Sedative-Hypnotic Drugs.

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1 Sedative-Hypnotic Drugs.

2 Anxiety Term used to describe both symptoms and disorders Occurs normally as signal of impending danger or threat Very common, occurs in many disorders in addition to the anxiety disorders Differentiated from fear on basis of whether there is a clear source of danger i.e. fight or flight response Adaptive value : helps to plan and prepare for threat moderate levels enhance learning and performance Maladaptive when chronic / severe

3 Anxiety Symptoms include : physiological symptoms of activated sympathetic nervous system (increased heart rate, increased respiration, sweating etc.) cognitive component (awareness of being frightened) behavioral components (urge to escape)

4 Anxiety Disorders (DSM-IV) Panic disorder with or without agoraphobia Agoraphobia without panic disorder Specific phobias Social phobia Obsessive compulsive disorder Posttraumatic stress disorder Acute stress disorder Generalized anxiety disorder Anxiety disorder due to a general medical condition Substance-induced anxiety disorder Anxiety disorder not otherwise specified

5 Anxiety Disorders: Prevalence 17% 13% Lifetime Prevalence 7.8% of Anxiety Disorders: 25% 5% 3.5% 2.5% Kessler RC, et al. Arch Gen Psychiatry 1994;51:8-19 Stein MB, et al. JAMA 1998;280: Kessler RC, et al. Arch Gen Psychiatry 1995;52:

6 Neurobiology of Anxiety Disorders CNS equilibrium is determined by a balance between excitatory and inhibitory neurotransmission Excitation -> Glutamate is prototypical NT. Inhibition -> GABA is prototypical NT. Inhibition via GABA is primarily mediated by the ionotropic GABA-A receptor. GABA binding to GABA-A results in an increase in neuronal Cl - conductance and subsequent neuronal hyperpolarization.

7 Neurobiology of Anxiety Disorders GABA Receptor Benzodiazepines major class of anxiolytic drugs. Act primarily via a selective binding sites on the GABA-A receptor. - high-affinity site. - low-affinity site. POTENTIATE the effects of GABA at the GABA-A receptor.

8 Anxiolytic drugs Benzodiazepines. Buspirone. Beta-blockers. Antideprassants.

9 Benzodiazepines Diazepam. Lorazepam Midozolam.

10 Mechanism of action All anxiolytic drugs decrease anxiety by reducing overactivity in the CNS.

11

12

13 Indications Anxiety Insomnia Sedation Muscle spasms Seizure disorders Adjuncts in anesthesia Adjuvant therapy for depression Alcohol (ethanol) withdrawal

14 Toxicity Somnolence, Confusion, Coma, and Diminished reflexes Do not cause hypotension and respiratory depression unless taken with other CNS depressants Treatment: symptomatic and supportive. Use Flumazenil as an antidote.

15 Diazepam It has varied uses: Treatment of anxiety. Anesthesia adjunct. Anticonvulsant therapy. Skeletal muscle relaxation.

16 Diazepam

17 Buspirone No sedative action. No risk of dependence. Nausea and headache.

18 Beta blockers: propranolol. Antidepressants.

19 Insomnia Insomnia can, however, cause feelings of anxiety, inability to concentrate. Reasons????????

20 physiology of sleep Sleep is defined as a transient, reversible, and periodic state of rest in which there is a decrease in physical activity and consciousness. Sleep architecture: Rapid eye movement (REM) sleep. Non-REM sleep. Prolonged sedative-hypnotic use lead to REM interference. On discontinuance of a sedative-hypnotic drug, REM rebound can occur.

21 Pharmacology overview Benzodiazepines. Nonbezodiazepines: Zaleplon and zolpidem. Ramelteon. Barbiturates.

22 Nonbenzodiazepines Nonbenzodiazepines function as benzodiazepine but are chemically distinct from them. Zaleplon and zolpidem.

23 Barbiturates: Four Categories Ultra short-acting Thiopental Short-acting Pentobarbital, secobarbital Intermediate-acting Butabarbital Long-acting Phenobarbital.

24 Barbiturates: Four Categories Ultra short-acting Anesthesia for short surgical procedures, other uses Short-acting Sedation/sleep induction and control of convulsive conditions Intermediate-acting Sedation/sleep induction and control of convulsive conditions Long-acting Sleep induction, epileptic seizure prophylaxis

25 Barbiturates: Mechanism of Action

26 Antihistamines : promethazine

27 Nursing Implications Give hypnotics 30 to 60 minutes before bedtime. benzodiazepines cause REM rebound. Instruct patients to avoid CNS depressants

28 Nursing Implications (cont d) Rebound insomnia may occur for a few nights after a 3- to 4-week regimen has been discontinued

29 Nursing Implications (cont d) Safety is important Keep side rails up, or use bed alarms Do not permit smoking Assist patient with ambulation (especially the elderly) Keep call light within reach Monitor for adverse effects

30 Drugs useful in the treatment of anxiety disorders. Generic name Trade name Half-life (hrs) Dosage (mg/day) Long-acting benzodiazepines Diazepam Valium Chlordiazepoxide Librium Clorazepate Tranxene Estazolam ProSom Prazepam Centrax Quazepam Doral Halazepam Paxipam Clonazepam* Klonopin Flurazepam+ Dalmane Short-acting benzodiazepines Oxazepam Serax Lorazepam Ativan Alprazolam Xanax Temazepam+ Restoril Triazolam+ Halcion Midazolam# Versed Non-benzodiazepine sedative/hypnotics Buspirone (BuSpar) Zolpidem (Ambien) Meprobamate (Miltown) Chloral hydrate (Noctec) Serotonin 1a agonist binds to benzodiazepine receptor * marketed as an anti-convulsant +marketed as a hypnotic #parenteral only

31 Statement from the British Committee for the Review of Medicines. All benzodiazepines are efficacious in the shortterm treatment of anxiety and insomnia. There is no evidence which can justify the particular use of any particular benzodiazepine in either anxiety or insomnia. The usual division of benzodiazepines into rigid treatment categories of antianxiety agents and hypnotics does not appear to be based on the known pharmacological or clinical properties of this group of compounds. Caveat different benzodiazepines have additional actions (i.e., muscle relaxants, anticonvulsants, anesthetics) and different half-lives.

32 Benzodiazepines - Properties Prototypical Benzodiazepine = Diazepam (Valium). Highly lipophilic well-absorbed orally and easily crosses the blood-brain and blood-placental barriers. Hepatic metabolism converted to hydrophilic metabolites for renal elimination. Metabolite = desmethyldiazepam Same metabolite for diazepam, chlordiazepam, prazepam, and clorazepate. Desmethyldiazepam itself is pharmacologically active as an anxiolytic. Desmethyldiazepam is converted to oxazepam in the liver. Short-acting metabolite. Directly glucuronidated (as is lorazepam and flurazepam) and excreted by the kidney.

33 Benzodiazepines - Properties Pharmacological Effects: Reduction of anxiety. Induction of sleep. Anesthesia some benzodiazepines. Respiratory depression not as great as observed with barbiturates. Adverse Effects primarily observed at plasma concentrations exceeding anxiolytic range. Expected side effects: sedation, ataxia, dependence. Impaired cognition and motor function. Confusion. Amnesia. Fatal overdose is uncommon, except when taken with alcohol.

34 Benzodiazepines - Properties Benzodiazepines may induce tolerance in some individuals. Discontinuation of benzodiazepine therapy in tolerant patients MUST be gradual. Avoid hyperexcitability and possible seizures (more common with short-acting benzodiazepines). Block sedative side-effects of benzodiazepines with flumazenil (benzodiazepine receptor antagonist). Precipitate withdrawal symptoms in patients dependent on benzodiazepines (i.e., anxiety, insomnia, convulsions).

35 Benzodiazepines - Indications Anxiety and Insomnia Sedation Mania Drug-induced hyperexcitability PCP intoxication. Spasticity Cerebral Palsy Tetanus toxin toxicity. Anesthesia Alcohol withdrawal syndrome. Seizures. Clonazepam in myoclonic disorders. Diazepam, midazolam, and lorazepam in status epilepticus. Only effective early during status epilepticus. Evidence for seizure-induced translation change in GABA-A subunit expression.

36 Benzodiazepines Mechanism of Action GABA Receptor GABA-A receptors highly variable (i.e., consist of different complements of alpha, beta, and gamma subunits). = different sensitivities to benzodiazepines. = α2 subunit is critical in sedative effects. Benzodiazepines do NOT activate the receptor directly. = increase frequency of chloride-channel opening produced by GABA.

37 Autoradiography of GABA-A Receptors. α2 subunit Data shows that α2 subunit is localized to limbic system = Sedation. α3 subunit Further evidence sitedirected mutagenesis against α2 subunit eliminates sedative effects of benzodiazepines.

38 Pharmacological Effects of Benzodiazepines are Concentration-Dependent. Nanomolar Concentrations Anxiolytic sedation via α2 subunit. Action effectively blocked by flumazenil. Micromolar Concentrations Anesthesia diazepam, midazolam, lorazepam. Activity due to binding of benzodiazepines to lowaffinity site on GABA-A receptor.

39 Practical Points regarding Benzodiazepines. Lowest effective dose for the shortest possible time. Minimizes dependence and withdrawal. Discontinuance withdrawal is most common with shortacting benzodiazepines. Cessation of long-acting drugs produces a tapering effect due to long elimination half-life. Patients on short-acting benzodiazepines need weeks to months to be weaned. Generally, benzodiazepines are safe drugs with few medical complications and do not interact adversely with other medications.

40 Newer sedative/hypnotic drugs. Different mechanisms of action as compared to benzodiazepines. Do not act on GABA-A receptors. May interact only with specific GABA-A receptor subunits. Designed to produce anxiolytic effects without undesirable side effects associated with benzodiazepines. Daytime sedation and drowsiness. CNS depression in combination with alcohol. Potential for dependence.

41 Buspirone (BuSpar ) Partial agonist at the serotonin 1a receptor. Relieves anxiety without producing sedation, impairment of motor skills, or memory loss. Does not induce withdrawal symptoms upon discontinuation. Does not act immediately. Can take up to 1 week to become effective. Used for chronic anxiety states. Pharmacokinetics: Rapidly absorbed orally. Rapid first-pass effect. Elimination half-life = 2-4 hrs. Metabolism is primarily hepatic.

42 Serotonin Pathways in the CNS

43 Serotonin and Anxiety Serotonin supported by efficacy of SSRIs major nuclei: CRN limbic/ prefrontal cortex structures Mediates fear/ anticipatory anxiety RRN prefrontal cortex, basal ganglia, thalamus, limbic cortex, substantia nigra, periaqueductal grey Modulates cognitive/ behavioural components strong feedback relationship with limbic cortex.

44 Zolpidem (Ambien ) Produces sedative properties by binding selectively to α1-subunit. Same site that also binds benzodiazepines. Evidence pharmacological effects blocked by flumazenil. Structurally unrelated to benzodiazepines. Used clinically for treatment of insomnia. Minimal muscle relaxing and anticonvulsant effects. Less potential for dependence and withdrawal. Pharmacokinetics: Elimination half-life = hrs. Largely metabolized in the liver.

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