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GASTRO-OESOPHAGEAL REFLUX DISEASE

GASTRO-OESOPHAGEAL REFLUX DISEASE. By Dr A S Maiyaki (FWACP) Gastroenterology Unit Department of Medicine Usmanu Danfodiyo University Teaching Hospital, Sokoto. INTRODUCTION.

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GASTRO-OESOPHAGEAL REFLUX DISEASE

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  1. GASTRO-OESOPHAGEAL REFLUX DISEASE By Dr A S Maiyaki (FWACP) Gastroenterology Unit Department of Medicine Usmanu Danfodiyo University Teaching Hospital, Sokoto

  2. INTRODUCTION • Dyspepsia is defined as upper abdominal or retrosternalpain,discomfort,heartburn,nausea vomiting or symptoms considered to be referable to the proximal alimentary tract. • It is a symptom complex rather than a specific disease • It is a common complaint among patients in both general and gastroenterology practice in Nigeria. • Functional dyspepsia needs to be clearly differentiated from dyspepsia with an organic cause.

  3. Definition • Is a clinical manifestation of excessive reflux of acid gastric contents into the oesophagus causing various degrees of symptomatic irritation to the oesophageal mucosa with symptoms lasting >6monthsGORD runs a chronic and relapsing courseTypical symptoms of GORD include heartburn, regurgitation and dysphagia.

  4. Epidemiology • Is a very common disorder of the upper GIT with an incidence rate of 10-38% of adults in the Western population • Based on hospitalization and death rates the prevalence of GORD has increased while that of PUD has been on the decrease. • GORD affects about 25-35% of the US population • Limited no of hospital based studies have reported on GORD and its complication in African countries.

  5. Ahmed et al reported 45% of patients with Erosive oesophagitis, Barrett’s 10.6% in a study of 105 Sudanese patients with heartburn. • In South Africa out of 216 consecutive Barrett’s only 5% were blacks despite the ratio of blacks to whites in the city being 5:1.(Mason et al) • OAUTHC prevalence of GORD 11 %(Oginni et al 2005) • Prevalence of GORD among clinical year Medical students in their clinical year was 26.3% College of Medicine UNN Enugu Campus( Nwokediuko 2009)

  6. RISK FACTORS • 1 Obesity • 2 Smoking • 3 Diet (fatty/spicy foods, peppermint, chocolate, citrus fruits, tomato based products, coffee) • 4 Hiatus hernia

  7. PATHOPHYSIOLOGY • -Results from an imbalance between defensive factors protecting the oesophagus (anti-reflux barriers, oesophageal acid clearance and tissue resistance) and aggressive factors from the stomach contents (gastric acidity and vol. and duodenal contents). • -Anti-reflux barriers consist of Lower oesophageal sphincter (LOS) and crura of the diaphragm. • Clearance of the oesophagus depends on the oesophageal peristalsis, saliva pH and gravity.

  8. Factors contributing to the pathogenesis of GORD include • Defective LOS • Hiatus hernia • Impaired oesophageal peristalsis • Delayed gastric emptying, gastric acid production as well as bile reflux. • Influence of H. pylori.

  9. CLINICAL PRESENTATION • Heartburn • Regurgitation • Dysphagia • Asthma • Chronic cough • Dental erosion • Obstructive sleep apnoea syndrome • Pulmonary fibrosis • COPD • Pneumonia • Pulmonary collapse • Intractable nausea • Non cardiac chest pain

  10. DIAGNOSTIC EVALUATION • Rest primarily on recognition of symptoms • Oesophagogastroduodenoscopy,capsule endoscopy(endoscopy negative,NERD and endoscopy positive) • Erosive oesophagitis (papillae extending into upper third of the oesophageal mucosa with or without the infiltration of inflammatory cells • The Los Angeles classification of Erosive Oesophagitis • Grade A: One or more mucosa break each <5mm in length • Grade B: There is at least one mucosal break >5mm long but not continuous between the tops of adjacent mucosal folds

  11. Grade C: At least one mucosal break that is continuous between the tops of adjacent mucosal fold but which is not circumferential. • Grade D: Mucosal breaks that involve at least75% of the oesophageal circumference • Savary-Miller grading of erosive oesophagitis.

  12. COMPLICATIONS • Stricture • Barrett’s oesophagus (columnar –lined epithelium with incomplete intestinal metaplasia with goblet cells in the oesophagus regardless of the length of the change. • Oesophageal adenocarcinoma

  13. EROSIVE OESOPHAGITIS

  14. Barrett’s Oesophagus

  15. Oesophageal Adenocarcinoma

  16. Oesophageal manometry • 24-hour pH monitoring • Multi-channel intra-luminal impedance

  17. MEDICAL AND SURGICAL TREATMENT • Well taken history is still paramount • Life style modification • Patient education • Elevation of the bed • Decrease fat intake • Cessation of smoking • Cessation of alcohol • Avoid recumbency 3hours postprandially

  18. MEDICAL TREATMENT • Antacids remain the drugs of choice for quick relief • Histamine-2-receptor antagonist(effective in controlling nocturnal acid secretion • Prokinetic agents (Domperidone) • 5HT3 agonist eg Tegaserod(has promotility and antinorciceptive effects) • Proton pump inhibitors (inhibit day time nocturnal and meal related stimulated acid secretion)

  19. SURGICAL MANAGEMENT • Patients who fail medical therapy or develop complications of GORD) • Barrett’s (antireflux treatment and mucosal ablation) • Laparascopic Nissen fundoplication • Toupet partial fundoplication • Belsey Mark iv repair • Hill posterior gastropexy repair

  20. SUGGESTIONS Un-investigated dyspepsia that may have an organic cause needs to be clearly differentiated from functional dyspepsia as management strategies differ. More upper gastro-intestinal endoscopy facilities should be provided in our hospitals to aid in defining the various causes of dyspepsia. Population based studies on GORD as it is a mimicker of many diseases

  21. THANKS FOR LISTENING • NAGODE

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