Case presentation pud

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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>
  9. 9. PEPTIC ULCER DISEASE
  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>

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