Peptic ulcer disease is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve lower esophagus, distal duodenum or jejunum.
Peptic ulcer disease (PUD) has various causes however Helicobacter pylori-associated PUD and NSAID-associated PUD account for the majority of the disease etiology.
Causes of Peptic Ulcer Disease
Helicobacter Pylori-Associated PUD
H. pylorus is a gram-negative bacillus that is found within the gastric epithelial cells. This bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori infection is more prevalent among those with a lower socioeconomic status and is commonly acquired during childhood. The organism has a wide spectrum of virulence factors allowing it to adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria leading to gastric ulceration.
Virulence Factors of Helicobacter pylori
Nonsteroidal anti-inflammatory drugs and aspirin use is the second most common cause of PUD after H. pylori infection. The gastric mucosa is normally protected by secretion of prostaglandin. NSAIDs block prostaglandin synthesis by inhibiting COX-1 enzyme resulting in a decrease in gastric mucus and bicarbonate production and a decrease in mucosal blood flow.
Apart from NSAIDs, bisphosphonates, potassium chloride, steroids, and fluorouracil have been implicated in etiology of PUD.
PUD is a global problem with a lifetime risk of development ranging from 5% to 10%. Overall, there is a decrease in incidence of PUD worldwide due to improved hygienic and sanitary conditions combined with effective treatment and judicious use of NSAIDs. Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers are more common in men than in the woman.
The mechanism of occurrence of PUD results from an imbalance between gastric mucosal protective and destructive factors. Risk factors predisposing to the development of PUD:
Gastric ulcers are most commonly located on the lesser curvature whereas duodenal ulcers are most common at the duodenal bulb. The ulcer is round to oval with a smooth base. Acute ulcers have regular borders while chronic ulcers have elevated borders with inflammation. An ulcer extends beyond the muscularis mucosa.
Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age. Gastric and duodenal ulcers can be differentiated from the timing of their symptoms in relation to meals. Common signs and symptoms include:
Diagnosis of PUD requires history taking, physical examination, and invasive/noninvasive medical tests.
A careful history should be obtained and noted for the presence of any complications. Patient reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion of PUD. The pain of gastric ulcers increases 2 to 3 hours after a meal and may result in weight loss whereas pain of duodenal ulcers decreases with meal resulting in weight gain. Any patient presenting with anemia, melena, hematemesis or weight loss should be further investigated for complications of PUD predominantly bleeding, perforation or cancer.
A physical exam may reveal epigastric abdominal tenderness and signs of anemia.
Anti-secretory drugs used for PUD include H2-receptor antagonists and the proton pump inhibitor (PPIs). H2 receptor blockers have been largely replaced by PPIs due to their superior healing and efficacy. PPIs block acid production in the stomach providing relief of symptoms and promote healing. Treatment may be incorporated with calcium supplements as long-term use of the PPIs can increase the risk of bone fractures. NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose. Corticosteroid, bisphosphonates, and anticoagulants should also be discontinued if possible. Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-induced peptic ulcers. First line treatment for H. pylori-induced PUD is a triple regimen comprising two antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole or amoxicillin are used for 7 to 14 days. Antibiotics and PPIs work synergistically to eradicate H. pylori.
Surgical treatment is indicated if the patient is unresponsive to medical treatment, noncompliant or at high risk of complications. Surgical options include vagotomy or partial gastrectomy.
The prognosis of PUD is excellent after the underlying cause is successfully treated. Recurrence of the ulcer may be prevented by maintaining good hygiene and avoiding alcohol, smoking, and NSAIDs.
Once a diagnosis of peptic ulcer disease is made, consult with a gastroenterologist and dietician.
Ulcers are differentiated from erosions based on size. Lesions less than 5 mm in diameter are termed erosions, whereas lesions greater than 5 mm in diameter are termed ulcers.
COX-2 selective NSAIDs are less likely to cause PUD as COX-2 is not expressed on the gastric mucosa. Therefore, in patients with a history of PUD, COX-2 selective NSAIDs are preferred.
A gastrin-producing endocrine tumor causes Zollinger-Ellison syndrome. It usually arises from the pancreas or duodenum. It results in multiple ulcers in the duodenum and jejunum. It can be diagnosed by measuring serum gastrin levels.
An evidence-based approach to peptic ulcer disease is recommended.
PUD is a very common disorder that affects millions of people. When left untreated, it has significant morbidity. The majority of patients with PUD present to their primary caregiver but others may present to the emergency department, urgent care clinic or an outpatient clinic. Because the presentation of PUD is often vague, healthcare workers including nurses need to be aware of this diagnosis. The abdominal pain can mimic a number of other pathologies and consequently lead to a delay in treatment. Once the diagnosis is made, the key is to educate the patient on lifestyle changes which include discontinuation of smoking, abstaining from alcohol and avoid consumptions of too many NSAIDs. The pharmacist should educate the patient on medication compliance to obtain symptom relief and a cure. For most patients with PUD who are treated with the triple regimen or PPI, the outcomes are excellent, but recurrence of symptoms is not uncommon. (Level II)