Snapshot A 65-year-old-male presents with complaints of epigastric pain and belching, which improves when he eats food but gets worse within a few hours after his meal. The pain is described as stabbing, intermittent, and concentrated at the epigastric region. He noticed a 5-lb. weight loss over the past 3 months and a dark color to his stools. Calcium carbonate seems to help with the pain. Introduction Clinical definition characterized by erosion and defects in the mucosal lining of the stomach, duodenum, and sometimes the lower esophagus that persists as a function of the acid or peptic activity in gastric juice gastric ulcers describe ulcers occurring at the stomach duodenal ulcers describe ulcers occurring at the duodenum duodenal ulcers abdominal pain is relieved with food intake the majority (90%) of cases are secondary to Helicobacter pylori lower risk of malignancy gastric ulcers abdominal pain is exacerbated with food intake the leading causes are H. pylori followed by nonsteroidal anti-inflammatory drugs (NSAIDs) use higher risk of malignancy Epidemiology demographics ulcer incidence increases with age H. pylori is the predominant cause of peptic ulcer disease (PUD) worldwide increasing prevalence of NSAID-related PUD due to widespread use of aspirin and NSAID risk factors NSAIDs smoking stress age Pathogenesis development of ulcers is secondary to the disruption of normal protective mechanisms of the gastric mucosa (e.g., bicarbonate) H. pylori secretion of urease creates an alkaline environment which allows for the survival of the bacteria inflammatory cytokines inhibit parietal cell acid secretion causing gastric ulcers at the pyloric antrum, somatostatin production is reduced and gastric production is increased, leading to metaplasia of the duodenal cells and causing duodenal ulcers NSAIDs mechanism of action blocks the function of cyclooxygenase-1 (COX-1), which is essential for the production of prostaglandins that stimulates the secretion of mucous that protects the gastric mucosa also inhibits stomach mucosa cell proliferation and mucosal blood flow other causes stress from serious illness gastric ischemia metabolic disturbances vasculitis gastrinoma (Zollinger-Ellison syndrome) Associated conditions Zollinger-Ellison syndrome suspect in patients with refractory duodenal ulcers Behcet disease Crohn disease Painful sores or ulcers in the lining of the stomach or duodenum breach in the mucosa with extension into the submucosa or deeper Occurs when gastric acid secretion outweighs mucosal defenses most commonly due to decreased mucosal barrier NSAIDs H. pylori smoking less commonly due to acid hypersecretion such as gastrinoma (Zollinger-Ellison syndrome) Presentation Symptoms abdominal pain most commonly at the upper quadrants belching vomiting weight loss poor appetite bloating hematemesis melena Physical exam abdominal tenderness peritoneal signs of perforation Imaging Esophagogastroduodenoscopy (EGD) gold standard of diagnosis indicated in patients who show no symptom improvement following few weeks of treatment allows for direct visual identification and allows for evaluation of the location and severity of the disease biopsy is important for the differentiation between benign ulcers and malignancy Abdominal and chest radiographs may be useful in detecting pneumoperitoneum secondary to perforation positive findings include air-fluid levels with bowel dilation or free air Studies Urease breath test best initial test noninvasive and allows for the detection of H. pylori infection Complete blood count often normal Differential Gastric malignancy differentiating factors lesions will appear different on endoscopy and will be confirmed via biopsy Chronic pancreatitis differentiating factors may have characteristic disease history and will present with calcifications on abdominal imaging Treatment Management depends on disease etiology and severity Lifestyle discontinue smoking and NSAIDs H. pylori induced PUD clarithromycin, amoxicillin, and pantoprazole for 7-14 days clarithromycin, amoxicillin, pantoprazole, and metronidazole for 7-14 days NSAID-induced PUD stop NSAID use introduce proton pump inhibitor (PPI) use Bleeding ulcers resuscitation with IV fluids and/or blood products IV PPI endoscopic therapy with either cautery, endoclip, or epinephrine injection Surgery indicated in patients with perforated ulcer and/or hemorrhage requires IV antibiotics and PPI prior to repair other indications include PUD refractory to medical therapy and Zollinger-Ellison syndrome Complications Bleeding Perforation manage with broad spectrum antibitoics, PPI, and emergency surgery perforated gastric ulcers may erode the left gastric artery perforated duodenal ulcers may erode the gastroduodenal artery Obstruction Malignancy