Gastric & Duodenal Disorders

By completing this question set, you will be able to trace the H. pylori pathogenic cascade — from urease-mediated survival to ↓somatostatin → ↑gastrin → ↑acid → ulcerogenesis — and select the correct diagnostic test for each clinical context, knowing that serology cannot confirm eradication. You will distinguish gastric from duodenal ulcers by pain timing, weight change, cancer risk, and bleeding vessel anatomy. You will explain why NSAIDs cause gastropathy through COX-1 inhibition and apply risk-stratified gastroprotection decisions. You will interpret a fasting serum gastrin level and explain why secretin paradoxically increases gastrin in a gastrinoma but not in normal physiology. You will trace the Type A gastritis cascade from autoimmune parietal cell destruction to achlorhydria to hypergastrinemia to ECL hyperplasia to Type I gastric carcinoids. You will distinguish intestinal from diffuse gastric adenocarcinoma by the Lauren classification, identify the five named metastatic sites, and apply the Correa cascade from H. pylori infection to intestinal-type adenocarcinoma. You will explain why H. pylori eradication can cure MALT lymphoma, and why the t(11;18) translocation predicts treatment failure. You will identify GIST by KIT mutation and CD117 immunohistochemistry and explain why imatinib is effective. You will distinguish gastric carcinoid Types I, II, and III by their pathophysiologic context and malignant potential.