GASTROESOPHAGEAL REFLUX DISEASE

• 1. Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manisfestations Diagnostic Evaluation Treatment Complications

2. 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 3. Physiologic GERD Postprandial Short lived Asymptomatic No nocturnal sx Pathologic GERD Symptoms Mucosal injury Nocturnal sx 4. GERD occurs in all ages but, most common in those older than 40 years of age. About 10-20% of people in western countries suffer from GERD symptoms on a weekly basis About 7% have symptoms daily. Except for NERD and pregnancy , no much difference in incidence between men and women. But for Barretts esophagus, prevalence is more in males particularly white adult males. 5. Primary barrier to gastro esophageal reflux is the lower esophageal sphincter LES normally works in conjunction with the diaphragm If barrier disrupted, acid goes from stomach to esophagus May be due to Spontaneous transient LES relaxations Transient increase in intra abdominal pressure An atonic LES 6. Drugs that reduce LES tone include calcium channel antagonists (e.g., nifedipine, verapamil, diltiazem), nitrates, anticholinergic agents(e.g.,tricyclic antidepressants , antihistamines), and oral contraceptives and estrogen. Foods that reduce LES tone include chocolate, fatty foods , onions, peppermint, and garlic Smoking(nicotine) reduces LES tone. 7. 2)DISRUPTION OF ANATOMICAL BARRIERS Associated with hiatal hernia The size of hiatal hernia is proportional to the frequency of LES relaxations Hypotensive LES pressures and large hiatal hernia- more chance of GERD following abrupt increase in intra abdominal pressure 3) ESOPHAGEAL CLEARANCE The GI acid produced spent too much time in contact with the esophageal mucosa Normally swallowing contributes to esophageal clearance by increasing salivary flow Saliva decreases with increasing age, so more often seen with elderly. 8. 4)MUCOSAL RESISTANCE The mucus secreated by the mucus secreting glands involves in the protection of esophagus The bicarbonate s moving from the blood to the lumen can neutralize acidic refluxate in the esophagus. On repeated exposure to the refluxate or due to some defect in normal mucosal defenses hydrogen ions diffuse into the mucosa, leading to cellular acidification and necrosis leading to esophagitis. 5)DELAYED GASTRIC EMPTYING An increase in gastric volume may increase both the frequency of reflux and the amount of gastric fluid available to be refluxed Physiologic Postprandial Gastro esophageal reflux occurs 9. 6)COMPOSITION OF REFLUXATE If the pH of the refluxate is less than 2, esophagitis may develop secondary to protein denaturation Also pepsinogen activated to pepsin at this pH may cause esophagitis. 10. Erosive esophagitis Responsible for 40-60% of GERD symptoms Severity of symptoms often fail to match severity of erosive esophagitis 11. Esophageal stricture Result of healing of erosive esophagitis May need dilation Common in the distal esophagus and are generally 1 to 2 cm in length. 12. Barretts Esophagus Columnar metaplasia of the esophagus,i.e replacement of the squamous epithelial lining of the esophagus by specialized columnar- type epithelium Associated with the development of adenocarcinoma Have a greater chance (30%) of developing esophageal stricture 13. Barretts Esophagus Acid damages lining of esophagus and causes chronic esophagitis Damaged area heals in a metaplastic process and abnormal columnar cells replace squamous cells This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma 14. 3 CLASSES OF SYMPTOMS TYPICAL SYMPTOMS May be aggravated by activities that worsen gastroesophageal reflux such as recumbent position, bending over, or eating a meal high in fat. Heartburnretrosternal burning discomfort Regurgitationeffortless return of gastric contents into the pharynx without nausea, retching, or abdominal contractions Water brash (hyper salivation) Belching 15. ATYPICAL SYMPTOMS In some cases, these extra esophageal symptoms may be the only symptoms present, making it more difficult to recognize GERD as the cause, especially when endoscopic studies are normal. Nonallergic asthma Hoarseness Pharyngitis Chest pain Dental erosions 16. ALARM SIGNS/SYMPTOMS These symptoms may be indicative of complications of GERD such as Barretts esophagus, esophageal strictures, or esophageal cancer Dysphagia Early satiety GI bleeding Odynophagia Vomiting Unexplained Weight loss Iron deficiency anemia Choking Continual pain 17. If classic/typical symptoms like heartburn and regurgitation exist in the absence of alarm symptoms the diagnosis of GERD can be made clinically and treatment can be initiated 18. H2RA or PPI Expect response in 2-4 weeks If no response Change from H2RA to PPI Maximize dose of PPI If PPI response inadequate despite maximal dosage Confirm diagnosis EGD(Esophagogastrodudenoscopy) 24 hour pH monitor 19. Endoscopy (with biopsy if needed) In patients with alarm signs/symptoms Those who fail a medication trial Those who require long-term treatment Important in distinguishing between esophagitis and Barrets metaplasia Absence of endoscopic features does not exclude a GERD diagnosis Confirmation can be achieved by provocative tests such as an acid perfusion test(Bernstein test), standard acid reflux test etc. 20. 24-hour pH monitoring Helps in establishing the presence of acid above the LES as the cause of symptoms or esophageal damage. Documents the amount of time the esophageal pH is low. Useful in patients who have not responded or who have had an incomplete response to empiric therapy, have symptoms with out evidence of mucosal injury, or have atypical symptoms. Trans-nasal catheter or a wireless, capsule shaped device 21. Patient with heartburn Iniate tx with H2RA or PPI H2RA taken BID Good response Frequent relapses On demand tx PPI taken QD Good response Maintenance therapy with lowest effective dose Symptoms persist Consider EGD if risk factors present (> 45, white, male and > 5 yrs of sx) Increase to max dose QD or BID Good response Confirm diagnosis EGD, ph monitor No Yes Yes No Yes Yes No No 22. Goals of therapy Alleviate or eliminate the patients symptoms. Decrease the frequency or recurrence and duration of gastro esophageal reflux. Promote healing of the injured mucosa. Prevent the development of complications. 23. Lifestyle modifications Avoid large meals Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic, peppermint Decrease fat intake Avoid lying down within 3-4 hours after a meal Elevate head of bed 4-8 inches Avoid meds that may potentiate GERD (CCB, alpha agonists, theophylline, nitrates, sedatives, NSAIDS) Avoid clothing that is tight around the waist Lose weight Stop smoking 24. Antacids Over the counter acid suppressants and antacids appropriate initial therapy Approx 1/3 of patients with heartburn-related symptoms use at least twice weekly More effective than placebo in relieving GERD symptoms 25. Histamine H2-Receptor Antagonists Competitively block the histamine receptors in gastric parietal cells, thereby preventing acid secretion More effective than antacids for relieving heartburn in patients with GERD Faster healing of erosive esophagitis Can use regularly or on-demand 26. AGENT DOSAGE Cimetadine 400-800mg twice daily Cimetidine(tab),Zydus Cadila Famotidine 20-40mg twice daily Famocid(tab), Sun Nizatidine 150mg twice daily Axid Ranitidine 150mg twice daily Aciloc(tab), Cadila 27. Proton Pump Inhibitors Effective not only with patients having erosive esophagitis or complications(Barrets esophagus), but also with non erosive GERD who have moderate to severe symptoms. Act by decreasing the basal and stimulated gastric acid secretion through inhibition of the final step of acid secretion by the parietal cell- the H+/K+ ATPase proton pump. Better control of symptoms with PPIs vs H2RAs and better remission rates Faster healing of erosive esophagitis with PPIs vs H2RAs 28. AGENT DOSAGE Esomeprazole 20-40mg daily Esomac(tab), Cipla Omeprazole 20mg daily Lomac(cap), Cipla Lansoprazole 15mg daily Lan(Cap), Intas Pantoprazole 40mg daily Pan-OD(tab), Burgeon Rabeprazole 20mg daily Rabeloc(tab), Cadila 29. H2RAs vs PPIs 12 week freedom from symptoms 48% vs 77% 12 week healing rate 52% vs 84% Speed of healing 6%/wk vs 12%/wk 30. Antireflux surgery Failed medical management Patient preference GERD complications Medical complications attributable to a large hiatal hernia Atypical symptoms with reflux documented on 24-hour pH monitoring 31. Postsurgery 10% have solid food dysphagia 2-3% have permanent symptoms 7-10% have gas, bloating, diarrhea, nausea, early satiety Within 3-5 years 52% of patients back on antireflux medications 32. Endoscopic treatment Relatively new No definite indications Select well-informed patients with well- documented GERD responsive to PPI therapy may benefit Three categories Radiofrequency application to increase LES reflux barrier Endoscopic sewing devices Injection of a nonresorbable polymer into LES area 33. Definition of GERD Epidemiology of GERD Pathophysiology of GERD Clinical Manisfestations Diagnostic Evaluation Treatment Complications 34. ?QUESTIONS?