Pharm 32 Objectives Flashcards by Ingrid Ericksen

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

5-HT1- Receptor Agonist (“Triptans”)

Ergotamine/Dihydroergotamine

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

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

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What is the MOA of Ergotamine/Dihydroergotamine?

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

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

Improve bioavailability by increasing the absorption of ergotamine
Exerting a mild vasoconstrictor effect.

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

Taken at the very onset of the migraine
Combined with a NSAID
No recent opioid use

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

Sumatriptan

- Nasal spray formulation or Sub Q injection.

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

Frovatriptan (t1/2 26 hrs)

- oral formulation

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

CV
CHD
HTN
Severe Hepatic impairment
PVD
Hypersensitivity to drug or components

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

N/V

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

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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What must you monitor when administering Ergotamine?

Must monitor for cold fingers and toes

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What are the main elements of management of erotism?

Institute basic life support/withdraw the offending agent
Supportive measures: management of GI sxs, warming of peripheral extremities, and tx of pain
Vasodilators and anti-coags

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What vasodilators and anticoags are administered for erotism?

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

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

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

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

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

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

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

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

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

Antihypertensives: BB, ACE-Inhibitors, ARBs, Thiazides

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What 2 types/sources of pain does acetaminophen relieve?

Frequent episodic tension HAs

2. Osteoarthritis pain

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What type of pain does acetaminophen not relieve?

Lower back pain

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

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

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What is the ASEs of Baclofen?

Rebound spasms if baclofen pump is d/c abruptly.

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

a2 adrenergic agonist

What is the ASEs of Tizanidine

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

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

General CNS depressant, some serotonergic effects

What is the ASEs of Cyclobenzaprine?

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.

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

General CNS depressant

What is the ASEs of Methocarbamol?

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

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

- 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.

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

Anti-inflammatory

What is the clinical use of topical Diclofenac

- solution form: knee osteoarthritis | - gel form: arthritis of upper and lower extremities and strains, sprains and contusions.

What is the ASEs of Diclofenac?

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

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

Imparts cooling effects by initially stimulating nociceptors and then desensitizing them

What is the clinical use of Methyl Salicylate?

Arthritis and mild MSK pain

What is the ASEs of Methyl Salicylate?

May cause burning sensation and skin irritation

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

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

What is the clinical use of Menthol?

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)

What is the ASEs of Menthol?

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

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

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

What is the clinical use of Capsaicin?

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

What is the ASEs of Capsaicin?

Burning sensation, do not use with active shingles

What may increase when using Capsaicin 8%?

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

How is Capsaicin 8% patch applied?

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.

What is the MOA of local anesthetics?

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

What are the common clinical uses of local anesthetics?

- Neuronal anesthesia and analgesia - Peripheral nerve blocks - Subcutaneous and tissue infiltration - Topical anesthesia.

What factors determine the onset of local anesthetics?

- 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

How does infected tissue affect the onset of local anesthetics?

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

Are local anesthetics weak or strong base?

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

What factors determine the duration of local anesthetics?

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

How is the ester-type local anesthetics metabolized?

Rapidly metabolism by plasma esterases and metabolized to PABA

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

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

How is the amide-type local anesthetics metabolized?

Metabolized by P-450 enzymes the liver

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

Much less potential than esters d/t different metabolite.

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

- 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.

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

- Allergic rxns | - Methemoglobinemia- more common with esters

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

- Slows systemic rate of absorption and prolongs the anesthetic effect. - Helps reduce systemic ASEs.

What is the MOA of epinephrine?

Vasoconstriction, and binds to a2-adrenergic receptor