Gastric and Duodenal Ulcers

Conventional Treatment of Active Duodenal and Gastric Ulcers and Long-Term Maintenance of Ulcer Healing... 

Acute treatment of duodenal and gastric ulcers PO 40 mg/day at bedtime Duodenal ulcer maintenance PO 20 mg/day at bedtime Gastroesophageal reflux disease PO 20 mg twice a day Esophagitis PO 2-40 mg twice a day. 

Graham DY, White RH, Moreland LW, Schubert TT, Katz R, Jaszewski R, Tindall E, Triadafilopoulos G, Stromatt SC, Teoh LS. Duodenal and gastric ulcer prevention with misoprostol in arthritis patients taking NSAIDs. Misoprostol Study Group. Ann Intern Med 1993 119(4) 257-62. 

Sucralfate [Carafate, Sulcrate). Sucralfate is a disaccharide that exerts a cytoprotective effect on the stomach mucosa.26,37 Although the exact mechanism is unclear, sucralfate may form a protective gel within the stomach that adheres to ulcers and shields them from the contents of the stomach. The protective barrier formed by the drug prevents further erosion and permits healing of duodenal and gastric ulcers. Sucralfate is well tolerated, although constipation may occur in some patients. 

Optimal therapy of patients with peptic ulcer disease (both duodenal and gastric ulcers) who are infected with K pylori requires antimicrobial treatment. To document infection with fcL pylori, endoscopic biopsy of the gastric mucosa or various noninvasive methods are available, including serologic tests and breath tests for urea. Figure 24.2 shows a biopsy sample with i . pylori closely associated with the gastric mucosa. Eradication of FL pylori results in rapid healing... 

Ranitidine (Zantac /GlaxoSmithKline) is a histamine H2-receptor antagonist that inhibits the release of gastric acid and is useful in the treatment of a variety of hypersecretory conditions [dyspepsia, heartburn, duodenal and gastric ulcers, and gastroesophageal reflux (GERD)]. Lansoprazole (Prevacid /TAP), omeprazole (Prilosec /AstraZeneca), and esomeprazole (Nexium /AstraZeneca) are benzimidazole... 

As mentioned earlier, blood losses from menstruation can result in iron deficiency and anemia. Other sources of blood loss arc important as well. The normal rate of blood loss in the feces is 0,5 to 1.0 ml/day. intestinal blood losses can increase in certain cancers. About 60% of the cancers of the colon and rectum lead to further blood losses of 2 to 10 ml/day. The fecal blood test is universally used to screen for the presence of cancer of the gastrointestinal tract- In the absence of periodic testing, cancer may first present as iron deficiency anemia. Duodenal and gastric ulcers, as well as hemorrhoids, arc extremely common sources of blood loss and can result in iron depletion. Aspirin, when consumed in large amounts, can provoke bleeding of the gastrointestinal tract, resulting In blood losses of 1 to 5 ml/day. 

Trade names Bralix Diporax Epirax Librax (Valeant) Libraxin Librocol Nirvaxal Quarzan Spasmoten Indications Duodenal and gastric ulcers Category Muscarinic antagonist Half-life N/A... 

I CONVENTIONAL TREATMENT OF ACTIVE DUODENAL AND GASTRIC ULCERS AND LONG-TERM MAINTENANCE OF ULCER HEALING... 

Pantoprazole, a substituted benzimidazole sulphoxide, is a proton-pump inhibitor recommended for the treatment of acid-related GI diseases such as reflux esophagitis and duodenal and gastric ulcers (see also Figure 72). 

Cimetidine 11 is used in the treatment of duodenal and gastric ulcers. It reduces gastric acid secretion by blocking the histamine receptor which stimulates gastric acid secretion (H2 receptor), but does not affect the H receptor. 

Isopropamide iodide is recommended for use in the treatment of peptic ulcer and various other states of gastrointestinal hyperactivity. It has also been advocated as an adjunct in the therapy of duodenal and gastric ulcer and invariably in the relief of visceral spasms. 

Chisholm MA. Pharmaootherapy of duodenal and gastric ulcerations. Am J Pharm Ed 1998 62 196-203. 

Prilosec is prescribed to treat duodenal and gastric ulcers the nurse would not question this medication. 

Both acid and pepsin contribute to aggressive factors enabling peptic ulcer disease or reflux erosions. The recent implication of H. pylori in generation of duodenal and gastric ulcer disease has added an additional element for consideration as an aggressive factor that can result in loss of epithelial integrity. 

Whether bacterial overgrowth plays a significant aetiopathogenetic role under the three conditions summarized in Table 3 is doubtful, because it can be expected in all three groups of patients and thus would hardly explain the variable cancer risk, especially the difference between duodenal and gastric ulcer patients. 

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