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G ASTRO E SOPHAGEAL R EFLUX D ISORDER

G ASTRO E SOPHAGEAL R EFLUX D ISORDER. Mahsa Khodadoostan MD. American College of Gastroenterology defines GERD as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus

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G ASTRO E SOPHAGEAL R EFLUX D ISORDER

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  1. GASTROESOPHAGEAL REFLUX DISORDER MahsaKhodadoostan MD

  2. American College of Gastroenterology defines GERD as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus • Physiologic reflux episodes typically occur postprandially, are short-lived, asymptomatic, and rarely occur during sleep • Pathologic reflux is associated with symptoms or mucosal injury, often including nocturnal episodes

  3. MECHANISMS OF REFLUX • Transient lower esophageal sphincter relaxations • Hypotensive lower esophageal sphincter • Hiatal hernia and the diaphragmatic sphincter • Obesity • Pregnancy and exogenous estrogen

  4. Transient lower esophageal sphincter relaxations • major differences between tLESRs and swallow-induced LES relaxation: • tLESRsoccur without an associated pharyngeal contraction • are unaccompanied by esophageal peristalsis • persist for longer periods (>10 sec) than do swallow-induced LES relaxations

  5. Hypotensive lower esophageal sphincter • Strain-induced reflux occurs when a hypotensive LES is overcome and "blown open" by an abrupt increase of intraabdominal pressure. Manometric data suggest that stress reflux is relatively unusual unless the LES pressure is less than 4 mmHg • During free reflux a fall in intraesophageal pH occurs without identifiable change in either intragastric or LES pressure. Free reflux is observed only when LES pressure is within 0 to 4 mmHg of intragastric pressure

  6. Hiatal hernia and the diaphragmatic sphincter

  7. Obesity • Obesity is a risk factor for GERD, erosive esophagitis, and esophageal adenocarcinoma

  8. Pregnancy and exogenous estrogen • Heartburn occurs in 30 to 50 percent of pregnancies

  9. ESOPHAGEAL ACID CLEARANCE • Esophageal emptying in GERD • Salivary function in GERD

  10. MECHANISMS OF AND DEFENSES AGAINST ESOPHAGEAL INJURY • Epithelial defense • Esophageal hypersensitivity

  11. CLINICAL MANIFESTATIONS • Heartburn • Regurgitation • Dysphagia • chest pain • Water brash or hypersalivation • Globus sensation • Odynophagia • Nausea

  12. The patient is a 40 years old man who comes to your office because of heartburn. • His symptoms were initiated since about 2 years ago, heartburn occur weekly • No alarm sign • Normal physical examination • What do you do ?

  13. DIAGNOSTIC EVALUATION • It is neither necessary nor practical to initiate a diagnostic evaluation in every patient with heartburn • In dysphagia Biopsies should target any areas of suspected metaplasia, dysplasia, or, in the absence of visual abnormalities, normal mucosa (at least five samples to evaluate for eosinophilic esophagitis) • Endoscopy should also be done to evaluate patients with a suspected esophageal GERD syndrome who have not responded to an empirical trial of twice daily PPI therapy

  14. Esophagoscopy • Grade A – one or more mucosal breaks each ≤5 mm in length • Grade B – at least one mucosal break >5 mm long, but not continuous between the tops of adjacent mucosal folds • Grade C – at least one mucosal break that is continuous between the tops of adjacent mucosal folds, but which is not circumferential • Grade D – mucosal break that involves at least three-fourths of the luminal circumference

  15. Ambulatory esophageal pH monitoring

  16. an endoscopy-negative patient being considered for surgical antireflux repair (pH study done after withholding antisecretory drug regimen for ≥ one week). • To evaluate patients after antireflux surgery who are suspected to have ongoing abnormal reflux (pH study done after withholding antisecretory drug regimen for ≥ one week). • to evaluate patients with either normal or equivocal endoscopic findings and reflux symptoms that are refractory to proton pump inhibitor therapy

  17. Esophageal pH recording is possibly indicated to detect refractory reflux in patients with chest pain after cardiac evaluation using a symptom reflux association scheme, preferably the symptom association probability calculation (pH study done after a trial of proton pump inhibitor therapy for at least four weeks). • Esophageal pH recording is possibly indicated to evaluate a patient with suspected otolaryngologic manifestations (laryngitis, pharyngitis, chronic cough) of gastroesophageal reflux disease after symptoms have failed to respond to at least four weeks of proton pump inhibitor therapy

  18. Esophageal pH recording is possibly indicated to document concomitant gastroesophageal reflux disease in an adult onset, nonallergic asthmatic suspected of having reflux-induced asthma (pH study done after withholding antisecretory drugs for ≥ one week). Note: a positive test does not prove causality! • Esophageal pH recording is not indicated to detect or verify reflux esophagitis (this is an endoscopic diagnosis). • Esophageal pH recording is not indicated to evaluate for "alkaline reflux."

  19. Esophageal manometry • for the evaluation of peristaltic function before antireflux surgery to exclude major motor disorders • It can also be used to ensure that ambulatory pH probes are placed correctly

  20. Bernstein test • determine symptom correlation with esophageal acidification in patients without endoscopic evidence of esophagitis • The test is done by alternately infusing saline or 0.1N HCl at a rate of 6 to 8 mL/min into the mid-esophagus via a nasogastric tube or manometric assembly • A positive test is defined as reproduction of the patient's symptoms with acid perfusion but not with saline. This test is ideal for determining acid sensitivity

  21. Radiologic techniques

  22. treatment?

  23. Mild symptomatic GERD : • lifestyle and dietary modifications along with antacids and nonprescription histamine-2 (H2) receptor antagonists • Patients with debilitating symptoms usually require more pharmacologically sustained acid-suppressive therapy

  24. LIFESTYLE MODIFICATIONS

  25. LIFESTYLE MODIFICATIONS • Head of bed elevation(important for individuals with nocturnal or laryngeal symptoms ) • Dietary modification : a core group of reflux-inducing foods (fatty foods, chocolate, peppermint, and excessive alcohol, which may reduce lower esophageal sphincter pressure) and then to suggest that the patient selectively avoid foods known to cause symptoms • Refraining from assuming a supine position after meals and avoidance of meals before bedtime • Avoidance of tight fitting garments • Wt loss • Promotion of salivation by chewing gum • Restriction of alcohol use and elimination of smoking

  26. ACID-SUPPRESSIVE MEDICATIONS • H2 receptor antagonists offer a therapeutic gain of 10 to 24 percent relative to the placebo • The different H2 receptor antagonist have equivalent efficacy if drug dose is adjusted for potency • An increased dose or prolonged course of an H2 antagonist is unlikely to produce relief for patients who continue to have heartburn after six weeks of treatment with a standard dose of an H2 antagonist • The proton pump inhibitors are more effective in healing esophagitis than the H2 receptor antagonists, with a therapeutic gain of 57 to 74 percent relative to placebo • proton pump inhibitors lead to more rapid healing and symptom relief than H2 receptor antagonists

  27. Nonerosivegastroesophagealreflux disease • patients with typical symptoms of GERD do not have esophagitis • hypersensitivity to physiologic degrees of acid reflux • patients have abnormal acid exposure but have not developed overt mucosal injury • others have heartburn not attributable to acid reflux, sometimes referred to as "functional heartburn“ • The first two groups, but not the third group of patients, may respond to antisecretory therapy

  28. ADJUNCTIVE THERAPY • Prokineticagents • Reflux inhibitors • TREATMENT OF HELICOBACTER PYLORI INFECTION

  29. UNDERLYING MECHANISMS OF PPI FAILURE

  30. Esophageal hypersensitivity and functional heartburn • Proper dosing • Compliance • Nocturnal acid breakthrough? • Reduced bioavailability • Differences in metabolism • Helicobacter pylori status • Drug resistance • Delayed healing • Weakly acidic or alkaline reflux • Residual acid reflux • Bile acid reflux • Psychological comorbidity

  31. MANAGEMENT • Optimizing therapy • Upper endoscopy • Esophageal pH testing • Esophageal manometry • Lifestyle modifications • Treatment of residual acid reflux : Changing PPIs versus doubling the dose Bedtime H2 receptor antagonist • Treatments aimed at reducing reflux • Treatment of esophageal hypersensitivity • Treatment of delayed gastric emptying • Fundoplication

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