PUD in the medical context is an acronym for Peptic Ulcer Disease, a condition characterized by open sores that develop on the inner lining of the digestive tract. These sores are localized defects that form in areas exposed to stomach acid and pepsin. The presence of these ulcers can range from being completely asymptomatic to causing significant discomfort and complications. The primary locations for these defects are the stomach and the first section of the small intestine.
What Peptic Ulcer Disease Is
Peptic Ulcer Disease is fundamentally an imbalance between the protective mechanisms of the gastrointestinal lining and the destructive forces of digestive acids and enzymes. The inner layer of the stomach and small intestine is naturally coated with a thick, protective mucus layer and bicarbonate, which neutralize acid and shield the underlying tissue. When this defense system is compromised, the highly acidic gastric contents begin to erode the mucosa.
An ulcer that forms within the stomach lining is called a gastric ulcer, while one found in the duodenum, the first part of the small intestine, is a duodenal ulcer. The erosion must extend through the muscularis mucosa to be classified as a true ulcer, distinguishing it from a more superficial erosion. The resulting defect exposes the sensitive tissue beneath to further damage from hydrochloric acid and pepsin, leading to inflammation and the characteristic open sore.
The Primary Drivers of Ulcer Formation
The vast majority of peptic ulcers are caused by one of two primary factors: infection with the bacterium Helicobacter pylori or the regular use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). These two agents compromise the mucosal barrier through distinct biological pathways. H. pylori is a spiral-shaped bacterium that has adapted to survive the harsh, acidic environment of the stomach by producing an enzyme called urease. Urease converts urea into ammonia, which creates a less acidic microenvironment, allowing it to colonize the lining.
Once colonized, H. pylori expresses virulence factors that cause chronic inflammation and directly damage the protective mucus layer. The resulting inflammation impairs the stomach lining’s ability to secrete bicarbonate and mucus, thereby weakening its defense against acid.
The second major cause is the chronic use of NSAIDs. These common pain relievers damage the gastroduodenal mucosa primarily by inhibiting the cyclooxygenase-1 (COX-1) enzyme. The COX-1 enzyme is responsible for synthesizing protective prostaglandins, which maintain mucosal blood flow and stimulate the production of mucus and bicarbonate.
By blocking COX-1, NSAIDs deplete these protective prostaglandins, leading to a diminished mucus layer and reduced blood flow to the lining. This makes the tissue vulnerable to acid damage. When both H. pylori infection and NSAID use are present, the risk of developing an ulcer increases due to the synergistic effect of the two risk factors.
Identifying Common Symptoms
The most common sign of a peptic ulcer is a dull, burning, or gnawing pain in the upper abdomen, often located between the breastbone and the navel. This pain is frequently intermittent, coming and going for days or weeks. The timing of the pain in relation to eating can often help differentiate the location of the ulcer.
Pain from a duodenal ulcer is often aggravated when the stomach is empty and may be temporarily relieved by eating food or taking antacids. Conversely, pain from a gastric ulcer may worsen shortly after eating a meal as the stomach produces more acid for digestion. Other associated symptoms include a feeling of fullness after eating only a small amount, bloating, belching, and nausea.
Many individuals with peptic ulcers, particularly older adults, may experience no symptoms at all until a serious complication, such as bleeding or perforation, occurs.
Diagnosis and Treatment Pathways
Diagnosing Peptic Ulcer Disease begins with a detailed review of the patient’s symptoms and medical history, particularly any history of NSAID use or prior ulcer disease. To confirm the diagnosis and determine the cause, physicians commonly use non-invasive methods to detect H. pylori. These tests often involve a urea breath test or a stool antigen test, which check for the presence of the active bacterial infection.
The most definitive diagnostic procedure is an upper endoscopy, also known as esophagogastroduodenoscopy (EGD). During this procedure, a flexible tube with a camera is passed through the mouth to visualize the stomach and duodenum. This allows the physician to directly inspect the ulcer and take biopsies to check for H. pylori and rule out malignancy, especially with gastric ulcers.
Treatment is tailored to the underlying cause of the ulcer. For ulcers caused by H. pylori, the standard treatment involves a combination of two antibiotics to eradicate the bacteria, paired with a Proton Pump Inhibitor (PPI). This medication works by reducing the amount of acid produced by the stomach, allowing the damaged tissue to heal.
If the ulcer is primarily due to NSAID use, the most important step is to stop taking the offending medication and administer a course of acid-suppressing medication, typically a PPI, for several weeks to promote healing. In cases of complicated ulcers, such as those with bleeding or perforation, endoscopic or surgical intervention may be required.