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Medical Pharmacology:  CNS Pharmacology Lecture, slide 2

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  • Stages of CNS depression

  • Classification of central nervous system depressants

  • Possible biochemical mechanism of action of anxiolytics, sedatives and hypnotics 

  • Effects on cardiovascular, respiratory and central nervous systems.

  • Comparative Advantages and disadvantages of  sedative-hypnotic classes 

  • Anxiolytics

  • Hypnotics

  • Specific Drug Classes

    • Ethanol

    • Barbiturates

    • Benzodiazepines

    • Others

  • Preoperative Medications: The Role of Sedative Hypnotics and Other Drugs and Issues

    • Benzodiazepines

    • Opioids

    • Antihistamines (including both sedative uses & effects on gastric acid secretion)

    • Patients who should receive prophylaxis against aspiration

    • Antiemetic Drugs

    • Antacids

    • Proton Pump Inhibitors

    • Anticholinergic Agents

    • Steroids

    • Antibiotics

    • Insulin

    • Preoperative medication differences between adults and children

     

 

 

Major drugs and drug classes used to treat anxiety

  • Chlordiazepoxide (Librium), Diazepam (Valium), Oxazepam (Serax), Clorazepate (Tranxene), Lorazepam (Ativan),Alprazolam (Xanax), Halazepam (Paxipam)

Major drugs and drug classes used to treat anxiety: Barbituratres and non-barbiturates in management of anxiety

  • Benzodiazepines are commonly used for management of generalized anxiety disorder. Most, but not all, clinical research studies have shown that benzodiazepines are more effective than placebo in treating anxiety.

  • Factors that have promoted the popularity of these drugs include:

    •  Safety

    •  Pharmacology

    •  Patient demand.

  • Benzodiazepines may be more efficacious and certainly safer in management of anxiety compared to barbiturates.

  • Barbiturates and non-barbiturates such as meprobamate have been used in the past to manage anxiety. However, these drugs are now rarely used.

  • Barbiturates are also infrequently used for this indication because of:

    • Excessive sedation/intoxication at anxiolytic dosages

    • Tolerance

    • Physical dependence

    • Potentially life-threatening withdrawal reactions

    • Life-threatening toxicity with overdosage.

Buspirone

  • Buspirone, which has selective affinity of 5-HT1A, is a relatively new anxiolytic.

  • Buspirone seems most effective in mild anxiety and is not effective compared to benzodiazepines and certain antidepressant agents in treatment of panic disorder.

  • Buspirone does not exhibit cross-tolerance with benzodiazepines or other sedative-hypnotics.

Baldessarini, R. J., Drugs and the Treatment of Psychiatric Disorders, In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 421-427]

Pharmacological hypnosis: major drugs /drug classes

Introduction

  • If non-pharmacological treatment of insomnia (such as moderate exercise) is not effective, drugs may have to be used.

  • Untreated chronic insomnia may have many adverse effects including a four-fold increase in serious accidents.

  • In addition to use of pharmacological agents, management of insomnia should include (a) a search for an underlying cause, elimination of "performance anxiety" related to falling asleep, adjusting the patient's biological clock such that sleepiness corresponds to the time of attempted sleep, and suppression of the use of alcohol or over-the-counter sleep aids

Benzodiazepines

  • Hypnotics that act at benzodiazepine receptors and newer agents such as zolpidem (Ambien) are preferable to barbiturates because of:  greater therapeutic index, less disruption of sleep patterns, less danger of overdosage toxicity, less abuse liability 

  • In the absence of daytime anxiety benzodiazepines with short half-lives (no active metabolites or only short-acting metabolites) are preferable.

  • Triazolam (Halcion) is an example of a short-acting agent that has been used as a hypnotic. 

    • Short acting benzodiazepines may, however cause amnesia, early morning awakening, rebound daytime anxiety

  • Some patients who have insomnia also have daytime anxiety.

    • To manage those patients a longer-acting benzodiazepine may be appropriate.

      • Use of these agents may result in: next-day cognitive impairment or delayed cognitive impairment as metabolites accumulate

Barbiturates and non-barbiturates for hypnosis

  • Barbiturates and non-barbiturates such as meprobamate have been used in the past for pharmacological hypnosis.

  • However, these drugs should be avoided:

    •  Liabilities associated with barbiturate use include abuse potential, physical potentially life-threatening withdrawal reactions, dependence, and  life-threatening toxicity with overdosage.

Ethanol

  • Ethanol should not be used to manage insomnia because of numerous adverse effects.

    • For insomnia, despite reducing sleep latency, it may cause sleep fragmentation.

[Hobbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 385-386

 

 

Specific Drugs and Classes

 

  • Ethanol: absorption, metabolism of ethanol, its effects on major organs system, contraindications, acute and chronic toxicities, the mechanism of action of disulfiram

  • *Note:  Chronic ethanol abuse has anesthesia implications.  In consideration of a variety of surgeries including colonic surgery, prostatectomy, ankle surgery, and surgical intervention to treat subdural hematoma, perioperative morbidity increases by 200%-300%.

    • Frequently observed complications include  bleeding, cardiopulmonary insufficiency,  and infection.

    • Underlying mechanisms for these complications include:

      • subclinical cardiac insufficiency,  hemostatic imbalance, immune system deficiencies, and possibly in accentuated stress response to surgery or alcohol abstinence (withdrawal).

*Mushlin, P.S. and S. Gelman, "Anesthesia and the Liver", in Clinical Anesthesia (4/e), edited by Paul G. Barish, Bruce F. Cullen and Robert K. Stoelting, Lippincott Williams & Wilkins, p 1084, 2001

Absorption, Metabolism

Absorption:

  • Ethanol is rapidly absorbed from stomach, small intestine and colon but the rate of absorption from the stomach is influenced by the food content.

  • Ethanol evenly distributed throughout all fluids and tissues, after absorption.

  • Placental permeability ensures access of ethanol to the fetus.

Metabolism:

  • Most ethanol molecules are oxidized, with the rate of oxidation insensitive to ethanol concentration (zero-order kinetics).

  • Most ethanol oxidation occurs in the liver and is catalyzed by alcohol dehydrogenase. 

    • The product is acetaldehyde which is then converted to acetyl CoA.

  • To a limited extent, in humans, ethanol is also oxidized by mixed function oxidases in liver microsomal membranes.

  • Genetic polymorphisms occur for both alcohol and aldehyde dehydrogenase.

Mechanism of Action

  • Ethanol (along with anesthetics) enhances GABA-mediated synaptic inhibition.

  • Ethanol inhibits glutamate-activated ion channels (excitatory) (predominately the NMDA glutamate receptors at mild intoxicating ethanol concentrations.)

  • Ethanol may also act by affecting 5-HT3 receptors.

    • Activation of these receptors results in excitation of inhibitory interneurons.

    • Serotonin's action at the 5-HT3 receptor subtype is enhanced by ethanol.

Ethanol: Drug-Drug Interactions

  • Ethanol enhances CNS depression caused by other sedative-hypnotics.

  • Ethanol interferes with metabolism of drugs that utilize the same hepatic oxidase system.

    • For example the clearance of phenytoin is prolonged due to competition with ethanol for the same mixed-function hepatic oxidase system.

    • By contrast, with chronic use, ethanol causes induction of hepatic metabolizing enzymes and can, in this case, increase clearance of many drugs (e.g. phenytoin (Dilantin), Tolbutamide (Orinase)).

  •   Chronic consumers of ethanol are susceptible to acetaminophen hepatoxicity probably due to accumulation of toxic metabolites and glutathione depletion.

 

Ethanol:  Organ Systems: Pharmacological Effects

 

Ethanol: Central Nervous System

Ethanol: Acute effects 

  • Ethanol is a CNS depressant.

    • Depression of inhibitory CNS systems may be responsible for apparent stimulation that is observed initially.

    • With moderate intoxication, mood swings, outgoing, and expansive behavior occur.

    • General impairment of statements function becomes evident with increased intoxication.

    • Large amounts of ethanol may lead to severe (even lethal) respiratory depression.

Ethanol: Chronic effects

  • Chronic and excessive ethanol use results in brain damage, memory loss, sleep disturbances.

  •  Increased risk of seizures. 

  •  Neuropsychiatric disturbances including Wernicke's encephalopathy. 

    • (Wernicke's encephalopathy is due to a nutritional thiamine deficiency. This syndrome is not observed only in alcoholics.  Common causes include chemotherapy-associated prolonged vomiting with lack of nourishment, eating disorders, elderly patients who had been living alone and who have not been maintaining adequate nutrition [Wernicke's may be precipitated in the hospital by glucose administration to patients who is deficient in thiamine.]

" Wernicke-Korsakoff encephalopathy. Note pigmentation of gray matter around third ventricle. Occurs with Vitamin B1 deficiency, most often in chronic alcoholics."--image from educational materials (pathology) University of Texas (Houston)


"Mammillary Gross Wernicke's encephalopathy. Note bodies black mammillary body from acute congestion and hemorrhage indicating the acute form of Wernicke's" --image from educational materials (pathology) University of Texas (Houston)

 

 

Ethanol: Cardiovascular System

Ethanol: Acute Effects:

  • Ethanol causes a generalized vasodilation (due to both central effects and effects on the vascular bed)

  • Moderate doses, however, can cause a vasoconstrictive effect in the heart and brain.

  • In severe intoxication, cardiovascular depression occurs secondary to central vasomotor effects and respiratory depression.

 Ethanol: Chronic Effects:

  • With chronic use, significant and irreversible damage to the myocardium may occur.

    • This effect is one of the most important causes of cardiomyopathy.

 

Gastrointestinal Tract:

  • Ethanol increases gastric secretions by (a) direct action on the stomach (may increase gastrin), (b) psychological mechanism (if the individual likes it), (c) stimulating sensory endings in the buccal and gastric mucosae.

  • At high ethanol concentrations (80 proof [40% alcohol]), direct gastric mucosal irritation occurs resulting in congestive hyperemia and inflammation.

    • These concentrations can result in an erosive gastritis.

  • Gastric damage caused by aspirin is significantly worsened by ethanol.

  • Chronic, excessive ethanol consumption may cause either diarrhea or constipation.

  • Ethanol may also predispose to chronic pancreatitis because of both increased secretion and pancreatic ductal obstruction.

 

Liver

  • Chronic use of ethanol promotes hepatic cirrhosis and is associated with an increased risk of cancer and drug toxicity (acetaminophen).

  • Acute use probably does not produce lasting hepatic changes.

 

Miscellaneous organ effects

  •   Teratogenic effects:

    • Fetal alcohol syndrome consists of many dysfunction. including low IQ, microcephaly, facial abnormalities.

    • Ethanol appears to be the most frequent cause of teratogenically-caused mental deficiency in the West.

  • Sexual Functions:

    • Inebriation interferes with coitus, decreasing sexual responsiveness in both men and women.

    • Chronic ethanol abuse may lead to impotence, sterility, testicular atrophy, and gynecomastia.

    • Feminization in males is due to both hyperestrogenization with reduced rate of testosterone production (due to hepatic damage) and by ethanol's induction of hepatic metabolizing enzymes, increasing the rate of testosterone inactivation.

  • Renal: Increased diuresis due to reduction in ADH and hence a decrease in tubular water reabsorption.

 

Disulfiram

  •  Disulfiram (Antabuse) inhibits aldehyde dehydrogenase which results, following ethanol ingestion, in an increased acetaldehyde concentration.

  • The resulting "acetaldehyde syndrome" consists of facial flush, headache, hypotension, marked uneasiness, confusion, vomiting and other symptoms.

    • These unpleasant effects are the basis of the use of disulfiram as part of the treatment of chronic alcoholism.

  • Disulfiram is converted to ethyldithiocarbamate a very effective chelator of copper and other metals. As a result, ethyldithiocarbamate inhibits the activity of dopamine beta-hydroxylase, alcohol dehydrogenase, and other metalloenzymes.

  Contraindications to Ethanol Use

  •  Hepatic disease, gastrointestinal ulcer, cardiac or skeletal myopathy, pregnancy,  individuals previously addicted to ethanol

Hobbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 386-392.

 

Barbiturates

  • Mechanism of action 

    • Molecular: Barbiturates activate inhibitory GABAA while inhibiting excitatory AMPA receptors.

    • AMPA receptors are the subtype of glutamate receptors sensitive to kainate or quisqualate.

    • Barbiturates interact differently than benzodiazepines at GABA receptors. For example, the gamma subunit is not required for barbiturate activity.

    •  The combination of these receptor effects may result in the profound CNS depression that occurs with higher barbiturate doses.

 

  • Pharmacokinetics/Redistribution

    • Barbiturates are usually orally administered and are rapidly and well absorbed.

    • Intravenous administration is used for:

      • Treatment of status epilepticus (phenobarbital)

      • Anesthesia induction/maintenance (methohexital (Brevital), thiopental (Pentothal)).

    • Barbiturates are highly lipid soluble and the i.v. barbiturate anesthesia induction agent are the most lipid soluble.

      • After i.v. injection these agents undergo rapid redistribution from the brain to other tissues.

    • Redistribution is the major mechanism  for termination of CNS action.

    • Most barbiturates undergo extensive hepatic metabolism prior to renal excretion.

    • Renal excretion is favored by osmotic diuresis and/or alkalinization of the urine.

    • Barbiturate metabolism is more rapid in young adults compared to children or the elderly.

    • Half-lives may be increased in pregnancy (due to increased volume of distribution)

    • Barbiturate half-lives can be increased in patients with chronic liver disease, such as cirrhosis.

     

Effects of barbiturates on major organ systems

 

Cardiovascular System

  • In sedative or doses for pharmacological hypnosis, barbiturates have minimal cardiovascular effects

  • When thiopental (Pentothal) is used in general anesthesia, following pre-anesthetic medication,  plasma renal flow, cerebral blood flow, and CSF pressure decrease.

  • Significant depression of myocardial contractility occurs in barbiturate poisoning.

 

Central Nervous System

  • Barbiturates depress respiratory drive.

    • At doses somewhat (three times) higher than required for pharmacological hypnosis, neurogenic drive is abolished and the hypoxic respiratory drive is reduced and the chemoreceptor drive is attenuated.

    • At still higher doses, the hypoxic drive is abolished.

 

Liver

  • Acutely, barbiturates combine with cytochrome P-450 and produce competitive inhibition of metabolism of a number of drugs and endogenous agents (such as steroids)

  • Chronically, barbiturates increase activities of cytochrome P-450 oxidases and glucuronyl transferases and therefore increase the metabolism (due to enzyme induction) of many drugs, steroids, vitamins K & D, cholesterol, bile salts. The extent of the increase is about two-fold

  • Part of barbiturate tolerance is due to increased hepatic metabolism of barbiturates, induced by barbiturates.

  • Non-microsomal enzyme system are also induced, including:

    •  d-aminolevulinic acid (ALA) synthetase. The effect of barbiturates on ALA synthetase that produces exacerbation in patients with intermittent porphyria.

    • aldehyde dehydrogenase

Hibbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 374-377.]

 

Therapeutic Uses: Barbiturates

  • IV anesthesia: Thiopental (Pentothal) and methohexital (Brevital)

  • Convulsions: emergency treatment (eclampsia, tetanus, status epilepticus), but benzodiazepines are preferable.

  • Epilepsy

  • Rarely used as a sedative due to the availability of safer benzodiazepine agents.

 

 

Barbiturate Overdosage/Adverse Effects

 

 

 Adverse Effects:

  •  Drowsiness, impaired judgment, impaired motor skills

  •  Significant CNS/respiratory depression with high dosage.

  •  Paradoxical excitement

  •  If barbiturates are given for pain, restlessness, excitement, or delirium may result

  •  Hypersensitivity: allergic reaction in patients who are predisposed to angioedema, urticaria, and asthma

  •  Drug interactions: combination with other sedative agents can result in severe CNS depression.

Untoward effects:

  • Absolutely contraindicated in acute intermittent porphyria or porphyria variegata because barbiturates increase porphyrin synthesis.

  •  i.v. administration can produce cardiovascular collapse; overdosage can cause severe respiratory depression.

  Management of barbiturate poisoning

  • Severe intoxication is associated with coma and depressed respiration

  • Treatment is supportive with CNS stimulants contraindicated (increases mortality)

  • Hemodialysis or hemoperfusion may be needed

  • Complicating factors include:

    •  Circulatory collapse

    •  Shock

    •  Dehydration

    •  Renal failure.

[Hibbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 374-377.]

 

 

 

Benzodiazepines: the primary use of the following agents

  • Diazepam (Valium)

  • Alprazolam (Xanax)

  • Chlordiazepoxide (Librium)

  • Clonazepam (Klonopin)

    •  Clonazepam is used (a) in seizure disorders: absence seizures, myoclonic seizures in children (b) as adjunctive treatment in acute mania and in (c) certain movement disorders.

    •   Adverse Effects: 

      • Common: Drowsiness, lethargy

      • Less common: Muscular incoordination, ataxia

      • Other: hypotonia, dysarthria, dizziness, behavior disturbances including hyperactivity, irritability, difficulty in concentration.

      • Seizures may occur if drug is discontinued abruptly.

    • [Hobbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) The McGraw-Hill Companies, Inc.,1996, pp. 372-373.;McNamara, J.O. Drugs Effective in the Therapy of the Epilepsies, In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 479]

       

  • Flurazepam (Dalmane)

    • Flurzepam has been prescribed for insomnia.

    • Flurazepam has long-acting metabolites.

    •   Adverse Effects: 

      • Presence of long-acting metabolites may cause daytime sedation, which may be undesirable.

       

  • Triazolam (Halcion)

    • Triazolam is used to induce sleep.

    • Triazolam is short-acting with no active metabolites

    • Adverse Effects: Tolerance may develop and rebound insomnia has been reported.

[Dopheide, J.A.. Sleep Disorders, In, Applied Therapeutics: The Clinical Use of Drugs, (Young, L.Y. and Koda-Kimble, M.A.,eds) Applied Therapeutics, Inc., 1995, p 74-5);[Harvery, R.A, Champe, P.C., Mycek, M.J., Gertner, S.B. and Perper, M.M., Anxiolytic and Hypnotic Drugs, In: Lippincott's Illustrated Reviews: Pharmacology, J.B. Lippincott Co, 1992, p 94]

 

  • Flumazenil (Romazicon, benzodiazepine antagonist*)

    • Primary use is for management of benzodiazepine overdosage.

    • Additional use in the reduction of benzodiazepine effects in general anesthesia or diagnostic procedures. Competitively antagonizes the binding and allosteric effects of benzodiazepines.

    • Benzodiazepine-induced electrophysiological and behavioral effects are antagonized.

    • Fumazenil is available only for intravenous administration (because of high first-pass effect)

    • Adverse Effects: 

      • In comatose patients, intoxicated with alcohol, flumazenil may increase risk of seizures.

      • In comatose patients due to tricyclic antidepressant agents, flumazenil increases seizure risk.

[Hobbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives: Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 372-373.]

 

Benzodiazepines: Effects on Organ Systems and Side Effects

 

Cardiovascular System

  •  Except in overdosage, cardiovascular effects of benzodiazepines in normal subjects are minor.

  •  If used as preanesthetic medication, all benzodiazepines decrease blood pressure and increase heart rate.

    •  In this setting diazepam increases coronary flow (perhaps by increasing adenosine concentration).

 

Respiratory System

  • At pharmacological hypnotic doses, benzodiazepines do not affect respiration in normal subjects.

  • At higher doses, such as those used for endoscopy or when given as preanesthetic medication, benzodiazepines somewhat depress alveolar ventilation due to a decrease in hypoxic drive. (as noted above)

    •  These effects are worse in patients with COPD (chronic obstructive pulmonary disease).

    •  In the presence of other CNS depressant drugs, severely benzodiazepine intoxicated patients may require assisted respiration.

  •  If a patient, however, has a sleep-related breathing syndrome such as obstructive sleep apnea (OSA), benzodiazepines may be contraindicated.

    • In this setting benzodiazepines may decrease muscle tone in the upper airway and accentuate the effect of apneic episodes on:

      •  Alveolar hypoxia

      •  Pulmonary hypertension

      •  Cardiac demand.

 

Central Nervous System

  • With increasing doses, benzodiazpines can progressive cause sedation, then hypnosis and then stupor.

  • Since awareness persists, benzodiazepines do not cause general anesthesia

  • Anti-anxiety / sedative-hypnotic properties

  • Some benzodiazepines are effective muscle relaxants (clonazepam (Klonopin)) , whereas most others ( diazepam (Valium)) are not.

 

[Hibbs, W.R, Rall, T.W., and Verdoorn, T.A., Hypnotics and Sedatives; Ethanol In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 364-367.]

 

Other Agents

Buspirone (BuSpar)

  • Buspirone is a non-benzodiazepine anxiolytic drug.

  • Site of action: 5-HT1A receptor subtype.

  • No anticonvulsant activity.

  • No interaction with benzodiazepine binding sites

  • No influence on interaction of GABA with the GABA receptor.

  • Not effective in management of severe anxiety/panic disorder.

  • No cross-tolerance with other sedative-hypnotic drugs

  • No muscle relaxant properties.

  • Minimal adverse effects

  Baldessarini, R. J., Drugs and the Treatment of Psychiatric Disorders, In, Goodman and Gillman's The Pharmacologial Basis of Therapeutics,(Hardman, J.G, Limbird, L.E, Molinoff, P.B., Ruddon, R.W, and Gilman, A.G.,eds) TheMcGraw-Hill Companies, Inc.,1996, pp. 425]

 

Anxiolytic-Sedative Hypnotic Drug List

Benzodiazepines

  • Alprazolam (Xanax)j

  • Clonazepam (Klonopin)

  • Diazepam (Valium)

  • Lorazepam (Ativan)

  • Triazolam (Halcion)

  • Flumazenil* (Romazicon)

*receptor antagonist

 

Barbiturates/
Anesthetics

  • Pentobarbital (Nembutal)

  • Phenobarbital (Luminal)

  • Thiopental (Pentothal)

Non-Depressant Anxiolytic

Buspirone (BuSpar)

Treatment of alcoholism

Disulfiram

 

 
 
 
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