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Peptic Ulcer
     Fatimah Abdullah
         6th year MS, KFU
Objectives
    Definition.
    Pathophysiology.
    Etiology.
    Clinical Picture.
    Management.
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.
The gastroduodenal mucosal integrity is
determined by protective (defensive) &
damaging (aggressive) factors.
•   Bicarbonate            •   Helicobacter pylori
•   Mucus layer            •   NSAIDs
•   Prostaglandins         •   Pepsins
•   Mucosal blood flow     •   Bile acids
•   Epithelial renewal     •   Smoking and alcohol


Defensive                  Aggressive

     Mucosal damage  erosions & ulcerations
H. Pylori Infection
  NSAIDs
   Smoking & Alcohol
   Acid Hypersecretion
  Stress
Family History of PUD.
Duodenal Ulcer Gastric ulcer
   Age      Any age specially 30-40 middle age 50-60

   Sex      More in male              More in male

Occupation Stress job eg. Manager     Same

   Pain     Epigastric , discomfort   Epi. Can radiate to
                                      back
  Onset     2-3 hours after eating & Immediately after
            midnight                 eating
  Agg.by    Hunger                    Eating
Duodenal Ulcer Gastric ulcer
Relived by    Eating                        Lying down or vomiting

Duration      1-2 months                    Few weeks

Vomiting      Uncommon                      Common(to relieve the
                                            pain)
Appetite      Good                          Pt. afraid to eat

Diet          Good , eat to relieve the pain Avoid fried food

Weight        No wt. loss                   wt. Loss

Hematemesis   40%                           60%

Melena        60%                           40%
Stool fecal occult blood.

CBC   CBL.
Rapid Urease test, urea
breath test  H. Pylori.
Upper GI Endoscopy.

Barium meal X-Ray.
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.
Life Style Change.

Medical.

Surgical.
Discontinue NSAIDs

Smoking cessation.

 Alcohol cessation.

 Stress reduction.
Antacids
H2-receptor blocking
 agents.
Proton pump inhibitors.
Cytoprotective and
 antisecretory drugs.
Antibiotics.
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.
Indications:
   Failure of medical treatment.

   Development of complications

   High level of gastric secretion and
     combined       duednal and gastric ulcer.

                 Principle:
                  Reduce acid and pepsin
               secretion.
Vagotomy:
 Truncal Vagotomy with drainage.

  Highly selective Vagotomy.

     Combination of vagal
       denervation (vagotomy) +
       anterctomy.
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.
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.
Combination of vagotomy+
anterctomy:
     Combination of vagal denervation &
     removal of the major area of gastric
     production.
Gastrointestinal continuity is restored by
gastroduodenal (Billroth 1) anastomosis
OR gastrojejunal (Billroth 2)
anastomosis.
Dehiscence.
Stenosis of
 anastomosis.
Bleeding.
Injury to neighbour
 tissues.
Dumping syndrome
Hemorrhage

Perforation peptic ulcer

Gastric outlet obstruction
Peptic ulcer

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Peptic ulcer

  • 1. Peptic Ulcer Fatimah Abdullah 6th year MS, KFU
  • 2. Objectives Definition. Pathophysiology. Etiology. Clinical Picture. Management.
  • 3. 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. The gastroduodenal mucosal integrity is determined by protective (defensive) & damaging (aggressive) factors.
  • 5. Bicarbonate • Helicobacter pylori • Mucus layer • NSAIDs • Prostaglandins • Pepsins • Mucosal blood flow • Bile acids • Epithelial renewal • Smoking and alcohol Defensive Aggressive Mucosal damage  erosions & ulcerations
  • 6. H. Pylori Infection NSAIDs Smoking & Alcohol Acid Hypersecretion Stress Family History of PUD.
  • 7.
  • 8. Duodenal Ulcer Gastric ulcer Age Any age specially 30-40 middle age 50-60 Sex More in male More in male Occupation Stress job eg. Manager Same Pain Epigastric , discomfort Epi. Can radiate to back Onset 2-3 hours after eating & Immediately after midnight eating Agg.by Hunger Eating
  • 9. Duodenal Ulcer Gastric ulcer Relived by Eating Lying down or vomiting Duration 1-2 months Few weeks Vomiting Uncommon Common(to relieve the pain) Appetite Good Pt. afraid to eat Diet Good , eat to relieve the pain Avoid fried food Weight No wt. loss wt. Loss Hematemesis 40% 60% Melena 60% 40%
  • 10. 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 In all patients with “Alarming symptoms” endoscopy is required. Dysphagia. Weight loss. Vomiting. Anorexia. Hematemesis or Melena.
  • 12.
  • 14. Discontinue NSAIDs Smoking cessation. Alcohol cessation. Stress reduction.
  • 15. Antacids H2-receptor blocking agents. Proton pump inhibitors. Cytoprotective and antisecretory drugs. Antibiotics.
  • 16. 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. Indications: 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. Vagotomy:  Truncal Vagotomy with drainage. Highly selective Vagotomy. Combination of vagal denervation (vagotomy) + anterctomy.
  • 19. 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.
  • 21.
  • 22. 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. 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. Dehiscence. Stenosis of anastomosis. Bleeding. Injury to neighbour tissues. Dumping syndrome