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Neurologic & Psych > EXAM #2 Pharmacology Headache Dr. Pond > Flashcards

EXAM #2 Pharmacology Headache Dr. Pond Flashcards

1
Q

What are the primary forms of headache?

A

-Migraine
-Tension-type
-Cluster

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2
Q

Characteristics of Migraine

A

-unilateral
-pulsatile
-disabling
-N/V
-Photophobia and Phonophobia

-more common in women (3x)

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3
Q

Migraine POUND

A

Pulsatile
One day duration (4-72h)
Unilateral
->start on one side, and may progress to both sides
Nausea, vomitting
Disabling intensity
-> aggravated by or avoidance of movement
->photophobia, phonophobia

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4
Q

Characteristics of Tension-type headache

A

-bilateral
-dull
-hatband pattern

  • more common in women
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5
Q

Characteristics of Cluster Headache

A

-unilateral
-pulsatile
-usually around one eye
-can cause a droopy eyelid
-severe (most severe of the 3 types)
-nasal congestion

-more common in men

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6
Q

What is a secondary headache?

A

Headache secondary to another disease
-infectious
-neoplastic
-drug-induced
-idiopathic

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7
Q

What are the types of migraine?

A

common migraine (without aura)
migraine with aura (aura can be a visual sensation or pattern, omen for the migraine)

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8
Q

Theories of migraine pathogeneisis

A

-dysfunction in brain nuclei involved in the central control of nociception (pain stimuli detection)

-altered cortical excitability (may explain why antiseizure drugs work for migraine)

-cortical spreading depression theory (mouse model): depolarization spreads across the brain (2-3 mm/min followed by depression; the spreading of depression may activate the trigeminovascular system -> causing the aura symptoms

-Neurogenic inflammation: neurons produce neuropeptides -> inflammatory response -> dialtion of trigeminovascular system (blood vessels that go the meninges)

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9
Q

What are the neuopeptides that are thought to cause an inflammatory response and vasodilation to the meninges?

A

-substance P
-neurokinin A
-Calcitonin Gene-Related Peptide (CGRP) - major

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10
Q

Which nerve is involved in the pathophysiology of migraine?

A

Trigeminal nerve (largest cranial nerve, cranial nerve 5)

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11
Q

What controls the output and input of trigeminal nerves?

A

Trigeminal nucleus in the brain stem

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12
Q

What may cause the pain in migrain?

A

Neuropeptides released into

-meninges (causing vasodilation)

-the brain stem -> gets to the thalamus and higher brain center (causing pain, photophobia, and photosonia)

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13
Q

What are Eicosanoids and where are they derived from?

A

-signal molecules

-made by oxidation of fatty acids

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14
Q

Eicosanoids are converted to …. by the enzyme…

A

->Inflammatory stimuli

to Arachidonic acid

by Phospholipase A2 (can be blocked by Corticosteroids - annexin A1)

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15
Q

Which molecules are responsible for inflammation and pain?

A

Prostanoids
-Prostaglandins
-> causes Inflammation, pain, fever

-Prostacyclin (PGI2)
-Thromboxane (TXA2)

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16
Q

Which enzyme converts Arachidonic acid to Prostanoids?

A

Cyclooxygenase (COX-1, COX-2)

blocked by Aspirin, NSAIDs

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17
Q

Which of the COX enzymes is induced and which one is constitutive?

A

COX-1 = constitutive

COX-2 = unducible -> involved in cancer, inflammation, pain

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18
Q

Location of COX-3

A

CNS

-it is a splice variant of COX-1
-not found in humans yet (only in animal models)

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19
Q

Which COX-isoenzymes are blocked by Aspirin?

A

All
COX-1, COX-2

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20
Q

Which COX-isoenzymes are blocked by NSAIDs?

A

Nonselective NSAIDs are fe ibuprofen, naproxen
selective: Celecoxib -> COX-2

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21
Q

What are the symptoms that are relieved by Aspirin and NSAIDs?

A

-Anti-inflammatory
-Analgesic -> Pain
-Antipyretic -> fever

-Antithrombotic (NSAID reversible, Aspirin irreversible)
-Anticancer

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22
Q

How does Acetaminophen work?

A

-not well understood
-weak COX inhibitor in CNS
-> inhibits prostaglandin synthesis in cells with low rate of synthesis and low levels of peroxide

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23
Q

How is Acetaminophen different from an NSAID or
Aspirin?

A

It reduces fever and pain
-but it doesnt have the anti-inflammatory and antithrombotic effect

24
Q

When does Acetaminophen tend to inhibit COX-2?

A

When levels of Arachidonic are low
-> which is in the CNS
-> Acetaminophen works more in the CNS rather than peripheral

25
Which CYP enzymes become active with chronic or high alcohol consumption?
MEOS (microsomal ethanol oxidizing systems) -> Two of them are CYP2E1 and CYP3A4 -alcohol BAC above 0.1%
26
What effect does MEOS have on Acetaminophen?
they convert Acetaminophen to toxic intermediates
27
What converts toxic intermediates of Acetaminophen to non-toxic intermediates?
Glutathione-conjugation (GSH-conjugation)
28
How does alcohol consumption cause liver toxicity?
alcohol depletes Glutathione, which is required to convert toxic intermediates into non-toxic intermediates -the toxicity is actually seen with a very high acetaminophen dose and very high or chronic alcohol consumption
29
Antidote for Acetaminophen liver toxicity
N-acetylcysteine -> replesnishes glutathione
30
How may Caffeine be involved in pain regulation?
-they are Xanthines MOA: -inhibit Phosphodiesterase (PDE converts the cAMP to AMP; cAMP is the signal molecule???) -adenosine receptor antagonist on afferents (nothing to with pain? -> FYI: inhibitory -> the blockage causes a stimulatory effect) -altering nociceptive pathways by blocking adenosine receptors -some evidence of COX-inhibition
31
Which NT receptors are involved in migraine?
Serotonergic receptors (5-HT-1F) across the brain -also on trigermnial nerve terminal -> modualting the release of CGRP (neuropeptides causing pain and vasodilation)
32
What is the effect that Serotonin receptors have on the release of CGRP?
5-HT receptors have an inhibitory effect -> activation of the receptor will block the release of the CGRP (inflammatory peptides)
33
MOA of Ergot alkaloids
5-HT1B/ 1D / 1F agonist -vasoconstriction (1B) -inhibition of CGRP release -blockage of trigeminal nerve transmission
34
Which form of Ergot alkaloids is a nasal spray, IV, IM, SC?
dihydroergotamine -Ergotamine is sublingual only
35
ADE and BBW of Ergot alkaloids
-GI (nausea, diarrhea) -leg cramps -serious CV risk and cerebral hemorrhage risks BBW: serious interaction with CYP3A4 inhibitors and macrolides -> elevates ergot levels - ischemia risk (vasoconstriction)
36
Which of the serotonergic receptors are thogut to cause vasoconstriction of the arterioles of the meninges?
1B on arterioles of the meninges (5-HT-1B) -> direct vasoconstriction when activated (agonized) -> CGRP will cause vasodilation when binding on CGRP receptors on the arterioles
37
Which of the serotonergic receptors are thogut to prevent release of neuropeptides (from trigeminal terminals) such as CGRP and cause inflammation?
1D/1F on presynaptic receptors (5-HT-1D or 5-HT-1F) by agonizing these receptors the release of neuropeptides (such as CGRO) is inhibited and vasodilation is blocked -also decrease in pain transmission through the brain
38
MOA of Triptans
Agonists of 5-HT- receptors (1B/1D/1F) (5-hydroxytryptamine receptors) Sumatriptan: is the first and most studied
39
Which Triptan is useful for pateints who suffer from migraine-induced N/V?
Zolmitriptan ->it has an intranasal formulation
40
What are the effects of the Triptans?
-direct vasoconstriction -reduced release of the neuropeptides -reduced pain transmission
41
What are the common side effects of Triptans?
-dizziness -parestheisa (sensation of tingeling) -abnormal sensation -rebound headache (when overused) serious ADE: -chest pain -unilateral weakness -changes in eyesight
42
DDI with Triptans
Serotonin syndrome: other serotinon drugs -MAOIs, Ergots -CYP 3A4: almotriptan, eletriptan, naratriptan -CYP 1A2: frovatriptan, zolmitriptan -CYP 2D6: almotriptan
43
Which drug only targets 5-HT-1F receptors?
Lasmiditan -blocks neuropeptide release on the presynaptic receptor -but does not cause vasoconstriction of the arteriole on the meninges
44
Which patient population benefits from Lasmitidan?
-helpful in patients with CV risk, bc it bypasses the vasoconstriction effect -Lasmitidan is not quite as effective
45
Which drugs target CGRP receptors?
-gepants Ubrogepant! Rimegepant! Olcegepant, Atogepant, Zavegepant
46
MOA OF CGRP receptor antagonist?
blocking CGRP receptors on the blood vessels ->preventing vasodilation blocking CGRP receptors on neurons ->block inflammation and pain transmission ADE: somnolence, N/V
47
What is the role of CGRP antagonists in therapy?
-some used for prophylaxis -some for acute migrain or both -cluster headache (similar pathophysiology as migraine)
48
Which drugs are used for migraine prophylaxis?
non-selective ß-blockers (propranolol) -antiepileptics: valproic acid, Topiramate -Botulinum toxin type A -Tricyclic antidepressants -CGRP antibodies (expensive)
49
Why Propranolol - what is their target?
Propranol is non-selective -> targeting ß1 and ß2 ß1 causes increased HR and contractility in the heart -> block it to reduce HR and contractility for HTN patients ß2 causes vasodilation -> block it to reduce pain? how does vasodilation cause migraine???
50
How are ß-blockers thougt to help with migraine prophylaxis?
-Non-selective ß antagonists without intrinsic sympathomimetic activity -Blocks ß-mediated vasodilation -May inhibit ϐ1 receptors in the thalamus -May inhibit generators of migraine pain -Inhibit firing of noradrenergic neurons in LC -Serotonergic modulation
51
How are antiepileptics thought to help with migraine prophylaxis?
-preventing hyperexcitability of the cerebral cortex -> valporic acid, topiramate
52
How does Botulinum toxin A (Botox) thougt to help with migraine prophylaxis?
a toxin produced by bacteria -> the toxin is a dichain peptide with a heavy and light chain -the light chain contains a Zn-containing endopeptidase -> that cleaves synaptosomal protein (SNAP-25) responsible for vesicle docking on the presynaptic neuron -> no release of neuropeptides (FYI in face-lifting: block of acetlycholine releas which would cause muscle contraction) "FAILED EXOCYTOSIS"
53
Which protein is cleaved by Botox?
SNAP-25 -on of the SNARE proteins that fuse and cause vesicle to bind to the membrane -> NT release into the cleft -> in this case CGRP, neurokinin A, substance P cant be released
54
ADE of Botox
BBW: relaxing effect of muscles (blocking ACh) can spread, and swallowing and breathing difficulties can cause death ADE: headache, respiratory infection, upper eyelid drop, nausea, difficulty swallowing
55
Which monoclonal antibodies block the CGRP receptor?
Erenumab
56
Which monoclonal antibodies block the CGRP molecules?
-Fremanezumab -Galcanezumab -Eptinezumab (IV) ->prevent CGRP from binding to CGRP receptors ->injectables: SC or IV, long-lasting (prophylaxis) ADE: injection site reaction, hypersensitivity, constipation

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