Barbiturates causing

Barbiturates do not raise the pain threshold and have no analgesic property. In anesthetic doses, they depress all areas of the CNS, including the hypothalamic thermoregulatory system, respiratory center, and vasomotor centers, as well as the polysynaptic pathways in the spinal column. In addition, some, such as phenobarbital, but not all, are anticonvulsants. In toxic doses, barbiturates cause oliguria. 

CNS Barbiturates cause drowsiness, impaired concentration, and mental and physical sluggishness. 

Barbiturates cause significant centrally mediated respiratory depression and overdose or rapid... 

The pharmacological effects of the barbiturates is invariably marked by a decrease with regard to the normal functional activities in the brain. It has been duly observed that at the prevailing therapeutic dose levels in vivo the barbiturates cause a distinct marked enhancement of the GABAergic inhibitory response, in a mechanism very much akin to that shown by the benzodiazepines, that is, by influencing conductance at the site of chloride channel. It is pertinent to mention here that at comparatively higher concentration barbiturates would display six marked and pronounced pharmacological actions ... 

The barbiturates also cause a physical dependence different from the opioid narcotics. In an individual addicted to barbiturates, the barbiturates should not be withdrawn abruptly but, rather, tapered slowly. Sudden withdrawal of the barbiturates can precipitate extreme agitation and grand mal seizures. This can lead to a spasm of the respiratory musculature, producing impaired respiration, cyanosis, and possibly, death (42). As a rule, drug dependence is followed by tolerance, in which increasing doses are required to obtain the same pharmacological effect. Because barbiturates cause tolerance and, often, dependence, their use as a hypnotic rarely is justified. 

The barbiturates are substituted pyrimidine derivatives with an ureide configuration (Fig. 20.4). They are lipophilic weak acids (pKa 7-8) that are weii distributed into brain (see Appendix A for the respective pKa values). Although many barbiturates dispiay sedative-hypnotic activity (see Chapter 19), oniy a few have antiseizure properties. Paradoxically, many barbiturates cause convulsions at larger doses. The barbiturates clinically useful as AEDs are phenobarbital, mephobarbital, and primidone (Fig. 20.8). In laboratory animals, phenobarbital is effective by several tests in nontoxic doses. It is active against electrically induced seizures (MES), and it elevates the threshold for pentylenetetrazole stimulation. The mechanism of antiseizure action for the barbiturates... 

Ingestion of carbon tetrachloride can be fatal to humans, death resulting from acute liver or kidney necrosis. Chronic exposure may cause liver and kidney damage. Exposure to a 10-ppm concentration for several weeks produced accumulation of fat in the livers of experimental animals (ACGIH 1986). Substances such as ethanol and barbiturates cause potentiation of toxicity of carbon tetrachloride. Skin contact can cause dermatitis. 

A. All barbiturates cause generalized depression of neuronal activity in the brain. Interaction with a barbiturate receptor leads to enhanced gamma-aminobutyric acid (GABA)-mediated chloride currents and results in synaptic inhibition. Hypotension that occurs with large doses is caused by depression of central sympathetic tone as well as by direct depression of cardiac contractility. 

Methohexital [18652-93-2] (Brevital), C 4H gN202, (2) is a barbiturate iv anesthetic iaduction agent that has a slightly faster onset than thiopentone and less accumulation. The recovery from anesthesia is also slightly faster and better. However, iaduction is associated with an iacreased iacidence of excitatory phenomena. Methohexital also causes respiratory and cardiovascular depression and is unstable ia solution, necessitating reconstitution before use (99). 

Note The reaction for barbiturates according to variant I is increased in sensitivity if the chromatogram is exposed to direct sunlight or UV light after it has been sprayed this causes the background coloration to fade almost completely and the blue zones stand out more distinctly [4]. 

A thiazole derivative that incorporates a fragment of the amphetamine molecule shows some CNS stimulant activity more specifically, the compound antagonizes the depression caused by overdoses of barbiturates and narcotics. Reaction of benzalde-hyde with sodium cyanide and benzenesulfonyl chloride gives the toluenesulfony1 ester of the cyanohydrin (141). Reaction of this with thiourea leads directly to aminophenazole (143) It is probable the reaction proceeds by displacement of the tosylate by the thiourea sulfur to give 142 addition of the amino group to the nitrile followed by tautomerization affords the observed product. ... 

Propyl-methyl-carbinyl allyl barbituric acid (also called allyl 1-methyl-butyl barbituric acid) may be prepared as follows 1 mol of propyl-methyl-carbinyl barbituric acid is dissolved in a suitable vessel In a 10 to 35% aqueous solution of 1 mol of potassium hydroxide. To this are added somewhat in excess of 1 mol of allyl bromide, and alcohol equal to about 10% of the total volume of the solution. The vessel Is agitated for 50 to 75 hours. At the end of this time, the solution, which may still exhibit two layers, is concentrated to about one-half its volume to remove the excess allyl bromide and the alcohol. On cooling, an oily layer, which is propyl-methyl-carbinyl allyl barbituric acid, separates out as a sticky viscous mass. It is dried, washed with petroleum ether, and dissolved in the minimum amount of benzene. Any unreacted propyl-methyl-carbinyl barbituric acid, which does not dissolve, is filtered off. The addition of petroleum ether to the clear filtrate causes the propyl-methyl-carbinyl allyl barbituric acid to precipitate as an oily mass. 

Acetaminophen may alter blood glucose test results, causing falsely lower blood glucose values. Use with the barbiturates, hydantoins, isoniazid, and rifampin may increase the toxic effects and possibly decrease the therapeutic effects of acetaminophen. The effects of the loop diuretics may be decreased when administered with acetaminophen. Hepatotoxicity has occurred in chronic alcoholics who are taking moderate doses of acetaminophen. 

Barbiturates have litde or no analgesic action, so the nurse does not give these drug if die patient has pain and cannot sleep. Barbiturates, when given in the presence of pain, may cause restiessness, excitement, and delirium. 

MONITORING AND MANAGING RESPIRATORY DEPRESSION These drugs depress the CNS and can cause respiratory depression. The nurse carefully assesses respiratory function (rate, depth, and quality) before administering a sedative, Vs, to 1 hour after administering the drug, and frequently thereafter. Toxic reaction of the barbiturates can cause severe respiratory depression, hypoventilation, and circulatory collapse. 

A. barbiturates, if given in the presence of pain, may cause excitement or delirium... 

As with the barbiturates, the most common adverse reaction seen with the use of clonazepam (Klonopin), clorazepate (Tranxene), and diazepam (Valium) is sedation in varying degrees. Additional adverse effects may include anorexia, constipation, or diarrhea. Some adverse reactions are dose dependent, whereas others may diminish in intensity or cause few problems after several weeks of therapy. 

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. 

There are similarities between the biological actions of inhalants and those of alcohol and barbiturates (Bowen et al. 1996b). For example, acute administration of inhalants affects motor coordination (Moser and Balster 1981) and induces anxiolysis, whereas chronic administration is associated with physical dependence and withdrawal (Bowen et al. 1996a Evans and Balster 1991, 1993). In addition, some inhalant drugs have anticonvulsant properties (Wood et al. 1984). Like other CNS-depressant agents, inhalants have biphasic effects on spontaneous locomotor activity in rodents, with increased activity seen at lower doses and diminished locomotion seen at higher doses (Cause et al. 1985 Kjellstrand et al. 1985). 

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