Management.

Primary (first-line) H. pylori eradication therapy: H+/K+ ATPase inhibitors (omeprazole), amoxicillin or metronidazole, clarithromycin.

Second-line H. pylori eradication therapy: H+/K+ ATPase inhibitors (omeprazole, lansoptrazole), tetracycline, bitsmuth, metronidazole.

Other inhibitors of gastric secretion: H2-receptors antagonists drugs (cimitidine, ranitidine, famotidine), M-cholin-receptor antagonists drugs.

Antacids.

Table 3. Treatment of Peptic Ulcers
Treatment	Comment	Options
radication of Helicobacter pylori	Treatment duration is 10 to 14 days (although courses lasting 1 to 7 days have been reported to have comparable effectiveness Eradication rates 80 to 90 % or higher	Omeprazole 20 mg 2t daily or lansoprazole 30 mg 2td plus amoxicillin 1 g 2td or metronidazole 500 mg 2td (if allergic to penicillin) plus clarithromycin 500 mg 2td
Ranitidine bismuth citrate (Tritec)* 400 mg 2td plus clarithromycin 500 mg 2td or metronidazole 500 mg 2td plus tetracycline 500 mg 2td or amoxicillin 1 g 2td
Levofloxacin 500 mg daily plus amoxicillin 1 g two times daily plus pantoprazole 40 mg two times daily
Bismuth subsalicylate 525 mg (2 tablets) 4 times daily plus metronidazole 250 mg 4t daily plus tetracycline 500 mg 4t daily plus H2 blocker for 28 days or proton pump inhibitor for 14 days
Histamine H2 blockers	70 to 80 % healing in duodenal ulcer after 4 weeks, 87 to 94 % after 8 weeks	Ranitidine 150 mg 2t daily or 300 mg at night Famotidine 20 mg 2t daily or 40 mg at night Cimetidine 400 mg 2t daily or 800 mg at night
Proton pump inhibitors	Treatment duration is 4 weeks for duodenal ulcer and 8 weeks for gastric ulcer 80 to 100 % healing	Omeprazole 20 mg daily Lansoprazole 15 mg daily Rabeprazole 20 mg daily Pantoprazole 40 mg daily
Sucralfate (Carafate)	Treatment duration is 4 weeks Effectiveness similar to H2 blockers	1 g 4 times daily
Surgery	Rarely needed	Duodenal ulcer: truncal vagotomy, selective vagotomy, highly selective vagotomy, partial gastrectomy Gastric ulcer: partial gastrectomy with gastroduodenal or gastrojejunal anastomosis

Complications of gastric resection Early satiety and vomiting. Rapid gastric emptying leads to distension of the proximal small intestine as the hypertonic contents draw fluid into the lumen. This leads to abdominal discomfort and diarrhoea after eating. Autonomic reflexes release a range of gastrointestinal hormones which lead to vasomotor features such as flushing, palpitations, sweating, tachycardia and hypotension ('early dumping'). Patients should therefore avoid large meals with high carbohydrate content.

Late dumping syndrome. Symptoms of dumping occur 90-180 minutes after eating. The pathogenesis is broadly similar to early dumping, but in addition reactive hypoglycaemia occurs and may cause mental confusion. Rapid emptying of carbohydrates into the proximal small intestine results in an exaggerated release of insulin with subsequent reactive hypoglycaemia.

Secondary prevention of PU – by H+/K+ ATPase inhibitors.

Complications

Obstruction - Gastric outlet obstruction (GOO) is not a single entity; it is the clinical and pathophysiological consequence of any disease process that produces a mechanical impediment to gastric emptying.

The major benign causes of GOO are PUD, gastric polyps, ingestion of caustics, pyloric stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars. Pancreatic cancer is the most common malignancy causing GOO. Outlet obstruction may occur in 10-20% of patients with pancreatic carcinoma. Other tumors that may obstruct the gastric outlet include ampullary cancer, duodenal cancer, cholangiocarcinomas, and gastric cancer. Metastases to the gastric outlet also may be caused by other primary tumors.

Intrinsic or extrinsic obstruction of the pyloric channel or duodenum is the usual pathophysiology of GOO; as previously noted, the mechanism of obstruction depends upon the underlying etiology.

Nausea and vomiting are the cardinal symptoms of GOO. Vomiting usually is described as nonbilious, and it characteristically contains undigested food particles. In the early stages of obstruction, vomiting may be intermittent and usually occurs within 1 hour of a meal. Early satiety and epigastric fullness are common. Weight loss is late, is most significant in patients with malignant disease. Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer.

Physical examination often demonstrates the presence of chronic dehydration and malnutrition. A dilated stomach may be appreciated as a tympanitic mass in the epigastric area and/or left upper quadrant.

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