Gastroesophageal Reflux Disease (GERD)

1. Gastroesophageal Reflux Disease (GERD) Dr. MahaArafah

2. Objectives Upon completion of this lecture the students will : • Understand the Pathophysiology of reflux esophagitis. • Know clinical features of reflux esophagitis • Describe the pathology (gross and microscopic features) of reflux esophagitis • Know the complications of reflux esophagitis

3. Anatomic radiographic landmarks of the lower esophageal sphincter (LES).

4. Gastroesophageal Reflux Disease (GERD) • Gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people, particularly after a meal. • Gastroesophageal reflux disease (GERD) occurs when the amount of gastric juice that refluxes into the esophagus exceeds the normal limit, causing symptoms with or without associated esophageal mucosal injury.

6. Definition • American College of Gastroenterology (ACG) • Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagus • Often chronic and relapsing • May see complications of GERD in patients who lack typical symptoms

7. Physiologic vs Pathologic • Physiologic GER • Postprandial • Short lived • Asymptomatic • No nocturnal sx • Pathologic GERD • Symptoms • Mucosal injury • Nocturnal sx

8. GERD Pathophysiology • Abnormal lower esophageal sphincter • or • Increase abdominal pressure

9. GERD Pathophysiology • Abnormal lower esophageal sphincter • Functional (frequent transient LES relaxation) • Mechanical (hypotensive LES) • Foods (eg, coffee, alcohol), • Medications (eg, calcium channel blockers), • Location .......... hiatal hernia • or B. Increase abdominal pressure The most common cause of (GERD). decrease the pressure of the LES. obesity Pregnancy increased gastric volume

10. Pathophysiology • Primary barrier to gastroesophageal reflux is the lower esophageal sphincter • LES normally works in conjunction with the diaphragm • If barrier disrupted, acid goes from stomach to esophagus

11. Summary of Pathogenesis of GERD • impaired lower esophageal sphincter-low pressures or frequent transient lower esophageal sphincter relaxation • hypersecretion of acid • decreased acid clearance resulting from impaired peristalsis or abnormal saliva production • delayed gastric emptying or duodenogastric reflux of bile • salts and pancreatic enzymes.

12. Clinical Manisfestations • Most common symptoms • Heartburn—retrosternal burning discomfort • Regurgitation—effortless return of gastric contents into the pharynx without nausea, retching, or abdominal contractions Atypical symptoms….coughing, chest pain, and wheezing.

13. Extraesophageal manifestations of GERD • Otolaryngeal: • hoarsness/laryngitis • Ch. Sore throat • Other: • Noncardial chest pain

14. Diagnostic Evaluation • If classic symptoms of heartburn and regurgitation exist in the absence of “alarm symptoms” the diagnosis of GERD can be made clinically and treatment can be initiated

15. Esophagogastrodudenoscopy • Endoscopy (with biopsy if needed) • In patients with alarm signs/symptoms • Those who fail a medication trial • Those who require long-term tx • The procedure lacks sensitivity for identifying pathologic reflux • Absence of endoscopic features does not exclude a GERD diagnosis • Allows for detection, and management of esophageal injury or complications of GERD

16. pH • 24-hour pH monitoring • Accepted standard for establishing or excluding presence of GERD for those patients who do not have mucosal changes • Trans-nasal catheter or a wireless, capsule shaped device

17. Complications • Erosive esophagitis • Stricture • Barrett’s esophagus

18. Complications • Erosive esophagitis • Responsible for 40-60% of GERD symptoms • Severity of symptoms often fail to match severity of erosive esophagitis

19. Esophagitis Eosinophils and neutrophils Elongation of lamina propria papillae basal zone hyperplasia,

20. Complications • Esophageal stricture • Result of healing of erosive esophagitis • May need dilation

21. Complications • Barrett’s Esophagus • Intestinal metaplasia of the esophagus • Associated with the development of adenocarcinoma 8-15%

22. Pathophysiology of Barrett’s Esophagus • Acid damages lining of esophagus and causes chronic esophagitis • Damaged area tries to heal in a metaplastic process and damaged squamous cells are replaced by metaplastic columnar cells defined by the presence of goblet cells (intestinal metaplasia) • This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma • Many patients with Barrett’s are asymptomatic

23. Complications dysplasia Barrett’s esophagus adenocarcinoma

24.  The risk of cancer in Barrett's esophagus is estimated to be 40 to 100 times • Endoscopic surveillance is recommended for all patients with Barrett's esophagus. Endoscopy is performed every 2 years, and biopsies are taken from the area of abnormal mucosa. • If the biopsies reveal low-grade dysplasia, then the frequency of endoscopies is increased.

25. If high-grade dysplastic changes are seen and confirmed by a second pathologist, then the risk of subsequent adenocarcinoma is greater than 25%, and surgical resection should be considered.

26. Summary

27. Treatment • H 2 receptor Blockers • Proton pump inhibitors Antireflux surgery