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Sedative-hypnotic drugs effects

CNS-depressant effects Zolpidem, like other sedative/hypnotic drugs, has CNS-depressant effects. Because of the rapid onset of action, only ingest immediately prior to going to bed. Zolpidem had additive effects when combined with alcohol therefore, do not take with alcohol. [Pg.1180]

Respiratory ejects Although preliminary studies did not reveal respiratory depressant effects at hypnotic doses of zaleplon in healthy subjects, observe caution if zaleplon is prescribed to patients with compromised respiratory function because sedatives/hypnotics have the capacity to depress respiratory drive. Depression As with other sedative/hypnotic drugs, administer zaleplon with caution to patients exhibiting signs or symptoms of depression. Suicidal tendencies may be present in such patients and protective measures may be required. Intentional overdosage is more common in this group of patients therefore, prescribe the least amount of the drug that is feasible for the patient at any one time. [Pg.1184]

Buspirone is as effective as the benzodiazepines in the treatment of general anxiety. However, the full anxiolytic effect of buspirone takes several weeks to develop, whereas the anxiolytic effect of the benzodiazepines is maximal after a few days of therapy. In therapeutic doses, buspirone has little or no sedative effect and lacks the muscle relaxant and anticonvulsant properties of the benzodiazepines. In addition, buspirone does not potentiate the central nervous system depression caused by sedative-hypnotic drugs or by alcohol, and it does not prevent the symptoms associated with benzodiazepine withdrawal. [Pg.356]

Another chemical class of sedative-hypnotic drugs, the barbiturates, also binds to receptors associated with the GABA-chloride ionophore, but these drugs appear to prolong rather than intensify GABA s effects. Fig. 24.4 shows the presumed drug receptor-GABA-chloride ionophore relationship. [Pg.357]

The benzodiazepines (BZDs), which were introduced nearly 40 years ago, were hailed as a breakthrough because they have fewer of the drawbacks of prior anxiolytics and sedative-hypnotics, are effective in a range of disorders, and are safe in combination with most drugs (except other sedatives), as well as alone in overdose, and are generally mild in terms of side effects. For these reasons, BZDs quickly became, and remain, among the most widely prescribed drugs worldwide. [Pg.229]

Buspirone causes less psychomotor impairment than benzodiazepines and does not affect driving skills. The drug does not potentiate effects of conventional sedative-hypnotic drugs, ethanol, or tricyclic antidepressants, and elderly patients do not appear to be more sensitive to its actions. Nonspecific chest pain, tachycardia, palpitations, dizziness, nervousness, tinnitus, gastrointestinal distress, and paresthesias and a dose-dependent pupillary constriction may occur. Blood pressure may be significantly elevated in patients receiving MAO inhibitors. [Pg.473]

Benzodiazepines, barbiturates, and most older sedative-hypnotic drugs exert calming effects with concomitant reduction of anxiety at relatively low doses. In most cases, however, the anxiolytic actions of sedative-hypnotics are accompanied by some depressant effects on psychomotor and cognitive functions. In experimental animal models, benzodiazepines and older sedative-hypnotic drugs are able to disinhibit punishment-suppressed behavior. This disinhibition has been equated with antianxiety effects of sedative-hypnotics, and it is not a characteristic of all drugs that have sedative effects, eg, the... [Pg.478]

Buspirone Mechanism uncertain Partial agonist at 5-HT receptors but affinity for D2 receptors also possible Slow onset (1-2 weeks) of anxiolytic effects t minimal psychomotor impairment—no additive CNS depression with sedative-hypnotic drugs Generalized anxiety states Oral activity forms active metabolite short half-life Toxicity Tachycardia paresthesias t gastrointestinal distress Interactions CYP3A4 inducers and inhibitors... [Pg.486]

Nontolerant individuals who consume alcohol in large quantities develop typical effects of acute sedative-hypnotic drug overdose along with the cardiovascular effects previously described (vasodilation, tachycardia) and gastrointestinal irritation. Since tolerance is not absolute, even chronic alcoholics may become severely intoxicated if sufficient alcohol is consumed. [Pg.499]

An understanding of common mechanisms of death due to poisoning can help prepare the care-giver to treat patients effectively. Many toxins depress the central nervous system (CNS), resulting in obtundation or coma. Comatose patients frequently lose their airway protective reflexes and their respiratory drive. Thus, they may die as a result of airway obstruction by the flaccid tongue, aspiration of gastric contents into the tracheobronchial tree, or respiratory arrest. These are the most common causes of death due to overdoses of narcotics and sedative-hypnotic drugs (eg, barbiturates and alcohol). [Pg.1248]

Finally, some patients may die before hospitalization because the behavioral effects of the ingested drug may result in traumatic injury. Intoxication with alcohol and other sedative-hypnotic drugs is a common contributing factor to motor vehicle accidents. Patients under the influence of hallucinogens such as phencyclidine (PCP) or lysergic acid diethylamide (LSD) may suffer trauma when they become combative or fall from a height. [Pg.1249]

The extensive clinical use of triazolam has led to reports of serious central nervous system effects including behavioral disinhibition, delirium, aggression, and violence. While behavioral disinhibition may occur with sedative-hypnotic drugs, it does not appear to be more prevalent with triazolam than with other benzodiazepines. Disinhibitory reactions during benzodiazepine treatment are more clearly associated with the use of very high doses and the pretreatment level of patient hostility. [Pg.527]

Thiopental may reduce hepatic blood flow and glomerular filtration rate, but it produces no lasting effects on hepatic and renal function. Barbiturates may exacerbate acute intermittent porphyria by inducing the synthesis of hepatic ALA synthase (see Chapter 22 Sedative-Hypnotic Drugs). Thiopental has precipitated porphyric crisis when used as an induction agent in susceptible individuals. [Pg.600]

Finally, very rapid onset benzodiazepines have been widely reported as a means of "date rape," by using a small tasteless dose of the drug to make the victim incapable of protecting herself (or himself). This produces intoxication but not dependence. The drug most commonly used in this situation has been flunitrazepam (Rohypnol, "roofies," not available in the USA) and more recently GHB. The amnesia-producing effects of the benzodiazepines (see Chapter 22 Sedative-Hypnotic Drugs) make the victim unable to describe the events after she or he has recovered. [Pg.728]


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See also in sourсe #XX -- [ Pg.206 , Pg.206 ]




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