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Therapeutic level

The anainoacridines, tacrine (19) and its 1-hydroxy metaboUte, velnacrine (20), are reversible inhibitors of AChE. Tacrine was synthesi2ed in the 1940s and has been used clinically for the treatment of myasthenia gravis and tardive dyskinesia (115). Placebo-controUed studies have indicated modest efficacy of tacrine to treat AD dementia (122,123) and in 1993 the dmg was recommended for approval by the PDA under the trade name Cognex. Tacrine (19) has been shown to interact with sites other than AChE, such as potassium channels (124) and muscarinic receptors. However, these interactions are comparatively weak and are not thought to contribute to the biological activity of the dmg at therapeutic levels (115). [Pg.98]

Older tricyclic antidepressants are set in italics. The specificity of action of tricyclic antidepressants (in particular of amitritpyline, imipmmine, doxepine, noitriptyline, maprotiline) is limited because at therapeutic levels ihese drugs also block receptors (H t-histamine, a,-adrenergic, muscarinic). [Pg.841]

As the drag circulates in the blood, a certain blood level must be maintained for the dragp to be effective When the blood level decreases below the therapeutic level, the drag will not produce the desired effect. Should the blood level increase significantly over the therapeutic level, toxic symptoms develop. Specific therapeutic blood levels are discussed in the subsequent chapters when applicable. [Pg.7]

Pharmacodynamics is a discipline within the broader topic of pharmacology, which focuses on how a drug brings about a particular response, and the effective levels that are required in order to elicit such a response. Some of these basic data will have emerged from the research-based activities that initiate the development of most drugs today. However, considerable additional studies are required to establish detailed dose-response curves so that the optimum therapeutic level can be chosen. [Pg.59]

The detection and determination limits are less than 0.1 and 0.2 mg hydrochlorothiazide per liter body fluid and thus appreciably lower than the therapeutic levels which are reported to be between 0.2 and 1.6 mg/1. [Pg.56]

Seeman, P (1992) Dopamine receptor sequences therapeutic levels of neuroleptics occupy D2 receptors, clozapine occupies D4. Neuropsychopharmacology 7 261-284. [Pg.374]

Once the loading dose of the AED is administered, it is important to remember to initiate maintenance doses to ensure that therapeutic levels are sustained. Chronic and idiosyncratic side effects as well as potential drug interactions should be considered if the patient will continue AED therapy indefinitely. All drug therapy should be adjusted for any hepatic or renal disease states. Table 28-1 summarizes the drug doses used in SE, and Table 28-2 provides an example of an algorithm for the treatment of patients in SE. Published studies comparing these treatment strategies are summarized in Table 28-3. [Pg.465]

Drug Name (Brand Name) Loading Dose Administration Rate Therapeutic Level Side Effects Comments... [Pg.466]

I with seizures and require anticonvulsant therapy. Phenytoin is the most frequently used agent, with a loading dose of 15 mg/kg followed by 300 mg by mouth daily (titrated to therapeutic levels between 10 and 20 mcg/mL). Diazepam 5 mg intravenously may be used for rapid control of persistent seizures. Prophylactic anticonvulsants have been used frequently, but a recent meta-analysis did not support their use.23 Thus, because adverse effects and drug interactions are common, the routine use of prophylactic anticonvulsants is not recommended. [Pg.1478]

J Schemer, WA Altemeier. Experimental study of factors inhibiting absorption and effective therapeutic levels of declomycin. Surg Gynecol Obstet 114 9-14, 1962. [Pg.75]

There are a number of drugs that would be of benefit for the treatment of diseases in the interior of the eye, but for which therapeutic levels cannot be achieved by topical administration [217]. Until recently the only... [Pg.446]

As has been pointed out earlier in this chapter, the dietary consumption and historical medicinal use of carotenoids has been well documented. In the modern age, in addition to crocin, 3.7, and norbixin, 3.8, several carotenoids have become extremely important commercially. These include, in particular, astaxanthin, 3.6 (fish, swine, and poultry feed, and recently human nutritional supplements) lutein, 3.4, and zeaxanthin, 3.3 (animal feed and poultry egg production, human nutritional supplements) and lycopene, 3.2 (human nutritional supplements). The inherent lipophilicity of these compounds has limited their potential applications as hydrophilic additives without significant formulation efforts in the diet, the lipid content of the meal increases the absorption of these nutrients, however, parenteral administration to potentially effective therapeutic levels requires separate formulation that is sometimes ineffective or toxic (Lockwood et al. 2003). [Pg.51]

Cartwright [124] reported that miconazole was slightly absorbed from epithelial and mucosal surface. The drug is well absorbed from the gastrointestinal tract, but caused nausea and vomiting in some patients. The drug may be given intravenously but was associated phlebitis. Up to 90% of the active compound was bound to plasma protein. Distribution into other body compartments was poor. Metabolism was primarily in the liver, and only metabolites were excreted in the urine. At therapeutic levels, they were relatively nontoxic both locally and systematically, but occasionally produced disturbances on the central nervous system. [Pg.62]

C for 1 h. A 100 pL portion of the solution was injected onto a column (15 cmx 3.2 mm) of LiChroscob RP-18 (7 pm) for HPLC at room temperature, using acetonitrile-0.033 M phosphate buffer of pH 8.2 (1 2) containing 0.05% of ethyle-nediamine as the mobile phase (eluted at 1 mL/min). Fluorimetric detection involved excitation at 338 nm and measurement at 540 nm (or with a 430 nm cutoff filter). For 50 300 ng of drug injected on to the column, the coefficient of variation was 7-8%. The method permits a simple determination of (z>)-penicilla-mine in serum at therapeutic levels. [Pg.146]

The effects of Li+ upon this system have been reviewed in depth by Mork [131]. Animal studies originally demonstrated that Li+ inhibits cAMP formation catalyzed by adenylate cyclase in a dose-dependent manner [132]. The level of cAMP in the urine of manic-depressive patients changes with mental state, being abnormally elevated during the switch period between depression and mania it is proposed that Li+ s inhibitory effect upon adenylate cyclase activity may correct this abnormality. Subsequent research, in accord with the initial experiments, have shown that Li+ s interference with this second messenger system involves more than one inhibitory action. At therapeutic levels, Li+ inhibits cAMP accumulation induced by many neurotransmitters and hormones, both in... [Pg.25]

Lithium toxicity can occur with serum levels greater than 1.5 mEq/L, but the elderly may have toxic symptoms at therapeutic levels. Severe toxic symptoms may occur with serum concentrations above 2 mEq/L, including vomiting, diarrhea, incontinence, incoordination, impaired cognition, arrhythmias, and seizures. Permanent neurologic impairment and kidney damage may occur as a result of toxicity. [Pg.788]


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See also in sourсe #XX -- [ Pg.8 ]




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