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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.
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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 mucus neck & surface cells Mucus & HCO3 parietal cells (oxyntic) H+ secretion & intrinsic factor Peptic cells (chief, zymogen) Pepsinogen secn
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
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
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
Peptic ulcer disease - cont. • Epithelial barrier • Depends of abundant vascular supply and continual, rapid regeneration of epithelial cells (~3 days)
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
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
Diagnostic procedures • Barium radiologic studies • Gastric analysis of acid secretion • Aspirate gastric juices with nasogastric tube • Endoscopy • Photography • Biopsy • Exfoliative cytology
Differential Diagnosis • Gallbladder disease • Pancreatitis • Functional indegestion • Reflux oesphagitis
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
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
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
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
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
Peptic ulcer disease - cont. • Intractability • Medical therapy fails to control symptoms adequately, resulting in frequent, rapid recurrences • Typically surgery is recommended
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
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
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
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)
GI Pathology Gastric peptic ulcer • Associations: Chronic gastritis, Helicobacter pylori (50-60%) • Peak incidence = 50's • Location = Lesser curvature, antrum