Gastritis and Peptic Ulcer Disease Year 4 Paediatrics Notes

Gastritis and Peptic Ulcer Disease Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.2 / MUNGE / GIT -- Slide 1 Gastritis and Peptic Ulcer Disease Dr Rose Munge Slide 2 Introduction Peptic ulcer disease, results from inflammation caused by an imbalance between cytoprotective and cytotoxic factors in the stomach and duodenum. It manifests with varying degrees of gastritis or frank ulceration.\n The pathogenesis of peptic ulcer disease is multifactorial- the final common pathway for the development of ulcers is the action of acid and pepsin-laden contents of the stomach on the gastric and duodenal mucosa and the inability of mucosal defense mechanisms to allay those effects. Slide 3 Peptic ulcers are defined as deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall. Gastric ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb. Can be classified as primary peptic ulcers, which are chronic and more often duodenal, or secondary, which are usually more acute in onset and are more often gastric. Slide 4 Primary ulcers are most often associated with Helicobacter pylori infection; idiopathic primary peptic ulcers account for up to 20% of duodenal ulcers in children.\n Secondary peptic ulcers can result from stress caused by sepsis, shock, or an intracranial lesion (Cushing ulcer), or in response to a severe burn injury (Curling ulcer). Secondary ulcers also the result of using aspirin or nonsteroidal anti inflammatory drugs (NSAIDs); hypersecretory states like Zollinger-Ellison syndrome, short bowel syndrome, and systemic mastocytosis are rare causes of peptic ulceration Slide 5 Pathogenesis Acid Secretion By 3-4 yr of age, gastric acid secretion approximates adult values.\n Acid initially secreted by the oxyntic cells of the stomach has a pH of approximately 0.8, whereas the pH of the stomach contents is 1-2.\n Excessive acid secretion is associated with a large parietal cell mass, hypersecretion by antral G cells, and increased vagal tone, resulting in increased or sustained acid secretion in response to meals and increased secretion during the night. Slide 6 The secretagogues that promote gastric acid production include acetylcholine released by the vagus nerve, histamine secreted by enterochromaffin cells, and gastrin released by the G cells of the antrum.\n Mediators that decrease gastric acid secretion and enhance protective mucin production include prostaglandins Slide 7 Pathogenesis cont. Mucosal Defense 1. A continuous layer of mucous gel that serves as a diffusion barrier to hydrogen ions and other chemicals covers the gastrointestinal (GI) mucosa.\n Mucus production and secretion are stimulated by prostaglandin E2. 2. The epithelium forms a second-line barrier, the characteristics of which are determined by the biology of the epithelial cells and their tight junctions.\n Another important function of epithelial cells is to secrete chemokines when threatened by microbial attack. Slide 8 Secretion of bicarbonate into the mucous coat, which is regulated by prostaglandins, is important for neutralization of hydrogen ions.\n If mucosal injury occurs, active proliferation and migration of mucosal cells occurs rapidly, driven by epithelial growth factor, transforming growth factor-α, insulin-like growth factor, gastrin, and bombesin, and covers the area of epithelial damage. Slide 9 Clinical Manifestations The presenting symptoms varies with the age of the patient. Hematemesis or melena is reported in up to half of the patients with peptic ulcer disease.\nSchool-age children and adolescents present with epigastric pain and nausea, similar to the presentation generally seen in adults. Dyspepsia, epigastric abdominal pain, and fullness are also seen in older children.\nInfants and younger children usually present with feeding difficulty, vomiting, crying episodes, hematemesis, or melena.\nIn the neonatal period, gastric perforation can be the initial presentation. Slide 10 The classic symptom of peptic ulceration, epigastric pain alleviated by the ingestion of food, is present only in a minority of children.\nMany present with poorly localized abdominal pain, which may be periumbilical.\nThe majority of patients with periumbilical or epigastric pain or discomfort do not have a peptic ulcer, but rather a functional GI disorder, such as irritable bowel syndrome or nonulcer (functional) dyspepsia.\nPatients with peptic ulceration rarely present with acute abdominal pain from perforation or symptoms and signs of pancreatitis from a posterior penetrating ulcer. Occasionally, bright red blood per rectum may be seen if the rate of bleeding is brisk and the intestinal transit time is short.\nVomiting can be a sign of gastric outlet obstruction. Slide 11 The pain is often described as dull or aching, rather than sharp or burning, as in adults.\nIt can last from minutes to hours; patients have frequ