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Neuro > Pharm 32 Objectives > Flashcards

Pharm 32 Objectives Flashcards

1
Q

What drug classes are most effective for abortive therapy of migraine?

A

5-HT1- Receptor Agonist (“Triptans”)

Ergotamine/Dihydroergotamine

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2
Q

What is the MOA of 5-HT1- Receptor Agonist (“Triptans”)?

A
  • Vasoconstriction of painfully dilated meningeal, dural, cerebral and pial vessels
  • Inhibit dural vasodilation
  • Inhibit trigeminal nuclear excitability.
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3
Q

What is the MOA of Ergotamine/Dihydroergotamine?

A

Ergot alkaloids activate serotonin 5-HT1 receptors which produce vasoconstriction.

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4
Q

What are the 2 reasons why caffeine is co-administered with ergotamine for migraine treatment?

A
  1. Improve bioavailability by increasing the absorption of ergotamine
  2. Exerting a mild vasoconstrictor effect.
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5
Q

What 3 factors increase/decrease the effectiveness of triptans to treat migraines?

A
  1. Taken at the very onset of the migraine
  2. Combined with a NSAID
  3. No recent opioid use
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6
Q

What triptan drug and formulation is rapid-acting, and therefore potentially more effective as migraine and cluster headache abortive therapies?

A

Sumatriptan

- Nasal spray formulation or Sub Q injection.

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7
Q

What triptan drug and formulation is longer-acting, and therefore potentially more useful for menstrual or other similarly timed recurring migraines?

A

Frovatriptan (t1/2 26 hrs)

- oral formulation

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8
Q

What are the CI of the ergot alkaloids and -triptans?

A
  • CV
  • CHD
  • HTN
  • Severe Hepatic impairment
  • PVD
  • Hypersensitivity to drug or components
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9
Q

What are some MODERATE signs, symptoms, and potential consequences of ergotism?

A

N/V

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10
Q

What are some SEVERE signs, symptoms, and potential consequences of ergotism?

A
  • Distal vasoconstriction (fingers/toes) first
  • Itching and burning limb pain
  • Loss of limb sensation
  • Gangrene and auto-amputation of charcoal-black limbs
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11
Q

What must you monitor when administering Ergotamine?

A

Must monitor for cold fingers and toes

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12
Q

What are the main elements of management of erotism?

A
  1. Institute basic life support/withdraw the offending agent
  2. Supportive measures: management of GI sxs, warming of peripheral extremities, and tx of pain
  3. Vasodilators and anti-coags
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13
Q

What vasodilators and anticoags are administered for erotism?

A
  • Nitroprusside and or phentolamine
  • Augmenting vasodilators: CCB-nifedipine
  • Unfractionated heparin IV or LMWH SQ to inhibit thrombosis
  • SL nitro if coronary artery spams then IV nitro
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14
Q

What is the 1st and 2nd line for tension HA tx?

A

1st: Acetaminophen 1,000mg
2nd: Ibuprofen, naproxen, aspirin

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15
Q

What is the 1st and 2nd line for tension HA prevention?

A

1st: Amitriptyline
2nd: Tizanidine (antispastic/ muscle relaxer)

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16
Q

What is the 1st and 2nd line for cluster HA tx?

A

1st: 5-HT1 agonist - rapid onset nasal or sub Q
2nd: Oxygen, 7-12L/min by non-rebreather mask

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17
Q

What is the 1st and 2nd line for cluster HA prevention?

A

1st: Verapamil (high does 360-960 mg/day)
2nd: Lithium (900 mg/day)

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18
Q

What drug class is associated w/ reduced HA incidence, generally speaking?

A

Antihypertensives: BB, ACE-Inhibitors, ARBs, Thiazides

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19
Q

What 2 types/sources of pain does acetaminophen relieve?

A
  1. Frequent episodic tension HAs

2. Osteoarthritis pain

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20
Q

What type of pain does acetaminophen not relieve?

A

Lower back pain

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21
Q

What is the MOA of the muscle relaxant/antispasmodic agent: Baclofen?

A

GABA-B receptor agonist, peripheral GABA receptor, reduces motor neuron excitability/spasticity.
- relieves clonus, flexor spasms, and muscle rigidity.

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22
Q

What is the ASEs of Baclofen?

A

Rebound spasms if baclofen pump is d/c abruptly.

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23
Q

What is the MOA of the muscle relaxant/antispasmodic agent: Tizanidine?

A

a2 adrenergic agonist

24
Q

What is the ASEs of Tizanidine

A

Can lower B/P, dry eyes, dry mouth, blurred vision.

25
Q

What is the MOA of the muscle relaxant/antispasmodic agent: Cyclobenzaprine?

A

General CNS depressant, some serotonergic effects

26
Q

What is the ASEs of Cyclobenzaprine?

A

Antimuscarinic effects: (dry mouth, blurred vision, photophobia, tachy, difficulty urinating)

  • risk for serotonin syndrome
  • Don’t use in pts with hx of allergy to TCAs and caution if added to opioids.
27
Q

What is the MOA of the muscle relaxant/antispasmodic agent: Methocarbamol?

A

General CNS depressant

28
Q

What is the ASEs of Methocarbamol?

A

Antimuscarinic effects: (dry mouth, blurred vision, photophobia, tachy, difficulty urinating) BUT less than cyclobenzaprine
- High risk in elderly and rarely used in peds - only used in tx for tetanus

29
Q

What is the place in therapy for muscle relaxants in acute and chronic pain?

A
  • For acute MSK pain they should be used as adjunct to NSAIDs, and/or opioids, and PT.
  • Not indicated for long term use, more beneficial for acute tx.
30
Q

What is the MOA of the counterirritant and local analgesic: Diclofenac?

A

Anti-inflammatory

31
Q

What is the clinical use of topical Diclofenac

A
  • solution form: knee osteoarthritis

- gel form: arthritis of upper and lower extremities and strains, sprains and contusions.

32
Q

What is the ASEs of Diclofenac?

A 
CV events
GI effects
HTN
CHF
Premature closure of ductus arteriosus in pregnancy, 
SJS
TEN
33
Q

What is the MOA of the counterirritant and local analgesic: Methyl Salicylate?

A

Imparts cooling effects by initially stimulating nociceptors and then desensitizing them

34
Q

What is the clinical use of Methyl Salicylate?

A

Arthritis and mild MSK pain

35
Q

What is the ASEs of Methyl Salicylate?

A

May cause burning sensation and skin irritation

36
Q

What is the MOA of the counterirritant and local analgesic: Menthol?

A

Imparts cooling effects by initially stimulating nociceptors and then desensitizing them.

37
Q

What is the clinical use of Menthol?

A

Cough
Sore throat
Muscles and joint pain and aches (menthol + camphor- Icy Hot)
Temporary relief of pain and itching associated with minor skin irritations
(bites, burns, cuts, poison ivy, eczema, psoriasis, dry skin)

38
Q

What is the ASEs of Menthol?

A

Burning sensation if applied to mucous membranes, broken, damages, burned and swollen skin, may worsen burns, avoid in peds

39
Q

What is the MOA of the counterirritant and local analgesic: Capsaicin?

A

Activates peripheral nociceptors and cause depletion of substance P in neurons.

40
Q

What is the clinical use of Capsaicin?

A

Minor aches and pains of muscle/joins - arthritis, backache, sprains, post herpetic neuralgia.

41
Q

What is the ASEs of Capsaicin?

A

Burning sensation, do not use with active shingles

42
Q

What may increase when using Capsaicin 8%?

A

May increase B/P d/t pain during or right after tx

43
Q

How is Capsaicin 8% patch applied?

A

RX only and used in the medical office.

- A single 1 hr patch can provide 3 months of relief form pain associated with post herpetic neuralgia.

44
Q

What is the MOA of local anesthetics?

A

Suppresses pain by blocking Na channels on afferent pain nerves w/o depression of nervous system.

45
Q

What are the common clinical uses of local anesthetics?

A
  • Neuronal anesthesia and analgesia
  • Peripheral nerve blocks
  • Subcutaneous and tissue infiltration
  • Topical anesthesia.
46
Q

What factors determine the onset of local anesthetics?

A
  • Injection near a nerve of interest
  • pKa of the drug
  • pH of surrounding tissues
  • Lipophilicity of the drug (more lipid soluble=diffuse faster)
  • Susceptibility/size of the nerve
  • Binding of local anesthetic to sites on VG Na+ channels
47
Q

How does infected tissue affect the onset of local anesthetics?

A

Infected tissue is more acidic and will reduce the fraction of unionized drug even further

48
Q

Are local anesthetics weak or strong base?

A

Weak bases with pH generally > 7.4, they are mostly ionized at pH 7.4.

49
Q

What factors determine the duration of local anesthetics?

A
  • Slow diffusion of local anesthetic molecules in and out of the whole nerve
  • Rate of dissociation from the Na+ channels (slower = longer duration)
50
Q

How is the ester-type local anesthetics metabolized?

A

Rapidly metabolism by plasma esterases and metabolized to PABA

51
Q

What is the cross allergenic potential of the ester-type local anesthetics?

A

Higher incidence of hypersensitivity rxns d/t the metabolite, PABA.

52
Q

How is the amide-type local anesthetics metabolized?

A

Metabolized by P-450 enzymes the liver

53
Q

What is the cross allergenic potential of the amide-type local anesthetics?

A

Much less potential than esters d/t different metabolite.

54
Q

What are the primary ASEs of local anesthetics that are d/t class effects as an extension of their MOA?

A
  • CNS depression and spinal HAs
  • Autonomic blockage; urinary or fecal incontinence
  • CV: bradycardia, heart block, reduced contractile force, cardiac arrest, and hypoTN
  • Neuro: first sx: metallic taste, ringing in ears, HA,
  • Severe tox: agitation, lethargy, seizures, general CNS depression.
55
Q

What are the primary ASEs of local anesthetics that are d/t idiosyncratic reactions?

A
  • Allergic rxns

- Methemoglobinemia- more common with esters

56
Q

What is the the rationale for co-administration of epinephrine with local anesthetics?

A
  • Slows systemic rate of absorption and prolongs the anesthetic effect.
  • Helps reduce systemic ASEs.
57
Q

What is the MOA of epinephrine?

A

Vasoconstriction, and binds to a2-adrenergic receptor

Neuro (14 decks)

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