Gastritis and Peptic Ulcer Disease (PUD) Acute and Chronic Gastritis Etiology and Pathophysiology o Gastritis is inflammation of the gastric lining, or mucosa, of the stomach Can be chronic or acute, w/ some symptoms being localized to area and some being diffuse Gastritis occurs because of a breakdown in the gastric mucosal barrier, which normally protects the stomach from the corrosion of hydrochloric acid and pepsin. Tissue edema occurs w/ disruption of capillary walls and plasma can leak into gastric lumen Hemorrhage may occur w/ corrosion of gastric lining Causes of gastritis: variety of factors including certain drugs, foods, microorganisms, and pathophysiologic conditions o Factors broken down: Drugs: Corticosteroids: inhibit prostaglandins (gastric mucosal protectant), increasing risk of gastritis NSAIDS: can erode stomach lining Dietary factors: Alcohol Spicy, irritating foods Caffeine Microorganisms: H. Pylori Salmonella organisms Staphylococcus organisms Pathophysiological conditions: Burns Large hiatal hernia Physiologic stress Reflux of bile and pancreatic secretions Renal failure (uremia) Sepsis Shock Other: Smoking cigarettes Endoscopic procedures NG Tube Psychologic stress Radiation exposure Peptic Ulcer Disease Pathophysiology Is erosion of the stomach’s lining (gastric mucosa, submucosa, and/or muscularis) resulting from digestive action of HCl and pepsin o When mucosa becomes damaged histamine is released, further secretion of HCl and pepsin Can be acute or chronic ulcers: o Acute: associated with superficial erosion and minimal inflammation Resolves quickly when cause is identified and removed o Chronic: ulcer of long duration, eroding through the muscular wall w/ the formation of fibrous tissue Continuously present for many months or intermittently throughout a person’s lifetime More common than acute ulcers (PEPTIC) Gastritis and Peptic Ulcer Disease: Clinical Manifestations Treatment of Gastritis Peptic Ulcer Disease: medical care Conservative treatment of PUD consists of adequate rest, drug therapy, lifestyle changes (smoking cessation and dietary management), and long-term follow-up care. The aim of treatment is to decrease gastric acidity and enhance mucosal defense mechanisms. Acute exacerbations w/o complications treatment: o NPO (to include regular mouth care) o NG suction with intermittent not constant suction o Adequate rest promotes ulcer healing o IV fluid replacement o Drug therapy o PPIs o H2-receptor blockers o Antibiotics for H. pylori infection o Cytoprotective drugs o Antacids o Anticholinergics (used rarely) Acute exacerbations w/ complications treatment: o Hemorrhage: frequent vital signs, lab values (possible blood transfusions), maintain NG patency, o Perforation: notify healthcare provider immediately, frequent vital signs (q 15 min), NPO, maintain IV rate or increase, antibiotic therapy, ready the patient for possible OR o Gastric Outlet Obstruction: NG suction with regular irrigation to maintain patency, IV fluids o Stomach lavage (possible) Education for PUD and Gastritis SUMMARY: