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Case presentation pud

  1. 1. Peptic Ulcer Disease Andrea M. Wilkins-Daly BSc.,PharmD October 2009
  2. 2. Peptic Ulcer Disease <ul><li>Peptic Ulcer - an imbalance between aggressive factors (gastric acid and pepsin) + </li></ul><ul><li>protective factors (gastric mucus, bicarbonate, prostaglandins). </li></ul><ul><li>Peptic ulcers are chronic most often solitary, lesions that occur in any portion of gastrointestinal tract exposed to the aggressive action of acid-peptic juices. </li></ul>
  3. 3. Pathophysiology <ul><li>Duodenal Ulcer – H.pyloric (95%) </li></ul><ul><li>- NSAIDS </li></ul><ul><li>Gastric Ulcer – NSAIDS </li></ul><ul><li>H.pyloric </li></ul>
  4. 4. ROLE OF H. Pylori INFECTION <ul><li>H. pylori infection is present in almost all patients with duodenal ulcers and 70% cases with gastric ulcers. </li></ul><ul><li>Duodenal ulcers - Usually associated with gastritis confined to the antrum. </li></ul><ul><li>Gastric ulcers - Usually associated with pangastritis (inflammation of the entire stomach) </li></ul><ul><li>. </li></ul>
  5. 5. Other factors causing PUD <ul><li>- high gastrin level and excess acid production . Gastrinoma may cause multiple peptic ulceration as in Zollinger Ellison syndrome. There is increased parietal cell mass. </li></ul><ul><li>impaired mucosal defense . The gastric acid and pepsin levels are normal and no H.pylori are present. </li></ul><ul><li>Chronic use of NSAIDs (aspirin) causes suppression of mucosal prostaglandin and direct irritative topical effect. </li></ul><ul><li>Repeated use of corticosteroid and Chemotherapy in high dose. </li></ul><ul><li>Cigarette smoking impair healing and favour recurrences. </li></ul><ul><li>Alcoholic cirrhosis. </li></ul><ul><li>Psychological stress, ischemia. </li></ul>
  6. 6. Sites of Peptic Ulcer <ul><li>Duodenum: First portion ( few cms from the pyloric ring). Anterior wall is more often affected. </li></ul><ul><li>Stomach: Usually antrum. Lesser curvature (common) . Anterior and posterior wall and greater curvature (less common). </li></ul><ul><li>In the margins of a gastroenterostomy (stomal ulcer) </li></ul><ul><li>In the duodenum, stomach or jejunum of patients with Zollinger-Ellison syndrome. </li></ul>
  7. 7. Mechanism of H pyloric <ul><li>M echanism – H pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus) </li></ul><ul><li>- breakdown of mucosal defense </li></ul><ul><li>****Show H plyoric Slide**treatment options </li></ul>H
  8. 8. Mechanism Of H pyloric <ul><li>Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion. </li></ul><ul><li>Inflammation of the gastric mucosa. </li></ul><ul><li>Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration. </li></ul><ul><li>Ulcers occur at sites of chronic inflammation </li></ul><ul><li>Eg - Antrum </li></ul>
  10. 10. Duodenal Ulcer Duodenal Ulcer
  11. 11. DU in 65yo male
  12. 12. DU in 35 yo female
  13. 13. Duodenal ulcer
  14. 14. Pathophysiology
  15. 15. Case Presentation <ul><li>Mr. Sloley is a 45 year old male who </li></ul><ul><li>presents to your clinic with epigastric </li></ul><ul><li>abdominal pain x 2 weeks. </li></ul><ul><li>What is your initial differential diagnosis at this point given the limited information? </li></ul>
  16. 16. Case Presentation <ul><li>Mr Sloley History </li></ul><ul><li>PMH: HTN stable, Osteoarthritis in knees, treated for an ulcer 3 years ago </li></ul><ul><li>Meds: Hydrochlorothiazide, ibuprofen prn </li></ul><ul><li>Soc HX: Married, employed as bank manager, smokes 1ppd x 20years, drinks 2 beers per day, and 2-4 cups coffee per day </li></ul><ul><li>What risk factors can you identify for PUD? </li></ul>
  17. 17. Diagnosis of H pyloric <ul><li>Breath Tests & Stool antigen tests </li></ul><ul><li>- Urea Breath Test ( 95-100% specificity) </li></ul><ul><li>-In office test (breath) </li></ul><ul><li>Urea Blood test – Less Specific </li></ul><ul><li>Endoscopy – culture of organism to determine antibiotic therapy </li></ul><ul><li>Serologic test – not reliable (persisting antibiodies) </li></ul>
  18. 18. PUD Diagnosis <ul><li>Initial Differential Diagnosis </li></ul><ul><li>More Common: </li></ul><ul><li>Gastroesophageal reflux disease </li></ul><ul><li>Nonulcer dyspepsia/ Gastritis </li></ul><ul><li>Ulcer disease </li></ul><ul><li>Gastroenteritis </li></ul><ul><li>Biliary colic or cholecystitis </li></ul><ul><li>Pancreatitis </li></ul><ul><li>Irritable bowel disease </li></ul>
  19. 19. Case Study <ul><li>Mr. Sloley is a 45 year old male who presents to your clinic with epigastric abdominal pain x 2 weeks. He describes it as a burning pain which is non-radiating and is worse after he eats. He has frequent belching with bloating sensation but denies nausea, vomiting, diarrhea, constipation, or weight loss. He has tried Maalox which do help a little. </li></ul><ul><li>Which symptoms support the possible diagnosis of PUD? </li></ul>
  20. 20. Case Presentation <ul><li>Signs and Symptoms of PUD </li></ul><ul><li>Epigastric pain is most common symptom </li></ul><ul><li>Pain described as gnawing, burning or annoying </li></ul><ul><li>May radiate to the back (consider penetration) </li></ul><ul><li>Pain occurs when stomach is empty </li></ul><ul><li>Relieved by food, antacids (duodenal), Dyspepsia including belching/ bloating </li></ul><ul><li>Hematemesis or melena with GI bleeding </li></ul>
  21. 21. Gastric Ulcers <ul><li>Pts with Gastric or Duodenal ulcers have similar symptoms </li></ul><ul><li>Lacks pattern </li></ul><ul><li>Pain occurs at anytime of day: frequently immediately or within 1-3 hrs after a meal </li></ul><ul><li>Mortality rate is higher in these patients </li></ul><ul><li>10% of pts with PUD present with complications and have no prior Hx of pain </li></ul>
  22. 22. Treatment Goals <ul><li>Relieve symptoms </li></ul><ul><li>Healing of ulcer </li></ul><ul><li>Eliminating cause of ulcer </li></ul>
  23. 23. Treatment <ul><li>No single medication works to get rid of H pylori infection. </li></ul><ul><li>2 combinations are available Triple or Dual Therapy </li></ul><ul><li>Ideal treatment regimen for H pyloric has not been identified </li></ul>
  24. 24. Treatment Options <ul><li>PPI* + clarithromycin (500 mg bid) + amoxicillin (1 gm bid ) x 10-14 days </li></ul><ul><li>Eradication rate 70-85% </li></ul><ul><li>PPI* + clarithromycin (500 mg bid) + metronidazole (500 mg bid) x 10-14 days Eradication rate 70-85%, use with penicillin  allergy </li></ul>
  25. 25. Treatment Options <ul><li>Bismuth subsalicylate 525 mg qid + metronidazole 250 mg qid), tetracycline (500 mg bid), ranitidine 150 mg bid or PPI* x 10-14 days </li></ul><ul><li>Eradication rate 75-90%, use with penicillin  allergy </li></ul>
  26. 26. Treatment Options <ul><li>PPI* + amoxicillin (1 gm bid) x 5 days, then PPI + clarithromycin 500 mg bid + tinidazole  500 mg bid x 5 days </li></ul><ul><li>Eradication rates > 90%, efficacy shown only in European studies </li></ul>
  27. 27. Treatment Options <ul><li>FDA approved regimens Bismuth 525 mg qid + metronidazole 250 qid, tetracycline 500 mg qid x 2 weeks + H2RA x 4 weeks Lansoprazole* 30 mg bid + clari 500 mg bid + amoxicillin 1 gm bid x 10 days *Substitute omeprazole 20 mg bid x 10 d or esomeprazole 40 mg qd x 10d or rabeprazole 20 mg bid x 7 days </li></ul>
  28. 28. Treatment <ul><li>H. Pylori Triple Therapy Treatment </li></ul><ul><li>Triple therapy for 14 days is treatment of choice </li></ul><ul><li>Two forms of triple therapy: PPI–based and bismuth-based </li></ul><ul><li>PPI based = PPI + 2 antibiotics for 2 wk, cont PPI for additional 2 weeks. </li></ul><ul><li>Bismuth-based = bismuth subsalicylate and 2 antibiotics, for 2 weeks with addition of H2- blocker to optimize ulcer healing. </li></ul>
  29. 29. Treatment <ul><li>For NDAID-related PUD – removal of offending agent </li></ul><ul><li>Use of an anti-secretory agent therapy for relieve of symptoms </li></ul><ul><li>If H pyloric present- eradication therapy </li></ul><ul><li>Prevention of PUD – H2RA or PPI or misprostol with pt with chronic NSAID use at risk for developing PUD </li></ul>
  30. 30. Treatment <ul><li>Patient Counseling – adherence to therapy, proper dosing, side-effects </li></ul><ul><li>Surgery –reserved pts with refractory ulcers or hemorrhage </li></ul>
  31. 31. NEW DEVOLPMENTS <ul><li>Supplementation with vitamin C enhances the success of Helicobacter pylori eradication efforts, researchers from Iran report. </li></ul><ul><li>**PLEASE REMEMBER TO READ CPT MANUAL ON DRUGS AND S/E </li></ul>