1 / 36

Peptic Ulcer disease

Peptic Ulcer disease. Anatomy . Stomach Regions. Anatomy – cont. Stomach – cont. Layers of walls Serosa Muscularis Submucosa Mucosa. Anatomy – cont. Stomach – cont. Glands in mucosa Cardiac glands Gastric glands Chief cells Parietal cells Mucous neck cells gastrin. Gastric pit.

farica
Télécharger la présentation

Peptic Ulcer disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Peptic Ulcer disease

  2. Anatomy • Stomach • Regions

  3. Anatomy– cont. • Stomach – cont. • Layers of walls • Serosa • Muscularis • Submucosa • Mucosa

  4. Anatomy– cont. • Stomach – cont. • Glands in mucosa • Cardiac glands • Gastric glands • Chief cells • Parietal cells • Mucous neck cells • gastrin

  5. Gastric pit mucus neck & surface cells Mucus & HCO3 parietal cells (oxyntic) H+ secretion & intrinsic factor Peptic cells (chief, zymogen) Pepsinogen secn

  6. Functions of gastric secretions • Digestion of proteins ( pepsinogen & HCl) • Protection of stomach ( HCO3- & mucus) • Absorption of vitamin B12 ( intrinsic factor) • Destroy bacteria & other micro-organisms (HCl) ~ 3 li per day

  7. Peptic ulcer disease • General consideration • Peptic ulcers result from the corrosive action of acid gastric juice • Ulcers may occur in oesophagus, stomach,duodenum, jejunum or ileum from ectopic gastric mucosa • Can be anywhere in GI tract exposed to acid-pepsin gastric juice • Other factors also contribute • H. pylori • Mucosal bicarbonate secretion • Stress • Genetics

  8. GI Pathology Helicobacter pylori

  9. Peptic ulcer disease - cont. • Pathogenesis • Two factors prevent stomach from digesting itself • Gastric mucosal barrier • First line of defense • NSAIDS cause in changes mucosa that my facilitate its digestion by pepsin • Destruction of barrier believed to be important factor in pathogenesis of gastric ulcers • Results of back diffusion of H+ injuring underlying tissues • Antrum more susceptible to back diffusion than fundus • Duodenum resistant to ulceration due to Brunner’s glands which produce a highly alkaline secretion

  10. Peptic ulcer disease - cont. • Epithelial barrier • Depends of abundant vascular supply and continual, rapid regeneration of epithelial cells (~3 days)

  11. Peptic ulcer disease - cont. • Other factors • 10-12 % incidence in population • Duodenal ulcers occur in much younger group than gastric 20-40 years • Males affected 3X as often as women • Duodenal ulcers 10X as common as gastric • >90% of duodenal ulcers are on anterior or posterior wall within 3 cm of pyloric ring • 40-60% have family history

  12. Peptic ulcer disease - cont. • Clinical features • Principle feature is chronic, intermittent epigastric pain – typically relieved by food • ~25% have bleeding (more common with duodenal) • Other signs and symptoms • Vomiting • Red or “coffee-ground” emesis • Nausea • Anorexia • Weight loss • Pain-food-relief pattern may not be typical of gastric ulcers – food sometimes aggravates

  13. Diagnostic procedures • Barium radiologic studies • Gastric analysis of acid secretion • Aspirate gastric juices with nasogastric tube • Endoscopy • Photography • Biopsy • Exfoliative cytology

  14. Differential Diagnosis • Gallbladder disease • Pancreatitis • Functional indegestion • Reflux oesphagitis

  15. Peptic ulcer disease - cont. • Medical treatment • Primary consideration is to inhibit or buffer acid to relieve symptoms and promote healing • Antacids – increase pH so pepsin isn’t activated • Dietary management – small frequent meals, avoid alcohol and caffeine • Anticholinergics – inhibit vagal stimulation • Antimicrobial therapy • Physical and emotional rest • Ulcers caused by H. pylori are successfully treated with antimicrobial agents, bismuth salts, and H2 blockers • 65-95% eradication rates

  16. 10 Day Regimen • clarithromycin 500 mg bid X 10 • amoxicillin 1 gram bid X 10 • omeprazole 20 mg bid X 10 • in patients with current ulcer, continue omeprazole 20 mg/day for 18 days

  17. kPeptic ulcer disease - cont. • Complications • Hemorrhage • Most frequent complication – 15-20% • Most common in ulcers of the posterior wall of duodenal bulb due to proximity of arteries • Symptoms depend on severity • Anemia • Occult blood in stool • Black and tarry stool • Hematemesis • Shock • Mortality up to 10% - higher for patients over 50

  18. Peptic ulcer disease - cont. • Perforation • Approximately 5% of all ulcers perforate - accounts for 65% of deaths from peptic ulcers • Usually on anterior wall of duodenum or stomach • Thought to be due to excess acid and often a result of NSAIDS • Characteristic presentation • Sudden onset of excruciating pain in upper abdomen – chemical peritonitis • Patient fears to move or breath • Abdomen becomes silent to auscultation and board like rigidity to palpation • Treatment – immediate surgery

  19. Peptic ulcer disease - cont. • Obstruction • Obstruction of gastric outlet in ~5% of patients • Due to inflammation and edema, pylorospasm or scarring • More often with duodenal ulcers • Symptoms • Anorexia • Nausea • Bloating after eating • Pain and vomiting when severe • Treatment • Restore fluids and electrolytes • Decompress stomach with nasogastric tube • Surgical correction - pyloroplasty

  20. Peptic ulcer disease - cont. • Intractability • Medical therapy fails to control symptoms adequately, resulting in frequent, rapid recurrences • Typically surgery is recommended

  21. Peptic ulcer disease - cont. • Surgical treatment – for patients who do not respond to therapy • For duodenal ulcers aim is to permanently reduce stomach’s capacity to secrete acid and pepsin • Vagotomy • Cut vagal branches to stomach • Eliminates cephalic phase • Several techniques • Antrectomy • Removal of entire antrum • Eliminates gastric phase • Vagotomy plus antrectomy • Eliminates both cephalic and gastric phases

  22. Peptic ulcer disease - cont. • Partial gastrectomy • Removal of distal 50-75% of stomach • Gastric remnant anastamosed to duodenum (Billroth I) or jejunum (Billroth II) • For gastric ulcers • Usually partial gastrectomy and a gastroduodenal anastomosis • Normally do not do vagotomy as patients have normal to low acid production

  23. Normal Stomach

  24. Esophagus & Stomach Normal

  25. Gastric Ulcer

  26. Peptic ulcer - Endoscopy

  27. Duodenal Peptic Ulcer

  28. Gastric Ulcer

  29. GI PathologyDuodenal Peptic Ulcers, Gross

  30. GI PathologyGiant gastric ulcer

  31. GI Pathology Gastric Peptic Ulcer • Gross • Lesser curvature is the most common location in the stomach; greatest frequency is in the first part of the duodenum • Less than three centimeters in diameter • Round to oval in shape • Punched-out area with clean base • Margins are usually level with surrounding mucosa or slightly elevated due to edema; the mucosa is undermined at the edges

  32. GI Pathology Gastric Peptic Ulcer • Up to 50% of those with gastric peptic ulcer have concurrent duodenal ulcer • These ulcers typically occur at mucosal junctions exposed to acid and pepsin (e.g., body of stomach/antrum)

  33. GI Pathology Gastric peptic ulcer • Associations: Chronic gastritis, Helicobacter pylori (50-60%) • Peak incidence = 50's • Location = Lesser curvature, antrum

  34. GI PathologyAnatomy of the stomach

More Related