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Flashcards in Pharm 11 Deck (34)
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MOA of local anesthetics (LA's)

Block voltage-dependent sodium channels

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This may enhance activity of local anesthetics

Hyperkalemia

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This may antagonize activity of local anesthetics

Hypercalcemia

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Almost all local anesthetics have this property and sometimes require the administration of vasoconstrictors (ex. Epinephrine) to prolong activity

Vasodilation

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Local anesthetic with vasoconstrictive property, favored for head, neck, and pharyngeal surgery

Cocaine

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Longer acting local anesthetics which are less dependent on vasoconstrictors

Tetracaine and bupivacaine

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These LA's have surface activity

Cocaine and benzocaine

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Most important toxic effects of most local anesthetics

CNS toxicity

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Commonly abused LA which has cardiovascular toxicity including severe hypertension with cerebral hemorrhage, cardiac arrhythmias, and myocardial infarction

Cocaine

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LA causing methemoglobinemia

Prilocaine

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Structurally related to acetylcholine, used to produce muscle paralysis in order to facilitate surgery or artifical ventilation. Full doses lead to respiratory paralysis and require ventilation

Neuromuscular blocking drugs

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These drugs strongly potentiate and prolong effect of neuromuscular blockade (NMB)

Inhaled anesthetics, especially isoflurane, aminoglycosides, and antiarrhythmic

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These prevent the action of Ach at the skeletal muscle endplate to produce a "surmountable blockade," effect is reversed by cholinesterase inhibitors (ex. neostigmine or pyridostigmine)

Nondepolarizing type antagonists

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Agent with long duration of action and is most likely to cause histamine release

Tubocurarine

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Non-depolarizing antagonist has short duration

Mivacurium

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Agent blocking muscarinic receptors

Pancuronium

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Agent undergoing Hofmann elimination (breaking down spontaneously)

Atracurium

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Depolarizing blocker --> continuous depolarization --> muscle relaxation and paralysis, also causes muscle pain postoperatively and myoglobinuria may occur

Succinylcholine

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During Phase I these agents worsen the paralysis by succinylcholine, but during phase II they reverse the blockade produced by succinylcholine

Cholinesterase inhibitors

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Agents acting in the CNS or in the skeletal muscle, used to reduce abnormally elevated tone caused by neurologic or muscle end plate disease

Spasmolytic drugs

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Facilitates GABA presynaptic inhibition

Diazepam

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GABA agonist in the spinal cord

Baclofen

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Similar to clonidine and may cause hypotension

Tizanidine

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Agent used for acute muscle spasm

Cyclobenzaprine

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Agent used in drug therapy of Parkinson's instead of Dopamine which has low bioavailability and does not cross the BBB

L-dopa

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This is combined with L-dopa, inhibits DOPA decarboxylase (active only peripherally) which allows lower effective doses of L-dopa and allows for fewer SE's (GI distress, postural hypotension, and dyskinesias)

Carbidopa

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Clinical response that may fluctuate in tx of Parkinson's dx

"On-off-phenomenon"

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Anti-Parkinson's drug which increases intraocular pressure and is contraindicated in closed angle glaucoma

Levodopa

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Ergot alkaloid that is a partial agonist at D2 receptors in the brain, used for patients who are refractory or cannot tolerate levodopa, causes erythromelalgia

Bromocriptine

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Non ergot agents used as first-line therapy in the initial management of Parkinson's

Pramipexole and ropinirole

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Sedative-Hypnotics action

Reduce inhibition, suppress anxiety, and produce relaxation

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Additive effects when Sedative-Hypnotics used in combination with these agents

CNS depressants

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Common mechanism by which overdose result in death

Depression of medullary and cardiovascular centers

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The most important sign of withdrawal syndrome

Excessive CNS stimulation (seizures)