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17 Cards in this Set
- Front
- Back
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mechanism of action of local anesthetics
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Na channel blockers
stop propagation of action potentials |
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types of local anesthetics
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aminoesters, amides
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how are aminoesters metabolized
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hydrolyzed by plasma esterases
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how are amide local anesthetics metabolized?
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biotransformation in the liver
*may be contraindicated in patients with liver dz, as will increase duration of action |
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what two types of toxicity are associated with local anesthetics?
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neurotoxicity- descending CNS depression, muscle twitching, convulsions, respiratory depression, death
cardiovascular toxicity- hypotension, dysrhythmia, cardiovascular collapse |
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what are the amide local anesthetics?
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Lidocaine, Mepivacaine, Bupivicaine
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Which local anesthetics are approved by the FDA and marketed for use in animals?
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Mepivacaine, Proparacaine
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Which local anesthetics are aminoesters?
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Benzocaine, Proparacaine
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How do competitive neuromuscular blockers work?
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compete for binding sites with ACh
stop stimulation of the post-synaptic membrane |
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How do depolarizing neuromuscular blockers work?
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bind to post-synaptic receptors
cause initial depolarization and action potential, prevent repolarization *may see initial muscle fasciculation followed by flaccid paralysis |
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What are the competitive neuromuscular blockers?
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Atracurium, Vecuronium, Pancuronium
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What are the depolarizing neuromuscular blockers?
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Succinylcholine
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Which NBs are metabolized by the liver and excreted by the kidneys?
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Vecuronium, Pancuronium
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Which NBs are degraded by plasma cholinesterases?
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Atracurium, Succinylcholine
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What is different about competitive vs depolarizing NBs?
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depolarizing NBs cannot be reversed with cholinesterase inhibitors and DO cause initial depolarization of the post-synaptic membrane
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What is a danger of reversing a competitive NB using a cholinesterase inhibitor?
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they also act at muscarinic receptors and may cause unwanted side effects
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Why can NBs not be used alone for surgery etc?
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NO analgesic effect
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