Peptic ulcer


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Peptic ulcer

  1. 1. PEPTIC ULCER Dr. S. Parasuraman Faculty of Pharmacy, AIMST University, Malaysia
  2. 2. The gastrointestinal tract (GIT, alimentary tract, gut) • It consists of an irregular tube about 6 m long, extending from the mouth to the anus. • The upper GIT Which includes the mouth, oesophagus and stomach. • The lower GIT Which comprises the duodenum, jejunum, ileum, colon, rectum and anus. • The accessory organs liver, gallbladder and pancreas
  3. 3. Abnormalities of the GIT • Dysphagia: – Difficulty swallowing, caused by obstruction of the esophagus – Obstruction may be caused by • tumors, congenital narrowing • Neurologic disorders such as brain injury stroke or Parkinson’s disease may affect voluntary swallowing or peristalsis of the esophagus • Dyspepsia – Epigastric fullness, discomfort, indigestion • Odynophagia – Painful swallowing usually associated with dysphagia • Heartburn – Burning sensation retrosternally associated with reflux
  4. 4. Abnormalities of the GIT • Anorexia – Loss of appetite • Haematemesis – Vomiting blood (could be red or altered “coffee ground”) • Melaena – Passing of black tarry, offensive stool (usually due to upper GI bleeding) • Haematochezia – Passing blood through rectum (PR bleeding) • Gastritis – Inflammation of the gastric mucosa – Acute gastritis – Chronic gastritis
  5. 5. Abnormalities of the GIT • Peptic ulcers A peptic ulcer is an abnormal area of mucosa that has been damaged by the pepsin and hydrochloric acid of gastric juice, with consequent inflammation of the underlying and surrounding tissue. Erosion may subsequently occur into the lamina propria and submucosa to cause bleeding. – Most of peptic ulcer occur either in the duodenum, or in the stomach – Ulcer may also occur in the lower oesophagus due to reflexing of gastric content – Rarely in certain areas of the small intestine
  6. 6. Epidemiology • Peptic ulcers are common and it has been estimated that up to 10% of the population has an ulcer and annual incidence of symptomatic peptic ulcer about 0.3%. • Duodenal ulcers are four times as common as gastric ulcers and occur mainly in the duodenal cap. • Gastric ulcers occurs mostly in the lesser curvature of the stomach. These are benign, some time develop as a tumors (5%). • Gastric malignancy is common in Japan, Chile, Finland and Iceland than other world countries (because of environmental and diet factor).
  7. 7. Aetology Aetology of peptic ulcer disease is multifactorial. • Infection with the bacteria Helicobacter pylori occurs in 80 to 95% of patients with peptic ulcer disease. • H. pylori infection impairs the protective mechanisms of the G.I. tract against low pH and digestive enzymes and leads to ulceration of the mucosa. • Stress — Emotional, trauma, surgical. • Injury or death of mucus-producing cells. • Chronic use of NSAIDs • Smocking • Alcohol and diet • Hypercalcemia (↑gastric secretion)
  8. 8. Aetology • Excess acid production in the stomach. The old hypothesis that ulceration is caused simply by hyperacidity is not tenable. About 70% of gastric ulcers and 50% of duodenal ulcers are not associated with abnormally high acid production. • Genetic factor: The lifetime prevalence of developing ulcer disease in first-degree relatives of ulcer patients is about three times greater than the general population. 20-50% of duodenal ulcer reported a positive family history. • Ulcers are also more common in blood group O subjects and in those who do not secrete blood group antibodies into gastric secretions.
  9. 9. Classification of peptic ulcer • Peptic ulcers classified based on region or location of illness – – – – Stomach (called gastric ulcer) Duodenum (called duodenal ulcer) Esophagus (called Esophageal ulcer) Meckel's Diverticulum (called Meckel's Diverticulum ulcer) Modified Johnson Classification of peptic ulcers Type I: Ulcer along the lesser curve of stomach Type II: Two ulcers present - one gastric, one duodenal/prepyloric Type III: Prepyloric ulcer Type IV: Proximal gastroesophageal ulcer Type V: Anywhere (associated with chronic NSAID use)
  10. 10. Sites of peptic ulcer • Duodenum: First portion, Anterior wall • Stomach: usually antrum, lesser curvature (common), anterior and posterior wall, greater curvature (less common) • Meckel’s diverticulum In the margins of a gastroenterostomy (stomal ulcer) • In the duodenum, stomach or jejunum of patients with Zollinger- Ellison syndrome. • Within or adjacent to a Meckel’s diverticulum. ZES
  11. 11. Symptoms of peptic ulcer Symptoms of peptic ulcer very with location of the ulcer and the patient age. • Abdominal discomfort • Pain or nausea (pain is located in the epogastrium; not radiate) Waterbrash • Waterbrash • Loss of appetite and weight loss • Hematemesis (vomiting of blood) Rarely, ulcer lead to a gastric or duodenal perforation. Hematemesis
  12. 12. Manifestations of peptic ulcer disease • Episodes of remission and exacerbation • Pain that for duodenal ulcers is often relieved by eating or antacids • G.I. bleeding and possible hemorrhage (20 to 25% of patients) • Perforation of ulcers with significant mortality • Obstruction of G.I. tract
  13. 13. Complications of peptic ulcer • Gastrointestinal bleeding. (Sudden large bleeding can be life threatening) • Cancer (Helicobacter pylori as the etiological factor making it 3-6 times likely to develop stomach cancer) • Perforation (hole in the wall) • Penetration.
  14. 14. Diagnosis of peptic ulcer
  15. 15. Diagnosis of peptic ulcer • Radiological Diagnosis: Barium x-ray or upper GI series is a widely used for diagnosis. Barium x-ray is difficult to analysis and less sensitive and accurate. • Laboratory test: – Noninvasive urea breath test. – Patient with refractory or recurrent peptic ulcer may have underlying H. pylori infection, histopathology investigation may req. – Serologic test for detecting H. pylori (levels of IgG and IgA ELISA test) – Stool antigen test for non-invasive detecting the presence of H. pylori. • Endoscopic diagnosis
  16. 16. Drugs for Treatment of Peptic Ulcer Disease • Antibiotics for eradication of H. pylori, if present (amoxicillin, clarithromycin) • Antacids (magnesium hydroxide, aluminum hydroxide) • H2 receptor antagonists (ranitidine, cimetidine) • Proton-pump inhibitors (omeprazole) • Mucosal protective agents (bismuth, sucralfate)
  17. 17. Management of peptic ulcer The objectives of management are to: • relieve pain and discomfort • accelerate healing • prevent recurrence and complications
  18. 18. Thank you
  19. 19. Helicobacter pylori & Ulcer • H. pylori -- causes chronic and indolent inflammation by damaging the mucosal defense system by reducing the thickness of the mucus gel layer, diminishing mucosal blood flow, and interacting with the gastric epithelium throughout all stages of the infection. • H. pylori infection can also increase gastric acid secretion by producing various antigens, virulence factors, and soluble mediators
  20. 20. Helicobacter pylori & Ulcer
  21. 21. Zollinger–Ellison syndrome • Tumors of the gastrinsecreting endocrine cells of the pancreas or, less frequently, the duodenal wall. • Leads to excessive acid production by the G.I. tract. • Development of serious and aggressive peptic ulcers. • Complications can include perforation, hemorrhage and obstruction. • Treatment may include resection of tumor, administration of H2 receptor antagonists, anticholinergics and antacids.