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Diagnosis and management of PUD

Diagnosis and management of PUD. Ermias (MD). History. Abdominal pain (epigatric burn) Common for DU, GU, NUD 10% present with complications with out antecedent pain, eg after NSAID DU – 90min-3hr after meal, past midnight, - relieve with food, antacids

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Diagnosis and management of PUD

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  1. Diagnosis and management of PUD Ermias (MD)

  2. History • Abdominal pain (epigatric burn) • Common for DU, GU, NUD • 10% present with complications with out antecedent pain, eg after NSAID • DU – 90min-3hr after meal, past midnight, - relieve with food, antacids • GU – worse with meal, nausea and weight loss are common • Mechanism of pain • Acid induced chemoreceptor activation in duodenum • Enhanced duodenal sensitivity to bile acids and pepsin • Altered gastro-duodenal motility

  3. History conti… • Alterations in pain may show complications • Persistent dyspepsia radiating to the back - penetrating ulcer to pancreas • Sudden onset severe generalized pain – peritonitis due to perforation (6-7%) • Worsening vomiting with meals – GOO (1-2%) • Tarry stool, coffee ground vomits - bleeding (15%)

  4. Physical examination • Epigastric tenderness • 20 % slightly to the right of the mid line • In complications • Tachycardia, hypotension • Signs of peritonitis • Succussion splash

  5. DDx • NUD (functional, essential) • Proximal GI tumors • GERD • Pancreaticobiliary diseases • Crohn’s disease (gastro-duodenal)

  6. diagnosis • Empiric tx as NUD (<45 yrs age) • Ba studies • Single contrast -80%, double contrast 90% sensitivity • See as well defined crater • Negative in <0.5cm ulcer, post op or scars • Endoscopy • Photography, tissue biopsy, source of blood loss, detection of small ulcers • H. pylori • Serum gastrin, gastric acid analysis - ZES

  7. H. Pylori detections • INVASIVE (ENDOSCOPY/BIOPSY REQUIRED) • Rapid urease – (80–95/95–100) - Simple, false negative with recent use of PPIs, antibiotics, or bismuth compounds • Histology – (80–90/>95) - Requires pathology processing and staining; • Culture - Time-consuming, expensive, allows determination of antibiotic susceptibility • NON-INVASIVE • Serology – (>80/>90) - Inexpensive, convenient; not useful for early follow-up • Urea breath test – (>90/>90) - Simple, rapid; useful for early follow-up; false negatives with recent therapy • Stool antigen – (>90/>90) - Inexpensive, convenient; promising for eradication

  8. treatment • Schwartz – “no acid no ulcer” (old dictum) • New concept • Eradication of H. pylori, • prevention of NSAID induced ds.

  9. Acid neutralizing • Antacids – symptomatic relief • Al(OH)3 Mg(OH)2 • CaCO3, NaHCO3 • H2 receptor blockers – for active ulcer tx with H pylori eradication (4-6wk) • Antiandrogenic, cyt P450 inhibitor, • Elevation of transaminases, cr, prolactin; pancytopenia • Proton pump inhibitors • Irreversibly inhibit H+K+ATPase • Rapid onset and prolonged half life • Hypergastrinemia, carcinoid tumors (in animals), hypochlorhydria (interfere with drug absorption)

  10. Cytoprotective agents • Sucralfate • Complex sucrose salt of Al(OH)3 and sulfate • Forms viscous paste in the stomach • Gives physicochemical barrier from further tissue injury • Induce trophic effect on growth factors • Stimulate mucous and bicarbonate secretion • Enhance prostaglandin secretion • SE – constipation, neurotoxicity (Al) in renal failure

  11. Bismuth preparations(colloidal bismuth subcitrate, subsalicylate) • Anti H pylori effect • Mech. for ulcer not clear • Prostaglandin analogues – misoprostal • Enhance mucous bicarbonate secretion, stimulate mucosal blood flow, decrease mucosal cell turn over • Se – diarrhea, uterine bleeding and contraction • 200ug QID

  12. Therapy of H pylori • Dramatic decrease in ulcer recurrence • GU 59% - 4% • DU 67% - 6% • Aim of initial eradication – 85-90% • Efficacy, pt tolerance, resistance pattern, cost • dual tx not recommended < 80% eradication • Unnecessary tx – drug resistance • Infection recurrence in 6 mnth is likely from recrudescence than reinfection

  13. TRIPLE THERAPY 1.  Bismuth subsalicylate plus    Metronidazole plus    Tetracycline 2.  Ranitidine bismuth citrate plus    Tetracycline plus    Clarithromycin or metronidazole 3.  Omeprazole (lansoprazole) plus    Clarithromycin plus    Metronidazole or    Amoxicillin QUADRUPLE THERAPY Omeprazole (lansoprazole)Bismuth subsalicylateMetronidazoleTetracycline 2 tablets qid250 mg qid500 mg qid 400 mg bid500 mg bid500 mg bid 20 mg bid (30 mg bid)250 or 500 mg bid500 mg bid1 gr bid 20 mg (30 mg) daily2 tablets qid250 mg qid500 mg qid

  14. Tx of NSAID related gastric injury • Stop the injurious agent • Use acid inhibitory agent (PPI, H2 blocker) • Prevention – misoprostol, PPI • Use of COX -2 inhibitors

  15. Clinical Setting Active ulcer     NSAID discontinued NSAID continued Prophylactic therapy H. pylori infection Recommendation H2 blocker or PPIPPI MisoprostolPPISelective COX-2 inhibitor Eradication if active ulcer or a past history of peptic ulcer disease

  16. UGIE 4wk

  17. GU vs DU • GU (body, fundal) – likely to be malignant • Repeat endoscopy and biopsy at 8-12 wk • Non healing DU (8wk), GU (12wk) – refractory • Causes: • Poor compliance • NSAID use • Cigarette smoking • Malignancy • Gastric hyper secretary state (ZES) • Ischemia, Crohn’s ds, Amyloidosis, Sarcoidosis, Lymphoma, Eosinophilic gastroenteritis, CMV infection, Tuberculosis, syphilis

  18. surgery • Elective and emergency • Medically refractory ulcer and complicated ulcers (bleeding, perforation and GOO) • Surgical mx decreased with increased endoscopic interventions • Procedures: • 1. vagotomy with drainage • 2. highly selective vagotomy • 3. vagotomy with antrectomy

  19. complications • Depend on the extent of anatomic modification • Complications of intra abdominal procedure • Recurrent ulcerations • Afferent loop syndrome • Dumping syndrome • Post vagotomy diarrhea • Bile reflux gastropathy • Maldigestions and malabsorption • Gastric adenocarcinoma

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