Sedative-Hypnotic Drugs Overview

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Questions and Answers

What is the primary mechanism by which barbiturates exert their CNS depressant effects?

  • Blockade of dopamine transporters
  • Inhibition of serotonin receptors
  • Activation of GABA receptors leading to chloride channel opening (correct)
  • Stimulation of adrenergic receptors

Which of the following is NOT a clinical application of barbiturates?

  • Anesthesia
  • Treatment of epilepsy
  • Management of anxiety disorders (correct)
  • Insomnia and sedation

What is the primary effect of sedative-hypnotic drugs on the central nervous system (CNS)?

  • They enhance excitatory neurotransmitter activity.
  • They produce dose-dependent CNS depressant effects. (correct)
  • They primarily produce stimulant effects.
  • They increase anxiety levels in individuals.

What adverse effect is associated with high tolerance levels to barbiturates?

<p>Severe cardiovascular depression (D)</p> Signup and view all the answers

Which of the following terms describes the phenomenon where a drug's removal evokes unpleasant symptoms?

<p>Dependence (B)</p> Signup and view all the answers

What is the primary pharmacokinetic characteristic of most sedative-hypnotic drugs like barbiturates?

<p>Good absorption from the gastrointestinal tract due to lipid solubility (A)</p> Signup and view all the answers

Which type of neurotransmitter is GABA classified as?

<p>Inhibitory neurotransmitter (C)</p> Signup and view all the answers

What makes barbiturate withdrawal symptoms particularly dangerous?

<p>There is no known antidote and can result in death (D)</p> Signup and view all the answers

What is the primary mechanism of action by which barbiturates produce their effects?

<p>They facilitate and prolong the inhibitory effects of GABA. (A)</p> Signup and view all the answers

Which of the following is NOT classified as a type of sedative-hypnotic drug?

<p>Opioids (B)</p> Signup and view all the answers

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Study Notes

Sedative-Hypnotic Drugs

  • Sedative-hypnotic drugs are a group of drugs that depress the central nervous system (CNS).
  • They produce dose-dependent effects, meaning the effects increase with the amount of drug taken.
  • Sedatives reduce excitement and calm the person.
  • Hypnotics produce sleep resembling normal sleep.

Benzodiazepines

  • Benzodiazepines are a major subgroup of sedative-hypnotic drugs.
  • Other sedative-hypnotic drugs include barbiturates and miscellaneous agents.

Key Terms

  • Addiction: A state where the drug user feels compelled to use the drug and experiences anxiety without it.
  • Anesthesia: Loss of consciousness with no response to pain.
  • Anxiolytic: A drug that reduces anxiety, a type of sedative.
  • Dependence: A state where removing the drug causes unpleasant, potentially life-threatening symptoms, often the opposite of the drug's effects.
  • REM Sleep: Phase of sleep with rapid eye movements; most dreaming takes place during REM sleep.
  • Tolerance: A decrease in drug effect requiring an increase in dosage to maintain the same response.

Neurotransmitters

  • Excitatory Neurotransmitters: Activate nerve cells.
    • Acetylcholine
    • Glutamate
  • Inhibitory Neurotransmitters: Inhibit nerve cell activity.
    • GABA (Gamma-Aminobutyric Acid)
    • Glycine

Barbiturates

  • Barbiturates are a class of sedative-hypnotic drugs.
  • Different types of barbiturates have varying durations of action:
    • Phenobarbital: Long-acting
    • Secobarbital: Short-acting
    • Thiopental: Ultra-short-acting

Mechanism of Action (Barbiturates)

  • Barbiturates depress neuronal activity in the midbrain reticular formation, enhancing and prolonging the inhibitory effects of GABA receptors.
  • They bind to multiple isoforms of the GABA A receptor.
  • Barbiturates increase the duration of GABA-mediated chloride (Cl-) channel opening (hyperpolarization).
  • They may also block the excitatory neurotransmitter glutamic acid and, at high concentrations, sodium channels.

GABA Receptor

  • Barbiturates activate GABA receptors.
  • Activation of GABA receptors opens chloride channels.
  • Increased duration of GABA-gated channel opening leads to hyperpolarization of cells.
  • Hyperpolarization of cells results in CNS depression.

Clinical Applications (Barbiturates)

  • Anesthesia (Thiopental).
  • Insomnia and sedation (Secobarbital).
  • Seizure disorders (Phenobarbital).

Pharmacokinetics (Sedative-Hypnotics)

  • Most sedative-hypnotic drugs are lipid-soluble and well absorbed from the gastrointestinal tract.
  • They distribute well to the brain.
  • The CNS effects of thiopental are terminated by rapid redistribution of the drug from the brain to other highly perfused tissues.
  • Renal excretion eliminates the drug from the body.

Adverse Effects (Barbiturates)

  • Drowsiness, severe respiratory and cardiovascular depression.
  • Tolerance: The body needs more of the drug to have the same effect.
  • Dependence liability: Higher than benzodiazepines.
  • Enzyme induction: Can lead to multiple drug interactions.
  • Withdrawal symptoms are more severe than opioid withdrawal and can be fatal (no antidote).
  • Contraindicated in pregnancy.

Experimental Methods (Sedative-Hypnotic Drug Effects)

  • Mouse/Rat Experiment:
    • Weigh two mice or rats.
    • Inject one animal with normal saline (control) and the other with Phenobarbital (50 mg/kg) or Thiopental (30 mg/kg).
    • Record the observations and time of occurrence in a table.

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