Gastrointestinal Ulcer

Gastrointestinal Ulcers (Peptic Ulcer)

GI Ulcers can occur along the GI tract, typically the stomach, duodenum and sometimes the lower oesophagus. They are the result of an erosion occurring in the mucosal lining, the reason for which varies but can include NSAID usage (i.e. Ibruprofen) and Helicobacter Pylori (H. Pylori) infection. The prevalence of gastric ulcers in particular is increasing.


Gastric and Duodenal Ulcers arise due an imbalance between the protective mechanisms of the stomach /duodenum, and factors that cause injury to the lining of these structures. IN H. Pylori infection, chronic gastritis results in excess secretion of gastric acid by the parietal cells. This causes erosion of the mucosa and subsequently results in a gastric ulcer. Similarly, excessive use of Non-steroidal anti-inflammatory drugs (NSAIDS) such as Ibroprofen and  Naproxen, inhibit COX-1, which in turn affects prostaglandin production, resulting in less secretion of the protective mucous lining the stomach; the end result is a mucosal lining less resistant to gastric acid and the formation of an ulcer


Symptoms of Gastric/ Stomach Ulcer – Typically patients with a gastric ulcer will present with burning epigastric pain that is made worse by eating. When describing the site of epigastric pain it is noted that patients often point with a single finger to the site of pain. Nausea may also occur, whilst vomiting is infrequent but would often improve pain.

Symptoms of Duodenal Ulcer – As with Gastric Ulcers, burning epigastric pain is the common complaint. Often those suffering with a duodenal ulcer complain of pain that is worse at night, and is relieved by eating as the pyloric sphincter closes when eating food. Equally pain may increase when eating. It is noted that relationship of pain to food is often unreliable.

Symptoms of Oesphageal Ulcer – Typically oesophageal ulcers occur as a consequence of Gastro-Oesophageal Reflux Disease (GORD), and often presents with dysphagia, sore throat and acid reflux type symptoms.

On Examination

Examination is likely to reveal epigastric tenderness in line with the presenting complaint, with no other abnormal findings associated with GU/ DU.


Helicobacter Pylori Non-Invasive investigations:

Serological blood tests have a relatively high sensitivity and specificity. They are capable of detecting H. Pylori IgG antibodies thus confirming a bacterial cause of the ulcer. Antibodies may remain in the blood up to a year post treatment thus serology is an inappropriate test for the confirmation of H. Pylori eradication.

The C-Urea Breath Test involves the patient swallowing Urea labeled with either Carbon-13 or Carbon-14. If H. Pylori is present the substance will be split by Urease, an enzyme produced by H. Pylori. The expelled breath will contain the remaining isotope and thus can be measured using specialist instruments. This test can be used as confirmation of eradication of the infection.

Image result for c-urea breath test

Stool antigen test can be used to determine the presence of H.Pylori in a stool sample. The test is highly sensitive and can be used as evidence of successful eradication of the infection.

Invasive investigations:

Oesophagogastroduodenoscopy (OGD) is recommended in all patients over the age of 55. A biopsy is taken to investigate the cause of the ulcer and to confirm H. Pylori as a cause if suspected. Endoscopy is also used as an exclusion for cancer, particularly in patients whom display ‘red flag symptoms’; such symptoms prompt OGD investigations regardless of age.


Treatment for H. Pylori involves a triple ‘eradication therapy’ consisting of a PPI (Proton Pump Inhibitor) such as Omeprazole and two antibiotics such Clarithromycin and Amoxicillin, all taken BD. In patients allergic to Penicillin, Amoxicillin may be substituted for Metronidazole.

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