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[null,null,"Autore",null,"Choudhuri Gourdas"]
[null,null,"Titolo",null,"Gastroenterology and Hepatology : Bench to Bedside / / edited by Gourdas Choudhuri, Anil C Anand, P Piramanayagam"]
[null,null,"Pubbl/distr/stampa",null,"Singapore : , : Springer Nature Singapore : , : Imprint : Springer, , 2024"]
[null,null,"ISBN",null,"981-9992-87-7"]
[null,null,"Edizione",null,"[1st ed. 2024.]"]
[null,null,"Descrizione fisica",null,"1 online resource (0 pages)"]
[null,null,"Disciplina",null,"616.33"]
[null,null,"Soggetti",null,"Diagnosis"]
[{"$nulls":4},"Internal medicine"]
[{"$nulls":4},"Gastrointestinal system"]
[{"$nulls":4},"Medical genetics"]
[{"$nulls":4},"Internal Medicine"]
[{"$nulls":4},"Gastrointestinal System"]
[{"$nulls":4},"Clinical Genetics"]
[null,null,"Lingua di pubblicazione",null,"Inglese"]
[null,null,"Formato",null,"Materiale a stampa"]
[null,null,null,"Livello bibliografico","Monografia"]
[null,null,"Nota di contenuto",null,"Intro -- Foreword -- Acknowledgments -- Introduction -- Contents -- Chapter 1: Esophagus -- 1.1 Lower Esophageal Sphincter -- 1.1.1 Anatomy -- 1.1.2 Embryology -- 1.1.3 Physiology -- 1.2 Wall Layer of the Esophagus -- 1.3 Esophageal Constrictions -- 1.4 Blood Supply of the Esophagus -- 1.5 Portosystemic Anastomosis -- 1.6 Lymphatic Drainage of Esophagus -- 1.7 Esophageal Rings -- 1.7.1 A Ring -- 1.7.2 B Ring -- 1.7.3 Corrugated Ringed Esophagus -- 1.8 Esophageal Webs -- 1.9 Esophagus in Portal Hypertension -- 1.9.1 Changes in Portal Hypertension -- 1.10 Tracheo-Esophageal Fistula -- 1.10.1 Diagnosis -- 1.10.2 Treatment -- 1.11 Transient Lower Esophageal Sphincter Relaxation -- 1.11.1 Definition -- 1.11.2 Physiology -- 1.11.3 Events Associated with TLESRs -- 1.11.4 Control of TLESRs -- 1.11.5 Neural Pathway-Mediating TLESRs -- 1.12 Refractory GERD -- 1.12.1 Refractory Gastroesophageal Reflux Disease Without Esophagitis -- Nocturnal Gastric Acid Breakthrough (NAB) -- Non-acid Gastroesophageal Reflux -- Missed Gastroesophageal Reflux Disease -- Functional Heartburn -- Wrong Diagnosis -- 1.12.2 Refractory Gastroesophageal Reflux Disease with Esophagitis -- Pill-Induced Esophagitis -- Autoimmune Skin Diseases -- Acid Hypersecretion -- Eosinophilic Esophagitis -- Genotypic Differences -- 1.12.3 Newer "]
[{"$nulls":4},"Treatment in Gastroesophageal Reflux Disease -- Extended Release Proton Pump Inhibitors -- Potassium-Competitive Acid Blocker -- TLESR Reducers -- Mucosal Protectant -- 1.13 Achalasia Cardia -- 1.13.1 Normal Esophageal Motor Innervation -- 1.13.2 Pathogenesis of Primary Achalasia -- 1.14 Eosinophilic Esophagitis -- 1.14.1 Endoscopic Findings -- 1.14.2 Histologic Characteristics -- 1.14.3 Treatment Options -- 1.15 Genetic Polymorphism in GERD -- 1.15.1 Introduction -- 1.15.2 Various Types of Polymorphism in Gastroesophageal Reflux Disease."]
[{"$nulls":4},"1.16 Biomarkers for Barrett's Esophagus -- 1.16.1 Diagnosis -- 1.17 Esophageal High-Resolution Manometry: Recent Updates on Chicago Classification 4.0 -- 1.17.1 Procedure -- 1.17.2 Classification of Esophageal Motility Disorders as per Chicago Classification 4.0 (Fig. 1.6) -- 1.18 24-Hour pH Impedance: Lyon Consensus and What Has Changed -- 1.18.1 Indications -- 1.18.2 Testing On or Off Proton Pump Inhibitors -- 1.18.3 Interpretation of pH and pH-Impedance Monitoring -- 1.18.4 Reflux-Symptom Association -- 1.18.5 Novel Metrics -- 1.19 Combined Multichannel Intraluminal Impedance and Esophageal Manometry -- 1.19.1 Indications -- 1.19.2 Principle -- 1.19.3 Patient Protocol -- 1.19.4 Technique -- 1.19.5 Impedance Results Parameters -- 1.19.6 Clinical Application -- 1.20 Third-Space Endoscopy and Its Clinical Utility -- 1.20.1 Third-Space Endoscopy Procedures -- 1.20.2 Principles of Third-Space Endoscopy -- 1.21 Esophageal Stents -- 1.21.1 Indications -- 1.21.2 Types -- 1.21.3 Technique -- 1.21.4 Adverse Events -- Early -- Late -- Chapter 2: Stomach -- 2.1 Embryology -- 2.2 Anatomy and Physiology -- 2.2.1 Gastric Mucosal Anatomy -- Oxyntic or Parietal Glands -- Parietal Cells (Oxyntic Cells) -- Chief Cells -- Endocrine Cells -- D Cells -- Somatostatin -- Enterochromaffin Cells -- Serotonin -- Enterochromaffin-Like Cells or ECL Cells -- Pyloric Glands -- G-Cells -- Gastrin -- Physiology of Gastric Acid Secretion -- Mechanism of Acid Production -- 2.3 Gastric Mucosal Barrier -- 2.3.1 Components of Gastric Barrier -- 2.3.2 Prostaglandins and Their Role in Gastric Mucosal Defense -- 2.4 Gastric Motility -- 2.4.1 ICC -- 2.4.2 Gastric Motility in Response to Solid Meal -- Receptive Relaxation -- Trituration -- Linear Phase of Gastric Emptying -- 2.4.3 Gastric Motility in Response to Liquid Meal -- 2.5 Gastrin -- 2.6 Ghrelin -- 2.6.1 Clinical Relevance."]
[{"$nulls":4},"Prader-Willi Syndrome -- Bariatric Surgery -- 2.7 Gastric Microbiota -- 2.7.1 Non-H. pylori Helicobacter Species -- 2.7.2 Clinical Relevance -- Gastric Non-H. Pylori Helicobacter Species -- Enterohepatic Non-H. Pylori Helicobacter Species -- 2.8 Acid Pocket -- 2.8.1 Mechanism -- 2.8.2 Gastroesophageal Reflux Disease and Acid Pocket -- 2.8.3 Management -- 2.9 H. pylori and Pathogenesis of Peptic Ulcer -- 2.9.1 H. pylori -- Transmission -- Bacteriology -- Adaptation of H. pylori to Stomach -- 2.9.2 Pathogenesis of H. pylori-Induced Mucosal Injury -- 2.9.3 Immune-Mediated Injury -- 2.9.4 Host Genetics and H. Pylori Pathogenicity -- 2.9.5 Pathogenesis of Duodenal Ulcer -- 2.10 NSAID and Gastric Mucosal Injury -- 2.11 Pathophysiology of Functional Dyspepsia -- 2.11.1 Pathophysiology of FD -- 2.12 Gastric Cancer Stem Cell -- 2.13 Pathogenesis and Molecular Classification of Gastric Cancer -- 2.13.1 Histologic Subtypes -- 2.13.2 Newer Molecular Classification of Gastric Cancer -- 2.14 H. pylori Treatment Guidelines: The Maastricht V/Florence Consensus Report -- 2.14.1 Indications for Testing for H. pylori -- 2.14.2 Diagnosis -- Tests for Identification of H. pylori -- 2.14.3 Treatment -- First-Line Treatment (Table 2.3) -- First-Line Treatment Failure: Management -- Second-Line Treatment Failure: Management -- Treatment in Patients with Penicillin Allergy -- "]
[{"$nulls":4},"Tests for Confirmation of H. pylori Eradication -- 2.15 Morphology of Superficial Neoplastic Lesions: Paris Classification -- 2.15.1 Historical Perspective -- 2.15.2 Practical Considerations -- 2.15.3 Endoscopic Staging Based on Morphology -- 2.15.4 Superficial Neoplastic Lesions in Columnar Epithelium Barrett's Esophagus -- 2.15.5 Superficial Neoplastic Lesions in Sub-cardiac Stomach -- 2.15.6 Superficial Neoplastic Lesions in the Colon -- 2.16 Proton Pump Inhibitors: Indications and Side Effects."]
[{"$nulls":4},"2.16.1 Indications -- 2.16.2 Side Effects -- 2.17 Prokinetics: Mechanism and Side Effects (Table 2.8) -- 2.18 Newer Antiplatelets and Anticoagulants: What the GI Physician Needs to Know -- 2.18.1 Risk of GI Bleeding with Newer Antiplatelets -- 2.18.2 Procedures Associated with the Risk of GI Bleed (Table 2.9) -- 2.18.3 Recommended Modification of Antiplatelet or Anticoagulant Use Before the Planned Procedure -- 2.18.4 Strategies for Reversal/Antidote to Newer Anticoagulants During a Life-Threatening Bleed -- Chapter 3: Small Intestine -- 3.1 Development and Malrotation -- 3.1.1 Timeline of Development (Table 3.1) -- 3.1.2 Intestinal Malrotation -- 3.2 Meckel's Diverticulum -- 3.2.1 Surgical Anatomy of Meckel's Diverticulum -- 3.2.2 Types -- Histology -- Clinical Presentation -- Treatment -- 3.3 Enteric Nervous System -- 3.3.1 Functions of Myenteric Plexus -- 3.3.2 Functions of Submucosal Plexus -- 3.4 Villi -- 3.4.1 Function -- 3.5 Microvilli -- 3.5.1 Location -- 3.5.2 Structure -- 3.5.3 Functions -- 3.5.4 Glycocalyx -- 3.5.5 Destruction of Microvilli -- 3.6 Intra-Epithelial Lymphocytes -- 3.6.1 The Upper Limit of the Normal Range of IELs -- 3.6.2 Associated Diseases with Increased IELs -- Increased IELs and Celiac Disease -- Increased IELs and Refractory Sprue -- Increased IELs and Non-celiac Disease-Associated Disorders -- 3.7 Microfold Cells -- 3.7.1 Structure and Function -- 3.7.2 Pathology -- 3.7.3 Development -- 3.8 Paneth Cells -- 3.8.1 Relationship with Stem Cells -- 3.8.2 Sensing Microbiota -- 3.8.3 Secretions -- Defensins -- 3.8.4 Other Secretions -- 3.9 Zona Occludens -- 3.9.1 Physiological Regulation by Na+/Nutrient Cotransport -- 3.9.2 Influence of Cytokines -- Interferon -- Hepatocyte Growth Factor -- Tumour Necrosis Factor -- Other Cytokines -- 3.9.3 Modulation by Leukocytes and Bacteria -- 3.10 Toll-like Receptors."]
[{"$nulls":4},"3.11 Migrating Myoelectric Complexes -- 3.12 Intestinal Pacemaker -- 3.12.1 Interstitial Cells of Cajal -- 3.12.2 Functions -- 3.12.3 Types -- 3.13 Gut Mucosal Barrier and Conditions with Increased Gut Permeability -- 3.13.1 Anatomy of Gut Mucosal Barrier -- 3.13.2 Physiology of Solute Transport Across the Gut Mucosal Barrier and Their Regulation -- Transport via TJ -- 3.13.3 Diseases Associated with Increased Gut Permeability -- 3.14 Small Intestinal Permeability (SIP) and Its Assessment -- 3.14.1 Factors That Determine Permeability -- 3.14.2 Measurement of Small Intestinal Permeability -- 3.14.3 Principles -- 3.14.4 Methods of Measurement -- 3.14.5 Clinical Relevance -- 3.15 Mucosal Defence -- 3.16 Immunoglobulin A -- 3.16.1 Structure (Fig. 3.4) -- 3.16.2 Functions -- 3.16.3 Clinical Significance -- Immunoglobulin A Deficiency -- Immunoglobulin A and Celiac Disease -- 3.17 Defensins -- 3.17.1 Clinical Importance -- 3.18 Enterokinase -- 3.18.1 Application -- 3.18.2 Enterokinase Deficiency -- 3.19 Cholecystokinin -- 3.19.1 Functions -- 3.19.2 Clinical Significance -- 3.20 Secretin -- 3.20.1 Functions -- 3.20.2 Clinical Uses -- 3.21 Incretins -- 3.21.1 Sources -- 3.21.2 Actions -- 3.21.3 Clinical Use -- 3.22 Vitamin B12 Absorption -- 3.22.1 Sources -- 3.22.2 Physiology -- 3.22.3 Diagnosis of Cobalamin Deficiency -- Peripheral Blood Film -- Serum B12 Levels -- 3.22.4 Schilling Test -- "]
[{"$nulls":4},"Principle -- 3.22.5 Treatment -- 3.23 Iron Absorption and Metabolism -- 3.23.1 Iron Absorption and Transport -- 3.23.2 Iron Transport Across the Apical Membrane of Enterocytes -- 3.23.3 Iron Transport Across the Basolateral Membrane of Enterocytes -- 3.23.4 Regulation of Iron Stores -- 3.24 Copper Metabolism -- 3.24.1 Absorption of Copper -- 3.24.2 Copper Transport -- 3.24.3 Role of Copper -- 3.24.4 Copper Deficiency: Causes and Diagnosis -- 3.24.5 Copper Toxicity."]
[{"$nulls":4},"3.24.6 Disease Associated with Copper Metabolism."]
[null,null,null,"Sommario/riassunto","The book aims to be a handy compendium to the very voluminous texts of gastroenterology and hepatology existing in the knowledge market and provides the reader with an easy understanding of the bench knowledge (basic sciences) as they apply to bedside practice (clinical gastroenterology). With introduction and contributions from Prof Eamon Quigley, Former president of World Gastroenterology Organization and American College of Gastroenterology, the book covers the recent advances in the basic sciences that form an important pillar of the knowledge, thereby linking basic sciences such as anatomy, physiology, biochemistry, molecular medicine, etc. to clinical conditions, diseases and new therapeutic approaches in gastroenterology and hepatology. The book is written in a simple easy to read format, with a lot of diagrams and flowcharts, making it a handy guide. It also discusses in-depth about very common clinical conditions encountered in hospital settings such as ulcerative colitis, pseudomembranous colitis, colonic cancer, amebiasis, and various other syndromes and diseases. This book is a useful read for fellows and trainees in Gastroenterology and Hepatology, as well as gastroenterologists, hepatologists and physicians interested in digestive disorders. ."]