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NS II Exam II AP > Drugs- Migraine/Headaches (Kinder) > Flashcards

Drugs- Migraine/Headaches (Kinder) Flashcards

1
Q

Migraine headache

A

Unilateral in 60-70%;
bifrontal or global in 30%

Gradual in onset, crescendo pattern; pulsating; moderate or severe intensity; aggravated by routine physical activity

Patient prefers to rest in a dark, quiet room, more commonly women

lasts 4-72 hours

Nausea, vomiting, photophobia, phonophobia; may have aura

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2
Q

tension headache

A

MC type of headache

Bilateral, head band configuration
Pressure or tightness which waxes and wanes

“hat band pattern)

Patient remains active or rests
Variable duration
No associated symptoms usually

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3
Q

cluster headache

A

Always unilateral, usually begins around the eye or temple

Pain begins quickly, reaches a crescendo within minutes; pain is deep, continuous, excruciating, and explosive in quality

Patient remains active
30-180 minutes duration

Ipsilateral lacrimation and redness of the eye; stuffy nose; rhinorrhea; pallor; sweating

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4
Q

what is the pathophysiology of migraines?

A

(1) Involves the trigeminal nerve distribution to intracranial and possibly extracranial arteries.
(2) These nerves release peptide neurotransmitters, especially calcitonin gene-related peptide (CGRP), an extremely powerful vasodilator, as well as substance P and neurokinin A.
(3) Along with promoting vasodilation, these peptide neurotransmitters lead to dural plasma extravasation resulting in neurogenic inflammation.

(4) Mechanical stretching caused by perivascular edema may be immediate cause of activation of pain nerve endings in the dura.

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5
Q

what are common triggers for migraine

A

(1) Food: alcohol, caffeine/caffeine withdrawal, chocolate, monosodium glutamate, aspartame.
(2) Environment: flickering lights, high altitude, strong smells/fumes, tobacco smoke, weather.
(3) Behavioral: excess/insufficient sleep, fatigue, menstruation, skipped meals, strenuous activity, stress.

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6
Q

where is serotonin found in the body

A

iii) Over 90% of serotonin in body found in enterochromaffin cells in the GI tract.
iv) In blood, serotonin found in platelets. Concentrated via an active serotonin transport mechanism (SERT) similar to that in membrane of serotonergic nerve endings.

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7
Q

what is monoamine oxidase’s effect on serotonin

A

v) Monoamine oxidase (MAO) oxidizes/inactivates serotonin. Immediate product of metabolism, 5-hydroxyindoleacetaldehyde, further oxidized to 5-hydroxyindoleacetic acid (5-HIAA).

5-HIAA may serve as a measure of serotonin synthesis; 24 hour excretion used as a diagnostic test for tumors synthesizing excessive quantities of serotonin (carcinoid tumor).

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8
Q

why is serotonin important in migraines

A

b/c its actions are involved in the perception of pain

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9
Q

what are the effects of serotonin in the heart

A

ii) CV: contraction of vascular smooth muscle (5-HT2), vasoconstrictor except skeletal muscle and heart where it causes dilation of blood vessels, venoconstriction, small direct positive chromotropic and inotropic effects on heart, promotes platelet aggregation (activation of 5-HT2 receptors).

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10
Q

GI effects of serotonin

A

iii) GI: increases tone and peristalsis (5-HT2), motility enhancing or “prokinetic” effect (5-HT4).

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11
Q

what are the effects of serotonin on skeletal muscle and what is serotonin syndrome

A

iv) Skeletal muscle: serotonin syndrome associated with skeletal muscle contraction (precipitated when MAO inhibitors given with serotonin agonists, especially antidepressants such as selective-serotonin reuptake inhibitors, SSRIs).

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12
Q

the “Triptan” drugs used in migraine are working at what receptor by what mechanism of action

A

b) MOA: activates 5-HT1D/1B receptors on presynaptic trigeminal nerve endings inhibiting release of vasodilating peptides;

stimulates vasoconstriction preventing vasodilation/stretching of pain endings.

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13
Q

MOA of triptans

A

b) MOA: activates 5-HT1D/1B receptors on presynaptic trigeminal nerve endings inhibiting release of vasodilating peptides; stimulates vasoconstriction preventing vasodilation/stretching of pain endings.

serotonin AGONISTS

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14
Q

what is the prototype triptan

A

sumatriptan

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15
Q

which triptans are metabolized by MAO-A and why is this clinically significant

A

sumatriptan, zolmitriptan, and rizatriptan

do NOT take these drugs if also on a MOA inhibitor

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16
Q

which triptans are metabolized by CYP450

A

eletriptan, naratriptan, and frovatriptan

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17
Q

which triptan is metabolized by both MAO-A and CYP450

A

almotriptan

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18
Q

what is the therapeutic use of triptans

A

d) Therapeutic use: currently 1st line for acute mild-to-severe migraine attacks in most patients. Also used as rescue therapy when nonspecific medications ineffective.

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19
Q

in what pt’s are triptans contraindicated

A

coronary artery disease, angina, ischemic heart disease, uncontrolled hypertension.

do NOT use within 24 hours of ergotamine derivative

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20
Q

what are some ADR’s of triptans

A

chest pain- due to coronary spasm (1-5 % of pt’s)

e) ADRs: most are mild – altered sensations (tingling, warmth), dizziness, muscle weakness, fatigue, flushing, drowsiness, nausea, sweating, neck pain.

injectable sumatriptan can cause injection site reaction

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21
Q

dihydroergotamine (DHE)

A

ergot alkaloid

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22
Q

ergotamine

A

ergot alkaloid

a) Ergots produced by Claviceps purpurea, fungus that infects grasses and grains; prototype: ergotamine.

23
Q

what is the MOA of ergot alkaloids

A

c) MOA: cause constriction of peripheral and cranial blood vessels; may also effect presynaptic trigeminal nerve endings, inhibiting release of vasodilating peptides; agonist activity at 5-HT1D/1B receptors.

24
Q

how can you speed the absorption of and peak blood levels of ergot alkaloids (ergotamine, DHE)

A

caffeine

25
Q

what is a more dangerous toxic effect of using ergot alkaloids

A

prolonged vasospasm usually associated with over-dosage

May result in gangrene and require amputation. Vasospasm refractory to most vasodilators but infusion of large doses of nitroprusside or nitroglycerin has been successful in some cases.

ii) Bowel infarction has also been reported and may require resection.

26
Q

what are the contraindications for using ergot alkaloids (ergotamine and DHE)

x5

A

obstructive vascular diseases (CAD)

collagen diseases

uncontrolled HTN

hepatic or renal dysfunction

pregnancy

27
Q

what are some commonly used analgesics/NSAIDs used in migraines and what is the MOA

A

acetaminophen
aspirin
ibuprofen
naproxen

b) MOA: appear to prevent neurogenic mediated inflammation in the trigeminovascular system through inhibition of prostaglandin synthesis.

some of these agents are combined with caffeine or barbituate (butalbital)

28
Q

what are some ADR’s when using NSAID’s

A

acute - GI symptoms (n/v/d)
CNS- somnolences , dizziness

medication overuse headaches

caution in pt’s with ulcer disease, renal dysfunction, or hypersensitivy to aspirin

29
Q

butalbital

A

barbituate

(a) MOA: increases GABAA channel opening time resulting in membrane hyperpolarization.

used in combonation with NSAID’s for migraines

(b) Potential for abuse and tolerance (some combinations are controlled substances); CNS depressant.

30
Q

Metoclopramide

A

Aka Reglan

antiemetic

31
Q

Prochlorperazine (compazine)

A

antiemetic

32
Q

MOA of metoclopramide and prochlorperazine

A

b) MOA: block D2-like (D2, D3, and D4) dopamine receptors in the chemoreceptor trigger zone and solitary tract nucleus.
c) Therapeutic use: useful adjuncts for nausea/vomiting that accompany migraine headache and medication side effects used to treat attacks (e.g. ergotamine).
i) Single dose given 15-30 minutes prior to abortive therapy often sufficient.

side effects –> drowsy and dizzy

33
Q

what 4 classes of drugs are used in prophylactic treatment of migraines

A

B-blockers - propranolol

CCB blockers - verapamil (Non DHP)

Antidepressants - amitriptyline (Elavil)

Anticonvulsants- topiramate (topamax)

34
Q

Two b-blockers used in migraines and what is the MOA

A

propranolol
metoprolol

ii) MOA: may raise migraine threshold by modulating adrenergic or serotonergic neurotransmission in cortical or subcortical pathways.

35
Q

what are the ADR’s of b-blockers

A

iv) ADRs: drowsiness, fatigue, sleep disturbances, vivid dreams, memory disturbance, depression

36
Q

in what pt’s must you use caution with b-blockers

A

congestive heart failure

peripheral vascular disease,

AV conduction disturbances,

asthma,

depression

and diabetes

37
Q

what is the mOA of CCB blocker verapamil in migraine prophylaxis

A

ii) MOA: inhibits Ca2+ entry from select voltage-sensitive areas of vascular smooth muscle, produces relaxation of vascular smooth muscle and vasodilation.
iii) Therapeutic use: evidence for CCB efficacy in migraine prophylaxis is weak and use is off label. Has shown beneficial effects when used as prophylaxis for cluster headache.

38
Q

which antidepressant agents are used in prophylactic treatment of migraine headaches

A

amitriptyline (tricyclic),

venlafaxine (serotonin/norepinephrine reuptake inhibitor),

39
Q

how do antidepressants work in prophylactic migraine therapy

A

may result in down regulation of central 5HT2 receptors, increased levels of synaptic norepinephrine, and enhanced opioid receptor actions.

40
Q

what are the ADR’s of antidepressants in migraine prophylaxis

A

iv) ADRs: tricyclic antidepressants sedating, agents often given in evening. Venlafaxine may cause nausea, vomiting, drowsiness.

41
Q

what 3 anticonvulsants are used in migraine prophylactic treatment

A

topiramate- blocks Na channels and increases GABA action

valproate- Na+ channel inactivation

divalproex sodium

42
Q

MOA of anticonvulsants used in migraine prophylactic treatment

A

ii) MOA: enhance y-aminobutyric acid (GABA) mediated inhibition, modulate excitatory neurotransmitter glutamate, and inhibit of sodium and calcium ion channel activity.
(1) Particularly useful in patients with comorbid seizures, anxiety disorder, or bipolar disorder.

43
Q

treatment for mild-to-moderate migraine attacks

A

NSAIDs/simple analgesics

i) May also be used in severe attacks if patient previously responded to medication.
c) If poor response to NSAID/simple analgesic, try combination product: acetaminophen/aspirin/caffeine

44
Q

if a migraine is associated with nausea and vomiting, what is the treatment plan

A

antiemetic pre-treatment useful.

i) Consider other routes of administration: suppository, parenteral, or intranasal, if available.

45
Q

if a patient is NOT responsive to NSAID’s simple analgesics what is next

A

triptan

i) Poor response to triptan: increase triptan dose, trial a different triptan, or switch medication class.
e) Triptan drugs first line for mild-to-severe migraine attacks.

46
Q

what if a migraine is unresponsive to triptan

A

f) Severe migraine attacks, if unresponsive to triptan, use intravenous antiemetic and ergot alkaloid.

47
Q

preventative therapies are administered on a daily basis if ….

A

i) Migraine recurs with significant disability despite acute therapy
ii) Attacks are frequent (> 2 episodes/week) with risk of developing medication overuse headache
iii) Symptomatic therapies ineffective or CI or produce serious ADRs
iv) Patient prefers prophylaxis to limit number of attacks

48
Q

choice of preventative therapy depends of pt’ comorbidities:

what do you give if pt has headaches that recur in predictable pattern (menses) ?

A

NSAID or triptan at time of vulnerability

49
Q

choice of preventative therapy depends of pt’ comorbidities:

what do you give if pt has headaches and HTN

A

B blocker

CCB if BB contraindicated

50
Q

choice of preventative therapy depends of pt’ comorbidities:

what do you give if pt has headaches and depression/insomnia?

seizure disorder?

A

tricyclic antidepressant

or

anticonvulsant

51
Q

treatment of mild to moderate tension type headache

A

simple analgesics (+/- caffeine) and NSAIDs

52
Q

prevention of tension type headache

A

antidepressant

53
Q

cluster headache abortive therapy

A

oxygen, triptan, ergot alkaloid

54
Q

prophylaxis of cluster headache

A

verapamil, lithium, prednisone, topiramate, frovatriptan

NS II Exam II AP (7 decks)

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