Peptic ulcer disease usually involves the mucosal lining of stomach or duodenum (first layer of the inner lining of the stomach or duodenum). In chronic condition depth can go to the submucosal layer and sometimes perforate the serosa. One of the commonest causes of both gastric and duodenal ulcers is Helicobacter Pylori (H pylori) infection. However it can also be due to gastric acid overproduction.
The prevalence of duodenal ulcers is four times that of gastric ulcers. Damage from Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs usage, gastric acid and pepsin can lead to peptic ulcer disease. The lining of the stomach and duodenum normally protect themselves from damage with mucus, intestinal blood flow and bicarbonate. However, if these are lacking the damaging substance like gastric acid (composed of hydrochloric acid, potassium chloride and sodium chloride) will lead to breaks in the stomach and duodenum wall.
Signs and symptoms
Patients presenting with peptic ulcer disease will most usually present with abdominal pain. This mainly will be in the epigastric region (the upper abdominal region) without any radiation. The pain is usually described as dull ache or burning sensation. Other symptoms that patients will complain about are nausea, loss of appetite, diarrhoea, and weight loss. In addition, they may experience vomiting, and this sometimes may be haematemesis. Those with long-term dyspepsia, symptoms such as heartburn, belching, fullness, and a history of gastro-oesophageal reflux disease can be vulnerable to peptic ulcer disease. There are no particular signs on physical examination however epigastric tenderness can be elicited on abdominal palpation.
ALARM Symptoms include:
- Loss of weight
- Recent onset of progressive symptoms
- Swallowing difficulty
These symptoms are important to investigate as stomach cancer could present like this.
Peptic ulcers can be caused by a bacteria Helicobacter pylori (H pylori). Interestingly in 2005 a Nobel prize was awarded to Barry J. Marshall and J. Robin Warren for their discovery of "the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease”. In addition to H pylori, non-steroidal anti-inflammatory drugs (NSAIDs) contribute to ulcer formation, as well as aspirin, alcohol, and other less common causes are things like caffeine, tobacco smoking, radiation therapy, physical stress due to illness, Crohn's disease, liver disease and in addition to these, Zollinger-Ellison syndrome is a risk factor too. This is a gastrin secreting tumour of the pancreas leading to increased acid production in the stomach.
Diagnosis can be made clinically, however for confirmation of diagnosis, investigations such as oesophago-gastro-duodenoscopy (OGD) and barium swallow abdominal x-rays can be carried out. Endoscopy is diagnostic test for peptic ulcer disease. If the patient is above the age of 45 with any of the alarm symptoms present or if symptoms do not resolve after a few weeks of treatment it is essential to investigate with endoscopy.
Full blood count needs to be checked for signs of microcytic anaemia.
When testing for H Pylori, the urea breath test is the gold standard for detecting H pylori because it is a rapid and non-invasive diagnostic technique. Blood tests to measure antibodies and stool antigen test can also be useful. A stool heme test is also an option to check for occult blood, this is usually negative. The CLO test (campylobacter like organism) is a biopsy test which detects the presence of H. Pylori in the stomach and duodenum. A biopsy is taken from the gastric antrum, and the tissue is placed onto a urea containing mediator. If H. Pylori is present, the indicator changes colour, as the urease produced by the bacteria converts the urea to ammonia, and hence the medium becomes more alkaline (the change is from yellow to red).
Lifestyle changes are important to advise to the patients of peptic ulcer, such as avoiding drinking alcohol and medications like aspirin and NSAIDS, to quit smoking is also essential.
Medical therapy includes acid reducing medication such as H2 antagonists (examples are ranitidine, cimetidine and famotidine) or proton pump inhibitor’s (examples are omeprazole, lansoprazole and rabeprazole) which can be taken for four weeks.
In the case where H pylori is present, the most effective treatment for this is called triple therapy. This is a combination of two antibiotics such as Clarithromycin and Amoxicillin, (Amoxicillin can be replaced with Metronidazole for those allergic to penicillin) and a proton pump inhibitor such as Omeprazole.
Endoscopy is required for bleeding peptic ulcers, where cautery or clipping is used to stop the bleed. Emergency surgery is used for a perforated peptic ulcer. This requires urgent repair of the perforation.
For follow up those treated for gastric ulcer disease will need an endoscopy six to eight weeks after treatment was initiated. Those with H Pylori need to be checked four weeks after the end of their treatment regime.
Perforation is a severe complication occurring when the wall of the stomach or duodenum has fully eroded through where the ulcer was. This is more likely to occur in elderly patients. It is empirical to urgently treat as it can lead to shock or peritonitis. The initial part of the duodenum runs anterior to the gastroduodenal artery, which is a direct branch of the common hepatic artery, and supplies the duodenum. If the duodenal ulcer forms in the posterior wall, the ulcer can erode through the vessel and result in significant intra-abdominal bleeding. Assessing and managing the patient for signs of shock following blood loss is essential.
Upper gastrointestinal bleeding is a complication that can occur if there is overt bleeding, emergency treatment is required to prevent shock. In this case endoscopy is performed straight away. Obstruction and malignant transformation within the ulcer are also potential complications, which is why all ulcers are biopsied if they look even remotely suspicious on endoscopy.