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1) Protection of the Stomach:

Living stomach is protected in 5 ways from harsh acidic and enzymatic environment it creates: 1) Mucous coat: - thick, highly alkaline mucus resists the actions of acids & enzymes. 2) Epithelial cell replacement: - Stomach epithelial cells live only 3-6 days - are then sloughed off into the chyme & digested with food - replaced as rapidly by cells division in gastric pits. 3) Tight Junctions: - Epithelial cells joined by tight junctions - Prevent gastric juice from seeping between them & digesting the connective tissue of lamina propria and beyond. 4) Bicarbonate secretions: - Produced by epithelial cells in stomach & duodenum - Creates neutral PH environment into boundary zone of adherent mucus 5) Prostaglandin synthesis: - Stimulated by stretching of stomach, and is produced by mucous cells. - Favours production of bicarbonates and mucous & inhibit acid secretion by parietal cells.

2) Peptic Ulcer Disease (PUD): Gastritis inflammation of stomach Can lead to a peptic ulcer pepsin + HCL erode stomach wall. Occur commonly in duodenum Occasionally in oesophagus If untreated they can perforate the organ: Cause fatal haemorrhage or peritonitis Most fatalities occur in people over 65 No evidence between peptic ulcer and stress:

Stress-Related Ulcers. Stress ulcers are ulcers of the stomach or duodenum that occur in

the context of a profound illness or trauma requiring intensive care. The etiology of stressrelated ulcers differs somewhat from that of other peptic ulcers, involving acid and mucosal ischemia. Because of limitations on the oral administration of drugs in many patients with stress-related ulcers, intravenous H2-receptor antagonists have been used extensively to reduce the incidence of GI hemorrhage due to stress ulcers. Now that intravenous preparations of proton pump inhibitors are available, it is likely that they will prove to be equally beneficial. However, there is some concern over the risk of pneumonia secondary to gastric colonization by bacteria in an alkaline milieu. In this setting, sucralfate appears to provide reasonable prophylaxis against bleeding without increasing the risk of aspiration pneumonia. This approach also appears to provide reasonable prophylaxis against bleeding, but is less convenient (Cook et al., 1998).
Hypersecretion of acid and pepsin -- sometimes involved Most involve acid-resistant gram (-) bacterium, Helicobacter Pylori Invades mucosa of stomach & duodenum Opens the way to chemical damage to tissues Risk factors: smoking; aspirin usage + other NSAIDS NSAIDS, supress synthesis of prostaglandins o Normally stimulate secretion of protective mucus + acidreducing bicarbonate o Aspirin is an acid that directly irritates gastric mucosa

Gross appearance: a) Clean, sharply demarcated and slightly elevated around the edges b) Most gastric ulcers are benign o Small percentage maybe malignant c) Duodenal ulcers are never malignant d) Four layers in sequence are noted in histologic sections of ulcers: 1- Necrotic debris 2- Inflammation with a predominance of neutrophils 3- Granulation tissue (repair tissue) 4- Fibrosis

3) Comparison between Gastric Ulcers and Doudenal Ulcers: Feature Percentage of ulcer cases Epidemiology Gastric Ulcers 25% Male-female ratio 1.5 to 2:1 Smoking does not cause PUD but delays healing Duodenal Ulcers 75% Male-female ratio 3:1 Women are most affected at or after menopause. Increased risk in cirrhosis, Chronic Obstructive Pulmonary Disease, renal failure, hyperparathyroidism 80% of cases Defective mucosal barrier due to H. pylori Mucosal ischemia (reduced PGE), bile reflux, delayed gastric emptying

Helicobacter pylori Pathogenesis

90-95% of cases Defective mucosal barrier due to H. pylori

Increased acid production (increased parietal cell mass)

Basal Acid Output and Maximal Acid Output normal to decreased Location Single ulcer on lesser curvature of antrum (same gastric cancer location) Bleeding (most commonly in left gastric artery) Perforation

Complications

Clinical findings Diagnosis

Burning epigastric pain soon after eating Endoscopy; biopsy for gastric ulcers is a must for malignancy check-up.

Basal Acid Output and Maximal Acid Output both increased Single ulcer on anterior portion of first part of duodenum followed by single ulcer on posterior portion (danger of perforation into pancreas) Bleeding (most commonly in gastroduodenal artery) Perforation (air under diaphragm, pain radiates to left shoulder) Gastric outlet obstruction, pancreatitis Burning epigastric pain 1-3 hours after eating Endoscopy; biopsy is not needed for duodenal ulcer is never malignant.

Treatment

Stop Smoking, alcohol, and NSAIDS. Avoid foods that may cause such symptoms. Eradicate H. Pylori; Use H2 antagonists, PPI, or antacids Surgery Method: anteroctomy or hemigasterectomy for ulcer removal without selective vagetomy.

Stop Smoking, alcohol, and NSAIDS. Avoid foods that may cause such symptoms. Eradicate H. Pylori; use H2 antagonists, PPI, or antacids Surgery Method: selective vagetomy