1. Fatimah Abdullah 6th year MS, KFU
Peptic Ulcer
Fatimah Abdullah
6th year MS, KFU

2. Objectives Definition. Pathophysiology. Etiology. Clinical Picture.
Management.

3. Definition
Break in the gastrointestinal mucosa exposed to the aggressive action of acid-peptic juices.
Common sites are the first part of the duodenum and the lesser curve of the stomach.

4. Pathophysiology
The gastroduodenal mucosal integrity is determined by protective (defensive) & damaging (aggressive) factors.

5. Mucosal damage  erosions & ulcerations
Pathophysiology
Bicarbonate
Mucus layer
Prostaglandins
Mucosal blood flow
Epithelial renewal
Defensive
Helicobacter pylori
NSAIDs
Pepsins
Bile acids
Smoking and alcohol
Aggressive
Mucosal damage  erosions & ulcerations

6. Etiology H. Pylori Infection NSAIDs Smoking & Alcohol
Acid Hypersecretion
Stress
Family History of PUD.

7. Clinical Presentation

8. Gastric ulcer Duodenal Ulcer middle age 50-60 Any age specially 30-40
More in male
Sex
Same
Stress job eg. Manager
Occupation
Epi. Can radiate to back
Epigastric , discomfort
Pain
Immediately after eating
2-3 hours after eating & midnight
Onset
Eating
Hunger
Agg.by

9. Gastric ulcer Duodenal Ulcer Lying down or vomiting Eating Relived by
Few weeks
1-2 months
Duration
Common(to relieve the pain)
Uncommon
Vomiting
Pt. afraid to eat
Good
Appetite
Avoid fried food
Good , eat to relieve the pain
Diet
wt. Loss
No wt. loss
Weight
60%
40%
Hematemesis
Melena

10. Investigations Stool fecal occult blood. CBC   CBL.
Rapid Urease test, urea breath test  H. Pylori.
Upper GI Endoscopy.
Barium meal X-Ray.

11. Any patient >50 y/o with new onset of symptoms
Investigations
Any patient >50 y/o with new onset of symptoms
In all patients with “Alarming symptoms” endoscopy is required.
Dysphagia.
Weight loss.
Vomiting.
Anorexia.
Hematemesis or Melena.

12. UGT Endoscopy

13. Management
Life Style Change.
Medical.
Surgical.

14. Life style modification
Discontinue NSAIDs
Smoking cessation.
Alcohol cessation.
Stress reduction.

15. Medications Antacids H2-receptor blocking agents.
Proton pump inhibitors.
Cytoprotective and antisecretory drugs.
Antibiotics.

16. Medications H. pylori Eradication Therapy: Triple therapy:
Proton pump inhibitor .
2 Antibiotics:
Metronidazole + Clarithromycin.
Clarithromycin + Amoxicillin.
In some regimens, H2-receptor blockers, e.g. ranitidine, are used instead of PPI.

17. surgical Reduce acid and pepsin secretion. Indications: Principle:
Failure of medical treatment.
Development of complications
High level of gastric secretion and combined duednal and gastric ulcer.
Principle:
Reduce acid and pepsin secretion.

18. surgical Vagotomy: Truncal Vagotomy with drainage.
Highly selective Vagotomy.
Combination of vagal denervation (vagotomy) + anterctomy.

19. Vagotomy Truncal vagotomy with drainage:
Resect the major trunk of the vagus to the stomach this will lead to:
Decrease acid and pepsin secretion.
Impair antral motility and drainage.
Two types of drainage:
Pyloroplasty.
Gastrojejnostomy.

20. Pyloroplasty Drainage

21. Gastrojejunostomy Drainage

22. Vagotomy It is a parietal cells vagotomy.
Highly selective vagotomy:
It is a parietal cells vagotomy.
It can be done with or without drainage.
It is done by cut a branch of vagus of the body and the fundus this will lead to decrease HCl production.

23. Vagotomy Combination of vagotomy+ anterctomy:
Combination of vagal denervation & removal of the major area of gastric production.

24. Gastrointestinal continuity is restored by gastroduodenal (Billroth 1) anastomosis OR gastrojejunal (Billroth 2) anastomosis.

25. Vagotomy Complications Dehiscence. Stenosis of anastomosis. Bleeding.
Injury to neighbour tissues.
Dumping syndrome

26. Complications of Disease
Hemorrhage
Perforation peptic ulcer
Gastric outlet obstruction

27. Thank you