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13 Cards in this Set
- Front
- Back
degrees of CNS depression in the progressive, dose-dependent manner
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calming->drowsiness (sedation)-> sleep (hypnosis) -> unconsciousness -> surgical anesthesia -> coma -> respiratory depression -> cardiovascular collapse
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BZD MOA
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interact w/ separate site that is associated w/ the Cl- channel -> enhances ability of GABA to open Cl- channels
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Barbiturates MOA
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interact w/ a distinct site associated w/ the Cl- channel and modify the actions of GABA
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High doses of barbiturates and alcohol are capable of activating...
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CL- influx even in the absence of GABA
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GABA produces many of its effects by interacting with specific receptors termed...
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GABA A receptors
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CNS effects/toxicity
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1)anterograde amnesia
2)disinhibtion of suppressed behavior (increased aggression and bizarre behaviors) 3)respiratory depression (not with BZDs) |
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Tolerance
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-readily develops to most effects
-cross tolerance and cross dependence to barbiturates and alcohol |
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Management of withdrawal
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1)long-acting BZD (diazepam) and gradually tapering over a period of several weeks
2)carbamazepine or valproic acid sometimes included in regimen to prevent seizures |
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Acute poisoning symptoms of barbiturates, alcohol, and inhalants
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1)severe CNS depression (coma and depressed respiration)
2)results in hypotension, shock, and circulatory collapse |
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Antidotes for poisoning
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1)flumazenil can reverse CNS effects of BZDs
2)no specific antidotes for barbiturate poisoning |
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pharmacological effects of inhalants
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1)non-specific depressants that produce a dose-dependent depression of CNS function
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Hazards associated with the use of inhalants
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1)acute poisoning (resp arrest and CV collapse)
2)suffocation 3)brain, lung, liver damage 4)immunosuppression, bone marrow suppression 5)cancer |
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Treatment of inhalant withdrawal
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long-acting BZDs followed by a gradual reduction in drug dose
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