Peptic Ulcer Disease I: Introduction

Peptic ulcer disease, or PUD, involves mucosal erosion in the esophagus, stomach, pylorus, or duodenum, appearing as acute or chronic ulcers.

Acute ulcers are short-term, with superficial erosion and minimal inflammation, and they heal quickly after the underlying cause is addressed.

Conversely, chronic ulcers persist for months, potentially penetrating the muscular wall and forming fibrous tissue.

The primary cause of PUD is H.pylori, transmitted via contaminated food, water, or contact with stool, saliva, or vomit.

H.pylori produces urease, converting urea to ammonia to reduce stomach acidity.

Once established, H.pylori triggers an immune response and releases toxins, resulting in mucosal inflammation and damage.

Next, NSAIDs contribute to PUD by inhibiting cyclooxygenase-1, an enzyme vital for prostaglandin production that protects mucosal integrity.

Reduced prostaglandin levels from NSAIDs increase the susceptibility of the gastric mucosa to damage from gastric juices.

Other contributing factors for PUD include alcohol, smoking, stress, Zollinger-Ellison syndrome, and medications like corticosteroids.