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به نام هستی بخش Dr.p.Falla abed Thorasic surgeon Objectives At the end of this presentation, the student should be able to: Review the anatomy and physiology of the stomach Discuss the pathophysiology, risk factors, signs and symptoms, complications and diagnosis of ulcers Given a drug associated with ulcer formation, discuss the proposed mechanism of ulceration Discuss the pathophysiology, risk factors, signs and symptoms, and complications of gastroesophageal disease (GERD) Acid Peptic Disorders Dyspepsia Peptic Ulcers Duodenal Ulcers Stress Ulcers Gastroesophageal Reflux Disease (GERD) Gastric Cancers Dyspepsia A constellation of upper abdominal symptoms Accounts for up 40 - 70% of GI complaints Significant societal costs Causes PUD, GERD, gastric cancer Food, medications, but commonly idiopathic Normal Stomach Anatomy Gastric Antrum Physiology: The Secretory Epithelial Cells 1. Mucus cells • Mucus 2. Parietal cells • HCL 3. Chief Cells • Pepsinogen 4. G cells • Gastrin Surface Epithelium Opening of gastric pit Parietal cell Chief Cell Parietal cell Gastric Acid and its Function Gastric Acid Contents HCl, salts, pepsin, mucus, water, intrinsic factor, bicarbonate Gastric Acid Function to kill micro-organisms to activate pepsinogen breaks down connective tissue in food Mucosal Defenses/Protection Mucus layer on gastric surface Mucosal Bicarbonate: Abundant in mucus layer Prevent barrier to damage acidic damage and auto digestion Prostaglandins are cytoprotective Increase blood flow and cell regeneration Mucosal integrity Maintained by tight cell junctions Epidemiology of Peptic Ulcer Disease (PUD) Development of PUD 4 -10% of Americans Gastric Ulcer peaks 55-65th year Duodenal Ulcer increases with age until 60 years Pathophysiology of Peptic Ulcer Disease (PUD) Luminal Aggressors • H. pylori • NSAIDs • Acid • Pepsin Mucosal Defenses • Bicarbonate • Mucus • Prostaglandin • Growth factor • Mucosal regeneration Goldin GF, et al. Gastr Endosco Clin Nor Am. 1996;6;505-526. Saggioro A, et al. Ital J Gastroenterol. 1994;269(suppl 1):3-9. Modlin IN, et al. Acid Related Diseases. 1998;317-362. Risk Factors/Aggressors of PUD Major Factors Helicobacter Pylori NSAIDs Cigarette smoking Acid and pepsin Other Factors Genetics ?Foods ?Stress Helicobacter Pylori Bacteria Gram –ve spiral bacterium 40% of patients >60 yrs are +ve for H.pylori Transmitted: possibly person to person Most common cause of antral gastritis Mechanism of gastric injury Cytotoxin Breakdown of mucosal defenses Adherence to epithelial cells Increase gastrin releasing peptide (GRP) Decrease bicarbonate secretion Drug Induced PUD Drug Action Iron, K+, Tetracyclines Corrosive to mucosa Reserpine. TCA, Anticholinergics sympathetic, parasympathetic tone – acid output Alcohol acid output (secretagogue) Causes gastritis, bleeding is possible, not thought to cause ulcer Caffeine acid production (even decaffeinated); No in ulcer formation, lowers (LES) so may cause GERD symptoms NSAIDS Inhibits prostaglandin synthesis (COX inhibition) Disrupts functional mucosal integrity mucosal blood flow cell regeneration Direct GI irritation Antiplatelet effect (causing bleeding) Ion trapping acid (basal and maximal stimulation) secretion Risk Factors for NSAID-Induced GI Injury History of ulcer or GI complications Increasing age Concomitant anticoagulation therapy Concomitant corticosteroid use High dose NSAID use or concomitant aspirin/NSAID use Conditions Associated with PUD Fig. 40-2. Feldman: Sleisenger & Fortran’s Gastrointestinal and Liver Disease, 7th ed. Smoking Impairs ulcer healing Promotes ulcer recurrence Increases the likelihood of ulcer complications Mechanisms Stimulate gastric acid secretion Stimulate bile salt reflux Causes alteration in mucosal blood flow Decrease mucus secretion Reduces prostaglandin synthesis Decrease pancreatic bicarbonate secretion Acid and Pepsin ? Mechanism of damage: gastrin releasing peptide (GRP) defect in inhibition of acid production mucosal bicarbonate secretion basal acid secretory drive postprandial acid secretory response sensitivity to secretagogues Effects of Diet and Stress Diet and Stress Action Diet Dyspepsia, may pain - not believed to cause ulcer or assist healing Physiologic stress ↓ mucosal blood flow, tissue hypoxia, mucosal lining degradation; e.g. ICU, sepsis, burn, trauma. Associated with multiple erosions & significant bleeding Psychological stress Similar # stressful events in ulcer vs. non-ulcer patients ↓ tolerance to discomfort Recent epidemiological data suggest possible role Gastric Ulcer Duodenal Peptic Ulcers Stages of Ulcer Formation Erosion Ulcer Chronic Ulcer Sclerosis Signs and Symptoms of GU or DU Epigastric pain Not well localized Annoying, burning, gnawing, aching Duodenal ulcers On an empty stomach During the night Between meals Relieved by food and antacids Episodic followed with symptomatic periods then no occurrence Complications of PUD Hematemesis Perforation Diarrhea Obstruction Nausea Vomiting Weight Loss Weakness Complications: PUD Stress Ulcer Duodenal Ulcer Gastric Ulcer Hemorrhage: Frequent, associated mortality Common in posterior wall of duodenal bulb, associated with melena Less common (associated with hematemesis, coffee grind emesis), melena Perforation: Common When in anterior wall of duodenum More common in anterior wall of stomach Obstruction: ? Common Rare Malignancy: Rare 7% Rare Objective Measures Melena Hct, Hgb Microcytic, hypochromic indices Pale conjunctiva BUN/Cr Ratio Heme +ve stool Diagnosis Gastric Ulcer/Duodenal Ulcer Upper endoscopy (gold standard) H. pylori Noninvasive: Urea breath test, serology Invasive: biopsy (histology, culture, rapid urease) NSAID- induced History Still need to rule out H pylori infection Gastroesophageal Reflux Disease (GERD) Reflux of gastric or intestinal contents Results in heartburn, “burping” bitter taste Signs and Symptoms Heartburn - hallmark symptom Typical: Belching, regurgitation Alarm symptoms: Atypical Weight loss Bleeding Choking Hoarseness, cough, wheeze Dysphagia (difficulty swallowing) Odynophagia (painful swallowing) Atypical chest pain Infants: spitting up, vomiting (uncommon: failure to gain weight, Fe def anemia, recurrent pneumonia, near SIDS) Spectrum of Gastroesophageal Reflux Disease (GERD) Acid reflux Esophagitis Esophageal ulceration Barrett’s esophagus Possible Extraesophageal Manifestations of GERD ENT Pharyngitis Otitis media Sinusitis Vocal cord granulomas Laryngitis Hoarseness Voice changes Chronic cough Dental enamel loss Pulmonary Chronic cough Asthma Idiopathic pulmonary fibrosis Chronic bronchitis Pneumonia Other Chest pain Sleep apnea Dental erosions GERD Pathophysiology Aggressive Factors Composition acid/pepsin -Volume of refluxate Loss of LES pressure -Inappropriate relaxation -Increase in intraabdominal pressure Defects in defense mechanisms -Anatomical -Mucosal resistance -Esophageal clearance -Gastric emptying Lower Esophageal Sphincter LES Closed LES Open Risk Factors Factors that decrease LES pressure Diet Alcohol Smoking Drugs Factors that increase intra-abdominal pressure Obesity Pregnancy Bending over Foods and Drugs Affecting LES RAISE LES Pressure LOWER LES Pressure Foods Proteins, carbohydrates Caffeine, Carminatives, Chocolates, Citrus, Garlic, Fat, Tomatoes Drugs Alpha-agonists Beta-blockers Cholinergics Cisapride Metoclopramide Alcohol, άantagonists, Anticholinergics Barbiturates Beta-agonists Calcium channel blockers Diazepam Dopamine Adapted from Gonzales et al. DICP 1990;24:1065 Meperidine Methylxanthines Narcotics Nicotine Nitrates Progesterone Prostaglandins Tricyclic antidepressants Estrogen Non Pharmacologic Interventions Helps 20% of patients Weight loss Small size food portions Loose fitting clothes Cigarette smoking cessation Avoid chocolate, alcohol, peppermint, fatty meals, spicy meals, citric juices, cola, beer Avoid meals 2 hours before lying down Elevate the head of the bed with a 6-8” block Elevation of Head of Bed Complications of GERD Infants: Failure to Thrive Esophagitis (histopathological changes) Gradations Grade I- erythema, edema Grade II- isolated erosions Grade III- confluent erosions, superficial ulceration Grade IV- erosions, deep ulcers, stricture Peptic stricture Worsening obstructive lung disease Barrett’s esophagus Malignancy GERD and Cancer Risk Esophageal adenocarcinoma 8 times higher in patients with heartburn, regurgitation, or both at least once a week Esophageal carcinoma 11 times higher in patients with nighttime symptoms of GERD Lagergren J, et al. New Engl J Med. 1999;240:825-831 GERD in Obstructive Lung Disease Lung Effects Reflux Effects Acid aspiration Chronic airflow trapping, irritates airways diaphragmatic flattening may reduce VagallyLES competency mediated Lung Dx: -ve bronchospasm intrathoracic pressure/+ abdominal via transient pressure acid reflux Bronchodilators LES pressure