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Gastroenterology and Hepatology : Bench to Bedside / edited by Gourdas Choudhuri, Anil C Anand, P Piramanayagam.

Springer Medicine eBooks 2024 Available online

Springer Medicine eBooks 2024
Format:
Book
Author/Creator:
Choudhuri, Gourdas.
Contributor:
Anand, Anil C.
Piramanayagam, P.
Language:
English
Subjects (All):
Diagnosis.
Internal medicine.
Gastrointestinal system.
Medical genetics.
Internal Medicine.
Gastrointestinal System.
Clinical Genetics.
Local Subjects:
Diagnosis.
Internal Medicine.
Gastrointestinal System.
Clinical Genetics.
Physical Description:
1 online resource (0 pages)
Edition:
1st ed. 2024.
Place of Publication:
Singapore : Springer Nature Singapore : Imprint: Springer, 2024.
Summary:
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. .
Contents:
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 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.
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.
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
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.
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.
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
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.
3.24.6 Disease Associated with Copper Metabolism.
ISBN:
981-9992-87-7
OCLC:
1434170696

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