Principles of Clinical PharmacologyArthur J. Atkinson Jr., Darrell R. Abernethy, Charles E. Daniels, Robert Dedrick, Sanford P. Markey Elsevier, 2011. gada 28. apr. - 568 lappuses This revised second edition covers the pharmacologic principles underlying the individualization of patient therapy and contemporary drug development, focusing on the fundamentals that underlie the clinical use and contemporary development of pharmaceuticals. Authors drawn from academia, the pharmaceutical industry and government agencies cover the spectrum of material, including pharmacokinetic practice questions, covered by the basic science section of the certifying examination offered by the American Board of Clinical Pharmacology. This unique reference is recommended by the Board as a study text and includes modules on drug discovery and development to assist students as well as practicing pharmacologists.
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No grāmatas satura
1.–5. rezultāts no 83.
iv. lappuse
... acid-free paper. Copyright © 2007, Elsevier Inc. All rights reserved. Except chapters 1, 2, 3, 4, 5, 11, 12, 14, 15, 16, 23, 24, 30, 31, 34, Appendix I and II which are in the public domain. No part of this publication may be reproduced ...
... acid-free paper. Copyright © 2007, Elsevier Inc. All rights reserved. Except chapters 1, 2, 3, 4, 5, 11, 12, 14, 15, 16, 23, 24, 30, 31, 34, Appendix I and II which are in the public domain. No part of this publication may be reproduced ...
4. lappuse
... acid metabolite is formed by oxidation of the t-butyl side chain of the parent drug. of drug action. Hence, pharmacokinetics and pharmacodynamics constitute two major subdivisions of pharmacology. Since as many as 70 to 80% of adverse ...
... acid metabolite is formed by oxidation of the t-butyl side chain of the parent drug. of drug action. Hence, pharmacokinetics and pharmacodynamics constitute two major subdivisions of pharmacology. Since as many as 70 to 80% of adverse ...
26. lappuse
... acids, the exponent in this equation becomes pH−pKa. In Figure 3.2, published experimentally determined values for log Doct are compared with estimates of log Φ. Equation 3.2 was rearranged to calculate Φ from literature values for fu ...
... acids, the exponent in this equation becomes pH−pKa. In Figure 3.2, published experimentally determined values for log Doct are compared with estimates of log Φ. Equation 3.2 was rearranged to calculate Φ from literature values for fu ...
37. lappuse
... acid analogs that are absorbed from the small intestine by the large neutral amino acid (LNAA) transporter. Similarly, some amino-β-lactam antibiotics, captopril, and other angiotensin-converting enzyme inhibitors are absorbed via an ...
... acid analogs that are absorbed from the small intestine by the large neutral amino acid (LNAA) transporter. Similarly, some amino-β-lactam antibiotics, captopril, and other angiotensin-converting enzyme inhibitors are absorbed via an ...
38. lappuse
... Acid Hydrolysis Drug in Small Particles Muscle, Fat, etc. Metabolism FIGURE 4.1 Summary of biopharmaceutic and physiologic processes that affect the rate and extent of absorption of an orally administered drug dose. Further explanation ...
... Acid Hydrolysis Drug in Small Particles Muscle, Fat, etc. Metabolism FIGURE 4.1 Summary of biopharmaceutic and physiologic processes that affect the rate and extent of absorption of an orally administered drug dose. Further explanation ...
Saturs
1 | |
9 | |
DRUG METABOLISM AND TRANSPORT | 141 |
ASSESSMENT OF DRUG EFFECTS | 273 |
OPTIMIZING AND EVALUATING PATIENT THERAPHY | 323 |
DRUG DISCOVERY AND DEVELOPMENT | 421 |
APPENDIX I Abbreviated Tables of Laplace Transforms | 527 |
APPENDIX II Answers to Study Problems | 529 |
Index | 537 |
Citi izdevumi - Skatīt visu
Principles of Clinical Pharmacology Arthur J. Atkinson Jr.,Arthur J. Atkinson Ierobežota priekšskatīšana - 2001 |
Principles of Clinical Pharmacology Arthur J. Atkinson Jr.,Charles E. Daniels,Robert Dedrick,Charles V. Grudzinskas,Sanford P. Markey Priekšskatījums nav pieejams - 2001 |
Bieži izmantoti vārdi un frāzes
absorption acid activity addition administration adverse agents analysis approach binding blood body cancer cause cells changes Chapter clearance Clin Pharmacol Ther clinical compartment compounds concentration decrease described determined differences digoxin disease distribution dose drug development effect elimination enzyme Equation errors estimate et al evaluation example expression factor Figure flow function gene half-life hepatic human identified important increased individuals infusion inhibition inhibitors initial interactions kinetics levels liver measured mechanism medication metabolism metabolites methods molecular needed normal observed occur oral organic P-glycoprotein parameters patients pharmacokinetics pharmacology Phase plasma population potential predicted pregnancy protein reactions receptor reduced relationship relative renal reported response result risk selection shown specific studies substrate Table therapeutic therapy tion tissue toxicity transport treated treatment trials tumor volume women
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