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  1. GASTROESOPHAGEAL REFLUX DISEASE • DEFINITIONS • GASTROESOPHAGEAL REFLUX: GER • Effortless movement of gastric contents from stomach to esophagus PHYSIOLOGIC, very frequent during day and night, post prandial with no symptoms or tissue injury. • GASTROESOPHAGEAL REFLUX DISEASE: GERD Damage to the esophageal mucosa inducing symptoms and esophageal inflammation.
  2. EPIDEMIOLOGY • ALL AGES, peak prevalence 35 – 45 years • In USA 44% of adults once a month 7% of adults once a week
  3. PATHOPHYSIOLOGY Contact of the noxius refluxate with the esophageal mucosa during enough time to produce damage IMBALANCE BETWEEN: OFFENSIVE FACTORS DEFENSIVE SYSTEM OFFENSIVE FACTORS: HCL acid – PEPCIN (their secretion is not increased but they are in the wrong place) DEFENSIVE SYSTEM: Antireflux Barrier Esophageal Clearance Tissue Resistance
  4. PATHOPHYSIOLOGY 1. Antireflux Barrier: Lower Esophageal Sphincter: LES The right crus of the diaphragm • High pressure zone of 2-3 cm between 2 low pressure zones (esophagus-stomach)
  5. Pathophysiology • In GERD • Low tone LES • Transiant LES relaxation episodes :TLESR • 80% of GERD episodes • Vagaly mediated non cholinergic inhibitory reflex induced by gastric stimulation (distention , inflammation
  6. Substances Influencing LES Pressure Increases LES pressure Decreases LES pressure Hormones Gastrin Secretin Motilin Cholecystokinin Substance P Glucagon Somatostatin Gastric inhibitory polypeptide Vasoactive inhibitory polypeptide Progesterone Medications Metoclopramide Theophylline Domperidone Prostaglandins E2 and I2 Cisapride Serotonin Histamine Morphine Antacids Meperidine Prostaglandin F2α Calcium channel blockers Diazepam Food Protein Fat Chocolate Ethanol Oil of peppermint Neural agents α-Adrenergic agonists α-Adrenergic antagonists β-Andrenergic antagonists β-Adrenergic agonists Cholinergic agonists Cholinergic antagonists
  7. PATHOPHYSIOLOGY 2. Esophageal acid clearance: Washes down acid/pepsin • Abnormal peristaltis: low amplitude non propagating contractions • Non reducible hiatal hernia: trapping acid and propelling it back • Impaired bicarbonate secretion by salivary and esophageal glands to neutralize acid
  8. PATHOPHYSIOLOGY 3. Tissue resistance: Stops H+ back diffusion • Preepithelial: Bicarbonate secretion, weak defense • Epithelial: Cell membrane Intercellular tight junction Intracellular H+ Buffering • Post epithelial: Blood supplies Bic, Oxygen, Nutrients and removes H and CO2
  9. Epithelial defense mecanism
  10. In summary • TLESR allow acid/pepsin to come in contact with the mucosa,the impared clearance increases contact time so noxius agente overcome the normal tissue resistance
  11. Impaired mucosal defence de Caestecker, BMJ 2001; 323:736–9. Johanson, Am J Med 2000; 108(Suppl 4A): S99–103. salivary HCO3 Hiatus hernia Impaired LOS (smoking, fat, alcohol) – transient LOS relaxations – basal tone H+ Pepsin Bile and pancreatic enzymes oesophageal clearance of acid (lying flat, alcohol, coffee) acid output (smoking, coffee) intragastric pressure (obesity, lying flat) bile reflux gastric emptying (fat) Pathophysiology of GORD
  12. CLINICAL FEATURES A. ESOPHAGEAL SYMPTOMS • HEART BURN • Regurgitation • Dysphagia – Odynophagia • Pain – “Non cardiac chest pain” B. EXTRA ESOPHAGEAL SYMPTOMS • Pulmonary: Bronchospasm, cough, bronchitis, pneumonia, Asthma. • Oral: Gingivitis, tooth decay, waterbrach. • Throat: Hoarsness, laryngitis, globus sensation. • Ear: Pain.
  14. Spectrum of GERD Symptomatic GERD – the real world 60%+ 35% 5% NERD Esophagitis Complicated erosive reflux disease
  15. THE SPECTRUM OF GERD NON EROSIVE REFLUX DISEASE: • No Endoscopic Lesions • Histological Alterations: - Mucosal infiltration by granulocytes - Basal cell hyperplasia - Dermal pegs elongation
  16. Normal esophagus
  17. THE SPECTRUM OF GERD EROSIVE ESOPHAGITIS: Endoscopic findings: erythema, erosions, ulcers, strictures. BARRETT ESOPHAGUS: Squamous epithelium replaced by columnar epithelium
  18. LA classification for esophagitis Grade A Grade B Grade C Grade D
  19. stricture
  20. DIAGNOSIS A. CLINICAL DIAGNOSIS B. DOCUMENTATION OF mucosal injury: • Barium swallow: Normal in NERD and Barrett. May show Reflux episodes, oesophagitis, ulcers , strictures and Hiatal Hernia • Esophago gastro duodenoscopy:Normal in NERD but gold standard in esophagitis and Barrett • Bernestein test:esophageal infusion of HCl C. Quantification of reflux: 24 hour PH monitoning
  21. pH Recording
  22. Scoring system to characterize patterns of reflux Parameters Evaluated During pH Monitoring Percentage of recording time when intraesophageal pH was below 4.0 in the upright position or recumbent position Percentage of recording time with pH below 4.0 for the total 24-hour period Total number of reflux episodes Number of episodes longer than 5 minutes Duration of longest episode
  23. BARRETT’S ESOPHAGUS • Healing process: colomnar epithelium • 3 types of cells: cardial, junctionnal, intestinal • Goblet cell epithelium • Prevalence of Barrett: < 10% • Risk of cancer only in Goblet cell type: 1/200 patient/year 30 – 120 times more than the normal population Higher in long segment >3cm  Endoscopy is gold standard + biopsies
  24. Barrett‘s esophagus
  25. Carcinoma of the esophagus
  26. Esophageal stent
  27. OTHER TYPES OF ESOPHIGITIS • Infectious esophagitis: Mainly in immunocompromised individuals : neutropenic, cancer patients, diabetics ,steroid treatment … Symptoms:Odynophagia, dysphagia , bleeding … - Viral: HSV 1, VZV, CMV, HIV - Bacterial: Mycobacterium tuberculosis, Cryptosporidium … - Candida: Normal oral flora but becomes pathogenic in immunocompomised patients Endoscopy: Ulcerations , vesicules in viral causes, white/yellow pseudomembranes in candida
  28. • Radiation: cancer therapy Early damage:erythema ,erosions, bleeding Late damage: strictures by ischemic changes • Corrosive: acid, alkali • Pill induced, drug induced: Tetracyclines, NSAId’s, KCL • Other: Pemphigus vulgaris, Stevens Johnson, GVH, crohn,Behcet