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48 Cards in this Set
- Front
- Back
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Overview of Sedative Hypnotics
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NE and 5HT are both for depression and pain. Enkeph, subP are the pain pathways. AcH affects memory. DA affects parkinson’s and controls muscle contractions. There is elevated DA in psychosis. GABA is a general inhibitory on CNS and is present in Spinal Cord. 2-4 hours is peak blood levels of drug, so will get peak cooperation
Enhances GABA |
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Mechanism of Barbiturates (BAR)
Thiopental (Pentothal) – ultra short duration, used as IV anesthetic |
Enhance actions of GABA (major inhibitory NT)
-Degree of CNS depression is dose related -Interact with other transmitters in CNS which explains greater degree of CNS depression (directly opens Cl channels at high doses) |
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Indications of Barbiturates (BAR)
Thiopental (Pentothal) – ultra short duration, used as IV anesthetic |
Daytime sedation (primary agents are BZD and Buspirone)
-Hypnosis (to relieve insomnia) – effectiveness limited to only a few days -Induction of anesthesia -Anti-epileptic (Phenobarbital, clonazepam (Klonopin) |
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Advantages of Barbiturates (BAR)
Thiopental (Pentothal) – ultra short duration, used as IV anesthetic |
Metabolites are inactive
Ulta short duration, used as IV |
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Disadvantages of Barbiturates (BAR)
Thiopental (Pentothal) – ultra short duration, used as IV anesthetic |
Cross placental barrier
-Low TI -Psychologic and Physiologic Dependence -Abuse potential -Withdrawal syndrome – more severe with chronic, high doses and with short-acting BARs Pharmacodynamic (CNS adaptation) and drug disposition tolerance (↑ activity of phase I (P450) drug-metabolizing enzymes |
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Mechanism of Pentobarbital (Nembutal) – intermediate half life (18-48 hrs) – hypnotic (rarely used today)
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Enhance actions of GABA (major inhibitory NT)
-Degree of CNS depression is dose related -Interact with other transmitters in CNS which explains greater degree of CNS depression (directly opens Cl channels at high doses) |
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Indications of Pentobarbital (Nembutal) – intermediate half life (18-48 hrs) – hypnotic (rarely used today)
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Daytime sedation (primary agents are BZD and Buspirone)
-Hypnosis (to relieve insomnia) – effectiveness limited to only a few days -Induction of anesthesia -Anti-epileptic (Phenobarbital, clonazepam (Klonopin) |
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Advantages of Pentobarbital (Nembutal) – intermediate half life (18-48 hrs) – hypnotic (rarely used today)
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Metabolites are inactive. Intermediate half life.
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Disadvantages of Pentobarbital (Nembutal) – intermediate half life (18-48 hrs) – hypnotic (rarely used today)
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Rarely used today.
Cross placental barrier -Low TI -Psychologic and Physiologic Dependence -Abuse potential -Withdrawal syndrome – more severe with chronic, high doses and with short-acting BARs -Pharmacodynamic (CNS adaptation) and drug disposition tolerance (↑ activity of phase I (P450) drug-metabolizing enzymes |
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Mechanism of Phenobarbital (Luminal) – long half life (4-5 days), used as sedative and anti-epileptic
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Enhance actions of GABA (major inhibitory NT)
-Degree of CNS depression is dose related -Interact with other transmitters in CNS which explains greater degree of CNS depression (directly opens Cl channels at high doses) |
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Indications of Phenobarbital (Luminal) – long half life (4-5 days), used as sedative and anti-epileptic
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Daytime sedation (primary agents are BZD and Buspirone)
-Hypnosis (to relieve insomnia) – effectiveness limited to only a few days -Induction of anesthesia -Anti-epileptic (Phenobarbital, clonazepam (Klonopin) |
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Advantages of Phenobarbital (Luminal) – long half life (4-5 days), used as sedative and anti-epileptic
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Metabolites are inactive.
Long half life. Used as sedative and anti-epileptic. |
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Disadvantages of Phenobarbital (Luminal) – long half life (4-5 days), used as sedative and anti-epileptic
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Cross placental barrier
-Low TI -Psychologic and Physiologic Dependence -Abuse potential -Withdrawal syndrome – more severe with chronic, high doses and with short-acting BARs -Pharmacodynamic (CNS adaptation) and drug disposition tolerance (↑ activity of phase I (P450) drug-metabolizing enzymes |
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Mechanism of Barbiturate-like drugs – Glutethimide, Ethchlorvynol, Methaqualone, Ethan
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Enhance actions of GABA (major inhibitory NT)
-Degree of CNS depression is dose related -Interact with other transmitters in CNS which explains greater degree of CNS depression (directly opens Cl channels at high doses) |
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Indications of Barbiturate-like drugs – Glutethimide, Ethchlorvynol, Methaqualone, Ethan
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Daytime sedation (primary agents are BZD and Buspirone)
-Hypnosis (to relieve insomnia) – effectiveness limited to only a few days -Induction of anesthesia -Anti-epileptic (Phenobarbital, clonazepam (Klonopin) |
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Advantages of Barbiturate-like drugs – Glutethimide, Ethchlorvynol, Methaqualone, Ethan
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Metabolites are inactive
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Disadvantages of Barbiturate-like drugs – Glutethimide, Ethchlorvynol, Methaqualone, Ethan
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Cross placental barrier
-Low TI -Psychologic and Physiologic Dependence -Abuse potential -Withdrawal syndrome – more severe with chronic, high doses and with short-acting BARs -Pharmacodynamic (CNS adaptation) and drug disposition tolerance (↑ activity of phase I (P450) drug-metabolizing enzymes |
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Mechanism of BZD diazepam (Valium):
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Type I
More selective in the suppression of anxiety than BAR and have a shallower dose-response curve. BZ1 and BZ2 are the sites of action of most BZD. Selective BZ1 agonists are selective hypnotics |
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Indications of BZD diazepam (Valium):
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Indicated for generalized anxiety disorder (GAD), Panic Disorder, OCD, Post traumatic stress disorder, Preanastethic medication and surgical adjunct, insomnia, skeletal muscle spasm, alcohol withdrawal, and epilepsy (stops continuous seizures).
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Advantages of BZD diazepam (Valium):
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It has higher TI than BAR so little respiratory depression, and little effect on P450 enzymes in liver. Has a smoother effect than BAR
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Disadvantages of BZD diazepam (Valium):
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Get dose-related drowsiness, ataxia, and anterograde amnesia. With CNS depressant drugs very dangerous.
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Mechanism of Oxazepam (Serax)
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Type II: Intermediate Half Life
Enhance actions of GABA (major inhibitory NT) -BZ1 and BZ2are site of action -Selective BZ1 agonists – “selective” hypnotics |
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Indications of Oxazepam (Serax)
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Anxiety (more selective than BAR)
-Preanesthetic medication and surgical adjunct -Insomnia (effective for a longer term) -Skeletal muscle spasm -Alcohol withdrawal -Epilepsy |
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Advantages of Oxazepam (Serax)
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Not metabolized by P450. Not so sensitive to the liver so can be used on patients with liver problems. Preferred by elderly
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Disadvantages of Oxazepam (Serax)
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a
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Mechanism of Triazolam (Halcion)
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Type III: Very short half life.
Enhance actions of GABA (major inhibitory NT) -BZ1 and BZ2are site of action -Selective BZ1 agonists – “selective” hypnotics |
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Indications of Triazolam (Halcion)
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Anxiety (more selective than BAR)
-Preanesthetic medication and surgical adjunct -Insomnia (effective for a longer term) -Skeletal muscle spasm -Alcohol withdrawal -Epilepsy |
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Advantages of Triazolam (Halcion)
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Less sedation
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Disadvantages of Triazolam (Halcion)
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Can get a lot of violence
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Mechanism of Flumazenil (Romazicon)
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Benzodiazapine antagonist
High affinity for CNS BZ receptors, but lacks efficacy (pure competitive antagonist) |
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Indications of Flumazenil (Romazicon)
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Use to reverse BZD anesthesia or treat overdose
-Does not affect CNS action of BAR, opiates or other CNS depressants |
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Advantages of Flumazenil (Romazicon)
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Very specific
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Disadvantages of Flumazenil (Romazicon)
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Agitation, confusion, dizziness
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Mechanism of Buspirone (Buspar)
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Benzodiazapine antagonist
May interact with dopamine or serotonin pathways -Lack of GABA interaction means lack of muscle relaxation, anti-epileptic and hypnotic activity |
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Indications of Buspirone (Buspar)
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Daytime sedation (primary agents are BZD and Buspirone)
-Hypnosis (to relieve insomnia) -Induction of anesthesia -Anti-epileptic (Phenobarbital, clonazepam (Klonopin) |
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Advantages of Buspirone (Buspar)
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Lower incidence of sedation, abuse potential, and withdrawal syndrome
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Disadvantages of Buspirone (Buspar)
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Tachycardia, miosis, paresthesia, tinnitus, chest pain
-Selective antianxiety action delayed 1-2 weeks |
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Advantage of Selective BZ1 agonists – Zolpidem (Ambien)
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Less anxiolytic, muscle relaxant or antiepileptic activity than other benzodiazepines
-Short half-life – no active metabolites – less daytime sedation -At low doses, produces very little REM suppression, tolerance or dependence |
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BAR and BZD: Similarities and Differences for Mechanism
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BAR: Open Cl channels in CNS neurons which increases GABA binding
BZD: Occupy BZD receptors which increases GABA binding |
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BAR and BZD: Similarities and Differences for Selectiveness
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BAR: Less selective
BZD: More slective in suppression of anxiety than BAR |
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BAR and BZD: Similarities and Differences Dose-Response Curves, TI
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BAR: Steeper, Low TI
BZD: Shallower, Higher TI |
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BAR and BZD: Similarities and Differences Placental Barriers
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BAR: Cross
BZD: Cross (Greater risk of teratogenic effects than BAR) |
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BAR and BZD: Similarities and Differences P450 Enzymes
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BAR: Induce or increase activity (Must inc dose overtime to achieve same level)
BZD: Litte effect on their activity. |
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BAR and BZD: Similarities and Differences Insomnia
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BAR: Effectiveness limited to only a few days. REM rebound upon discontinuance.
BZD: Effective for a longer term than BAR. Less REM suppression and rebound. |
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BAR and BZD: Similarities and Differences Daytime Sedation
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BAR: Declining use for BAR
BZD: Primary agent (along with buspirone) |
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BAR and BZD: Similarities and Differences Dependence
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BAR: Psychological and phsyiolgocial.
BZD: Lower risk of physiological dependence. |
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BAR and BZD: Similarities and Differences Withdrawal.
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BAR: Severe (disturbed sleep patterns, tremor, anxiety, agitation, confusion, hallucinations, convulsions. May be life threatening
BZD: Less severe (rebound anxiety, agitation, restlessness, sweating, irritability, delusions, and seizures.) |
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BAR and BZD: Similarities and Differences Metabolites
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BAR: Inactive
BZD: Some active which contribute to effects. |
