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13 Cards in this Set

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