Hypnotics depressants

This BZD sedative-hypnotic depresses the CNS at the limbic and subcortical levels of the brain. It potentiates the effect of GABA on its receptor, which increases inhibition and blocks cortical and limbic arousal. Temazepam is well absorbed through the gastrointestinal tract, with peak plasma levels in 1 to 3 hours. Onset of action occurs at 30 to 60 min. Temazepam is 98% protein bound, and its half-life ranges from 8 to 12 hours. 

TCA Sedative/hypnotics depression when used concomitantly... 

As a therapeutic class, hypnotics are nonselective CNS depressants that eflcit drowsiness and a natural sleep state from which the individual can be aroused. The effects of hypnotics are generally dose-dependent. 

Melatonin [73-31-4] C 2H N202 (31) has marked effects on circadian rhythm (11). Novel ligands for melatonin receptors such as (32) (12), C2yH2gN202, have affinities in the range of 10 Af, and have potential use as therapeutic agents in the treatment of the sleep disorders associated with jet lag. Such agents may also be usehil in the treatment of seasonal affective disorder (SAD), the depression associated with the winter months. Histamine (see Histamine and histamine antagonists), adenosine (see Nucleic acids), and neuropeptides such as corticotropin-like intermediate lobe peptide (CLIP) and vasoactive intestinal polypeptide (VIP) have also been reported to have sedative—hypnotic activities (7). 

Many patents have been issued on the use of pyrogaUol derivatives as pharmaceuticals. PyrogaUol has been used extemaUy in the form of an ointment or a solution in the treatment of skin diseases, eg, psoriasis, ringworm, and lupus erythematosus. GaUamine triethiodide (16) is an important muscle relaxant in surgery it also is used in convulsive-shock therapy. Trimethoprim (2,4-diamino-5-(3,4,5-trimethoxybenzyl)pyrimidine) is an antimicrobial and is a component of Bactrin and Septra. Trimetazidine (l(2,3,4-trimethoxybenzyl)piperazine (Vastarel, Yosimilon) is used as a coronary vasodilator. l,2,3,4-Tetrahydro-6-methoxy-l-(3,4,5-trimethoxyphenyl)-9JT-pyrido[3,4- ]indole hydrochloride is useful as a tranquilizer (52) (see Hypnotics, sedatives, ANTICONVULSANTS, AND ANXIOLYTICS). Substituted indanones made from pyrogaUol trimethyl ether depress the central nervous system (CNS) (53). Tyrosine-and glycine(2,3,4-trihydroxybenzyl)hydrazides are characterized by antidepressant and anti-Parkinson activity (54). 

Benzodiazepiaes have largely replaced barbiturates and barbiturate-like agents for use as anxiolytics and sedative—hypnotics. Because benzodiazepiaes rarely produce levels of CNS depression that require therapeutic iatervention, the need for analeptics has decreased considerably. 

Miscellaneous or nonbarbiturate sedatives and hypnotics have essentially the same mode of action as the barbiturates, that is, they depress the CNS. However,... 

Because narcoticanalgesicsdepressthe CNS(see Chap. 19), the nurse should not administer a barbiturate or miscellaneous sedativesand hypnoticsapproximately 2 hoursbefore or after administration of a narcoticanalgesic or other CNS depressant. If the time interval between administration of a narcotic analgesic and a sedative or hypnotic is less than 2 hours the patient may experien ce severe respiratory depres-son, bradycardia, and unresponsiveness. 

If the patient lias an order for a PRN narcotic analgesic or odier CNS depressant and a hypnotic, die nurse should consult die primary healdi care provider regarding die time interval between administration of tiiese drugp. Usually at least 2 hours should elapse between administration of a hypnotic and any odier CNS depressant, but this interval may vary, depending on factors such as die patient s age and diagnosis. 

Use With Alcohol. Alcohol is a CNS depressant, as are the sedatives and hypnotics. When alcohol and a sedative or hypnotic are taken together, there is an additive effect and an increase in CNS depression, which has, on occasion, resulted in death. The nurse must emphasize tiie importance of not drinking alcohol while taking this drug and stress that the use of alcohol and any one of these drains can result in serious effects. 

The antiemetics and antivertigo drug may have additive effects when used with alcohol and other CNS depressants such as sedatives, hypnotics, antianxiety drugp, opiates, and antidepressants. There may be additive anticholinergic effects (see Chap. 25) when administered with drag s that have anticholinergic activity such as the antihistamines, antidepressants, pheno-thiazines, and disopyramide The antacids decrease absorption of the antiemetics. 

The antidiarrheal drugs cause an additive CNS depression when administered with alcohol, antihistamines, narcotics, and sedatives or hypnotics. There are additive cholinergic effects when administered with other drugp having anticholinergic activity, such as antidepressants or antihistamines. Concurrent use of the antidiarrheals witii a monoamine oxidase inhibitor increases the risk of a hypertensive crisis. 

Respiratory drive and rhythm are depressed by barbiturates. Coughing, sneezing, hiccupping, and laryngospasm may occur during anesthesia with barbiturates. Sedative ot hypnotic doses of barbiturates teduce heatt tate and blood pressure to levels found in normal sleep. Anesthetic doses produce more pronounced effects. Barbiturates cross the placenta when used in labor, they can cause respiratoty depression in neonates. Anesthetic doses dectease force and frequency of uterine contractions among pregnant women. 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

Setting aside the general anaesthetics, which do not directly modify the function of any particular neurotransmitter, all the drugs that are used to induce sleep, i.e. the hypnotics , augment the function of GABA and so directly depress neuronal function and probably facilitate cortico-thalamic synchrony. Most of them are benzodiazepines... 

Hypnotics induce states of drowsiness and facilitate the onset and continuation of sleep resembling natural sleep [32]. Central nervous system (CNS) functions, in addition to the maintenance of wakefulness, are usually depressed by these drugs. Barbiturates, clinically... 

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