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" Pharmacology of Peptic Ulcer Disease "
edited by Martin J. Collen, Stanley B. Benjamin.
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BL
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| Record Number
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731411
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b551197
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| Main Entry
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edited by Martin J. Collen, Stanley B. Benjamin.
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| Title & Author
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Pharmacology of Peptic Ulcer Disease\ edited by Martin J. Collen, Stanley B. Benjamin.
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| Publication Statement
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Berlin, Heidelberg: Springer Berlin Heidelberg, 1991
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| Series Statement
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Handbook of experimental pharmacology, 99.
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(xxii, 464 pages 69 illustrations)
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| ISBN
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3642758584
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: 9783642758584
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| Contents
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1 Pharmacology of the Parietal Cell --;A. Introduction --;B. Anatomy of Gastric Mucosa --;C. Secretion by the Stomach --;I. General --;II. Secretion and Absorption by Surface Epithelial Cells --;D. Gastric Barrier --;E. Agents Thought to Affect Gastric Barrier function --;I. Sucralfate --;II. Prostaglandins --;III. Bismuth Compounds --;F. Ion Transport by the Parietal Cell --;I. Apical Surface --;II. Basal Lateral Surface --;III. Stimulation of Acid Secretion --;IV. Mechanism of Parietal Cell Stimulation --;G. Receptor Antagonists --;I. Muscarinic Antagonists --;II. H2 Antagonists --;H. Mechanism of Gastric Proton Pump --;I. Transport by ATPase --;II. Reaction Cycle --;III. Structure of Gastric H+, K+-ATPase --;J. Inhibitors of H+, K+-ATPase --;I. Omeprazole --;1. Effects on Acid Secretion --;2. Duration of Action --;3. Mechanism of Action --;II Reversible H+, K+-ATPase Inhibitors --;III. Clinical Use of Pump Inhibitors --;References --;2 Epidermal Growth Factor --;A. Introduction --;B. Perspective on Growth Factors --;C. Perspective on Mucosal Disease --;D. EGF Structure --;E. Structure-Activity Relationships --;F. Biological Effects --;G. Gastrointestinal Activity --;I. Developmental Effects of EGF --;II. Gastric Acid Secretion --;III. Trophic Effects --;H. Conclusion --;References --;3 Gastrin and Other Peptide Hormones --;A. Introduction --;B. The Molecular Heterogeneity of Gastrin --;C. Gastrin Release --;D. Autonomic Control of Gastrin Release --;E. Bombesin-Like Peptides --;F. Somatostatin --;G. Mechanism of Gastrin-Induced Gastric Acid Secretion --;H. Gastrin and Peptic Ulcer Disease --;J. Hypergastrinemic Syndromes --;K. Conclusion --;References --;4 The Role of Essential Fatty Acids in Gastric and Duodenal Protection and Ulcer Therapy --;A. Cytoprotection and Prostaglandins --;I. Definition of Cytoprotection --;II. Mucosal Sites of Cytoprotection --;1. Protection of the Mucosal Microvasculature --;2. Direct Protection of Gastric Mucosal Cells --;III. Metabolism of Natural and Synthetic Prostaglandins --;B. Arachidonic Acid Cascade and Prostaglandin Synthesis by Gastric and Duodenal Mucosa --;I. Arachidonic Acid Cascade --;II. Sources of Arachidonic Acid from Mucosal Pools --;III. Control of Mucosal Prostaglandin Synthesis --;C. Dietary Sources of Arachidonic and Linoleic Acids --;I. Food Sources --;II. Absorption of Dietary Essential Fatty Acids --;III. Distribution of Absorbed Essential Fatty Acids Between Organs --;IV. The Requirement for Detergents for the Intestinal or Gastric Absorption of Essential Fatty Acids --;D. Gastric Mucosal Synthesis of Endogenous Prostanoids from Dietary Essential Fatty Acids --;I. The Requirement for Detergents for Absorption of Dietary Essential Fatty Acids into the Gastric Mucosa --;II. The Requirement for Direct Gastric Mucosal Contact with Solubilized Essential Fatty Acids for Mucosal Protection --;III. Generation of Prostanoids by the Gastric Mucosa from Solubilized Essential Fatty Acids --;E. Gastric Mucosal Protection by Solubilized Essential Fatty Acids --;I. Angiogenic Effect of Essential Fatty Acids --;F. Dietary Intake of Essential Fatty Acids --;I. Animal Studies --;II. Human Intake of Dietary Essential Fatty Acids and Its Relationship to Peptic Ulcer Disease --;G. Potential Therapeutic Advantages of Dietary Essential Fatty Acids Over the Synthetic Prostaglandins --;I. Effect of Short-Term Treatment with Dietary Essential Fatty Acids on the Human Gastric Mucosa --;H. Summary and Conclusion --;References --;5 Helicobacter pylori --;A. Introduction --;B. Clinical Relevance of Helicobacter pylori --;I. Frequency in the General Population and Association with Chronic Gastritis and Peptic Ulcer Disease --;II. Causation --;1. Chronic Gastritis --;2. Peptic Ulcer Disease --;C. Attempts to Eradicate Helicobacter pylori --;I. Natural History --;II. Eradication of Helicobacter pylori Infections --;III. Methods to Confirm Eradication of Helicobacter pylori Infections --;IV. Bismuth Salts --;V. Antimicrobials as Monotherapy --;VI. Drug Combinations --;1. Triple Drug Combinations --;2. Double Drug Combinations --;VII. Toxicity of Antimicrobials and Bismuth Salts --;VIII. Experimental Therapeutic Approaches --;D. Eradication of Helicobacter pylori and Peptic Ulcer Disease --;I. Effect on Gastritis --;II. Effect on Healing of Duodenal Ulcers --;III. Effect on Relapse Rates of Duodenal Ulcers --;IV. Effect on Relapse Rates of Gastric Ulcers --;E. Whom to Treat and What to Expect? --;F. Summary and Conclusions --;References --;6 Development of a New Gastric Antisecretory Drug for Clinical Use --;A. General Considerations --;B. Etiology and Pathophysiology of Peptic Ulcer --;C. Scope for Pharmacological Intervention --;D. Clinical Development of a New Antisecretory Drug for Peptic Ulcer --;I. Phase I --;II. Phase II --;III. Phase III --;IV. Phase IV --;References --;7 Therapeutic use of Omeprazole in Man: Pharmacology, Efficacy, Toxicity, and Comparison with H2 Receptor Antagonists --;A. Introduction --;B. Pharmacology --;I. General --;II. Plasma Concentrations --;III. Inhibition of Acid Secretion --;IV. Other Actions of Omeprazole --;1. Effect on Secretion of Intrinsic Factor and Vitamin B12 Absorption --;2. Effect on Pepsin --;3. Effects on Motility --;4. Effects on Gastric Endocrine function --;C. Therapeutic Trials in Acid-Peptic Diseases --;I. Overview --;II. DuodenalUlcer --;1. Effect of Different Doses of Omeprazole --;2. Comparative Studies of Omeprazole and H2 Receptor Antagonists --;3. Relapse After Stopping Omeprazole Therapy --;4. Omeprazole Treatment for Ulcers Resistant to H2 Receptor Antagonists --;III. Gastric Ulcer --;1. Noncomparative Studies of Omeprazole --;2. Comparative Studies of Omeprazole and Ranitidine --;3. Relapse After Stopping Omeprazole Therapy --;4. Omeprazole Treatment for Ulcers Resistant to H2 Receptor Antagonists --;IV. Reflux Esophagitis --;1. Effect of Different Doses of Omeprazole --;2. Comparative Studies of Omeprazole and H2 Receptor Antagonists --;3. Relapse After Stopping Omeprazole Therapy --;4. Omeprazole Treatment for Reflux Esophagitis Resistant to H2 Receptor Antagonists --;V. Zollinger-Ellison Syndrome --;VI. Side-Effects and Toxicity --;D. Probable Role of Omeprazole in Acid-Peptic Diseases --;References --;8 Hypothesis of Peptic Ulcer: A Modern Classification of a Multifactorial Disease --;A. Introduction --;B. Histopathology of Peptic Ulcer --;I. Ulcer Histology --;II. Gastritis --;Definitions --;1. Endoscopic Gastritis --;2. Histologic Gastritis --;C. Schwarz's Balance --;I. Mucosal Defenses --;1. Measurement of the Barrier --;2. The Mucus Gel and pH Gradient --;3. Mucosal Healing --;4. Mucosal Bloodflow --;5. Other Mechanisms of Defense --;II. Aggressive Factors --;1. Hydrogen Ion --;2. Aspartic Proteinases --;3. Bile Acids --;4. Oxygen Free Radicals --;III. Risk Factors as Modifiers of Mucosal Defense --;1. Blood Groups --;2. Tobacco Use --;IV. Regulation of Mucosal Defenses: Prostaglandins and Epidermal Growth Factor --;1. Role of Prostaglandins in Mucosal Defense --;2. Epidermal Growth Factor and Other Factors --;D. Classification of Peptic Ulcer Disease --;E. Drug-Induced Ulcer Disease --;I. Nonsteroidal Anti-Inflammatory Drugs and Aspirin --;1. Mechanisms of NSAID-Induced Injury --;2. Lesions Associated with NSAID Ingestion --;3. Helicobacter pylori and NSAID Ingestion --;II Drug-Induced Ulcers --;Alcohol --;1. Mechanisms of Injury --;2. Ethanol ad Ulcers --;III. Drug-Induced Ulcers --;Steroids --;1. Corticosteroids and Ulcers --;2. Effects of Corticosteroids on the Mucosa --;F. Helicobacter pylori and Peptic Ulcer --;1. Helicobacter pylori --;2. The Effect of Helicobacter pylori on the Mucosa and the Host Response --;3. Helicobacter pylori- Associated Gastroduodenal Ulcers --;G. Ulcers Associated with Hypersecretory States --;H. Malignant Ulcers --;J. Other Types of Chronic Relapsing Peptic Ulcer --;K. Acute Mucosal Stress Ulceration --;L.
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Summary --;References --;9 Nonulcer Dyspepsia --;A. Introduction --;B. Definition --;C. Epidemiology --;D. Categories of Nonulcer Dyspepsia --;I. Gastroesophageal Reflux-Like Dyspepsia --;II. Dysmotility-Like Dyspepsia --;III. Ulcer-Like Dyspepsia --;IV. Aerophagia --;V. Idiopathic/Essential Dyspepsia --;E. Pathophysiology --;I. Gastric Acid --;II. Helicobacter pylori --;III. Motility --;IV. Psychosocial Factors --;V. Environmental Factors --;F. Diagnostic Approach --;G. Treatment --;H. Prognosis --;J. Conclusions --;References --;10 The Natural History of Duodenal Ulcer Disease: Has it been Altered by Drug Therapy? --;A. Introduction --;B. Incidence of Duodenal Ulcer --;Historical Perspectives --;I. Cohort Phenomena --;C. Recent Time Trends in the Incidence of Duodenal Ulcer --;D. Geographic Influences --;E. Recent Trends in Hospitalization and Surgery for Duodenal Ulcer --;F. Seasonal Variations in Duodenal Ulcer --;I. Seasonal Variations Studied Endoscopically --;G. Natural History of Duodenal Ulcer --;Pre-H2 Blocker Studies --;I. Scandinavian Studies --;II. European Studies --;III. CURE Study --;H. Duodenal Ulcer Disease in the H2 Blocker Era --;I. How Long Does a Duodenal Ulcer Stay Healed After Treatment? --;J. Role of Helicobacter pylori --;K Natural History of Untreated Ulcers --;L. Natural History of Unhealed Ulcers --;M. Can Drug Therapy Prevent Duodenal Ulcer Relapse? --;N. Other Agents for "Short-Term" Maintenance Therapy --;I. Antacids --;II. Anticholinergics --;III. Tricyclic Antidepressants --;IV. Sucralfate --;V. Bismuth --;VI. Omeprazole --;O. How Long Should Maintenance Therapy Be Continued? --;I. On-Demand Versus Intermittent Therapy --;P. Summary --;References --;11 Refractory Duodenal Ulcer --;A. Introduction --;I. Definition --;II. Adequate Treatment and Compliance --;III. Hypersecretory Disorders and Nonpeptic Ulcer Disease --;B. Factors Which Affect Healing and Recurrence --;I. Acid Hypersecretion --;1. Parietal Cell Sensitivity --;2.
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| Abstract
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Covered are the pharmacology of the parietal cell and the latest hypotheses for the development of acid-peptic disease including epidermal growth factor, gastrin and other peptide hormones, fatty acids and prostaglandins, helicobacter pylori, and gastric acid hypersecretion including Zollinger-Ellison syndrome.
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| Subject
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Medicine.
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| Subject
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Toxicology.
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| LC Classification
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QP905.E358 1991
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| Added Entry
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Martin J Collen
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Stanley B Benjamin
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