Peptic (=’acid-related’) ulcer = DU or GU or both!
- o Incidence: improving in line with improvements in living standards, still affects 10-15% in certain populations. Helicobacter pylori carriage and NSAIDs use are the major RFs.
- o Dyspepsia: abdo pain, worse at night, relived by food
- o Vomiting: due to oedema or stenosis of pylorus
- o GI bleeding: common in PU
- o Perforation: +peritonitis may be a complicating feature (=rigid, painful abdomen)
- o Endoscopy: 1st line for dyspepsia/upper GI bleeding. Can be therapeutic in bleeding with injections/banding
- o Testing for H.pylori: typically v difficult to culture – test via:
- o CLO test: for bacterial ‘urease’, from endoscopically obtained antral tissue. Urease hydrolyses ureamethane and carbon dioxide. Detected by a colour change in pH-sensitive indicators.
- o 13C-labelled urea breath test: radiolabelled urea is ingestedand 13CO2 is produced by hydrolysis, excreted in lungs and detected in mouth
- o Measurement of H.pylori antibodies in blood.
- o Detection of H.pylori alone is not sufficient for diagnosis of DU, because 20% (20yo) to 50% (50yo) population carry it anyway
- o Barium contrast radiology: less commonly used – flexi-endoscopes are preferred.
- Key difference – GU’s have potential to be malignant.
- P/c: same as PU although often less acid involved – so less dyspepsia
- Ix: endoscopy – because of increased risk of cancer – biopsy ulcer edge and re-scope 6/52 later.
- o STOP NSAIDs!
- o Use H2 receptor antagonists and PPIs – should heal in 4-6/52!
- o H.pylori eradication:
- o Regimens consist of a high dose PPI + two different antibiotics. Example = one week “triple therapy” consisting of omeprazole/lansoprazole and the antibiotics clarithromycin and amoxicillin.
- o Regimen is usually 70% successful.
- o Success can be proven using 13C-radiolabelled urea breath test
- o Surgery: required in those with perforation and recurrent or persistent bleeding. Elective surgery is not recommended.