum 6 per day, 10 per week.

71
Q

Ergotamine - elderly

A

Not recommended

72
Q

Ergotamine - protein binding

A

High

73
Q

Ergotamine - absolute F

A

Low

74
Q

Ergotamine - Metabolism

A

Substrate of CYP3A4
- Avoid CYP3A inhibitors like macrolides (elevated concentration)

75
Q

Ergotamine - common SEs

A

N/V

76
Q

Ergotamine - rare but notable SEs

A

MI, vascular ischaemia

77
Q

Why are opioids not recommended as treatment for migraine/headache?

A

Abusable, opioid overuse (worsening patient outcomes, MOH)

78
Q

Criteria for initiating preventive migraine treatment

A

Elevated headache frequency, increased symptom severity
- Attacks significantly interfere with patients’ daily routine
- ≥ 4 MHDs
- CI or failure to acute treatment
- Patient preference

79
Q

MOA of BBs in preventive migraine treatment

A

Reduces blood vessel dilation

80
Q

Gepants are _________.

A

Small molecules that are antagonists at CGRP receptors which bind to CGRP receptor and prevent signalling

81
Q

MOA of anti-CGRP antibodies

A

Prevents CGRP from interacting with its receptors

82
Q

MOA of anti-CGRP receptor antibodies

A

Bind to CGRP receptor and prevent signalling

83
Q

Example of CGRP mAbs

A

Erenumab

84
Q

When is Erenumab indicated?

A

Prophylaxis in adults who have at least 4 migraine days per month

85
Q

Erenumab - dosing

A

SubQ: 70 to 140 mg once monthly

54 CNS (13 decks)

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