Peptic ulcer (Clinical features, Investigation and Management) -physiology

Peptic Ulcer (Physiology)
-clinical features
-investigation
-management

1. Peptic Ulcer (Clinical Features, Investigation, Management) Maryam Jamilah Binti Abdul Hamid 082013100002 IMS Bangalore

2. Learning outcome We should be able to identify clinical features for peptic ulcer We should be able to know the investigation in peptic ulcer We should be able to list the management in patient with peptic ulcer.

3. Clinical features Duodenal Ulcer Abdominal pain in the epigastric region Pain worsens when stomach is empty (usually 2-5 hours after a meal) 11PM-2AM greatest acid secretion Feels better after eating/drinking but worsens 1 or 2 hours later Vomiting is rare unless pyloric stenosis is present

4. Gastric Ulcer Pain after eating Appetite changes (decrease) Weight loss Vomiting (after having a meal)

5. investigations NON-INVASIVE -serology -13C-urea breath tests -faecal antigen test INVASIVE -histology (biopsy) -rapid urease tests -microbiological culture

6. investigations Examination of blood Examination of stool Gastric function tests Radiological Investigation Endoscopy (diagnostic accuracy >95%)

7. management Changing of lifestyle Quit smoking Hurry, worry, curry Eat slowly Take meditation programme or any programme to release stress Don’t eat too much of spicy food Quit eating smoked food

8. Drugs/blocker for peptic ulcer Antacids H2- receptor blocking drugs M3-muscarinic receptors blocking drugs Proglumide Omeprazole

9. Sucralphate (basic aluminium salt of sucrose octasulphate ) Antibiotic Vagotomy

10. 1) Antacids -has aluminium hydroxide, magnesium hydroxide or calcium carbonate -form a gel that coats the mucosa and neutralize the acid 2 ) H2- receptor blocking drugs (Histamine receptors--> H1 & H2; H2 mediate the response of acid secreting cells) - eg : cimetidine , ranitidine, nizatidine & famotidine 3 ) M3-muscarinic receptors blocking drugs eg : atropine or specific anticholinergic drugs pirenzepine 4) Proglumide -block gastrin receptors 5 ) Omeprazole -inhibit gastric H+ - K+ ATPase 6 ) Sucralphate (basic aluminium salt of sucrose octasulphate ) -increase the resistance of mucosa to acid *by forming adherent protein and other complexes at the ulcer site 7 ) Antibodies -if Helicobacter pylori is the etiology 8 ) Vagotomy -decreased gastric juice secretion during all the phases ( cephalic,gastric,intestinal phases) -gastric tone decrease -motility decrease *motility of what? stomach or food? -emptying time increased from 2-3 hours to 12-24 hours or longer. *patient complains of fullness,nausea and bleching of large volume of gas (foul smelling) -usually comes with pyloroplasty (distension of pylorus to increase pyloric tone -----> usually this is done by vagus ) - prevent retention of gastric contents - alternately,removal of the gastrin secreting antral mucosa

11. COMPLICATION Perforated peptic ulcer Gastrointestinal bleeding Coffee ground vomiting Gastric Outlet Obstruction

12. Gastrointestinal bleeding Most common complication (~15% in >60 y/o) Mortality rate high 5-10% Higher incidence in elderly cz using NSAID Peritonitis *Coffee ground vomiting Perforated peptic ulcer 2 nd most common 6-7% Increasing secondary to increase on NSAID Duodenal ulcer: penetrate posterior into pancrease lead to pancreatitis Gastric ulcer: penetrate to left hepatic lobe ( Gastrocolic fistulas also being described) Gastric Outlet Obstruction Least common 1-2% A patient may have relative obstruction secondary to ulcer-related inflammation and edema in the peripyloric region Resolves when ulcer heals Fixed mechanical obstruction secondary to scar formation in the peripyloric area need endoscopic (balloon dilation) or surgical intervention Onset: nausea, early satiety, vomiting, increase postprandial abdominal pain & weight lost

13. References AK JAIN, MEDICAL PHYSIOLOGY TEXT BOOK, VOLUME 1, 3 RD EDITION HARRISON’S VOLUME 2 S DAS TEXTBOOK OF SURGERY