Benzodiazepine Poisoning
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Basics
Description
- Potentiates the activity of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter, by binding to its own specific site
- Also facilitates GABA binding to its site
- Results in chloride influx, membrane hyperpolarization, and inhibition of cellular excitation:
- Benzodiazepines (BZDs) increase the frequency of chloride channel opening
- Depresses spinal reflexes and reticular activating system
- Rapidly absorbed from GI tract:
- Highly protein bound
- Large Vd
- Most have hepatic metabolism, some have active metabolites
- Duration of action is inversely proportional to lipophilicity with highly lipophilic drugs penetrating the CNS more rapidly
- Duration of diazepam > lorazepam > midazolam
- Synergistic with other sedative–hypnotic medications (e.g., ethanol, barbiturates, propofol)
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Basics
Description
- Potentiates the activity of γ-aminobutyric acid (GABA), the major inhibitory neurotransmitter, by binding to its own specific site
- Also facilitates GABA binding to its site
- Results in chloride influx, membrane hyperpolarization, and inhibition of cellular excitation:
- Benzodiazepines (BZDs) increase the frequency of chloride channel opening
- Depresses spinal reflexes and reticular activating system
- Rapidly absorbed from GI tract:
- Highly protein bound
- Large Vd
- Most have hepatic metabolism, some have active metabolites
- Duration of action is inversely proportional to lipophilicity with highly lipophilic drugs penetrating the CNS more rapidly
- Duration of diazepam > lorazepam > midazolam
- Synergistic with other sedative–hypnotic medications (e.g., ethanol, barbiturates, propofol)
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