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

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Presentation on theme: "GASTRO-OESOPHAGEAL REFLUX DISEASE By Dr A S Maiyaki (FWACP) Gastroenterology Unit Department of Medicine Usmanu Danfodiyo University Teaching Hospital,"— Presentation transcript:

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 retrosternal pain,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 >6months GORD runs a chronic and relapsing course Typical 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) 5HT 3 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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