PEPTIC ULCER DISEASE (PUD)PEPTIC ULCER DISEASE (PUD)

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• UlcerUlcer 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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* 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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* 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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* 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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* 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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* Damaging agents:

• H. pylori• NSAIDs.• Aspirin. • Cigarette smoking.• Alcoholism.• Gastric hyperacidity.• Duodenal-gastric reflux..

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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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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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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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* 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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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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GU

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Gastric ulcerGastric ulcer

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Duodenal ulcerDuodenal ulcer

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* 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.18

Microscopic picture of peptic ulcer

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* 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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* 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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• 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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References:Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition.

ThanksThanks

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