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Nervous system drugs depression

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. [Pg.191]

All barbiturates have essentially die same mode of action. Depending on the dose given, tiiese drags are capable of producing central nervous system (CNS) depression and mood alteration ranging from mild excitation to mild sedation, hypnosis (sleep), and deep coma These drugs also are respiratory depressants the degree of depression... [Pg.237]

There is an increased risk for bone marrow suppression when levamisole or hydroxyurea are administered witii other antineoplastic dni. Use of levamisole witii phenytoin increases die risk of phenytoin toxicity. Pegaspargase may alter drug response of the anticoagulants. When procarbazine is administered with other central nervous system (CNS) depressants, such as alcohol, antidepressants, antihistamines, opiates, or the sedatives, an additive CNS effect may be seen. Procarbazine may potentiate hypoglycemia when administered witii insulin or oral antidiabetic dru . ... [Pg.594]

In Chapter 9 we were introduced to another class of drugs - central nervous system (CNS) depressants. This class of drugs includes many that are used for their anxiety-reducing properties. Alcohol is the most widely used of our recreational depressants, and its use has immense health costs for society. Furthermore, alcohol, unlike most of the other recreational drugs we have encountered, is legal in most countries. It produces a clear pattern of intoxication, with equally clear dose-related deficits. Intoxication depends on a number of factors including personality and other... [Pg.225]

It is a reduction/decrease in the activity of specialized cells. For example barbiturates depress central nervous system, quinidine depresses myocardium. Certain drugs stimulate one type of cells but depress others e.g. morphine stimulates the vagus and chemoreceptor trigger zone but depresses the vomiting and cough centres. Similarly acetylcholine stimulates intestinal smooth muscle but depresses SA node in the heart. [Pg.40]

More important than numerical data are the clinical implications of differences between the two countries. The largest differences have narrowed since the previous study, but important categories in which the U.S. still lagged behind Britain in December 1976 included cardiovascular drugs, peptic ulcer treatment, and central nervous system drugs—including therapies for depression, epilepsy, and migraine. [Pg.147]

Barbiturates are among the drugs classified as central nervous system (CNS) depressants. These drugs depress or slow down the activity of nerves that control emotions and bodily functions such as breathing. Barbiturates are prescribed as a sedative that calms the patient or as a hypnotic that helps a person sleep. Other uses include epilepsy treatment and anesthesia before surgery. [Pg.59]

There are three major classes of prescription drugs of abuse opioids, central nervous system (CNS) depressants, and stimulants. Opioids are medications often prescribed to treat pain. They work on special parts of the brain to relieve... [Pg.14]

Like Rohypnol, GHB is a central nervous system (CNS) depressant, which, when tested on animals, induces a sleep-like state in doses ranging from 0.1 to 1.5 milligrams per kilogram.33 Although many neurotransmitter systems are affected by treatment with GHB, evidence supports the hypothesis that GHB itself acts as a neurotransmitter. This implies that GHB is a naturally occurring chemical in the body that is necessary for normal nervous system functions. Administered as a drug, GHB has been shown to temporarily inhibit the release of dopamine in the brain.34 This inhibition is followed by a marked increase in the release of both dopamine and naturally occurring opioids, such as endorphins.35... [Pg.40]

Many of the examples quoted involve central nervous system drugs. This is very important, as gender-related prescription usage is heavily weighted in this area toward women. The FDA 1985 drug utilization report showed that for benzodiazepines, the increased usage in women outnumbers men by 2 1 (339 vs. 171 prescriptions/ 1000 women and men, respectively). Twice as many women are treated for depression and anxiety neurosis than men, first described by Raskin (1974), and confirmed by Weissman and Klerman (1977). It is by no means certain that this is solely due to biochemical differences, for women are more likely to seek help than men. Of importance from the prior discussion is that, if women are... [Pg.212]

What physical manifestations are seen with increasing central nervous system (CNS) depression (increasing dose of sedative-hypnotic drugs) ... [Pg.24]

The oxazohdinedion are contraindicated in patients with known hypersensitivity to the dru. Trimeth-adione is classified as a R nancy Cat ory D drug and is contraindicated during pr nancy and lactation. Trimethadione is used with caution in patients with eye disorders (, retinal or optic nerve disease), liver or kidney disease, and neurologic disorders. When trimethadione is used with otiier nervous system (CNS) depressants (, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. [Pg.258]

Meyer and Overton further expanded their theory and suggested that the correlation may be established and observed between lipid solubility and the central nervous system (CNS) depressant aetivity profde. The CNS-depressant activity is foimd to be directly proportional to the partition coefficient of the drug substance . [Pg.24]

Older medications, such as the barbiturates, are used as sedative-hypnotics, but toxicity limits their widespread use. For example, they can cause significant central nervous system (CNS) depression, physical dependence, and tolerance. Additionally, they are potent inducers of liver enzymes, which can lead to clinically significant drug interactions when these medications are administered with other drugs extensively metabolized by the liver. [Pg.736]


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See also in sourсe #XX -- [ Pg.297 , Pg.301 ]




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