Peptic ulcer

1. PEPTIC ULCER
Presented By:
Maryam Manzoor
Lecturer Pharmacology
Rashid Latif College of Pharmacy

2. Peptic ulcer
• A break in superficial epithelial cells penetrating down to
muscularis mucosa in areas exposed to acid and pepsin
and most often caused by H.pylori or by use of NSAIDS.
• Can be gastric and duodenal.

3. Duodenal vs Gastric
DUODENAL GASTRIC
INCIDENCE More common Less common
ANATOMY First part of duodenum –
anterior wall
Lesser curvature of
stomach
DURATION Acute or chronic Chronic
MALIGNANCY Rare Benign or malignant

5. Duodenal Ulcers
• duodenal sites are 4x as common as gastric sites
• most common in middle age
• peak 30-50 years
• associated with increased serum pepsinogen
• H. pylori infection common
• up to 95%
• smoking is twice as common

6. Gastric Ulcers
• common in late middle age
• incidence increases with age
• Use of NSAIDs - associated with a three- to four-fold increase
in risk of gastric ulcer
• Less related to H. pylori than duodenal ulcers – about 80%
• 10 - 20% of patients with a gastric ulcer have a concomitant
duodenal ulcer

7. • Duodenal ulcers: occurs 1-3 hours after a meal and may awaken patient
from sleep. Pain is relieved by food, antacids, or vomiting.
• Gastric ulcers: food may exacerbate the pain while vomiting relieves it.

8. Risk factors
• HELICOBACTER PYLORI
• Non Steroidal Anti-inflammatory Drugs
• Smoking
• Excess alcohol intake
• Genetic factors
• Zollinger Ellison syndrome – rare syndrome
caused by gastrin-secreting tumour
• Blood group O

9. Defensive Factors
* Mucus Production
* Bicarbonate Production
* High epithelial cell turnover
* Prostaglandins (PGE2) - stimulate mucus and bicarbonate
production, and blood flow

10. Symptoms of PUD
• Asymptomatic
• Epigastric pain
• Nausea
• Oral flatulence, bloating, distension and intolerance of fatty food
• Heartburn
• Pain radiating to the back

11. Pathogenesis of peptic ulcer:
Peptic ulcers are produced by an imbalance between the gastro-duodenal mucosal
defense mechanisms and damaging forces of gastric acid and pepsin, combined
with superimposed injury from environmental or immunologic agents.

12. Complications
• Hemorrhage
• Perforation
• Obstruction
• Cancer

13. Diagnostic Test and Procedures
a) Routine
* Routine lab tests are not useful in establishing the diagnosis of
uncomplicated PUD
* Hct, HgB, and stool hemoccult are useful to detect bleeding
b) H.pylori test
Histology
Culture
Biopsy/gram stain
Urea breath test
Serology

14. Diagnosis
• Breath Test: Carbon
14 Urea Test

15. Management
MEDICAL TREATMENT
a) Antisceretory/Anti-acid Agents
1) H2-blockers
2) Proton-pump inhibitors
3) Antacids
b) Cytoprotectives
1) Misoprostil
2) Sucralfate
c) H. pylori Agents

16. • Eradication of H.pylori (proton pump inhibitor in combination with
antibiotics)
• Cessation of NSAIDS.
• Criteria for reduction of the size of ulcer crater
• SURGICAL TREATMENT

17. ANTIMICROBIAL AGENTS
• To eradicate H pylori
• Triple therapy consisting of a PPI with either metronidazole or
amoxicillin plus clarithromycin,
• Quadruple therapy of bismuth subsalicylate and metronidazole plus
tetracycline plus a PPI, are administered for a 2-week course. This
usually results in a 90 percent or greater eradication rate.
• Bismuth salts do not neutralize stomach acid, but they inhibit
pepsin and increase the secretion of mucus, thus helping to form a
barrier against the diffusion of acid in the ulcer

18. H2 RECEPTOR BLOCKERS
• Although antagonists of the histamine H2 receptor block the actions of
histamine at all H2 receptors, their chief clinical use is to inhibit gastric
acid secretion, being particularly effective against nocturnal acid
secretion. By competitively blocking the binding of histamine to H2
receptors, these agents reduce the intracellular concentrations of cyclic
adenosine monophosphate and, thereby, secretion of gastric acid.
• The most common side effects are headache, dizziness, diarrhea, and
muscular pain.

19. Inhibitors of the H+/K+-ATPase proton
pump /// PPI’S
• These drugs bind to the H+/K+-ATPase enzyme system (proton pump) of
the parietal cell, thereby suppressing secretion of hydrogen ions into the
gastric lumen.
• Side effects include Headache, diarrhoea and abdominal pain, Skin rashes
and arthralgia

20. Prostaglandins
• Prostaglandin E2, produced by the gastric mucosa, inhibits secretion of
HCl and stimulates secretion of mucus and bicarbonate (cytoprotective
effect).
• misoprostol produces uterine contractions and is contraindicated during
pregnancy.
• Dose-related diarrhea and nausea are the most common adverse effects
and limit the use of this agent.

21. Antimuscarinic agents (anticholinergic
agents)
• Muscarinic receptor stimulation increases gastrointestinal motility and
secretory activity.
• Side effects include cardiac arrhythmias, dry mouth, constipation, and
urinary retention

22. Antacids
• Antacids are weak bases that react with gastric acid to form water and a
salt, thereby diminishing gastric acidity. Because pepsin is inactive at a pH
greater than 4, antacids also reduce pepsin activity.
• Aluminium hydroxide: constipation
• Magnesium hydroxide: diarrhea
• Hypophosphatemia
• Belching and flatulence as Sodium bicarb releases CO2.

23. Mucosal protective agents
• These compounds prevent mucosal injury, reducing inflammation, and
healing existing ulcers.
• Sucralfate :
• it is complex aluminum hydroxide and sulphated sucrose.
• Polymerized to form sticky gel that adheres to the ulcer base and protects
it.
• Form barrier against acid-pepsin.
• Needs acidic ph to act.
• Increase mucus-bicarbonate secretion.

24. • Bismuth subsalicylate:
• Preparations of this compound effectively heal peptic ulcers.
• They inhibit the activity of pepsin
• Increase secretion of mucus, and interact with glycoproteins in necrotic
mucosal tissue to coat and protect the ulcer crater.