Page 413 - Concise Pathology for Exam Preparation ( PDFDrive )

398
398 SECTION II Diseases of Organ Systems
Complications

Peptic ulcer and gastric carcinoma.

Q. Write briefly on the aetiology, pathology and complications
of peptic ulcer.

Ans. Peptic ulcer is a chronic (remitting and relapsing), often solitary lesion, present in any
part of GIT that is exposed to acid and peptic juices; usually, diagnosed in middle to old age.

Sites (in Decreasing Order)

• First portion of duodenum
• Antral region of stomach (98% of the peptic ulcers present in duodenum or stomach;
ratio of duodenal and gastric ulcers is about 4:1)
• Gastroesophageal junction
• Margins of gastrojejunostomy
• Duodenum, stomach and jejunum in Zollinger–Ellison syndrome
• Meckel’s diverticulum

Pathogenesis
Peptic ulcer results whenever defence mechanisms of stomach are impaired and/or damag-
ing factors become predominant.

Gastroduodenal defence mechanisms
• Mucous layer on surface
• Bicarbonate secretion into mucosa
• Adequate mucosal blood flow
• Apical surface membrane transport
• Epithelial regenerative capacity
• Prostaglandin secretion

Damaging factors
Gastric acid and peptic enzyme secretion is aggravated by:
• NSAIDs like aspirin (direct mucosal irritation and reduction in prostaglandin and bicar-
bonate secretion)
• Cigarette smoking and alcohol (impair blood flow and healing capacity of the mucosa)
• Ischaemia and shock (decreased oxygen delivery)
• Iron preparations (direct mucosal damage)
• Viral infections (direct mucosal damage)
• Ageing (reduced mucin and bicarbonate secretion)
• Urease secreting H. pylori and gastric injury associated with uraemia (inhibition of
gastric bicarbonate transporters by ammonium ions)
• Chemotherapy and chemicals (direct mucosal injury)
• Duodenal-gastric reflux
• Psychological stress
• Hyperkalaemia

Role of H. pylori in peptic ulceration
• It secretes urease, protease and phospholipase.
• Urease generates free ammonia that binds with H1 and decreases acidity; thus, coloniza-
tion and survival of the organism is favoured.
• Proteases damage the glycoprotein of gastric mucous.
• Phospholipases damage surface epithelial cells and also release leukotrienes and eicosanoids.

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