- 1 Summary
- 2 More Information
- More common in men than women
- DU’s and 2-3x as common as GU’s
- H. pylori infection
- Smoking –reduces prostaglandin synthesis
- Alcohol intake
- NSAID use – reduced prostaglandin synthesis
- Epigastric pain
- Although vomiting is rare, it may relieve pain
- Weight loss (patient may eat less to try and avoid pain)
- 50% of patients are asymptomatic
- Tiredness (anaemia)
- Pain may be worse at night
- Pain tends to be worse on eating, or just before eating, when acid is produced.
- Stool test – this is now the first line test. Tests for the presence of H. pylori, put PPI’s must be stopped a week before the test
- Urea breath test – if H pylori is present, any urea ingested will be converted to ammonia and then absorbed by the body. If you label the urea with an uncommon isotope (e.g. carbon13), then you can detect the isotope in the breath of the individual. If H. pylori is not present, the urea will not be turned into ammonia, and thus will pass through the GI tract undigested, and the unusual isotope will not be detected in the breath.
- Serum IgG – you can take a blood sample for IgG against H. pylori. Test is quite useful, but levels do not fall for many months after eradication, thus you cant use this test to see if treatment is successful.
- Endoscopy – should be done in anyone over 55, and/or with red flag symptoms. Enable biopsy (for cancer). Also, most patients are scoped 6 weeks after treatment for ulcer to check for cancer.
- FBC – to check for anaemia
- Fecal occult blood – not very specific
- Triple therapy – this is a PPI and two AB’s, e.g.:
- Omeprazole, metronidazole and clarithromycin – all given twice daily.
- The antibiotics are taken for 7 days, and the PPI for a further 3-4 weeks
- Haemorrhage – if the ulcer directly overlies a blood vessel
- Anaemia – due to blood loss
- Duodenal Ulcers more likely to perforate than Gastric Ulcers
- May be the first sign that an ulcer is present
- Pain – sudden onset – likely to be localised to epigastrium initially, but then generally. May radiate to the back, particularly in DU
- Absent bowel sounds
- Shallow breathing due to diaphragmatic irritation
- X-ray may show gas under the diaphragm
Presentation – Peptic Ulcer (not yet perforated)
- Abdominal pain in the epigastric region. For DU’s, the pain is when you are hungry, and GU’s the pain is when you eat. This is because when you are hungry, you produce acid in anticipation of food (the cephalic phase), which is then washed straight into the duodenum and isn’t buffered. When you eat, the food buffers the acid, and so the pain is reduced. In GU, the pain is greater when you eat due to the physical pressure of food on the ulcer. DU pain is present at night as well as in the day.
- Nausea may accompany the pain, and although vomiting is infrequent, it will often relieve the pain.
- Weight loss may be present, particularly in gastric ulcers.
- Left untreated, the symptoms of DU follow a spontaneous relapse and remission course
- Examination is not always that helpful, as there is nearly always general tenderness in all dyspepsia’s.
- History of NSAID’s / alcohol / steroids
- Urea breath test to test for presence of H. Pylori
- Patients will swallow urea that is labelled with an uncommon isotope – i.e. carbon 13 or 14. Usually Carbon 113 is used as it is non-radioactive. Then 10-30 minutes later, a breath sample is taken to measure the amounts of exhaled carbon dioxide containing the labelling isotope. The sample is measured using a mass-spectrometer, which is expensive, but is highly sensitive (97%) and specific (96%). This indicates that the urea has been split up and the carbon absorbed by the body. The urea is split by the enzyme urease which is present in H. Pylori, and thus this indicates the presence of H. Pylori.
- Often a baseline sample of carbon dioxide is taken before the labelling isotope is given and then the two results compared.
- There are also urea splitting bacteria in the colon that will cause the labelled carbon to be present in exhaled air about 5 hours after ingesting the urea.
- Serological tests for IgG. These are useful for confirming the presence of H. Pylori, but not as convenient as the breath test. They are about 90% specific. It can take over a year for IgG levels to fall below 50% of their original value even after H. Pylori eradication, so this is not a useful test to see if the infection has been eradicated. Antibodies can also be found in the saliva, but these are nowhere near as accurate as serology.
- Stool test. This is a highly sensitive (96%) and specific (97%) immunoassay that will detect the presence of H Pylori, and can also be used to see if H Pylori has been eradicated. PPI’s must be stopped one week before the test for eradication. This is now often the first line test.
- Endoscopy. (OGD) This will confirm the presence of an ulcer by sight, but a sample of gastric mucosa may also be taken. This can be tested in three ways:
- Put in a urea solution containing Phenol red. If H. Pylori is present, then the urea will be rapidly split to release ammonia, and the solution will increase in pH and change colour. This is known as the rapid urease test.
- Cultured and tests against various antibiotics
- Looked at histologically.
- FBC – to check for anaemia
- U+E – rarely shows up Zollinger-Ellison syndrome
- Faecal occult blood
- Barium meal test – sometimes used in patients who are unable to tolerate endoscopy.
- These are usually held responsible for the ulcers where H pylori infection is absent (about 25%). They inhibit cyclo-oxygenases (COX), which are enzymes that enable the production of prostanoids (prostaglandins and thromboxanes). There are 3 variants of COX, 1,,& 3. COX-1 is involved with protection of the gastric mucosa, and it is sometimes called the ‘housekeeping’ enzyme, due to its role in every day wear and tear repair.
- Ultimately, NSAID’s inhibit prostaglandin formation and so reduce the ability of the stomach to heal itself. Small abrasions to the lining of the stomach that occur all the time, and would normally heal are now less likely to heal. Pepsin may also act on these abrasions, and ulceration may possibly occur.
- The major repair pathways that prostaglandins affect are:
- Bicarbonate secretion into the mucous layer
- Tight junction maintenance between gastric cells to prevent lumen contents getting between the cells
- Gastric bloodflow – delivering lots of bicarbonate ions to buffer to acid to the gastric cells.
- Taking long term aspirin makes you 3x as more likely to get an ulcer, and other NSAID’s have a similar effect. Take them both together and your risk is 10x greater!
- The patient is under 55 and has tested positive for H. Pylori
- The patient is over 55 and testes have confirmed a gastric ulcer is responsible for their symptoms.
- The patient has no significant underlying pathologies (e.g. cancer) but H. Pylori is present. This is slightly controversial as it has been implicated in GORD, but it is still recommended.
- First line therapy – Triple therapy – patients will be treated with a proton pump inhibitor, and two antibiotics. An example would be:
- Omeprazole 20mg + metronidazole 400mg + clarithromycin 400mg All twice daily.
- Omeprazole 20mg + metronidazole 400mg + amoxicillin 1g All twice daily.
- There is very high resistance for metronidazole (25%) and that is why another antibiotic is taken. This regimen should be followed for 7 days, and then a PPI taken for a further 3-4 weeks.
10-15% of population
3-5% of population
Mostly anterior of first part of duodenum (the duodenal cap)
Mostly on lesser curve and antrum
Action of pepsin and / or acid on a normal abrasion in the duodenum, with abnormal healing. Increased acid and pepsin as a result of H. Pylori causing a depletion of Somatostatin reserves and a loss of natural feedback of acid production. Decreased bicarbonate secretion in duodenum ; possibly an effect of nitrates produced by of H. Pylori.
H. Pylori induced pangastritis, resulting in reduced effectiveness of gastric mucosal repair mechanisms.
- Haemorrhage – this is a result of an ulcer being in an ‘unlucky’ place, and as it gets deeper, it comes across a blood vessel. This can be quite serious if it is a relatively major vessel, and result in anaemia.
- Penetration of adjacent organs
- Sudden onset severe abdominal pain. At first pain may be localised to the upper abdomen, but it quickly spreads and becomes generalised.
- If the pain radiates to the back, then it is likely to be a posterior duodenal ulcer.
- Localised or generalised peritonitis. Very tender to the touch. You can tell if someone has peritonitis as opposed to a different cause of abdominal pain because if they have peritonitis they will want to lie very still, but with other causes of pain, they may ‘writhe’ around in pain.
- Signs of SIRS (systemic inflammatory response syndrome).
- Breathing will be shallow due to diaphragmatic pain and shock.
- The abdomen will be immobile with board like rigidity.
- Bowel sounds are absent, and the dullness over the liver may not be there due to the prescence of gas in the abdominal cavity
- After a few hours, the initial symptoms may die down, but there will still be the rigidity. Over a longer period of time, the patien’s condition will deteriorate due to peritonitis.
- Perforation has a mortality rate of 25% – this is dependent on the patient’s age and other factors.
- The main problem with a perforated ulcer is that it will cause peritonitis.
- X-ray may show gas under the diaphragm (in about 50% of cases)– pneumoperitoneum – shown below by the distinctive lines underneath the diaphragm. Don’t get this confused with air in the stomach, which is perfectly normal and most commonly seen after a recent meal. It is important when taking an x-ray like this that the patient has been sat upright for at least 10 minutes beforehand and is sat upright when the x-ray is taken Otherwise you will not be able to see any air! Sitting like this may be uncomfortable for the patient.
- After resuscitation then the perforation will be treated surgically – it will be closed by being sewn up, and then part of the greater omentum may also be sewn over the affected area – the omentum is still attached to the rest of itself! If this is not possible, then a pyloroplasty may be made from the perforation.
- A pyloroplasty is where the pyloric sphincter of the stomach is widened. It allows quicker emptying of the stomach in people at high risk of PUD and is sometimes performed before an ulcer has perforated. In this case it is performed because sealing up the perforation is too difficult, and it is a treatment that may have beneficial effects for the patient by reducing the risk of future ulcers.
Complications (of surgery)
- Chest infection from aspiration during intubation
- Wound infection
- Adhesions. These can occur years after surgery and will ofte4n cause obstruction of the bowel. They are much lea common with key hole surgery than with open surgery – probably due to the reduces physical moving of the bowel by this type of surgery.
- Keyloid scarring – this is where a big thick scar develops over the site of the incision and is virtually impossible to get rid of. You can get rid of it by cutting it off, but it is very likely to grow back again just the same.