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16 Cards in this Set
- Front
- Back
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Non-selective CNS depressants
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barbital, pentobarbital, secobarbital, phenobarbital, and thiopental
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Site of action
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synapses, not axons
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Barbiturate MOA
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enhances postsynaptic action of GABA at GABA-AR; can directly open GABA-AR Cl- channel; reduce response to glutamate
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Barbiturate SEs
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Depressed level of consciousness, decreased respiration, hyperreflexia at low doses, lose of reflexes at high doses
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Hepatic biotransformation
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pento and secobarbital
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Phenobarbital elimination
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1/3 to 1/4 in the urine and the rest is parahydroxylated in the liver
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Thiopental elimination
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due to redistribution
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Context-sensitive half-time
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longer period of which a drug was given, the longer the period to recovery
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propofol
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similar to thiopental; greater decrease in blood pressure and negative inotropic effect on mycardium
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etomidate
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like thiopental; relatively less effect on cardio function
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Ketamine MOA
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antagonist at NMDA glutamate receptors; increases sympathetic activity
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Barbiturate toxicities
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induce hepatic enzymes; additive or greater than normal CNS depression; stimulate porphyrin synthesis
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COPD and porphyria
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avoid barbiturates
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Tolerance
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Metabolic, functional, and cross
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withdrawal syndrome
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hyperexcitability of CNS
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Psychological dependence
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may elicit some
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