Dosage determination

Iron deficiency anemia The accompanying formula and table are applicable for dosage determinations only in patients with iron deficiency anemia they are not to be used for dosage determinations in patients requiring iron replacement for blood loss. 

Dosages determined that produced almost no toxicity in pregnant rats and offspring 495... 

The patient also was advised to change his dietary habits by avoiding large meals and eating several smaller or medium meals. He was treated with pancreatin, a medication containing a mixture of porcine pancreatic enzymes, including lipase, amylase, and proteases, with the dosage determined by units of lipase activity (Layer and... 

Use of dosage determinations based on body surfece area may be the most sensitive approach to approximating age-dependent variations in drug disposition. Several body snrface area dosing nomograms are available, including some that are condition specific (e.g., Marfan s disease). 

Absorption. The rate of absorption from the gastrointestinal tract after oral dosage determines the speed of the onset of action of a benzodiazepine. For a quick onset of action, the benzodiazepine must dissolve completely in the stomach and cross the stomach mucosa into the systemic circulation. The different dissolution and absorption kinetics of benzodiazepines will affect their onset of action. Once the benzodiazepine is in the systemic circulation, it must also cross the blood-brain barrier to enter the CNS. Therefore, the lipophilidty of the benzodiazepine is important in determining the entry into the CNS and the onset of clinical action. Most benzodiazepines are highly lipophilic with the 3-hydroxy-substi-tuted benzodiazepines (lormetazepam, loraz-epam, temazepam, and doxefazepam) triazolam is the least lipophilic. 

Interview patients to obtain information pertinent to product selection, dosage determination, and usage of current and past prescription and over-the-counter products. 

What is the intact nephron hypothesis, and how does it apply to dosage determinations in patients with renal dysfunction ... 

The optimum dosage determined for CIO2 was nearly equal to that of CI2. Paraoxon was the only intermediate oxidative product formed during the oxidation of parathion by CI2 or CIO2 at pH 7.4. Paraoxon is more resistant to oxidation by CI2 or CIO2 as compared with the parent... 

Fernando SL, Saunders BM, Sluyter R et al 2005 Gene dosage determines the negative effects of polymorphic alleles of the P2X7 receptor on adenosine triphosphate-mediated killing of mycobacteria by human macrophages. Infect Dis 192 149—155 Ferrari D, Los M, Bauer MK et al 1999 P2Z purinoreceptor ligation induces activation of caspases with distinct roles in apoptotic and necrotic alterations of cell death. FEBS Lett 447 71-75... 

Dosage determination is based on treatment objective. For example, one objective for chlorine dose may be to achieve a target residual at the end of the distribution system. The objective for hydro-fiuosilicic acid addition may be to achieve a required concentration. The objective for coagulant dose may be to achieve some minimum turbidity goal. 

Protein concentration is the most fundamental and one of the most important analytical end-points for a protein pharmaceutical. It is used for dosage determination, as a basis for specific biological activity calculations, to normalize sample concentrations for many release assays, to establish process yields, and it can be stability-indicating. 

For a particular toxic material the concentration and period of exposure (dosage) determine the hazard level. Data on hazards in some cases can be found in many documents, such as the Material Safety Data Sheets (MSDS) published by the manufacturer of the particular materials, in National Institute Occupational Safety and Health (NIOSH) publication NIOSH Pocket Guide to Hazardous Chemicals (DHHS, 1990), or Emergency Response Planning Guidelines for Air Contaminants (ERPGs) issued by the American Industrial Hygiene Association (1992). 

The toxic dosage determined by Kretzschmar and Leuschner in animal experiments was confirmed in our clinical investigations with patients. Oral doses of 50 to 120 mg vitamin A acid daily cause side-effects, such as severe headaches, dryness of the lips, etc. (Table 22.1). However, a dose of 10 to 20 mg is well tolerated by most patients. The clinically visible side-effects encountered with oral vitamin A acid at doses of 100 mg correspond to those observed with high doses of vitamin A palmitate. 

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