Pharmacology of Peptic Ulcer Disease - Taschenbuch

EAN (ISBN-13): 9783642758607
ISBN (ISBN-10): 3642758606
Gebundene Ausgabe
Taschenbuch
Erscheinungsjahr: 2011
Herausgeber: Springer Berlin

Buch in der Datenbank seit 2012-09-12T18:37:10+02:00 (Berlin)
Detailseite zuletzt geändert am 2024-01-31T11:24:22+01:00 (Berlin)
ISBN/EAN: 9783642758607

ISBN - alternative Schreibweisen:
3-642-75860-6, 978-3-642-75860-7
Alternative Schreibweisen und verwandte Suchbegriffe:
Autor des Buches: jensen, collen, rademaker, cölle, stanley, martin gardener, caldwell, cöllen, benjamin martin, graham benjamin, holländer, zollinger, hollander, fleischer, martin johnson
Titel des Buches: peptic ulcer, pep, handbook experimental pharmacology

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Daten vom Verlag:

Autor/in: Martin J. Collen; Stanley B. Benjamin
Titel: Handbook of Experimental Pharmacology; Pharmacology of Peptic Ulcer Disease
Verlag: Springer; Springer Berlin
464 Seiten
Erscheinungsjahr: 2011-12-13
Berlin; Heidelberg; DE
Gedruckt / Hergestellt in Niederlande.
Sprache: Englisch
106,99 € (DE)
109,99 € (AT)
118,00 CHF (CH)
POD
XXII, 464 p.

BC; Hardcover, Softcover / Medizin/Pharmazie; Pharmakologie; Verstehen; growth factor; pathophysiology; pharmacology; physiology; Pharmacology; BB

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. Helicobacterpylori 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. 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. Tolerance.- 3. Rebound Hypersecretion.- 4. Gastrin.- 5. Clinical Significance.- II. Smoking.- III. Nonsteroidal Anti-Inflammatory Drugs.- IV. Helicobacter pylori.- V. Ulcer Morphology.- C. Outcome of Refractory Duodenal Ulcer Treatment Trials.- I. Acid Suppression.- II. Mucosal Protective Agents.- III. Surgery.- D. Management.- I. General Advice.- II. Specific Treatment.- References.- 12 Idiopathic Gastric Acid Hypersecretion.- A. Introduction.- B. Method of Doing Gastric Analysis.- C. Definition of Idiopathic Gastric Acid Hypersecretion.- I. Statistical Definition.- II. Functional Definition.- D. Diseases Associated with Idiopathic Gastric Acid Hypersecretion.- I. Gastroesophageal Reflux Disease.- II. Duodenal Ulcer Disease.- III. Gastric Ulcer Disease.- IV. Nonulcer Dyspepsia.- E. Comparison of Idiopathic Gastric Acid Hypersecretion and Zollinger-Ellison Syndrome.- I. Characteristics.- II. Basal Acid Output, Maximal Acid Output, and Basal Acid Output/Maximal Acid Output Ratio.- F. Helicobacter pylori Associated with Idiopathic Gastric AcidHypersecretion.- G. Therapy for Idiopathic Gastric Acid Hypersecretion.- H. Other Data on Idiopathic Gastric Acid Hypersecretion.- I. Basal Acid Output in Children.- II. Basal Acid Output in Other Disorders.- J. Conclusions.- References.- 13 Zollinger-Ellison Syndrome: Advances in Diagnosis and Management.- A. Introduction.- B. Pathophysiology.- C. Clinical Features.- D. Provocative Tests.- E. Differential Diagnosis of Disorders with Increased Basal Acid Output and Increased Fasting Gastrin Concentration.- F. Medical Therapy.- I. H2 Receptor Antagonists.- 1. General.- 2. Absorption and Excretion of H2 Receptor Antagonists.- 3. Studies in Patients with Zollinger-Ellison Syndrome.- 4. Potency.- 5. Onset of Action.- 6. Duration of Action.- 7. Failure.- 8. Safety.- 9. Use.- 10. Use of Parenteral H2 Receptor Antagonists.- II. Omeprazole.- 1. General.- 2. Absorption, Metabolism, and Excretion.- 3. Onset of Action.- 4. Duration of Action.- 5. Potency.- 6. Failure..- 7. Use.- 8. Safety.- III. Anticholinergic Agents.- IV. Prostaglandins.- V. Somatostatin or SMS 201–995.- VI. Gastrin Receptor Antagonists.- G. Surgical Therapy.- H. Tumor Localization.- J. Treatment of Metastatic Disease.- References.- 14 The Pathophysiology and Treatment of Gastroesophageal Reflux Disease.- A. Introduction.- B. The Nosology of Reflux.- C. Why Do Humans Reflux?.- D. Variability of Tissue Response to Reflux.- E. Sequelae of Gastroesophageal Reflux.- F. Extraesophageal Manifestations of Reflux.- G. Testing in Gastroesophageal Reflux.- H. Treatment of Gastroesophageal Reflux.- J. Surgery in Gastroesophageal Reflux.- K Management in Real Life.- L. Summary.- References.- 15 Endoscopy in the Evaluation and Treatment of Acid-Peptic Disease.- A. Introduction.- B. Accuracy.- C. Safety.- D. UncomplicatedAcid-Peptic Disease.- I. Endoscopy as the Initial Diagnostic Modality.- II. Endoscopy Following a Radiologic Procedure.- 1. Negative Upper Gastrointestinal Series.- 2. Gastric Ulcer.- 3. Duodenal Ulcer.- III. Biopsy and Cytology.- IV. Disease Follow-up.- E. Gastrointestinal Bleeding from Acid-Peptic Disease.- I. Guidelines for Intervention.- II. Stigmata of Bleeding.- III. Endoscopic Hemostasis.- 1. Electrocoagulation.- 2. Photocoagulation.- 3. Heater Probe.- 4. Chemical Injection.- 5. Comparison of Hemostatic Modalities.- F. Gastric Outlet Obstruction.- G. Summary.- References.- 16 Videoendoscopy and Digital Imaging.- A. Introduction.- B. Charge-Coupled Devices and Videoendoscopy — How They Work..- I. Background.- II. CCD function.- III. Image Transfer.- IV. Microprocessor function.- V. Color.- 1. Background.- 2. Videoendoscopic Color Reproduction.- VI. Technical Evaluation.- VII. Clinical Use.- C. Practical Benefits and Advantages of Videoendoscopy.- I. Image Storage, Retrieval, and Transfer.- II. Teaching/Other.- D. Special Applications.- I. Measurement of Lesion Size.- II. Real-Time Image Analysis.- III. Image Modification.- IV. Chromoscopy and Infrared Imaging.- V. Mucosal Hemodynamics.- VI. Videoenteroscopy.- E. The Future.- References.