Peptic ulcer disease (PUD) refers to chronic lesions in the gastrointestinal tract caused by an imbalance between mucosal defenses and damaging agents, primarily Helicobacter pylori, NSAIDs, and lifestyle factors. Common locations include the duodenum and stomach, with symptoms presenting as epigastric pain that worsens with meals, nausea, and potentially significant weight loss. Complications of PUD can include hemorrhage, perforation, and, though rare, malignant transformation.

1. PEPTIC ULCER DISEASE (PUD)
PEPTIC ULCER DISEASE (PUD)
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2. • Ulcer
Ulcer is defined as a breach in the mucosa , which
extends through the muscularis mucosa into the
submucosa or deeper.
• Erosion
Erosion differs from an ulcer in being more
superficial and partially affecting the surface
epithelium).
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3. * Definition of peptic ulcer:
* Definition of peptic ulcer:
• Peptic ulcers are chronic most often solitary, lesions
that occur in any portion of the gastrointestinal tract
exposed to the aggressive action of acidic-peptic
secretion.
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4. * Sites of peptic ulcer:
* Sites of peptic ulcer:
• Duodenum (DU): First portion. Anterior wall is more often
affected.
• Stomach (GU): Usually antrum. Lesser curvature (common) .
• At the margins of a gastroenterostomy (stomal ulcer)
• In the duodenum, stomach or jejunum of patients with
Zollinger-Ellison syndrome.
• Within Meckel’s diverticulum that contains ectopic gastric
mucosa.
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5. * Pathogenesis of peptic ulcer
* Pathogenesis of peptic ulcer:
:
Peptic ulcers are produced by an imbalance between
the gastro-duodenal mucosal defense mechanisms and
damaging forces.
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7. * Mucosal defense mechanisms:
• Surface mucous secretion.
• Bicarbonate secretion into mucous.
• Tight adherence between epithelial cells to
prevent any acid leakage to the inside.
• Good blood supply to the mucosa
• Renewal of damaged epithelial cells.
• Elaboration of prostaglandins.
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8. * Damaging agents:
• H. pylori
• NSAIDs.
• Aspirin.
• Cigarette smoking.
• Alcoholism.
• Gastric hyperacidity.
• Duodenal-gastric reflux..
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9. Role of H. Pylori infection in the pathogenesis of
peptic ulcer:
H. pylori infection is present in almost all patients with
duodenal ulcers and 70% of cases with gastric ulcers.
* Mechanism:
1. H. pylori secretes damaging enzymes;
• Urease: breaks down urea to toxic compounds e.g.
ammonium chloride.
• Protease breaks down glycoprotein in the gastric
mucus).
• Phospholipases. Damage the cell membranes of surface
epithelial cells.
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10. 2. Bacterial lipopolysaccharide stimulate the surface
epithelial cells to release pro-inflammatory cytokines
e.g. IL-1, IL-6 and TNF. These attracts inflammatory cells
(Neutrophils) to the mucosa and promote the
inflammatory reaction
3. H. pylori release bacterial platelet-activating factor
promotes thrombotic occlusion of surface capillaries.
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11. 4. H. pylori enhances gastric acid secretion and impairs
duodenal bicarbonate production, thus reducing
luminal pH in the duodenum. This altered milieu seems
to favor gastric metaplasia (the presence of gastric
epithelium) in the first part of the duodenum.
- Such metaplastic foci provide areas for H. pylori
colonization.
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13. * Gross features:
* Gross features:
Site: Gastric ulcers are located at the antrum toward the
lesser curvature. The duodenal ulcer is usually located at
the 1st
part anteriorly.
Shape: Round, oval.
Size: Usually less than 2cm in diameter.
Lesions less than 0.3 cm are likely to be shallow
erosions.
Giant ulcers are usually greater than 3cm in
diameter.
Size does not differentiate benign from malignant
ulcer.
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14. Base of ulcer:
• Firm (formed of bundles of muscles and fibrous tissue).
Floor:
Clean (gastric juice digest any food particles at the floor.
Margin (Surrounding gastric mucosa):
Edematous and reddened due to gastritis.
Depth of the ulcer:
• Superficial ulcer penetrate the mucosa reaching up to the
muscularis mucosa.
• Deeply excavated ulcers having their bases on the muscularis
propria.
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15. GU
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16. Gastric ulcer
Gastric ulcer
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17. Duodenal ulcer
Duodenal ulcer
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18. * Microscopic features:
- Four distinct layers are present in a peptic ulcer in
the same sequence starting from the luminal side:
1. Necrotic debris.
2. Non-specific acute inflammatory reaction.
3. Granulation tissue.
4. Fibrosis: replacing the muscle wall and extending
into subserosa.
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19. Microscopic picture of peptic ulcer
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20. * Complications of PUD:
1. Hemorrhage: hematemesis or melena.
2. Perforation.
3. Healing by fibrosis: causing obstruction.
4. Malignant transformation: rare (0.5% of gastric
peptic ulcer).
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21. * Clinical presentation:
• A chronic, recurring lesion.
• Age: Most often diagnosed in middle aged to older adults.
• Pain:
- Epigastric burning or aching pain.
- Pain worse at night and 1 to 3 hours after meal during the day
specially in duodenal ulcer.
- Classically, the pain is relieved by alkalis or food (DU) or vomiting
(GU).
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22. • Nausea, vomiting, bloating, and significant weight loss
(raising the possibility of some hidden malignancy) are
additional manifestations.
• With penetrating ulcers, the pain is occasionally
referred to the back, the left upper quadrant, or chest.
This type of pain may be misinterpreted as being of
cardiac origin.
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