Anxyolitics& hypnotics


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Anxyolitics& hypnotics

  2. 2. <ul><li>Optimal </li></ul><ul><li>Performance </li></ul>Sedated Nervous Breakdown Performance Anxiety GOAL
  3. 3. <ul><li>Normal </li></ul><ul><ul><ul><ul><li> </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Relief from Anxiety </li></ul></ul></ul></ul><ul><ul><li>_________  _________________ </li></ul></ul><ul><ul><ul><li>SEDATION </li></ul></ul></ul><ul><ul><ul><li>(Drowsiness/decrease reaction time) </li></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><li>HYPNOSIS </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Confusion, Delirium, Ataxia </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> Surgical Anesthesia </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  Depression of respiratory and vasomotor center in the brainstem </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> COMA </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> DEATH </li></ul></ul></ul></ul></ul>
  4. 4. SEDATIVE/HYPNOTICS ANXIOLYTICS <ul><li>Major therapeutic use is to relief anxiety (anxiolytics) or induce sleep (hypnotics). </li></ul><ul><li>Hypnotic effects can be achieved with most anxiolytic drugs just by increasing the dose. </li></ul><ul><li>The distinction between a &quot;pathological&quot; and &quot;normal&quot; state of anxiety is hard to draw, but in spite of, or despite of, this diagnostic vagueness, anxiolytics are among the most prescribed substances worldwide. </li></ul>
  5. 5. Manifestations of anxiety : <ul><li>Verbal complaints. The patient says he/she is anxious, nervous, edgy. </li></ul><ul><li>Somatic and autonomic effects . The patient is restless and agitated, has tachycardia, increased sweating, weeping and often gastrointestinal disorders. </li></ul><ul><li>Social effects . Interference with normal productive activities. </li></ul>
  6. 6. Pathological Anxiety <ul><li>Generalized anxiety disorder (GAD) : People suffering from GAD have general symptoms of motor tension, autonomic hyperactivity, etc. for at least one month. </li></ul><ul><li>Phobic anxiety : </li></ul><ul><ul><li>Simple phobias. Agoraphobia, fear of animals, etc. </li></ul></ul><ul><ul><li>Social phobias. </li></ul></ul><ul><li>Panic disorders : Characterized by acute attacks of fear as compared to the chronic presentation of GAD. </li></ul><ul><li>Obsessive-compulsive behaviors : These patients show repetitive ideas (obsessions) and behaviors (compulsions). </li></ul>
  7. 7. Causes of Anxiety <ul><li>1). Medical : </li></ul><ul><ul><li>Respiratory </li></ul></ul><ul><ul><li>Endocrine </li></ul></ul><ul><ul><li>Cardiovascular </li></ul></ul><ul><ul><li>Metabolic </li></ul></ul><ul><ul><li>Neurologic . </li></ul></ul>
  8. 8. Causes of Anxiety <ul><li>2). Drug-Induced : </li></ul><ul><ul><li>Stimulants </li></ul></ul><ul><ul><ul><li>Amphetamines, cocaine, TCAs, caffeine. </li></ul></ul></ul><ul><ul><li>Sympathomimetics </li></ul></ul><ul><ul><ul><li>Ephedrine, epinephrine, pseudoephedrine phenylpropanolamine. </li></ul></ul></ul><ul><ul><li>AnticholinergicsAntihistaminergics </li></ul></ul><ul><ul><ul><li>Trihexyphenidyl, benztropine, meperidine diphenhydramine, oxybutinin. </li></ul></ul></ul><ul><ul><li>Dopaminergics </li></ul></ul><ul><ul><ul><li>Amantadine, bromocriptine, L-Dopa, carbid/levodopa. </li></ul></ul></ul>
  9. 9. Causes of Anxiety <ul><ul><li>Miscellaneous: </li></ul></ul><ul><ul><ul><li>Baclofen, cycloserine, hallucinogens, indomethacin . </li></ul></ul></ul><ul><li>3). Drug Withdrawal : </li></ul><ul><ul><ul><li>BDZs, narcotics, BARBs, other sedatives, alcohol. </li></ul></ul></ul>
  10. 10. Anxiolytics <ul><ul><li>Strategy for treatment </li></ul></ul><ul><ul><li>Reduce anxiety without causing sedation. </li></ul></ul>
  11. 11. Anxiolytics <ul><ul><li>Benzodiazepines (BZDs). </li></ul></ul><ul><ul><li>Barbiturates (BARBs). </li></ul></ul><ul><ul><li>5-HT 1A receptor agonists. </li></ul></ul><ul><ul><li>5-HT 2A , 5-HT 2C & 5-HT 3 receptor </li></ul></ul><ul><ul><li>antagonists. </li></ul></ul><ul><li>If ANS symptoms are prominent : </li></ul><ul><ul><li>ß-Adrenoreceptor antagonists. </li></ul></ul><ul><ul><li> 2 -AR agonists (clonidine). </li></ul></ul>
  12. 12. Anxiolytics <ul><li>Other Drugs with anxiolytic activity. </li></ul><ul><ul><li>TCAs (Fluvoxamine). Used for Obsessive compulsive Disorder. </li></ul></ul><ul><ul><li>MAOIs. Used in panic attacks. </li></ul></ul><ul><ul><li>Antihistaminic agents. Present in over the counter medications. </li></ul></ul><ul><ul><li>Antipsychotics (Ziprasidone). </li></ul></ul><ul><li>Novel drugs . (Most of these are still on clinical trials). </li></ul><ul><ul><li>CCK B (e.g. CCK 4 ). </li></ul></ul><ul><ul><li>EAA's/NMDA (e.g. HA966). </li></ul></ul>
  13. 13. Sedative/Hypnotics <ul><ul><li>A hypnotic should produce, as much as possible, a state of sleep that resembles normal sleep. </li></ul></ul>
  14. 14. Sedative/Hypnosis <ul><li>By definition all sedative/hypnotics will induce sleep at high doses. </li></ul><ul><li>Normal sleep consists of distinct stages, based on three physiologic measures: electroencephalogram, electromyogram, electronystagmogram. </li></ul><ul><li>Two distinct phases are distinguished which occur cyclically over 90 min: </li></ul><ul><li>1) Non-rapid eye movement (NREM). 70-75% of total sleep. 4 stages. Most sleep  stage 2. </li></ul><ul><li>2) Rapid eye movement (REM). Recalled dreams. </li></ul>
  15. 15. Properties of Sedative/Hypnotics in Sleep <ul><li>1) The latency of sleep onset is decreased (time to fall asleep). </li></ul><ul><li>2) The duration of stage 2 NREM sleep is increased. </li></ul><ul><li>3) The duration of REM sleep is decreased. </li></ul><ul><li>4) The duration of slow-wave sleep (when somnambulism and nightmares occur) is decreased. </li></ul><ul><li>Tolerance occurs after 1-2 weeks . </li></ul>
  16. 16. Other Properties of Sedative/Hypnotics <ul><li>Some sedative/hypnotics will depress the CNS to stage III of anesthesia. </li></ul><ul><li>Due to their fast onset of action and short duration, barbiturates such as thiopental and methohexital are used as adjuncts in general anesthesia. </li></ul>
  17. 17. Sedative/Hypnotics <ul><ul><li>Benzodiazepines (BZDs): </li></ul></ul><ul><ul><li>Alprazolam, diazepam, oxacepam, triazolam </li></ul></ul><ul><ul><li>2) Barbiturates: </li></ul></ul><ul><ul><li>Pentobarbital, phenobarbital </li></ul></ul><ul><ul><li>3) Alcohols: </li></ul></ul><ul><ul><li>Ethanol, chloral hydrate, paraldehyde, trichloroethanol, </li></ul></ul><ul><ul><li>4) Imidazopyridine Derivatives: </li></ul></ul><ul><ul><li>Zolpidem </li></ul></ul><ul><ul><li>5) Pyrazolopyrimidine </li></ul></ul><ul><ul><li>Zaleplon </li></ul></ul>
  18. 18. Sedative/Hypnotics <ul><ul><li>6) Propanediol carbamates: </li></ul></ul><ul><ul><li>Meprobamate </li></ul></ul><ul><ul><li>7) Piperidinediones </li></ul></ul><ul><ul><li>Glutethimide </li></ul></ul><ul><ul><li>Azaspirodecanedione </li></ul></ul><ul><ul><li>Buspirone </li></ul></ul><ul><ul><li>9)  -Blockers** </li></ul></ul><ul><ul><li>Propranolol </li></ul></ul><ul><ul><li>10)  2-AR partial agonist** </li></ul></ul><ul><ul><li>Clonidine </li></ul></ul>
  19. 19. Sedative/Hypnotics <ul><li>Others: </li></ul><ul><li>11) Antyipsychotics ** </li></ul><ul><li>Ziprasidone </li></ul><ul><li>12) Antidepressants ** </li></ul><ul><li>TCAs, SSRIs </li></ul><ul><li>13) Antihistaminic drugs ** </li></ul><ul><li>Dephenhydramine </li></ul>
  20. 20. Sedative/Hypnotics <ul><li>All of the anxiolytics/sedative/hypnotics should be used only for symptomatic relief. </li></ul><ul><li>************* </li></ul><ul><li>All the drugs used alter the normal sleep cycle and should be administered only for days or weeks, never for months. </li></ul><ul><li>************ </li></ul><ul><li>USE FOR </li></ul><ul><li>SHORT-TERM TREATMENT </li></ul><ul><li>ONLY!! </li></ul>
  21. 21. Sedative/Hypnotics <ul><li>Relationship between </li></ul><ul><li>Older vs Newer Drugs </li></ul><ul><li>Barbiturates Benzodiazepines </li></ul><ul><li>Glutethimide Zolpidem </li></ul><ul><li>Meprobamate Zaleplon </li></ul><ul><li>** All others differ in their effects and therapeutic uses. They do not produce general anesthesia and do not have abuse liability. </li></ul>
  23. 23. Sedative/Hypnotics <ul><li>The benzodiazepines are the most important sedative hypnotics. </li></ul><ul><li>Developed to avoid undesirable effects of barbiturates (abuse liability). </li></ul>
  24. 24. Benzodiazepines <ul><li>Diazepam </li></ul><ul><li>• Chlordiazepoxide </li></ul><ul><li>Triazolam </li></ul><ul><li>Lorazepam </li></ul><ul><li>Alprazolam </li></ul><ul><li>Clorazepate => nordiazepam </li></ul><ul><li>Halazepam </li></ul><ul><li>Clonazepam </li></ul><ul><li>Oxazepam </li></ul><ul><li>Prazepam </li></ul>
  25. 25. Barbiturates <ul><li>Phenobarbital </li></ul><ul><li>Pentobarbital </li></ul><ul><li>Amobarbital </li></ul><ul><li>Mephobarbital </li></ul><ul><li>Secobarbital </li></ul><ul><li>Aprobarbital </li></ul>
  26. 26. <ul><li>NORMAL </li></ul><ul><ul><ul><ul><li> </li></ul></ul></ul></ul><ul><ul><ul><ul><li>ANXIETY </li></ul></ul></ul></ul><ul><ul><li>_________  _________________ </li></ul></ul><ul><ul><ul><li>SEDATION </li></ul></ul></ul><ul><ul><ul><li>  </li></ul></ul></ul><ul><ul><ul><ul><li>HYPNOSIS </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Confusion, Delirium, Ataxia </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> Surgical Anesthesia </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  COMA </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>  </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> DEATH </li></ul></ul></ul></ul></ul>
  27. 27. Respiratory Depression Coma/ Anesthesia Ataxia Sedation Anxiolytic Anticonvulsant DOSE RESPONSE BARBS BDZs ETOH
  28. 28. Respiratory Depression Coma/ Anesthesia Ataxia Sedation Anxiolytic Anticonvulsant DOSE RESPONSE BARBS BDZs
  29. 29. GABAergic SYNAPSE GABA glutamate glucose Cl - GAD
  30. 30. GABA-A Receptor <ul><li>Oligomeric (  glycoprotein. </li></ul><ul><li>Major player in Inhibitory Synapses. </li></ul><ul><li>It is a Cl - Channel. </li></ul><ul><li>Binding of GABA causes the channel to open and Cl - to flow into the cell with the resultant membrane hyperpolarization. </li></ul>GABA AGONISTS BDZs    BARBs  
  31. 31. Mechanisms of Action <ul><li>1) Enhance GABAergic Transmission </li></ul><ul><ul><ul><li> frequency of openings of GABAergic channels. Benzodiazepines </li></ul></ul></ul><ul><ul><ul><li> opening time of GABAergic channels. Barbiturates </li></ul></ul></ul><ul><ul><ul><li> receptor affinity for GABA. BDZs and BARBS </li></ul></ul></ul><ul><li>2) Stimulation of 5-HT 1A receptors. </li></ul><ul><li>3) Inhibit 5-HT 2A , 5-HT 2C , and 5-HT 3 receptors. </li></ul>
  32. 32. Patch-Clamp Recording of Single Channel GABA Evoked Currents From Katzung et al., 1996
  33. 33. Benzodiazepines <ul><li>PHARMACOLOGY </li></ul><ul><li>BDZs potentiate GABAergic inhibition at all levels of the neuraxis. </li></ul><ul><li>BDZs cause more frequent openings of the GABA-Cl - channel via membrane hyperpolarization, and increased receptor affinity for GABA. </li></ul><ul><li>BDZs act on BZ 1 (  1 and  2 subunit-containing) and BZ 2 (  5 subunit-containing) receptors. </li></ul><ul><li>May cause euphoria, impaired judgement, loss of cell control and anterograde amnesic effects. </li></ul>
  34. 34. Pharmacokinetics of Benzodiazepines <ul><li>Although BDZs are highly protein bound (60-95%), few clinically significant interactions.* </li></ul><ul><li>High lipid solubility  high rate of entry into CNS  rapid onset. </li></ul><ul><li>*The only exception is chloral hydrate and warfarin </li></ul>
  35. 35. CNS Effects (Rate of Onset) Lipid solubility
  36. 36. Pharmacokinetics of Benzodiazepines <ul><li>Hepatic metabolism. Almost all BDZs undergo microsomal oxidation (N-dealkylation and aliphatic hydroxylation) and conjugation (to glucoronides). </li></ul><ul><li>Rapid tissue redistribution  long acting  long half lives and elimination half lives (from 10 to > 100 hrs). </li></ul><ul><li>All BDZs cross the placenta  detectable in breast milk  may exert depressant effects on the CNS of the lactating infant. </li></ul>
  37. 37. Pharmacokinetics of Benzodiazepines <ul><li>Many have active metabolites with half-lives greater than the parent drug. </li></ul><ul><li>Prototype drug is diazepam (Valium), which has active metabolites (desmethyl-diazepam and oxazepam) and is long acting (t½ = 20-80 hr). </li></ul><ul><li>Differing times of onset and elimination half-lives (long half-life => daytime sedation). </li></ul>
  38. 38. Biotransformation of Benzodiazepines From Katzung, 1998
  39. 39. Biotransformation of Benzodiazepines <ul><li>Keep in mind that with formation of active metabolites, the kinetics of the parent drug may not reflect the time course of the pharmacological effect. </li></ul><ul><li>Estazolam, oxazepam, and lorazepam, which are directly metabolized to glucoronides have the least residual (drowsiness) effects. </li></ul><ul><li>All of these drugs and their metabolites are excreted in urine. </li></ul>
  40. 40. Properties of Benzodiazepines <ul><li>BDZs have a wide margin of safety if used for short periods. Prolonged use may cause dependence. </li></ul><ul><li>BDZs have little effect on respiratory or cardiovascular function compared to BARBS and other sedative-hypnotics. </li></ul><ul><li>BDZs depress the turnover rates of norepinephrine (NE), dopamine (DA) and serotonin (5-HT) in various brain nuclei. </li></ul>
  41. 41. Side Effects of Benzodiazepines <ul><li>Related primarily to the CNS depression and include: drowsiness, excess sedation, impaired coordination, nausea, vomiting, confusion and memory loss. Tolerance develops to most of these effects. </li></ul><ul><li>Dependence with these drugs may develop. </li></ul><ul><li>Serious withdrawal syndrome can include convulsions and death. </li></ul>
  42. 42. Sedative/Hypnotics <ul><ul><li>They produce a pronounce, graded, dose-dependent depression of the central nervous system. </li></ul></ul>
  43. 43. Toxicity/Overdose with Benzodiazepines <ul><li>Drug overdose is treated with flumazenil (a BDZ receptor antagonist, short half-life), but respiratory function should be adequately supported and carefully monitored. </li></ul><ul><li>Seizures and cardiac arrhythmias may occur following flumazenil administration when BDZ are taken with TCAs. </li></ul><ul><li>Flumazenil is not effective against BARBs overdose. </li></ul>
  44. 44. Drug-Drug Interactions with BDZs <ul><li>BDZ's have additive effects with other CNS depressants (narcotics), alcohol => have a greatly reduced margin of safety. </li></ul><ul><li>BDZs reduce the effect of antiepileptic drugs. </li></ul><ul><li>Combination of anxiolytic drugs should be avoided. </li></ul><ul><li>Concurrent use with ODC antihistaminic and anticholinergic drugs as well as the consumption of alcohol should be avoided. </li></ul><ul><li>SSRI’s and oral contraceptives decrease metabolism of BDZs. </li></ul>
  45. 45. Pharmacokinetics of Barbiturates <ul><li>Rapid absorption following oral administration. </li></ul><ul><li>Rapid onset of central effects. </li></ul><ul><li>Extensively metabolized in liver (except phenobarbital), however, there are no active metabolites . </li></ul><ul><li>Phenobarbital is excreted unchanged. Its excretion can be increased by alkalinization of the urine. </li></ul>
  46. 46. Pharmacokinetics of Barbiturates <ul><li>In the elderly and in those with limited hepatic function, dosages should be reduced. </li></ul><ul><li>Phenobarbital and meprobamate cause autometabolism by induction of liver enzymes. </li></ul>
  47. 47. Properties of Barbiturates <ul><li>Mechanism of Action. </li></ul><ul><ul><li>They increase the duration of GABA-gated channel openings. </li></ul></ul><ul><ul><li>At high concentrations may be GABA-mimetic. </li></ul></ul><ul><li>Less selective than BDZs, they also: </li></ul><ul><ul><li>Depress actions of excitatory neurotransmitters. </li></ul></ul><ul><ul><li>Exert nonsynaptic membrane effects. </li></ul></ul>
  48. 48. Toxicity/Overdose <ul><li>Strong physiological dependence may develop upon long-term use. </li></ul><ul><li>Depression of the medullary respiratory centers is the usual cause of death of sedative/hypnotic overdose. Also loss of brainstem vasomotor control and myocardial depression. </li></ul>
  49. 49. Toxicity/Overdose <ul><li>Withdrawal is characterized by increase anxiety, insomnia, CNS excitability and convulsions. </li></ul><ul><li>Drugs with long-half lives have mildest withdrawal (. </li></ul><ul><li>Drugs with quick onset of action are most abused. </li></ul><ul><li>No medication against overdose with BARBs. </li></ul><ul><li>Contraindicated in patients with porphyria . </li></ul>
  50. 50. Sedative/Hypnotics <ul><ul><li>Tolerance and excessive rebound occur in response to barbiturate hypnotics. </li></ul></ul>NREM III and IV REM 1 2 3 NIGTHS OF DRUG DOSING SLEEP PER NIGHT (%) CONTROL WITHDRAWAL
  51. 51. Miscellaneous Drugs <ul><li>Buspirone </li></ul><ul><li>Chloral hydrate </li></ul><ul><li>Hydroxyzine </li></ul><ul><li>Meprobamate (Similar to BARBS) </li></ul><ul><li>Zolpidem (BZ 1 selective) </li></ul><ul><li>Zaleplon (BZ 1 selective) </li></ul>
  52. 52. BUSPIRONE <ul><li>Most selective anxiolytic currently available. </li></ul><ul><li>The anxiolytic effect of this drug takes several weeks to develop => used for GAD. </li></ul><ul><li>Buspirone does not have sedative effects and does not potentiate CNS depressants. </li></ul><ul><li>Has a relatively high margin of safety, few side effects and does not appear to be associated with drug dependence. </li></ul><ul><li>No rebound anxiety or signs of withdrawal when discontinued. </li></ul>
  53. 53. BUSPIRONE <ul><li>Side effects: </li></ul><ul><ul><li>Tachycardia, palpitations, nervousness, GI distress and paresthesias may occur. </li></ul></ul><ul><ul><li>Causes a dose-dependent pupillary constriction. </li></ul></ul>
  54. 54. BUSPIRONE <ul><li>Mechanism of Action: </li></ul><ul><ul><li>Acts as a partial agonist at the 5-HT 1A receptor presynaptically inhibiting serotonin release. </li></ul></ul><ul><ul><li>The metabolite 1-PP has  2 -AR blocking action . </li></ul></ul>
  55. 55. Pharmacokinetics of BUSPIRONE <ul><li>Not effective in panic disorders. </li></ul><ul><li>Rapidly absorbed orally. </li></ul><ul><li>Undergoes extensive hepatic metabolism (hydroxylation and dealkylation) to form several active metabolites (e.g. 1-(2-pyrimidyl-piperazine, 1-PP) </li></ul><ul><li>Well tolerated by elderly, but may have slow clearance. </li></ul><ul><li>Analogs: Ipsapirone, gepirone, tandospirone . </li></ul>
  56. 56. Zolpidem <ul><li>Structurally unrelated but as effective as BDZs. </li></ul><ul><li>Minimal muscle relaxing and anticonvulsant effect. </li></ul><ul><li>Rapidly metabolized by liver enzymes into inactive metabolites. </li></ul><ul><li>Dosage should be reduced in patients with hepatic dysfunction, the elderly and patients taking cimetidine. </li></ul>
  57. 57. Properties of Zolpidem <ul><li>Mechanism of Action: </li></ul><ul><ul><li>Binds selectively to BZ 1 receptors. </li></ul></ul><ul><ul><li>Facilitates GABA-mediated neuronal inhibition. </li></ul></ul><ul><ul><li>Actions are antagonized by flumazenil </li></ul></ul>
  59. 59. Properties of Other drugs . <ul><li>Chloral hydrate </li></ul><ul><li>Is used in institutionalized patients. It displaces warfarin (anti-coagulant) from plasma proteins. </li></ul><ul><li>Extensive biotransformation . </li></ul>
  60. 60. Properties of Other Drugs <ul><li> 2-Adrenoreceptor Agonists (eg. Clonidine) </li></ul><ul><ul><li>Antihypertensive. </li></ul></ul><ul><ul><li>Has been used for the treatment of panic attacks. </li></ul></ul><ul><ul><li>Has been useful in suppressing anxiety during the management of withdrawal from nicotine and opioid analgesics. </li></ul></ul><ul><ul><li>Withdrawal from clonidine, after protracted use, may lead to a life-threatening hypertensive crisis . </li></ul></ul>
  61. 61. Properties of Other Drugs <ul><li> -Adrenoreceptor Antagonists </li></ul><ul><li>(eg. Propranolol) </li></ul><ul><ul><li>Use to treat some forms of anxiety, particularly when physical (autonomic) symptoms (sweating, tremor, tachycardia) are severe. </li></ul></ul><ul><ul><li>Adverse effects of propranolol may include: lethargy, vivid dreams, hallucinations. </li></ul></ul>
  62. 62. OTHER USES <ul><li>1. Generalized Anxiety Disorder </li></ul><ul><li>D iazepam, lorazepam, alprazolam, buspirone </li></ul><ul><li>2. Phobic Anxiety </li></ul><ul><ul><ul><li>a. Simple phobia. BDZs </li></ul></ul></ul><ul><ul><ul><li>b. Social phobia. BDZs </li></ul></ul></ul><ul><li>3. Panic Disorders </li></ul><ul><li>TCAs and MAOIs, alprazolam </li></ul><ul><li>4. Obsessive-Compulsive Behavior </li></ul><ul><li>C lomipramine (TCA), SSRI’s </li></ul><ul><li>5. Posttraumatic Stress Disorder (?) </li></ul><ul><ul><ul><li>Antidepressants, buspirone </li></ul></ul></ul>
  63. 63. Other Properties of Sedative/Hypnotics <ul><li>BDZs on the other hand, with their long half-lives and formation of active metabolites, may contribute to persistent postanesthetic respiratory depression. </li></ul><ul><li>Most sedative/hypnotics may inhibit the development and spread of epileptiform activity in the CNS. </li></ul><ul><li>Inhibitory effects on multisynaptic reflexes, internuncial transmission and at the NMJ. </li></ul>
  64. 64. <ul><li>ANXYOLITICS </li></ul><ul><li>Alprazolam </li></ul><ul><li>Chlordiazepoxide </li></ul><ul><li>Buspirone </li></ul><ul><li>Diazepam </li></ul><ul><li>Lorazepam </li></ul><ul><li>Oxazepam </li></ul><ul><li>Triazolam </li></ul><ul><li>Phenobarbital </li></ul><ul><li>Halazepam </li></ul><ul><li>Prazepam </li></ul><ul><li>HYPNOTICS </li></ul><ul><li>Chloral hydrate </li></ul><ul><li>Estazolam </li></ul><ul><li>Flurazepam </li></ul><ul><li>Pentobarbital </li></ul><ul><li>Lorazepam </li></ul><ul><li>Quazepam </li></ul><ul><li>Triazolam </li></ul><ul><li>Secobarbital </li></ul><ul><li>Temazepam </li></ul><ul><li>Zolpidem </li></ul>