Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.

An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.

Peptic ulcers can also be classified by location, such as gastric ulcers in the stomach, duodenal ulcers in the small intestine, or esophageal ulcers in the esophagus.

Various factors contribute to PUD, primarily Helicobacter pylori (H. pylori), which may be acquired through ingesting contaminated food and water and person-to-person transmission, mainly through contact with stool, saliva, or vomit. Once ingested, H. pylori generates an enzyme called urease, which converts urea (a compound found naturally in the stomach) to ammonia to reduce stomach acidity, making it a more hospitable environment for the bacterium. After establishing in the gastric mucosa, H. pylori triggers an immune response and releases toxins, resulting in mucosal inflammation and damage.

Next is non-steroidal anti-inflammatory drugs or NSAID-associated PUD. NSAIDs inhibit cyclooxygenase-1 (COX-1) enzymes, which play an important role in the production of prostaglandins. Prostaglandins are essential for maintaining mucosal integrity, mucus and bicarbonate secretion, mucosal blood flow, cell turnover, and repair.

As a result, the inhibition of COX-1 by NSAIDs compromises these defense mechanisms, predisposing the gastric mucosa to be more susceptible to damage from acid and pepsin, which can lead to ulcer formation.

Beyond NSAIDs, other medications like corticosteroids such as prednisolone, and bisphosphonates such as alendronate, potassium chloride, and fluorouracil are implicated in PUD etiology. Smoking, chewing tobacco, and alcohol consumption can further irritate the gastric mucosa and induce acidity.

Peptic ulcer disease is also linked to a rare condition called Zollinger-Ellison syndrome (ZES). ZES involves the formation of tumors, both benign and malignant, in the pancreas and duodenum. These tumors produce excessive quantities of the hormone gastrin, leading to high levels of gastric acid and severe peptic ulcer disease.

Finally, psychological distress can impede the healing of ulcers, while familial tendency may also play a significant role. Individuals with blood type O are more prone to developing peptic ulcers compared to those with blood types A, B, or AB. The increased density of colonization of epithelial cells and heightened inflammatory responses to H. pylori in individuals of blood group O might contribute to an elevated susceptibility to peptic ulceration.