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|a Chansoma, Parakrama T.,
|e author.
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|a GERD :
|b a new understanding of pathology, pathophysiology, and treatment /
|c Parakrama T. Chandrasoma.
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|a Gastroesophageal reflux disease
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|a London :
|b Academic Press,
|c [2018]
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|c �2018
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|a 1 online resource
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|a text
|b txt
|2 rdacontent
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|2 rdamedia
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|a Includes index.
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|a Front Cover -- GERD -- Dedication -- GERDA: New Understanding of Pathology, Pathophysiology, and Treatment -- Copyright -- Contents -- Acknowledgments -- Introduction: Discovery: A Path to a New Solution for Gastroesophageal Reflux Disease -- 1. STATEMENT OF CONFLICT OF INTERESTS -- 2. PERIOD UP TO 1990: NO INTEREST IN DISCOVERY -- 3. THE DISCOVERY: 1990 TO THE PRESENT -- 3.1 The Material on Which Expertise Was Developed -- 3.2 Cardiac Epithelium Does Not Exist Normally -- 3.3 Autopsy Studies of the Region
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|a 3.4 The Normal Histologic State of the Esophagus and Stomach: The Zero Squamooxyntic Gap93.5 A Cellular Definition of Gastroesophageal Reflux Disease -- 3.6 Location of Cardiac Mucosa: Definition of the True Gastroesophageal Junction and the Definition of the Dilated Distal Esophagus -- 3.7 Correlation Between the Dilated Distal Esophagus and Damage to the Lower Esophageal Sphincter -- 4. ACCEPTANCE OF THE NEW CONCEPTS -- 4.1 The Value of Clinical Research -- 4.2 Impossible Contradictions -- 4.3 My Responsibility for the Failure of Acceptance
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|a 4.4 The Reason for This Book5. THE FUTURE THAT I HOPE FOR -- REFERENCES -- 1 -- Definition of Gastroesophageal Reflux Disease: Past, Present, and Future -- 1. POTENTIAL CRITERIA TO DEFINE GASTROESOPHAGEAL REFLUX DISEASE -- 1.1 Symptoms of Gastroesophageal Reflux Disease -- 1.2 The Empiric Proton Pump Inhibitor Test -- 1.3 Tests Based on Quantitating Gastroesophageal Reflux -- 1.4 Gross, Radiologic, and Endoscopic Mucosal Abnormalities Caused by Reflux -- 1.5 Cellular (Histopathologic) Changes Caused by Reflux -- 1.6 Criteria Based on Molecular (Genetic) Changes
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|a 1.7 Criteria Based on Detecting Lower Esophageal Sphincter Damage, the Cause of Gastroesophageal Reflux Disease (Fig. 1.7)2. PAST DEFINITIONS OF GASTROESOPHAGEAL REFLUX DISEASE BASED ON ULCERS AND EROSIONS -- 3. PRESENT (SYMPTOM-BASED) DEFINITIONS OF GASTROESOPHAGEAL REFLUX DISEASE -- 3.1 Common Unstandardized Definition of Gastroesophageal Reflux Disease in Practice -- 3.2 The Genval Working Group Definition, 1999 -- 3.3 The Montreal Definition and Classification of Gastroesophageal Reflux Disease, 200624 -- 4. PROBLEMS WITH PRESENT SYMPTOM-BASED DEFINITION
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|a 4.1 An Illusion of �a#x80;#x9C;Cure�a#x80;#x9D; of Gastroesophageal Reflux Disease4.2 Unnecessary Use of Proton Pump Inhibitors -- 4.3 Lack of Effort to Prevent Progression to Failure of Symptom Control in Gastroesophageal Reflux Disease -- 4.4 Failure to Prevent Esophageal Adenocarcinoma (Fig. 1.8) -- 4.5 Absence of Alternatives to Treating Gastroesophageal Reflux Disease -- 5. A NEW CELLULAR DEFINITION OF GASTROESOPHAGEAL REFLUX DISEASE -- 5.1 Pathogenesis of Gastroesophageal Reflux Disease -- 5.2 Reflux Esophagitis and Reflux Carditis
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|a Vendor-supplied metadata.
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|a Includes bibliographical references and index.
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|a GERD: A New Understanding of Pathology, Pathophysiology, and Treatment transforms the assessment of gastroesophageal reflux disease (GERD) from its present state, which is largely dependent on clinical definition and management, to a more objective scientific basis that depends on pathologic assessment. Sequential chapters in this single-author book describe the fetal development of the esophagus, the normal adult state, and the way exposure to gastric juice causes epithelial and lower esophageal sphincter damage at a cellular level. It allows recognition of the pathologic manifestations of lower esophageal sphincter damage and develops new histopathologic criteria for quantitating such damage. This understanding provides new pathologic criteria for definition and diagnosis of GERD from its earliest cellular stage. Algorithms based on measurement of sphincter damage can identify, even before the onset of clinical GERD, persons who will never develop GERD during life, those who develop GERD but remain with mild and easily controlled disease, and those who will progress to severe GERD with failure to control symptoms, Barrett esophagus and adenocarcinoma. Aggressive early intervention in the last group with the objective of preventing disease progression to its end points of uncontrolled symptoms and adenocarcinoma becomes feasible.
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|a Gastroesophageal reflux.
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650 |
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|a Gastroesophageal Reflux
|0 (DNLM)D005764
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650 |
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|a Reflux gastro-�sophagien.
|0 (CaQQLa)201-0058214
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650 |
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|a HEALTH & FITNESS
|x Diseases
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|2 bisacsh
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650 |
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|a MEDICAL
|x Clinical Medicine.
|2 bisacsh
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|a MEDICAL
|x Diseases.
|2 bisacsh
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650 |
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|a MEDICAL
|x Evidence-Based Medicine.
|2 bisacsh
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650 |
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7 |
|a MEDICAL
|x Internal Medicine.
|2 bisacsh
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650 |
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|a Gastroesophageal reflux
|2 fast
|0 (OCoLC)fst00938849
|
655 |
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4 |
|a Internet Resources.
|
776 |
0 |
8 |
|i Print version:
|a Chansoma, Parakrama T.
|t GERD.
|d London : Academic Press, [2018]
|z 9780128098554
|z 0128098554
|w (OCoLC)992433799
|
856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/book/9780128098554
|z Texto completo
|