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<ul><li><p>Pharmacology</p><p>Gary C. Rosenfeld, Ph.D.ProfessorDepartment of Integrated Biology and Pharmacology andGraduate School of Biomedical SciencesAssistant Dean for Education ProgramsUniversity of Texas Medical School at HoustonHouston, Texas</p><p>David S. Loose, Ph.D.Associate ProfessorDepartment of Integrated Biology and Pharmacology andGraduate School of Biomedical SciencesUniversity of Texas Medical School at HoustonHouston, Texas</p><p>With special contributions by</p><p>Medina Kushen, M.D.William Beaumont HospitalRoyal Oak, Michigan</p><p>Todd A. Swanson, M.D., Ph.D.William Beaumont HospitalRoyal Oak, Michigan</p></li><li><p>Acquisitions Editor: Charles W. MitchellProduct Manager: Stacey L. SebringMarketing Manager: Jennifer KuklinskiProduction Editor: Paula Williams</p><p>CopyrightC 2010 Lippincott Williams &Wilkins</p><p>351 West Camden StreetBaltimore, Maryland 21201-2436 USA</p><p>530 Walnut StreetPhiladelphia, PA 19106</p><p>All rights reserved. This book is protected by copyright. No part of this book may be reproduced in any form or byany means, including photocopying, or utilized by any information storage and retrieval system without writtenpermission from the copyright owner.</p><p>The publisher is not responsible (as a matter of product liability, negligence or otherwise) for any injury resultingfrom any material contained herein. This publication contains information relating to general principles ofmedical care which should not be construed as specific instructions for individual patients. Manufacturersproduct information and package inserts should be reviewed for current information, includingcontraindications, dosages and precautions.</p><p>Printed in the United States of America</p><p>Library of Congress Cataloging-in-Publication Data</p><p>Rosenfeld, Gary C.Pharmacology / Gary C. Rosenfeld, David S. Loose ; with special contributions by Medina Kushen,</p><p>Todd A. Swanson. 5th ed.p. ; cm. (Board review series)</p><p>Includes index.ISBN 978-0-7817-8913-4 (soft cover : alk. paper)1. PharmacologyExaminations, questions, etc. I. Loose, David S. II. Title. III. Series: Board review series.[DNLM: 1. PharmacologyExamination Questions. QV 18.2 R813p 2010]RM301.13.R67 20106150.1076dc22</p><p>2009010547</p><p>The publishers have made every effort to trace the copyright holders for borrowed material. If they haveinadvertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity.</p><p>Wed like to hear from you! If you have comments or suggestions regarding this Lippincott Williams &Wilkins title, please contact us at the appropriate customer service number listed below, or send correspondenceto [email protected]. If possible, please remember to include your mailing address, phone number,and a reference to the book title and author in your message. To purchase additional copies of this book call ourcustomer service department at (800) 638-3030 or fax orders to (301) 824-7390. International customers shouldcall (301) 714-2324.</p></li><li><p>Preface to the Fifth Edition</p><p>This concise review of medical pharmacology is designed for medical students, dental stu-dents, and others in the health care professions. It is intended primarily to help studentsprepare for licensing examinations, such as the United States Medical Licensing Exami-nation Step 1 (USMLE) or other similar examinations. This book presents condensed andsuccinct descriptions of relevant and current Board-driven information pertaining to phar-macology without the usual associated details. It is not meant to be a substitute for thecomprehensive presentation of information and difficult concepts found in standard phar-macology texts.</p><p>ORGANIZATION</p><p>The fifth edition begins with a chapter devoted to the general principles of drug action, fol-lowed by chapters concerned with drugs acting on the major body systems. Other chaptersdiscuss autocoids, ergots, anti-inflammatory and immunosuppressive agents, drugs usedto treat anemias and disorders of hemostasis, infectious diseases, cancer, and toxicology.</p><p>Each chapter includes a presentation of specific drugs with a discussion of their gen-eral properties, mechanism of action, pharmacologic effects, therapeutic uses, and adverseeffects. A drug list, tables, and figures summarize essential drug information included inall chapters.</p><p>Clinically oriented, USMLE-style review questions and answers with explanations fol-low each chapter to help students assess their understanding of the information. Similarly,a comprehensive examination consisting of USMLE-style questions is included at the endof the book. This examination serves as a self-assessment tool to help students determinetheir fund of knowledge and diagnose any weaknesses in pharmacology.</p><p>Key Featuresn Updated with current drug informationn End-of-chapter review tests feature updated USMLE-style questionsn 2-color tables and figures summarize essential information for quick recalln Updated drug lists for each chaptern Additional USMLE-style comprehensive examination questions and explanations</p><p>Gary C. Rosenfeld, Ph.D.David S. Loose, Ph.D.</p><p>v</p></li><li><p>Acknowledgments</p><p>The authors acknowledge and thank our colleagues for their support and contributions tothis book and our medical students for being our harshest critics.</p><p>vi</p></li><li><p>Contents</p><p>Preface v</p><p>Acknowledgments vi</p><p>1. GENERAL PRINCIPLES OF DRUG ACTION 1</p><p>I. DoseResponse Relationships 1II. Drug Absorption 6III. Drug Distribution 9IV. Drug Elimination and Termination of Action 10V. Biotransformation (Metabolism) of Drugs 11VI. Excretion of Drugs 14VII. Pharmacokinetics 15</p><p>Review Test 19</p><p>2. DRUGS ACTING ON THE AUTONOMICNERVOUS SYSTEM 26</p><p>I. The Peripheral Efferent Nervous System 26II. Parasympathomimetic Drugs 31III. Muscarinic-Receptor Antagonists 35IV. Ganglion-Blocking Drugs 38V. Skeletal Muscle Relaxants 38VI. Sympathomimetic Drugs 41VII. Adrenergic Receptor Antagonists 47</p><p>Review Test 52</p><p>3. DRUGS ACTING ON THE RENAL SYSTEM 60</p><p>I. Diuretics 60II. Nondiuretic Inhibitors of Tubular Transport 66</p><p>Review Test 68</p><p>vii</p></li><li><p>4. DRUGS ACTING ON THE CARDIOVASCULAR SYSTEM 72</p><p>I. Agents Used to Treat Congestive Heart Failure (CHF) 72II. Antiarrhythmic Drugs 78III. Antianginal Agents 83IV. Antihypertensive Drugs 85V. Drugs that Lower Plasma Lipids 91</p><p>Review Test 95</p><p>5. DRUGS ACTING ON THE CENTRALNERVOUS SYSTEM 100</p><p>I. SedativeHypnotic Drugs 100II. Antipsychotic (Neuroleptic) Drugs 105III. Antidepressant Drugs 109IV. Lithium 114V. Opioid Analgesics and Antagonists 115VI. Antiparkinsonian Drugs and Drugs Used to Treat Alzheimers Disease 121VII. Antiepileptic Drugs 125VIII. General Anesthetics 128IX. Local Anesthetics 133X. Drugs of Abuse 136</p><p>Review Test 145</p><p>6. AUTOCOIDS, ERGOTS, ANTI-INFLAMMATORYAGENTS, AND IMMUNOSUPPRESSIVE AGENTS 150</p><p>I. Histamine and Antihistamines 150II. Serotonin and Serotonin Antagonists 154III. Ergots 155IV. Eicosanoids 157V. Nonsteroidal Antiinflammatory Drugs (NSAIDs) 159VI. Drugs Used for Gout 167VII. Immunosuppressive Agents 168</p><p>Review Test 172</p><p>7. DRUGS USED IN ANEMIA AND DISORDERSOF HEMOSTASIS 175</p><p>I. Drugs Used in the Treatment of Anemias 175II. Drugs Acting on Myeloid Cells 179III. Drugs Used in Hemostatic Disorders 179</p><p>Review Test 186</p><p>viii Contents</p></li><li><p>8. DRUGS ACTING ON THE GASTROINTESTINAL TRACT 191</p><p>I. Antiemetics 191II. Anorexigenics and Appetite Enhancers 193III. Agents Used for Upper GI Tract Disorders 193IV. Prokinetic Agents 197V. Drugs Used to Dissolve Gallstones 197VI. Digestive Enzyme Replacements 198VII. Agents that Act on the Lower GI Tract 198</p><p>Review Test 202</p><p>9. DRUGS ACTING ON THE PULMONARY SYSTEM 206</p><p>I. Introduction to Pulmonary Disorders 206II. Agents Used to Treat Asthma and Other Bronchial Disorders 206III. Drugs Used to Treat Rhinitis and Cough 212</p><p>Review Test 214</p><p>10. DRUGS ACTING ON THE ENDOCRINE SYSTEM 216</p><p>I. Hormone Receptors 216II. The Hypothalamus 216III. The Anterior Pituitary 220IV. The Posterior Pituitary 222V. Drugs Acting on the Gonadal and Reproductive System 223VI. The Adrenal Cortex 232VII. The Thyroid 236VIII. The Pancreas and Glucose Homeostasis 238IX. The Calcium Homeostatic System 243X. Retinoic Acid and Derivatives 246</p><p>Review Test 249</p><p>11. DRUGS USED IN TREATMENT OF INFECTIOUSDISEASES 252</p><p>I. Infectious Disease Therapy 252II. Antibacterials 253III. Antimycobacterial Agents 265IV. Antifungal Agents 269V. Antiparasitic Drugs 271VI. Antiviral Drugs 275</p><p>Review Test 282</p><p>Contents ix</p></li><li><p>12. CANCER CHEMOTHERAPY 287</p><p>I. Principles of Cancer Chemotherapy 287II. Alkylating Agents 288III. Antimetabolites 292IV. Natural Products 295V. Miscellaneous Agents 298VI. Steroid Hormone Agonists and Antagonists and Related Drugs 300VII. Adjunct Agents 302</p><p>Review Test 304</p><p>13. TOXICOLOGY 309</p><p>I. Principles and Terminology 309II. Air Pollutants 311III. Solvents 313IV. Insecticides and Herbicides 313V. Fumigants and Rodenticides 315VI. Heavy Metal Poisoning and Management 315VII. Drug Poisoning 319</p><p>Review Test 321</p><p>Comprehensive Examination 324</p><p>Index 341</p><p>x Contents</p></li><li><p>chap t e r 1 General Principles ofDrug Action</p><p>I. DOSERESPONSE RELATIONSHIPS</p><p>A. Drug effects are produced by altering the normal functions of cells and tissues in the bodyvia one of four general mechanisms:1. Interaction with receptors, naturally occurring target macromolecules that mediate the effects</p><p>of endogenous physiologic substances such as neurotransmitters and hormonesa. Figure 1-1 illustrates the four major classes of drugreceptor interactions, using specific</p><p>examples of endogenous ligands.(1) Ligand-activated ion channels. Figure 1-1A illustrates acetylcholine interacting with a</p><p>nicotinic receptor that is a nonspecific Na+/K+ transmembrane ion channel. Interactionof a molecule of acetylcholine with each subunit of the channel produces a conforma-tional change that permits the passage of Na+ and K+. Other channels that are targets forvarious drugs include specific Ca2+ and K+ channels.</p><p>(2) G-proteincoupled receptors (Fig. 1-1BD). G-proteincoupled receptors compose thelargest class of receptors. The receptors all have seven transmembrane segments, threeintracellular loops, and an intracellular carboxy-terminal tail. The biologic activity of thereceptors is mediated via interaction with a number of G (GTP binding)-proteins.(a) Gas-coupled receptors. Figure 1-1B illustrates a b-adrenoceptor, which when acti-</p><p>vated by ligand binding (e.g., epinephrine) exchanges GDP for GTP. This facilitatesthe migration of Gas (Gastimulatory) and its interaction with adenylyl cyclase (AC).Gas-bound AC catalyzes the production of cyclic AMP (cAMP) from adenosine tri-phosphate (ATP); cAMP activates protein kinase A, which subsequently acts tophosphorylate and activate a number of effector proteins. The bg dimer may alsoactivate some effectors. Hydrolysis of the guanosine triphoshate (GTP) bound tothe Ga to guanosine diphosphate (GDP) terminates the signal.</p><p>(b) Gai (Ginhibitory)-coupled receptors (Fig. 1-1C). Ligand binding (e.g., somatostatin) toGai (Gainhibitory)-coupled receptors similarly exchanges GTP for GDP, but Gaiinhibits adenylyl cyclase, leading to reduced cAMP production.</p><p>(c) Gq (and G11)-coupled receptors (Fig. 1-1D). Gq (and G11) interact with ligand (e.g.,serotonin)-activated receptors and increase the activity of phospholipase C (PLC).PLC cleaves the membrane phospholipid phosphatidylinositol 4,5-bisphosphate(PIP2) to diacylglycerol (DAG) and inositol 1,4,5-triphosphate (IP3). DAG activatesprotein kinase C, which can subsequently phosphorylate and activate a number ofcellular proteins; IP3 causes the release of Ca</p><p>2+ from the endoplasmic reticuluminto the cytoplasm, where it can activate many cellular processes.</p><p>(3) Receptor-activated tyrosine kinases (Fig. 1-1E). Many growth-related signals (e.g., insu-lin) are mediated via membrane receptors that possess intrinsic tyrosine kinase activityas illustrated for the insulin receptor. Ligand binding causes conformational changes inthe receptor; some receptor tyrosine kinases are monomers that dimerize upon ligandbinding. The liganded receptors then autophosphorylate tyrosine residues, whichrecruits cytoplasmic proteins to the plasma membrane where they are also tyrosinephosphorylated and activated.</p><p>1</p></li><li><p>(4) Intracellular nuclear receptors (Fig. 1-1F). Ligands (e.g., cortisol) for nuclear receptorsare lipophilic and can diffuse rapidly through the plasma membrane. In the absence ofligand, nuclear receptors are inactive because of their interaction with chaperone proteinssuch as heat-shock proteins like HSP-90. Binding of ligand promotes structural changes inthe receptor that facilitate dissociation of chaperones, entry of receptors into the nucleus,hetero- or homodimerization of receptors, and high-affinity interaction with the DNA oftarget genes. DNA-bound nuclear receptors are able to recruit a diverse number of proteinscalled coactivators, which subsequently act to increase transcription of the target gene.</p><p>2. Alteration of the activity of enzymes by activation or inhibition of the enzymes catalyticactivity</p><p>3. Antimetabolite action in which the drug, acting as a nonfunctional analogue of a naturallyoccurring metabolite, interferes with normal metabolism</p><p>Na+ Acetylcholine</p><p>ACh nicotinic receptorIon channel</p><p>A</p><p>GTP</p><p>Multiple cellulareffects</p><p>Epinephrine -adrenoreceptor coupled to Gs</p><p>Gs GsAC AC</p><p>GDP</p><p> cAMP PKAATP</p><p>Other cellulareffects</p><p>B</p><p>SomatostatinSomatostatin receptor </p><p>coupled to Gi</p><p>Gi GiAC AC</p><p>GDP GTP</p><p> cAMPATP</p><p>Other cellulareffects</p><p>C</p><p>FIGURE 1-1. Four major classes of drugreceptor interactions, with specific examples of endogenous ligands. A. Acetyl-choline interaction with a nicotinic receptor, a ligand-activated ion channel. BD. Gcoupled receptors. B. Epinephrineinteraction with a Gas-coupled b-adrenoceptor. C. Somatostatin interaction with a Gai (Ginhibitory)-coupled receptor. D.Serotonin interaction with a Gq (and G11)-coupled receptor. E. Insulin interaction with a receptor-activated tyrosine ki-nase. F. Cortisol interaction with an intracellular nuclear receptor.</p><p>2 Pharmacology</p></li><li><p>4. Nonspecific chemical or physical interactions such as those caused by antacids, osmoticagents, and chelators</p><p>B. The graded doseresponse curve expresses an individuals response to increasing doses of agiven drug. The magnitude of a pharmacologic response is proportional to the number ofreceptors with which a drug effectively interacts (Fig. 1-2). The graded doseresponse curveincludes the following parameters:</p><p>1. Magnitude of response is graded; that is, it continuously increases with the dose up to the max-imal capacity of the system, and it is often depicted as a function of the logarithm of the doseadministered (to see the relationship over a wide range of doses).</p><p>GTP </p><p>Serotonin</p><p>Ca2+</p><p>GqGq</p><p>PLC PLC</p><p>GDP </p><p>ActivatesPKC</p><p>IP3 + DAGPIP2 </p><p>Serotonin receptor coupled to Gq</p><p>D</p><p>PO4 PO4Y Y Y Y</p><p>PI3-K</p><p>AKT</p><p>Multiple cellulareffects</p><p>IRS PO4IRS</p><p>Insulin</p><p>Insulin receptor</p><p>Insulin receptor-activated tyrosinekinase activity</p><p>E</p><p>FIGURE 1-1. (continued ).</p><p>Chapter 1 General Principles of Drug Action 3</p></li><li><p>2. ED50 is the dose that produces the half-maximal response; the threshold dose is that whichproduces the first noticeable effect.</p><p>3. Intrinsic activity...</p></li></ul>
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