Sympathomimetics seizures with

Aspirin, sympathomimetics, agents with muscarinic blocking actions, and drugs that cause muscle rigidity or seizures are all likely to cause hyperthermia at toxic doses. Hypothermia is more typical of overdoses with opioids or sedative-hypnotics. The answer is (C). 

Isolated seizures that are not epilepsy can be caused by stroke, central nervous system trauma, central nervous system infections, metabolic disturbances (e.g., hyponatremia and hypoglycemia), and hypoxia. If these underlying causes of seizures are not corrected, they may lead to the development of recurrent seizures I or epilepsy. Medications can also cause seizures. Some drugs that are commonly associated with seizures include tramadol, bupropion, theophylline, some antidepressants, some antipsy-chotics, amphetamines, cocaine, imipenem, lithium, excessive doses of penicillins or cephalosporins, and sympathomimetics or stimulants. 

The answer is b. (Kn.lzu.ng, p 5.38.) Crack is the free-base (nonsalt) form of the alkaloid cocaine. It is called crack because, when heated, it makes a crackling sound. Heating crack enables a person to smoke it the drug is readily absorbed through the lungs and produces an intense euphoric effect in seconds Use has led to seizures and cardiac arrhythmias. Some of cocaine s effects (sympathomimetic) are due to blockade of norepinephrine reuptake into presynaptic terminals it does not block receptors. Flashbacks can occur with use of LSD and mescaline but have not been associated with the use of cocaine. 

As with most data for reboxetine, this information primarily comes from summary papers rather than primary sources (473, 474). With this caveat, the adverse-effect profile of reboxetine is consistent with its pharmacology as an NSRI. Thus, it is similar to that of desipramine and maprotiline but without the risk of serious CNS (i.e., seizures, delirium) or cardiac (i.e., conduction disturbances) toxicity. The most common adverse effects of reboxetine are dry mouth, constipation, urinary hesitancy, increased sweating, insomnia, tachycardia, and vertigo. Whereas the first three adverse effects are commonly called anticholinergic, they are well known to occur with sympathomimetic drugs as well. In other words, these effects can be either the result of decreased cholinergic tone or increased sympathetic tone, although they tend to be more severe with the former than the latter. In contrast to TCAs, reboxetine does not directly interfere with intracardiac conduction. The tachycardia produced by reboxetine, however, can be associated with occasional atrial or ventricular ectopic beats in elderly patients. 

Correct answer = D. MAO inhibitors and aspirin can be taken concurrently. Hypertensive crisis may result from use (concurrently or within 2 weeks) of MAO inhibitors and indirect sympathomimetic amines, such as ephedrine. Concomitant use of MAO inhibitors and tricyclic antidepressants may result in mutual enhancement of effects with the possibility of hyperpyrexia, hypertension, seizures and death. Tyramine-containing foods, such as aged cheeses and beer, may precipitate a hypertensive crisis because of the accumulation and release of stored catecholamines from nerve endings. MAO inhibitors may lead to an exaggerated response to dopamine. 

Cocaine is a central nervous system stimulant that inhibits the peripheral reuptake of catecholamines, leading to increased sympathomimetic activity [129]. Its abuse is associated with a variety of medical problems. These include acute myocardial infarction, cardiac arrhythmias, cerebrovascular accidents, hyperpyrexia and stimulated sympathetic activity, seizures and coma, obstetrical comphcations, intestinal ischemia and a variety of psychiatric complications [128-131]. A number of reports in the mid to late 1980 s described patients who developed rhabdomyolysis while using cocaine [132-134]. Some of these patients experienced acute kidney injury [135-139]. While the exact incidence of acute kidney injury secondary to cocaine rhabdomyolysis is unknown, in one reported series it occurred... 

Molindone (50 to 75 mg/day) is indicated in the management of the manifestations of psychotic disorders. Molindone is strncturally nnrelated to the phenothiazines, butyrophenones, or thioxanthenes, but it resembles the piperazine phenothiazines in its clinical action. It causes sedation, possesses anticholinergic properties and, similar to flnphenazine, produces movement disorders. Molindone is metabolized, and the metabolites are excreted in the nrine. It lowers the seizure threshold and may cause seizures in patients with epilepsy and other seizure disorders. Concomitant nse with sympathomimetics, including epinephrine, phenylephrine, phenylpropanolamine, and ephedrine (often fonnd in nasal sprays), or appetite suppressants may decrease their stimulatory and pressor effects. Becanse of its alpha-blocking potential, molindone may canse epinephrine reversal—a hypotensive response to epinephrine. 

A a X 0 Q, 1 W s o a (D CQ PO/PR. Well absorbed, liver metabolism, kidney excretion. Dozens of standard and long-acting preparations available. Patients with seizure disorder, cardiovascular disorder or peptic ulcer disease. Sympathomimetics T risk of heart and CNS toxicity. Cimetidine, oral contraceptives and several antibiotics t half-life of theophylline - thus T toxicity. Phenobarbital and phenytoin induce metabolism of theophylline, thus i half-life. Dehdydration results from t diuresis with concurrent use of furosemide. Warn patients doubling a dose, even if one is missed, is very dangerous. Intoxication may cause seizures. Treat overdose with ipecac, activated charcoal, and a cathartic. 

Treat seizures (see p 22), coma (p 19), and arrhythmias (pp 12-15) if they occur. Caution Avoid the use of epinephrine or other sympathomimetic amines because of the risk of inducing or aggravating cardiac arrhythmias. Tachyarrhythmias caused by myocardial sensitization may be treated with propranolol (p 496), 1-2 mg IV, or esmolol (p 443), 0.025-0.1 mg/ kg/min IV. 

Serious adverse events are uncommon with the cannabinoid agonists. Their interactions with the central nervous system are complex and not well understood, but include sympathomimetic effects that can lead to tachycardia and, occasionally, postural hypotension, which may lead to cardiac events in susceptible patients. Psychotic reactions and seizures can he precipitated in some patients with a history or genetic predisposition to these disorders. 

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