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Peptic Ulcer Disease Dr Shatdal


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This presentation is ment for undergraduate medical student to revise PUD

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Peptic Ulcer Disease Dr Shatdal

  1. 1. Peptic Ulcer Disease Dr. Shatdal Chaudhary Assistant Professor (Internal Medicine) B.P. Koirala Institute of Health Sciences, Dharan
  2. 2.  An ulce r is defined as disruption of the mucosal integrity leading to a local defect or excavation due to active inflammation  Erosion: Damage within the mucosal layer  Ulce rs are defined as breaks in the mucosal surface >5 mm in size, with depth to the submucosa.  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
  3. 3. Gastroduodenal Mucosal Defense • 3-level barrier preepithelial, epithelial, and subepithelial elements • Mucus-bicarbonate layer serves as a physicochemical barrier • Surface epithelial cells provides defense  mucus production,  epithelial cell ionic transporters that maintain intracellular pH and HCO3 production  intracellular tight junctions
  4. 4. Gastroduodenal Mucosal Defense Role of Prostaglandins  Gastric mucosa contains abundant levels of PG  Play central role in epithelial defense/repair  Regulate release of mucosal HCO3 & mucus  Inhibit parietal cell secretion  Maintain mucosal blood flow  Epithelial cell restitution.
  5. 5. Synthesis of PGE2 & prostacyclin (PGI2)
  6. 6. Duodenal Ulcers  duodenal sites are 4x as common as gastric sites  most common in middle age  peak 30-50 years  Male to female ratio—5:1  Genetic link: 3x more common in 1st degree relatives  more common in patients with blood group O  associated with increased serum pepsinogen  H. pylori infection common  up to 95%  smoking is twice as common
  7. 7. Gastric Ulcers  common in late middle age  incidence increases with age  Male to female ratio—2:1  More common in patients with blood group A  Use of NSAIDs - associated with a three- to four-fold increase in risk of gastric ulcer  Less related to H. pylori than duodenal ulcers – about 70%  10 - 20% of patients with a gastric ulcer have a concomitant duodenal ulcer
  8. 8. H. Pylori HISTORY 1982- Waren and Marshall described first-named “campylobacter pyloridis” 1985: Association with peptic ulcer 1989: Named as ‘helicobacter ‘(helico-curved; bacter-staff)
  9. 9. Pathophysiology • H. pylo ri inf. is virtually always associated with chronic active gastritis. • But only 10–15% develop frank PUD.
  10. 10. Interplay between bacterial and host factors
  11. 11. Pathophysiology Tolerance of the acid conditions (pH 1-2) 1. Urease: urea -> CO2 + NH3, then NH3 + H+ -> NH4+, which provides buffering. 2. Residence in mucus and on the epithelial cells. 3. Capacity to create an ionic gradient at a low pH. 4. Release of factors that decrease acid secretion by parietal cells during early infection.
  12. 12. • H. pylori is able to fight off the stomach acid that does reach it with the enzyme urease. • Urease converts urea into bicarbonate and ammonia, which are strong bases. • These acid neutralizing chemicals around the H. pylori protect if from the acid in the stomach.
  13. 13. Natural history of H. pylori infection
  14. 14. Etiology • AThe most important contributing factors are H pylori, NSAIDs, acid, and pepsin. • Additional aggressive factors include smoking, ethanol, bile acids, aspirin, steroids, and stress. • Important protective factors are mucus, bicarbonate, mucosal blood flow, prostaglandins, hydrophobic layer, and epithelial renewal. – Increased risk when older than 50 d/t decrease protection
  15. 15. Causes of Ulcers Not Caused by Hp and NSAIDs Infection  Miscellaneous  Cytomegalovirus, Herpes simplex virus   Basophilia in myeloproliferative disease He lico bacte r he ilm anni    Duodenal obstruction (e.g., annular pancreas) Drug/Toxin    Infiltrating disease   Bisphosphonates   Ischemia Glucocorticoids (when combined with NSAIDs)   Radiation therapy   Chemotherapy   Sarcoidosis Potassium chloride   Crohn's disease   Mycophenolate mofetil   Idiopathic hypersecretory state
  16. 16. Clinical Features : DU  Abdominal pain  Typical pain pattern in DU occurs 90 min to 3 h after meal and is relieved by antacids or food.  Awakes the patient from sleep : the most discriminating symptom( 2/3rd of DU pt.)  Unfortunately, this symptom also present in 1/3rd of patients with NUD.
  17. 17. Clinical Features: GU  Pain pattern in GU may be different  Precipitated by food.  While vomiting relieves it.  Nausea and weight loss occur more commonly in GU patients.
  18. 18. Clinical features  Mechanism of pain in ulcer is unknown.  Possible explanations include  acid-induced activation of chemical receptors in the duodenum  enhanced duodenal sensitivity to bile acids and pepsin, or  altered gastroduodenal motility
  19. 19. On Examination  Epigastric tenderness  Guaic-positive stool resulting from occult blood loss  Succussion splash resulting from scaring or edema due to partial or complete gastric outlet obstruction  A succussion splash describes the sound obtained by shaking an individual who has free fluid and air or gas in a hollow organ or body cavity.  Usually elicited to confirm intestinal or pyloric obstruction.  Done by gently shaking the abdomen by holding either side of the pelvis. A positive test occurs when a splashing noise is heard, either with or without a stethoscope. It is not valid if the pt has eaten or drunk fluid within the last three hours.
  20. 20. Differential Diagnosis  Neoplasm of the stomach  Pancreatitis  Pancreatic cancer  Diverticulitis  Nonulcer dyspepsia (also called functional dyspepsia)  Cholecystitis  Gastritis  GERD  MI—not to be missed if having chest pain
  21. 21. PUD-Related Complications  Gastrointestinal Bleeding :15%  Perforation/ Peritonitis : 6–7%  Gastric Outlet Obstruction:1–2%  Gastric Carcinoma
  22. 22. Diagnostic Evaluation  Poor predictive value of abdominal pain for the presence of a gastroduodenal ulcer  Multiple disease that can mimic this disease  Most patients with symptoms s/o an ulcer have NUD;  Empirical therapy is appropriate for pts who are otherwise healthy and <45, before embarking on a diagnostic evaluation .
  23. 23. Diagnostic Evaluation Barium studies • Sensitivity for detecting a DU single-contrast Ba meals 80%: double-contrast 90%. • Sensitivity decreased in small ulcers (<0.5 cm), presence of previous scarring, or in postop pt.
  24. 24. Endoscopy  Most sensitive and specific .  Direct visualization of the mucosa,  Biopsy to rule out malignancy or Hp.  Identifies lesions too small to detect by Ba exam, for evaluation of atypical radiographic abnormalities, or to determine if an ulcer is a source of blood loss.
  25. 25. Tests for Detection of H. pylori Test Sensitivity/Sp ecificity, % Comments 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 provides histologic information Culture —/— Time-consuming, expensive ; 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 ; exposure to low- dose radiation with 14 C test Stool antigen >90/>90 Inexpensive, convenient; not established for eradication but promising
  26. 26. Peptic Ulcer Disease: Treatment Drug Type/Mechanism Examples Dose Acid-suppressing drugs Antacids H2 receptor antagonists Ranitidine Famotidine Nizatidine 300 mg hs 40 mg hs 300 mg hs Proton pump inhibitors Omeprazole Lansoprazole Rabeprazole Pantoprazole Esomeprazole 20 mg/d 30 mg/d 20 mg/d 40 mg/d 20 mg/d Mucosal protective agents Sucralfate Sucralfate 1 g qid Prostaglandin analogue Misoprostol 200 g qid Bismuth-containing compounds Bismuth subsalicylate (BSS)
  27. 27. Regimens for H. pylori eradication Drug Dose Triple Therapy 1. Bismuth subsalicylate plus 2 tablets qid Metronidazole plus 250 mg qid Tetracyclinea 500 mg qid 2. Ranitidine bismuth citrate plus 400 mg bid Tetracycline plus 500 mg bid Clarithromycin or metronidazole 500 mg bid 3. Omeprazole (lansoprazole) plus 20 mg bid (30 mg bid) Clarithromycin plus 250 or 500 mg bid Metronidazoleb or 500 mg bid Amoxicillinc 1 g bid
  28. 28. Regimens for H. pylori eradication Quadruple Therapy Omeprazole (lansoprazole) 20 mg (30 mg) daily Bismuth subsalicylate 2 tablets qid Metronidazole 250 mg qid Tetracycline 500 mg qid
  29. 29. Evaluation/Follow-up/ • H. Pylori Positive: retesting for tx efficacy • Urea breath test—no sooner than 4 weeks after therapy to avoid false negative results • Stool antigen test—an 8 week interval must be allowed after therapy. • H. Pylori Negative: • evaluate symptoms after one month. Patients who are controlled should cont. 2-4 more weeks.
  30. 30. Surgical Therapy Required for 1. Medically refractory disease: rare 2. Treatment of an ulcer-related complication
  31. 31. Specific Operations for Duodenal Ulcers 1. Vagotomy and drainage (by pyloroplasty, gastroduodenostomy, or gastrojejunostomy), 2. Highly selective vagotomy (which does not require a drainage procedure) 3. Vagotomy with antrectomy
  32. 32. Zollinger–Ellison Syndrome Severe peptic ulcer diathesis secondary to gastric acid hypersecretion due to unregulated gastrin release from a non- β cell endocrine tumor (gastrinoma)
  33. 33. Zollinger–Ellison Syndrome  Incidence varies from 0.1 to 1% of individuals presenting with PUD.  Males > females,  Ages 30 and 50 yrs.  Gastrinomas are classified into sporadic tumors (more common) and those associated with MEN type I
  34. 34. ZES: Clinical Manifestations  Peptic ulcer is the most common clinical manifestation  Suspicious Ulcers  in unusual locations (D2 & beyond)  refractory to standard medical therapy  recurrence after acid-reducing surgery  presenting with frank complications  in the absence of H. pylo ri or NSAID .
  35. 35. ZES: Clinical Manifestations  Diarrhea, found in up to 50%.  Gastrinomas can develop in the presence of MEN I syndrome in ~25% of patients.  AD disorder involves primarily 3 organs: parathyroid glands (80–90%), pancreas (40– 80%), and pituitary gland (30–60%).
  36. 36. ZES: Treatment  PPIs are the treatment of choice  Surgery