Dyspepsia: Gastric Ulcer & Duodenal Ulcer

Dyspepsia:Gastric Ulcer & Duodenal UlcerIzatty Lim0308188Batch 4

defined as having one or more symptoms of epigastric pain, burning, postprandial fullness, or early satiety.BloatingNausea Loss of appetite Dyspepsia

PUD

Type Itypically located near the angularis incisura on the lesser curvature, close to the border between the antrum and the body of the stomach. Patients with type I gastric ulcers usually have normal or decreased gastric acid secretion.Type IIa combination of stomach and duodenal ulcers and are associated with normal or increased gastric acid secretion.Type IIIprepyloric and are associated with normal or increased gastric acid secretion.Type IVoccur near the gastroesophageal junction, and gastric acid secretion is normal or below normal.

Types of Gastric Ulcer

Etiology:H. pylori bacteriumNSAID

Gastric Ulcer

H. pylori

70% of gastric ulcer patients are infected with H. pylori. Majority of colonised people remain healthy and asymptomatic.

uses adhesin molecules (BabA) to bind to Lewis b antigen on epeithelial cells.

induces an intense inflammatory and immune responseIL-1, IL-6, tumor necrosis factor, IL-8Production of ammonia by the enzyme ureaseToxic to epithelial cell Increase gastrin release from G cells Negative feedback loop for gastrin release is haltedstimulates increased acid production by parietal cells.

Pathophysiology

Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor, and, most notably, IL-8. IL-8 is produced by the mucosal epithelial cells, and it recruits and activates neutrophils.Several bacterial gene products are involved in causing epithelial cell injury and induction of inflammation. Epithelial injury is mostly caused by a vacuolating toxin called VacA, which is regulated by the cytotoxin-associated gene A (CagA). This gene is a component of the Cag pathogenicity island, a cluster of 29 genes, some of which encode pro-inflammatory proteins. In addition, H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. The organisms also elaborate phospholipases that damage surface epithelial cells. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucus, thus weakening the first line of mucosal defense.H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. This altered milieu seems to favor gastric metaplasia (the presence of gastric epithelium) in the first part of the duodenum. Such metaplastic foci provide areas for H. pylori colonization.Several H. pylori proteins are immunogenic, and they evoke a robust immune response in the mucosa. Both activated T cells and B cells can be seen in chronic gastritis caused by H. pylori. The B lymphocytes aggregate to form follicles. The role of T and B cells in causing epithelial injury is not established, but T-cell-driven activation of B cells may be involved in the pathogenesis of gastric lymphomas6

NSAIDDirect chemical irritation & COX enzyme inhibition, which prevent prostaglandin synthesisincreases secretion of hydrochloric acid and reduces bicarbonate and mucin production

Damage gastric and duodenal mucosal barrier increased risk of upper gastric ulcer, bleeding &perforation.

Pathophysiology

Suppression of mucosal prostaglandin synthesis, which increases secretion of hydrochloric acid and reduces bicarbonate and mucin production7

Smoking Increased risk of gastric ulcer and duodenal ulcer to a lesser extent.more likely to causing complication and less likely to heal if the patient continues to smoke.

Pathophysiology

recurrent abdominal pain localisation to the epigastriumRelation to foodEpisodic occurrance

Occasional vomitingAnorexia & nauseaCompletely silent presented with anaemia for the first timeRecurrent acute bleeding without ulcer painGnawing or burning sensation occurs shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer.

Diagnostic value of individual symptoms for PUD is poor.

Clinical Features

Upper GI endoscopyRapid urease testsFecal antigen testing detecting the presence ofH pyloriantigens in stoolsUrea breath test testing for the enzymatic activity of bacterial urease.Antibodies (IgG)X- raydetect free abdominal air when perforation is suspected. upper GI contrast studyextravasation of contrast indicates gastric perforationInvestigation

H. pylori eradicationproton pump inhibitor (PPI)based triple therapy.PPI, amoxicillin, and clarithromycin for 7-14 days. Amoxicillin should be replaced with metronidazole in penicillin-allergic patients only high rate of metronidazole resistance

NSAIDAmerican College of Gastroenterology (ACG ) guideline: test for H pylori done in patients who started long-term NSAID therapyNSAIDs should be immediately discontinued in patients with positive H pylori test results if clinically feasiblePatient with known history of ulcer and in whom NSAID use is unavoidable, the lowest possible dose and duration of the NSAID and co-therapy with a PPI or misoprostol are recommended.

Treatment

SurgicalRarely requiredChoice for a chronic non-healing gastric ulcer partial gastrectomy to exclude an underlying cancer.

Treatment

Duodenal ulcer and gastric ulcer both belong to the family of peptic ulcer disease.H. pylori infection is the major cause of duodenal ulcer followed by NSAIDThey share almost the same clinical features.

Duodenal Ulcer

Gastric UlcerSymptoms do not follow a consistent patternEating sometimes exacerbates rather than relieves pain

Gastric Ulcer vs Duodenal UlcerDuodenal UlcerTend to cause more consistent pain.Pain can awaken the patient at night.Pain is relieved by food, but recurs 2 to 3 hours after a meal

Complication

Harmon RC, Peura DA. Evaluation and Management of Dyspepsia [Internet]. Medscape. [cited 2015 May 24]. Available from: http://www.medscape.com/viewarticle/721062_1

Robbins basic Pathology. 9th Ed.

BS Anand. Peptic Ulcer Disease Treatment & Management [Internet]. [cited 2015 May 24]. Available from: http://emedicine.medscape.com/article/181753-treatment#aw2aab6b6b1aa

Davidsons Principle & Practice of Medicine. 22nd Ed.

References