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Barbiturates acute toxicity

The onset of symptoms of barbiturate toxicity may not occur until several hours after the drug is administered. Symptoms of acute toxicity include CNSand respiratory depression, constriction or paralytic dilation of the pupils tachycardia, hypotension, lowered body temperature, oliguria, circulatory collapse, and coma. The nurse should report any symptoms of toxicity to the primary health care provider immediately. [Pg.243]

Chen G, Ensor CR, Bohner B (1966) The neuropharmacology of 2-(o-chlorophenyl)-2-methylaminocyclohexanone hydrochloride. J Pharm Exp Ther 152 332-339 Child KJ, Currie JP, Davis B et al. (1971) The pharmacological properties in animals of CT1341 - a new steroid anaesthetic agent. Br J Anaesth 43 2-24 Christensen HD, Lee IS (1973) Anesthetic potency and acute toxicity of optically active di-substituted barbituric acids. Toxicol Appl Pharmacol 26 495-503 Domenjoz R (1959) Anaesthesist 8 16... [Pg.211]

H, D. Christensen and I. S. Lee, Anesthetic potency and acute toxicity of opticaUy active disubstituted barbituric acids, Toxicol. Appl. Pharmacol., 26 496-503 (1973). [Pg.63]

Reports of signs and symptoms by patients such as noted in the Acute Toxicity section should be regarded as the onset of toxicity. Administration of anesthetics should be halted and proper supportive care initiated. Benzodiazepines can be given prophy-lactically to prevent or decrease the expected seizure activity. If seizures have begun, then benzodiazepines or fast-acting barbiturates such as pentothal can be given intravenously. [Pg.129]

Severe anaphylactic reactions following intravenous administration of diazepam have been reported. Meprobamate causes toxicity similar to that of a barbiturate overdosage. Death may result from respiratory failure or hypotension. Limited information is available about the acute toxicity of Buspirone. Effects are merely extensions of pharmacological effects. Nausea, vomiting, dizziness, drowsiness, miosis, and gastric distention may be seen. [Pg.152]

Phenytoin. Phenytoin sodium is sodium diphenylhydantoin [630-93-3] which is stmcturally related to the barbiturates. It was originally introduced as an anticonvulsant (18) (see Hypnotics, sedatives, and anticonvulsants) and later found to have antiarrhythmic properties (19), although not approved by the PDA for any arrhythmic indications. Phenytoin is effective in the treatment of ventricular arrhythmias associated with acute MI and with digitalis toxicity (20). It is not very effective in treatment of supraventricular arrhythmias (20). [Pg.113]

Barbiturates. The hrst barbiturate, barbital, was introduced in 1903 and was followed a few years later by phenobarbital. The barbiturates effectively relieve anxiety, but they are never used as anxiolytics today due to toxicity and abuse concerns. However, several barbiturates, including phenobarbital (Luminal), secobarbital (Seconal), and pentobarbital (Nembutal), remain available and are occasionally used to treat epilepsy and rarely to manage acute alcohol withdrawal. [Pg.130]

It produces severe toxic manifestations. Either suicidal or accidental intake of toxic doses of barbiturates is characterized by depressed respiration, circulatory shock, pupils are initially constricted then dilated due to asphyxia, hypothermia, renal failure and pulmonary complications such as acute pulmonary edema. [Pg.71]

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting the respiration, preven-... [Pg.607]

SAFETY PROFILE Poison by ingestion, intraperitoneal, rectal, subcutaneous, and intravenous routes. Human systemic effects by intraarterial route acute arterial occlusion by rectal route respiratory depression, body temperature decrease, general anesthetic. An experimental teratogen. Experimental reproductive effects. An intravenous anesthetic. When heated to decomposition it emits toxic fumes of NOx and Na20. See also PENTOTHAL and BARBITURATES. [Pg.1078]

There is a broad spectrum of signs and symptoms associated with acute short-acting barbiturate toxicity. Lethargy, ataxia, nystagmus, diplopia, amnesia, slurred speech, confusion, hypotonia, hypotension, hypothermia, hypoglycemia, coma, respiratory depression, and death have been reported. Comatose patients may develop erythematous or hemorrhagic bullous skin lesions primarily over areas of pressure (e.g., elbows and knees). These lesions are commonly referred to as barb burns . Doses of 3-5 mg kg of most short-acting barbiturates will cause toxicity in children. The estimated potentially fatal dose in nondependent adults is 3-6 g. [Pg.212]

Acute intoxication resembles barbiturate toxicity. Clinical effects include dose-related central nervous system depression, nystagmus, ataxia, nausea and vomiting, dizziness, vertigo, and irritability. [Pg.2107]

Barbiturates (Phenobarbital, mephobarbital, primidone) Treat grand mal and acute episodes or status epilepticus, meningitis, toxic rations, and eclampsia... [Pg.231]

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting respiration, prevention of hypotension, as well as diuresis, hemodialysis and, in the event of phenobarbital poisoning, the administration of sodium bicarbonate. Tolerance does not develop from lethal doses. The abrupt withdrawal from barbiturates may cause tremors, restlessness, anxiety, weakness, nausea and vomiting, seizures, delirium, and cardiac arrest. [Pg.101]

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. [Pg.447]


See other pages where Barbiturates acute toxicity is mentioned: [Pg.1796]    [Pg.883]    [Pg.862]    [Pg.407]    [Pg.164]    [Pg.291]    [Pg.278]    [Pg.579]    [Pg.1811]    [Pg.2600]    [Pg.933]    [Pg.199]    [Pg.1023]    [Pg.1187]    [Pg.516]    [Pg.970]    [Pg.82]    [Pg.22]   
See also in sourсe #XX -- [ Pg.607 ]




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