This PPT covers the Pathophysiology of Peptic ulcer. It includes factors causing peptic ulcer, factors causing peptic ulcer, diagnosis and complications of peptic ulcer.

1. PREPARED BY: JEGAN. S. NADAR
PEPTIC ULCER

2. PEPTIC ULCER
❖ Ulcers are defined as a breach in the mucosa of the alimentary tract, which
extends through the muscularis mucosa into the submucosa or deeper.
❖ Peptic ulcers are chronic most often solitary, lesions that occur in any portion
of gastrointestinal tract exposed to the aggressive action of acid-peptic
juices.
❖ Typically occurs in stomach (Gastric ulcer) and 1st few cm of duodenum
(duodenal ulcer)
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3. SITES OF PEPTIC ULCERS
❖ Duodenum: First portion ( few cms from the pyloric ring). Anterior wall is
more often affected.
❖ Stomach: Usually antrum. Lesser curvature (common) . Anterior and posterior
wall and greater curvature (less common).
❖ In the margins of a gastroenterostomy (stomal ulcer)
❖ In the duodenum, stomach or jejunum of patients with Zollinger-Ellison
syndrome. Jegan Nadar

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6. 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.
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9. IMBALANCE (AGGRESSIVE)
Aggressive Factors
* H. pylori
* Acid Secretion
* Pepsinogen Secretion
* NSAIDS
* Cigarette smoking
* Corticosteroid use
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10. DEFENSIVE FACTORS
➢ Mucus Production
➢ Bicarbonate Production
➢ Mucosal blood flow - more important in the development of stress ulcer
➢ High epithelial cell turnover
➢ Prostaglandins (PGE2) - stimulate mucus and bicarbonate production, and
blood flow
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12. H. pylori
❖ H. pylori infection is present in almost all patients with duodenal ulcers and 70%
cases with gastric ulcers.
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13. Mechanism:
❖ H. pylori secretes urease (generates ammonia), protease (breaks down
glycoprotein in the gastric mucus) or phospholipases.
❖ Bacterial lipopolysaccharide attracts inflammmatory cells to the mucosa.
❖ A bacterial platelet-activating factor promotes thrombotic occlusion of surface
capillaries.
❖ Mucosal damage allows leakage of tissue nutrients in the surface
microenvironment , sustaining the bacillus.
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14. ❖ Damage of the protective mucosal layer. The epithelial cells are exposed to the
damaging effect of acid-peptic digestion.
❖ Inflammation of the gastric mucosa.
❖ Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to
peptic ulceration.
❖ Ulcers occur at sites of chronic inflammation. Eg - Antrum
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16. OTHER FACTORS CAUSING PEPTIC ULCER:
❖ Peptic ulcer caused due to high gastrin level and excess acid production.
Gastrinoma may cause multiple peptic ulceration as in Zollinger Ellison syndrome.
There is increased parietal cell mass.
❖ Peptic ulcers caused due to impaired mucosal defense .
❖ The gastric acid and pepsin levels are normal and no H.pylori are present.
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17. ❖ Chronic use of NSAIDs (aspirin) causes suppression of mucosal prostaglandin and
direct irritative topical effect.
❖ Repeated use of corticosteroid in high dose.
❖ Cigarette smoking impair healing and favour recurrences.
❖ Alcoholic cirrhosis.
❖ Personality, psychological stress, ischemia.
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21. Endoscopy

22. COMPLICATION
❖ Hemorrhage
❖ Perforation
❖ Penetration
❖ Obstruction
❖ Malignancy
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