PUD is the acronym for Peptic Ulcer Disease, a common condition affecting the gastrointestinal tract. This disease involves the formation of open sores within the lining of the stomach, esophagus, or the upper part of the small intestine. It develops when the digestive tract’s protective mechanisms are compromised, allowing corrosive stomach acid to damage the underlying tissue layers.
Defining Peptic Ulcer Disease
Peptic Ulcer Disease refers to a break in the inner lining of the gastrointestinal tract that extends beyond the superficial epithelial layer. The term “peptic” relates to the digestive enzyme pepsin and the stomach acid that contributes to tissue erosion. The digestive tract normally maintains a defense system featuring mucus and bicarbonate ions that neutralize the highly acidic environment.
An ulcer forms when this protective layer is weakened, allowing hydrochloric acid and pepsin to erode the mucous membrane and damage the muscular layers beneath. Peptic ulcers are categorized based on their location within the upper digestive system. A gastric ulcer forms within the stomach lining, while a duodenal ulcer develops in the duodenum, the first section of the small intestine.
Duodenal ulcers are the more frequently observed type, often occurring in the duodenal bulb. Although both types result from similar destructive mechanisms, gastric ulcers are sometimes associated with normal or reduced acid output, suggesting a primary defect in mucosal defenses. Conversely, duodenal ulcers are often linked to increased gastric acid secretion.
Primary Causes of PUD
The majority of Peptic Ulcer Disease cases are attributed to two distinct factors that disrupt the balance between protective factors and damaging stomach acid. The first and most common cause is infection with the bacterium Helicobacter pylori (H. pylori). This spiral-shaped microorganism is adapted to survive in the stomach’s acidic environment, where it colonizes the lining and releases enzymes that weaken the protective mucus layer.
The second major cause involves the regular use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs), such as ibuprofen and aspirin. NSAIDs damage the gastric mucosa through both topical injury and a systemic effect. Systemically, these medications inhibit the cyclooxygenase-1 (COX-1) enzyme, which produces prostaglandins.
Prostaglandins are responsible for maintaining mucosal blood flow, stimulating mucus and bicarbonate secretion, and promoting cellular repair. By inhibiting COX-1, NSAIDs suppress these protective functions throughout the digestive tract, leaving the lining defenseless against acid. The presence of both H. pylori infection and NSAID use significantly increases the risk of developing a peptic ulcer.
Recognizable Signs and How PUD is Identified
The most common sign of Peptic Ulcer Disease is a characteristic burning or gnawing epigastric pain in the upper abdomen. This discomfort often occurs between meals when the stomach is empty or may wake the individual during the night. For duodenal ulcers, pain may temporarily improve after eating as food neutralizes the acid, but returns a few hours later as the stomach empties.
Other symptoms include bloating, a feeling of fullness after eating a small amount of food, and unexplained nausea. Signs indicating bleeding mandate immediate medical attention, such as vomiting blood (hematemesis) or passing dark, tarry stools (melena). These alarm symptoms signal a potential complication requiring urgent intervention.
To definitively identify PUD, healthcare providers often rely on upper gastrointestinal endoscopy (EGD). During an EGD, a flexible tube with a camera is passed down the throat to visualize the lining of the esophagus, stomach, and duodenum. This allows the doctor to locate the ulcer and assess its severity.
Endoscopy also allows for biopsies, which are tissue samples taken to rule out malignancy and test for H. pylori using a rapid urease test. Non-invasive diagnostic methods for H. pylori infection include the urea breath test and the stool antigen test, which confirm an active infection.
Modern Treatment Approaches
Treatment for Peptic Ulcer Disease depends on identifying the underlying cause, typically H. pylori infection or NSAID use. For ulcers caused by H. pylori, the standard is combination therapy, often called “triple therapy,” to eradicate the infection. This regimen involves a course of two different antibiotics, such as amoxicillin and clarithromycin, combined with a Proton Pump Inhibitor (PPI).
The PPI dramatically reduces stomach acid production, creating an environment conducive to ulcer healing and enhancing antibiotic effectiveness. If antibiotic resistance is a concern or initial treatment fails, a different combination, such as bismuth-based quadruple therapy, may be prescribed. Post-treatment testing with a urea breath test or stool antigen test confirms successful eradication.
When PUD is linked to NSAIDs, the primary measure involves discontinuing the medication, if medically feasible. To allow the ulcer to heal, acid-suppressing medications are prescribed, most commonly PPIs, which are powerful suppressors of gastric acid secretion. Histamine H2-receptor antagonists (H2 blockers) are an alternative class of medication that also reduces stomach acid production.
If a patient must continue taking NSAIDs, the treatment plan includes long-term acid suppression therapy, such as a continuous daily PPI. This therapy is necessary to reduce the risk of ulcer recurrence and complications.