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Pharmacokinetics loading dose

Pryor FM, Gidal B, Ramsay RE, et al. Fosphenytoin pharmacokinetics and tolerance of intramuscular loading doses. Epilepsia 2001 42 245-250. [Pg.471]

Loading dose on first day of 200 mg. Reproduced with permission from Horadam VW, Sharp JG, Smilack JD, et al. Pharmacokinetics of amantadine hydrochloride in subjects with normal and impaired renal function. Ann Intern Med. 1981 94 454-458. [Pg.1309]

Life-threatening situations - Although clinical studies did not provide for a loading dose, it is recommended, based on pharmacokinetic data, that a loading dose of 200 mg 3 times/day be given for the first 3 days of treatment. [Pg.1683]

Quinine is derived from the bark of the cinchona tree, a traditional remedy for intermittent fevers from South America. The alkaloid quinine was purified from the bark in 1820, and it has been used in the treatment and prevention of malaria since that time. Quinidine, the dextrorotatory stereoisomer of quinine, is at least as effective as parenteral quinine in the treatment of severe falciparum malaria. After oral administration, quinine is rapidly absorbed, reaches peak plasma levels in 1-3 hours, and is widely distributed in body tissues. The use of a loading dose in severe malaria allows the achievement of peak levels within a few hours. The pharmacokinetics of quinine varies among populations. Individuals with malaria develop higher plasma levels of the drug than healthy controls, but toxicity is not increased, apparently because of increased protein binding. The half-life of quinine also is longer in those with severe malaria (18 hours) than in healthy controls (11 hours). Quinidine has a shorter half-life than quinine, mostly as a result of decreased protein binding. Quinine is primarily metabolized in the liver and excreted in the urine. [Pg.1124]

Krowke R, Chahoud I, Baumann-Wilschke I, et al. 1989. Pharmacokinetics and biological activity of 2,3,7,8-tetrachlorodibenzo-p-dioxin 2. Pharmacokinetics in rats using a loading-dose/maintenance-dose regime with high doses. Arch Toxicol 63 356-360. [Pg.644]

Pharmacokinetics Leflunomide is well absorbed after oral administration. It is extensively bound to albumin (>90 percent), and has a half-life of 14 to 18 days. [Note Because of its long half-life, loading doses are necessary (see p. 19).] Leflunomide is rapidly converted to the active metabolite. The metabolites are excreted in the urine and the feces. The active metabolite undergoes biliary recycling. [Pg.479]

Since there is a directly proportionate relationship between administered drug dose and steady-state plasma levels Equations 2.2 and 2.3 provide a straightforward guide to dose adjustment for drugs that are eliminated by first-order kinetics. Thus, to double the plasma levels the dose simply should be doubled. Con-versely to halve the plasma level, the dose should be halved. It is for this reason that Equations 2.2 and 2.3 are the most clinically important pharmacokinetic equations. Note that, as is apparent from Eigure 2.6, these equations also stipulate that the steady-state level is determined only by the maintenance dose and elimination clearance. The loading dose does not appear in the equations and does not influence the eventual steady-state level. [Pg.16]

Pharmacokinetics. Amiodarone is effective given orally its enormous apparent distribution volume (701/kg) indicates that little remains in the blood. It is stored in fat and many other tissues and the t) of 54 days after multiple dosing signifies slow release from these sites (and slow accumulation to steady state means that a loading dose is necessary, see Table 24.1). The drug is metabolised in the liver and eliminated through the biliary and intestinal tracts. [Pg.503]

For oral doses, the loading dose is usually twice that of the single dose. This is based on the pharmacokinetic principle that the accumulation factor is two when a drug is administered at every half-life. However, a loading dose should be cautiously used, particularly for those drugs... [Pg.1014]

A population pharmacokinetic study of intramuscular quinine (loading dose 20 mg/kg salt diluted 1 1 in water) in 120 Ghanaian children with severe malaria showed predictable profiles, which were within the target range for quinine (15-20 pg/ml) and independent of clinical and laboratory variables (1). Adverse events included skin induration or abscesses at the injection site (12%), all of which resolved without surgical intervention, and hypoglycemia (10%), a special risk in children who were hypoglycemic at presentation. [Pg.3002]

The use of quinine to treat cerebral malaria, and to a lesser extent severe malaria, has always been considered more risky than treatment of common cases of malaria. The changes in the pharmacokinetics of quinine caused by the malaria provide an explanation the standard dose of 10 mg/kg is usually well tolerated in patients with uncomplicated malaria but causes markedly higher plasma serum concentrations in patients with cerebral malaria. Total quinine clearance and total apparent volume of distribution are significantly lower in severe malaria, and after recovery, the pharmacokinetics return to normal. Probably the first loading dose should be as generally advised, but with a reduction in subsequent doses until the general condition has improved. Monitoring of plasma or red cell concentrations of quinine would of course be ideal, but this luxury is rarely available (SEDA-13, 816). [Pg.3006]

Fentanyl (0.001 mg/kg i.v.) can be used with xylazine (0.44 mg/kg i.v.) for anesthetic premedication. Fentanyl is sometimes used as an anesthetic adjunct during inhalation anesthesia to improve analgesia. The pharmacokinetics of fentanyl make it ideal for administration by constant rate infusion and it can be administered intra-operatively at a rate of 0.001-0.004 mg/kg/h after a 0.001 mg/kg loading dose. To prevent excitement or locomotory stimulation in recovery, the infusion should be discontinued 30 min prior to recovery or the horse should be sedated with xylazine (0.1 mg/kg i.v.) prior to recovery. [Pg.280]

Medicis JJ, Stork CM, Howland MA, et al. Pharmacokinetics following a loading dose plus a continuous infusion of pralidoxime compared with the traditional short infusion regimen in human volunteers. J Toxicol Clin Toxicol 1996 34 289-295. [Pg.147]

Because phenytoin has poor lipid solubility and enters the brain slowly, it may take up to 60 minutes before the pharmacodynamic effect is apparent. This delay in response is important when considering administration of a second mini-loading dose. For a review of the distribution and elimination pharmacokinetics of phenytoin, see Chap. 54. [Pg.1056]


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See also in sourсe #XX -- [ Pg.177 ]

See also in sourсe #XX -- [ Pg.340 ]




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