IPN 2022 May

Page 92


Peptic Ulcers

Peptic Ulcer Disease Peptic ulcers are ulcerations more than 5 mm in diameter that develop in the mucosal lining of the stomach or duodenum resulting from an imbalance between factors promoting mucosal damage (such as gastric acid, pepsin, Helicobacter pylori infection and non-steroidal anti-inflammatory drugs) and mechanisms promoting gastroduodenal defence such as prostaglandins, mucus, bicarbonate and mucosal blood flow. Interview with Theresa Lowry Lehnen (GPN, RNP, PhD) Clinical Nurse Specialist and Associate Lecturer South East Technological University (SETU)

Theresa Lowry Lehnen, Clinical Nurse Specialist and Associate Lecturer South East Technological University explains that ulcers smaller than 5mm in diameter or without depth are called erosions. “Most cases of PUD are associated with Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs),” she says.

Theresa explains, “Duodenal ulcers are four times more common than gastric ulcers and are also more common in males than females. Gastric ulcers are most commonly located on the lesser curvature and duodenal ulcers are most common at the duodenal bulb. Duodenal ulcers occur most frequently in the first portion of the duodenum (over 95%), with approximately 90% located within 3 cm of the pylorus and are usually less than or equal to 1 cm in diameter. Peptic ulcers are round or oval in shape with a smooth base. Acute ulcers have regular borders, while chronic ulcers have elevated borders with inflammation.”

Peptic ulcer disease (PUD) is a significant source of morbidity and mortality worldwide with a lifetime risk of development ranging from 5% to 10%. Epidemiological studies however, have shown a sharp decreasing trend in the past 20–30 years in the incidence, rates of hospital admissions and mortality associated with the condition, due to improved hygiene, more effective treatments including the widespread use of PPIs and judicious use of NSAIDs and aspirin.

According to Theresa, the mechanism of peptic ulcer disease results from an imbalance between gastric mucosal protective and destructive factors. In PUD there is usually a defect in the mucosa that extends to or beyond the muscularis mucosa. Once the protective superficial mucosal layer is damaged, the inner layers are susceptible to acidity and the ability of the mucosal cells to secrete bicarbonate is compromised. H. pylori can colonise the gastric mucosa and also impair the

secretion of bicarbonate, promoting the development of acidity and gastric metaplasia. Aetiology Common causes of PUD include, Helicobacter pylori bacteria, NSAID’s and other medications. Rare causes include, zollingerellison syndrome, malignancy, stress, viral infection, vascular insufficiency, radiation therapy, crohn’s disease and chemotherapy. She continues, “Nonsteroidal anti-inflammatory drug use is the second most common cause of peptic ulcer disease and approximately 25% of NSAID users will develop PUD. Aspirin users are also twice as likely to develop peptic ulcers as the general population. NSAIDs damage the gastroduodenal mucosa through both systemic and local mechanisms, but the systemic inhibition of cyclooxygenase 1 (COX-1) derived prostaglandins is regarded as the main mechanism. The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting the COX-1 enzyme, resulting in decreased gastric mucus and bicarbonate production and a decrease in mucosal blood flow. Other medications including corticosteroids, bisphosphonates, potassium chloride, and fluorouracil have been implicated in the aetiology of PUD. “About a fifth of PUD cases are not related to H. pylori, NSAIDs or aspirin, but the accuracy of this value has been challenged due to false negative H. pylori testing or under reported NSAID use. Idiopathic PUD may be due to an imbalance between factors that contribute to mucosal integrity and aggressive insults, including a hyper-secretory status.” Symptoms So what are the symptoms of peptic ulcer disease? Theresa notes, “Approximately twothirds of patients with PUD are asymptomatic. In symptomatic patients, the most common presenting symptom of peptic ulcer disease is epigastric pain, which may be associated with dyspepsia, bloating, abdominal fullness, nausea, or early satiety.



“Other signs include weight loss/ gain, haematemesis and melaena.

Signs and symptoms of PUD vary depending upon the age and location of the ulcer. Gastric and duodenal ulcers can be differentiated by the timing of their symptoms in relation to meals. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer, and 2-3 hours post prandial for patients with a duodenal ulcer. Nocturnal pain is common with duodenal ulcers. The most common complication of peptic ulcer disease is gastroduodenal bleeding. Perforation is a less frequent but potentially lifethreatening complication. Either of these may be the presenting symptom, particularly in patients taking NSAIDs.” Investigations and Diagnosis A detailed history including medication use and lifestyle factors, physical examination, invasive and non-invasive medical tests are important for an accurate diagnosis of PUD. “A careful history should be obtained and noted for the presence of any complications,” she adds. “Any patient presenting with anaemia, melaena, haematemesis or weight loss should be further investigated for complications including bleeding, perforation, or cancer. A physical exam may reveal epigastric abdominal tenderness and signs of anaemia. “Endoscopy is the gold standard for diagnosis of peptic ulcer disease. Although invasive, endoscopy allows for biopsy and includes a variety of methods for testing such as histology, culture, or rapid urease test. Endoscopy can be used to detect H. pylori and can also rule out malignancy. Less invasive options include a helicobacter pylori carbon-13 urea breath test or stool antigen test and a full blood count. The urea breath test has high specificity, however, false-negative results can occur in the case of PPI use. Other investigations to consider may include fasting serum gastrin level and urine NSAID screen. “Computed tomography can identify non-perforated peptic ulcers. However, many patients will need endoscopy, oesophagogastroduodenoscopy (OGD) for further evaluation. Barium endoscopy is an option for patients with contraindications