Pharmacology 2.6 Flashcards

1
Q

What is Calcitonin Gene-Related Peptide (CGRP)?

A
  • potent vasodilator

- functions in the transmission of pain

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2
Q

What is the MOA of triptans?

A
  • vasoconstriction of painful intracranial extra cerebral vessels
  • inhibition of vasoactive neuropeptide
  • inhibition of nococeptive NTs
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3
Q

How is the correct triptan chosen for each patient?

A
  • fast vs. slow onset of activity
  • formulation (oral, injection, nasal)
  • formulatory tier and availability (sumatriptan = generic)
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4
Q

What are the pharmacokinetics of triptans?

A
  • oral
  • nasal
  • subcutaneous (umatriptan)
  • rapid onset of action*
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5
Q

What are the adverse effects of triptans?

A
  • fatigue
  • dizziness
  • parasthesia
  • warm sensation
  • tightness (neck, chest, throat)
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6
Q

What are the contraindications of triptans?

A
  • liver/kidney disorder
  • MAO inhibitor therapy
  • hemiplegic migraine
  • basilar migraine
  • hypersensitivity to triptans
  • peripheral vascular disease
  • uncontrolled blood pressure
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7
Q

What is the MOA of ergot alkaloids?

A

-DHE and ergotamine constrict cranial vascular bed

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8
Q

Which drug is best ofr intractable migraines?

A

DHE

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9
Q

Which drug is effective at the beginning of a migraine attack?

A

ergotamine

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10
Q

What are the pharmacokinetics of ergotamine?

A
  • oral and suppository
  • high first pass effect
  • combined with caffeine helps bioavailability
  • excreted by liver
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11
Q

What are the pharmacokinetics of DHE?

A
  • SC, IV, IN, oral
  • metabolized by liver
  • excreted by feces
  • metabolites similar to parent compound
  • effects last longer than expected
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12
Q

What are the adverse effects of ergotamine?

A
  • decreased blood flow to brain, heart, extremities
  • diarrhea
  • nausea
  • vomitting
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13
Q

What are the contraindications of ergotamine?

A
  • obstructive vascular disease
  • collagen disease
  • hypertension
  • angina
  • history of heart attack/silent ischemia
  • liver/kidney disease
  • serious infection
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14
Q

What is the MOA of propranolol?

A
  • beta blocker

- MOA unknown

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15
Q

What is the first line drug for prevention of migraines?

A

propranolol

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16
Q

What are the effects of beta-1 receptors?

A
  • increase heart rate
  • increase contractility
  • increase nerve conduction
17
Q

What are the effects of beta-2 receptors?

A
  • bronchodilation
  • relaxation
  • vasodilation
18
Q

What are the effects of beta-3 receptors?

A

-relax bladder

19
Q

Which beta blocker is the primary therapeutic target for migraines?

A

beta-1

20
Q

Which drugs should be avoided in migraines with aura?

A
  • propranolol

- metoprolol

21
Q

What are the pharmacokinetics of propranolol?

A
  • oral
  • hepatic first pass effect
  • lipophilic
  • metabolized by liver
22
Q

What are the adverse effects of propranolol?

A
  • bradycardia
  • sedation
  • vivid dreams
23
Q

What are drug interactions with beta blockers?

A

verapamil

  • severe hypotension
  • bradycardia
  • heart failure
  • cardiac conductance abnormailities
24
Q

What is the therapeutic class of prochlorperazine?

A
  • antiemetic

- antipsychotic

25
Q

What are the therapeutic uses of prochlorperazine?

A
  • associated with migraines
  • vomiting
  • nausea
  • pain
26
Q

What are the pharmacokinetics of prochlorperazine?

A
  • oral
  • rectal
  • IV
27
Q

What are the adverse effects of prochlorperazine?

A
  • extrapyramidal (acute dystonic effects)

- akathisia (restlessness)

28
Q

Does prochlorperazine or sumatriptan reduce pain more?

A

Prochlorperazine

29
Q

What is the MOA of botulinum toxin A?

A
  • enzymatic removal of AAs in fusion proteins critical to the release of ACh
  • used for prevention of migraines
30
Q

What is the treatment of medication overuse headache (MOH)?

A
  • education

- detoxification