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peptic ulcer disease.pptx

  1. Peptic ulcer disease Ghadeer Ismail Eideh Supervised by Dr. Aref Rajabi From: step up to medicine
  2. Introduction 01 02 Clinical features 03 Diagnosis 04 Treatment 05 Causes Outlines
  3. Introduction 01
  4. A peptic ulcer is a sore on the lining of the stomach, small intestine or esophagus. Definition
  5. Intoduction • The term ‘peptic ulcer’ refers to an ulcer in the lower oesophagus, stomach or duodenum, in the jejunum after surgical anastomosis to the stomach or, rarely, in the ileum adjacent to a Meckel’s diverticulum. • Ulcers in the stomach or duodenum may be acute or chronic; both penetrate the muscularis mucosa but the acute ulcer shows no evidence of fibrosis.
  6. Causes Infectious cause H.Pylori (one of the most common cause) Drugs NSAID (one of the most common cause) Acid hypersecretory Zollinger-Ellison syndrome Other risk factor a. Smoking b. Alcohol use c. Emotional stress and dietary factors (such as coffee and spice intake)
  7. Gastric ulcer vs duodenal ulcer 02
  8. Types of gastric ulcers
  9. Clinical features 03
  10. a. Aching or gnawing in nature. b. Nocturnal symptoms and the effect of food on symptoms are variable. Epigastric pain Upper GI bleeding Clinical features May be complicated by upper GI bleeding.
  11. nausea/vomiting Early satiety, and weight loss Clinical features
  12. In some patients, the ulcer is completely ‘silent’, presenting for the first time with anemia from chronic undetected blood loss, as abrupt hematemesis or as acute perforation; in others, there is recurrent acute bleeding without ulcer pain. Clinical features
  13. DIAGNOSIS 04
  14. 1. Endoscopy a. Most accurate test in diagnosing ulcers. b. Essential in diagnosis of gastric ulcers because biopsy is necessary to rule out malignancy. c. Preferred when severe or acute bleeding is present (can perform electrocautery of bleeding ulcers). d. Can obtain endoscopic biopsy for diagnosis of H. pylori. Diagnosis
  15. 2. Barium swallow a. Sometimes used initially but is less reliable than endoscopy. b. Double-contrast techniques preferred due to improved accuracy. Diagnosis
  16. 3. Laboratory test—for diagnosis of H. pylori infection a. Biopsy: Histologic evaluation of endoscopic biopsy is the gold standard. b. Stool antigen test—High sensitivity and ease of testing makes this ideal for screening. c. Urease detection via urea breath test is highly sensitive and specific. It documents active infection and helps to assess the results of antibiotic therapy. Diagnosis
  17. d. Serology (lower specificity)—The presence of antibodies to H. pylori does not necessarily indicate current infection—antibodies to H. pylori can remain elevated for months or even years after eradication of infection. The following may lead to false-negative test results: PPIs, bismuth, many antibiotics, and upper GI bleeding. 4. Serum gastrin measurement—if considering Zollinger–Ellison syndrome as a diagnosis. Diagnosis
  18. • Gastric ulcers require a biopsy to rule out malignancy; duodenal ulcers do not require biopsy. • If a peptic ulcer is uncomplicated, a barium study or endoscopy is not needed initially. Initiate empiric therapy. However, if you suspect any of the complications of PUD, order confirmatory studies. Diagnosis
  19. Treatment 05
  20. 1. Medical—Majority of patients with PUD can be successfully treated by curing H. pylori infection, avoidance of NSAIDs, and appropriate use of antisecretory drugs. a. Supportive (patient directives) • Discontinue aspirin/NSAIDs. • Restrict alcohol use but do not restrict any foods. • Stop smoking, decrease emotional stress. • Avoid eating before bedtime (eating stimulates nocturnal gastric acid levels). Treatment
  21. b. Acid suppression therapy • PPIs—omeprazole (Prilosec), lansoprazole (Prevacid), block H+/K+ ATPase pump directly in parietal cell membrane. First line of therapy, most effective antisecretory agents. • H2 receptor blockers—cimetidine (Tagamet) and ranitidine (Zantac). Block histamine-based parietal cell acid secretion. Less effective than PPIs. • Antacids—somewhat outdated for primary therapy and more appropriately used for adjunctive therapy/symptomatic relief. Examples include aluminum hydroxide (Mylanta), calcium carbonate (Tums), bismuth subsalicylate (PeptoBismol). Treatment
  22. c. Eradicate H. pylori with triple or quadruple therapy (see Table 3-5). Once infection is cleared, the rate of recurrence is very low. • For initial therapy, triple therapy (PPI, amoxicillin, and clarithromycin) for 14 days. • Quadruple therapy (PPI, bismuth, metronidazole, and tetracycline) indicated for patients with risk factors for macrolide resistance. Treatment
  23. Treatment
  24. d. Cytoprotection • Sucralfate—facilitates ulcer healing. Must be taken frequently, is costly, and can cause GI upset. • Misoprostol—reduces risk for ulcer formation associated with NSAID therapy. Costly, and can cause GI upset (common side effect). Treatment
  25. e. Treatment regimens • If H. pylori test is positive, begin eradication therapy with either triple or quadruple therapy (see Table 3-6). Also begin acid suppression with antacids, an H2 blocker, or a PPI. • If the patient has an active NSAID-induced ulcer, stop NSAID use (may switch to acetaminophen). Also begin with either a PPI or misoprostol. Continue for 4 to 8 weeks, depending on severity. Treat the H. pylori infection as above if present. • Antisecretory drugs can be discontinued after 4 to 6 weeks in patients with uncomplicated ulcers who are asymptomatic. Patients at increased risk of recurrence (especially if underlying cause of ulcer is not reversed) may benefit from maintenance therapy. • H. pylori–negative ulcers that are NOT caused by NSAIDs can be treated with antisecretory drugs (either H2 blockers or PPI).
  26. 2. Surgical a.Rarely needed electively b. Required for the complications of PUD (bleeding, perforation, gastric outlet obstruction). Treatment
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