12.10: Peptic Ulcer Disease
- Page ID
- 100214
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A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus.
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List the causes of and treatments for peptic ulcer disease
Causes
A peptic ulcer, also known as peptic ulcer disease, is an erosion in the wall of the stomach, duodenum, or esophagus. The stomach protects itself from its own acidic gastric juice with a mucosal barrier made of mucus, bicarbonate, and tight junctions that seal the epithelial cells together. This barrier is highly effective but not flawless. When it becomes damaged, stomach acid can erode the mucosa. Small, shallow erosions usually heal on their own, but deeper injuries that extend into the tissue are called ulcers.
Helicobacter pylori
About 10% of Americans will develop a peptic ulcer during their lifetime. Contrary to popular belief, ulcers are not caused by stress or spicy foods. Most are linked to an infection of the stomach with Helicobacter pylori, a bacterium that can survive the acidic environment by neutralizing its immediate environment As many as 70–90% of peptic ulcers are associated with Helicobacter pylori (= H. pylori), a spiral-shaped bacterium that can live in the acidic environment of the stomach. (See image on the right.)
Roughly 30 to 40% of Americans carry this organism. People who are carriers for H. pylori often have no symptoms at all, even though the bacteria slowly thin the protective mucus layer of the stomach and duodenum and slightly inflame the lining. Carriers can unintentionally spread the infection to others, especially in childhood, through contaminated food or water or contact with saliva, vomit, or feces. Most carriers never develop problems, but some may eventually experience chronic gastritis, peptic ulcers, or, over many years, a small increase in gastric cancer risk. Because they feel fine, carriers are usually identified only when a family member tests positive or a clinician investigates unexplained stomach pain or anemia.
Why H. pylori Can Live in an Environment as Acidic as the Stomach
Helicobacter pylori survives in the stomach’s extreme acidity by creating a tiny “safe zone” around itself. It produces an enzyme called urease, which breaks down urea (a substance always naturally present in stomach fluid) into ammonia.
Ammonia is basic, so it neutralizes the acid immediately surrounding the bacteria. With this protective cloud, H. pylori can nestle into the mucus layer that coats the stomach wall, where the environment is less acidic than the stomach lumen. It also uses its spiral shape and flagella to burrow deeper into the mucus and avoid direct exposure to gastric acid. Together, these strategies allow H. pylori to survive and thrive in one of the harshest environments in the body.
H. pylori weakens the protective mucus layer that normally shields the stomach and duodenum from gastric acid. As the mucus thins, acid can damage the underlying tissue, leading to inflammation and ulcer formation. The exact route of transmission is still unclear, but the bacterium may spread through contaminated food or water, or through contact with the saliva, vomit, or feces of an infected person.
NSAIDs (Non-Steroidal Anti--Inflammatory Drugs)
NSAIDs such as aspirin, ibuprofen, and naproxen can also cause or worsen peptic ulcers because they reduce the production of protective mucus. Normally, the stomach is shielded from its own acid by a thick layer of mucus and bicarbonate, both of which are produced in response to prostaglandins. Prostaglandins are short-lived, hormone-like chemicals made from fatty acids that act locally in tissues to regulate inflammation, pain, blood flow, amongst much more.
NSAIDs block the enzyme (COX) that the body uses to make prostaglandins. When prostaglandin levels drop, three problems occur at the same time:
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Less protective mucus is produced.
The stomach surface becomes more exposed to acid. -
Less bicarbonate is secreted.
Acid is not neutralized as effectively. -
Blood flow to the mucosa decreases.
This slows healing and makes the tissue more vulnerable to damage.
With these defenses weakened, normal stomach acid can begin to injure the mucosa. Small erosions can progress into deeper ulcers, especially wit
h continued NSAID use. Over time, these ulcers may bleed or, in rare cases, perforate the stomach wall.
This is why long-term NSAID use is one of the leading causes of peptic ulcers, even in people without H. pylori infection.
Symptoms
Peptic ulcers can cause a range of symptoms. The most common is abdominal pain, especially near the stomach, often linked to mealtimes and sometimes appearing a few hours after eating. Other symptoms may include bloating, a sense of abdominal fullness, nausea, loss of appetite, weight loss, and sometimes heavy vomiting. If bleeding occurs, a person may vomit blood or pass melena, which are dark, tarry stools created when iron in hemoglobin is oxidized during digestion. In rare cases, an ulcer may perforate the stomach or duodenum and spill contents into the abdominal cavity, causing acute peritonitis, a medical emergency that requires immediate surgery.
Diagnosis
Doctors usually begin making a diagnosis based on the characteristic symptoms, especially stomach pain, which is often the first warning sign. In some cases, treatment is started right away without specific tests. If the symptoms improve within a few weeks, that improvement helps confirm that the initial diagnosis was correct.
If symptoms do not improve with treatment, or if they first appear in someone over age 45 or in a person with concerning signs such as unexplained weight loss, doctors may order diagnostic tests such as an endoscopy or a barium contrast x-ray. These tests help rule out other conditions, including stomach cancer, which can mimic ulcer symptoms. Doctors may also test further when ulcers are unusually resistant to treatment, unusually located, or when there is concern that the stomach is producing too much acid due to an underlying disorder.
An esophagogastroduodenoscopy (EGD) — often called an upper endoscopy or gastroscopy — is the most direct way to evaluate a suspected ulcer. With this procedure, the clinician can see the ulcer, determine its exact location and severity, and, if no ulcer is present, often identify another cause for the symptoms.
If a peptic ulcer perforates, air from inside the gastrointestinal tract can leak into the peritoneal cavity, which normally contains no air. This escaped air rises and collects under the diaphragm when the patient is standing, making it visible on an erect chest x-ray. The presence of this “free gas” on imaging is a classic sign of a perforated ulcer and requires immediate medical attention.
Treatment
Younger patients with ulcer-like symptoms are often treated first with antacids. These medications help neutralize stomach acid by raising the pH or by blocking acid secretion from gastric cells, which reduces irritation of the stomach lining. Patients who use NSAIDs may also be prescribed a prostaglandin analogue to replace the protective prostaglandins that NSAIDs suppress, helping prevent peptic ulcers from forming.
When H. pylori infection is present, the most effective therapy is “triple therapy,” which combines two antibiotics (such as clarithromycin, amoxicillin, tetracycline, or metronidazole) with a proton pump inhibitor. Antacids may also be added. In more severe or resistant cases, a third antibiotic can be included. Clearing the H. pylori infection usually relieves symptoms and allows ulcers to heal, although some patients may require retreatment if the infection returns.
A perforated peptic ulcer is a medical emergency and requires immediate surgical repair. Most actively bleeding ulcers require urgent endoscopy so the bleeding vessel can be treated by cautery, injection, or clipping.