Ulcers Flashcards
What is grouped under peptic ulcers?
They aren’t the same but for treatment wise grouped together: gastric and duodenal
If someone presents with epigastric pain and a burning sensation after meals, what investigations are done?
Which results indicate what?
Carbon-urea breath test
- Involves giving the patient a lot of urea – H. pylori metabolises urea to nitrogen
- If you get increased levels of nitrogen, this means the H. pylori infection is present -> positive
Stool antigen test
- This involves testing for H. pylori antigens within the stool of the patient
As a result of these investigations, we can diagnose the patient with a H. Pylori positive peptic ulcer.
What % of duodenal and gastric ulcers are due to H.pylori?
98-100% of duodenal ulcers are a result of H. pylori infection, and 70-80% of gastric ulcers arise due to H. pylori infection.
What is H.pylori?
H. pylori is a motile spirochete that is able to move around (it has flagella allowing it to do this)
In the vast majority of people, H. pylori is a commensal bacteria
Only 3% of people in the world will develop a peptic ulcer as a result of H. pylori
How does H. pylori cause infection?
- A mucus layer protects the stomach epithelium from the acidic environment
- H. pylori can dissolve our mucus layer using urease enzyme: this allows H. pylori to access epithelia
- This causes epithelial cell death: H. pylori releases exotoxins -> increased inflammatory reaction
- Eventually, there is damage to the mucus layer, epithelial layer, and then to the interstitial layer
- This results in ulceration within the region of damage
- Increased acidity -> peptic ulcer
- There is also a shift in balance of certain cell types in the stomach
- You get more cells that produce protons, which causes an increased acidity -> further ulceration
How is H. pylori treated?
Amoxicillin & Clarithromycin/Metronidazole
- The two drug combination (i.e. amoxicillin + clarithromycin/metronidazole) is very effective
- These are given with the intention to wipe out the H. pylori infection causing the ulcer
- Once the H. pylori infection is removed, the stomach is amazing at healing itself
What is given to help treat the ulcer?
Proton Pump Inhibitor (PPI) – reduces acid production, given for 7 days
What happens when the carbon urea test and stool test are positive, an endoscopy is done and the ulcer is found to be complicated (bleeding, perforation etc)?
- Antibiotics for H Pylori (amoxicillin & clarithromycin/metronidazole)
- All 3 can be given in the case of an individual with recurrent peptic ulcers
- Consider adding quinolone or tetracycline. These may be added alongside the first line antibiotics
This is a big attempt to remove the H. pylori infection that wouldn’t budge the first time - Addition of BISMUTH (pain)
- Proton Pump Inhibitor (omeprazole) – 4-12 weeks
What do proton pump inhibitors do?
- The proton pumps that exist on the apical surface of parietal cells release protons. This is the final end point that results in an increase in acidity of the stomach
- Proton pump inhibitors, such as omeprazole, are known to be very effective at reducing the activity of proton pumps, and thence reducing stomach acidity
What affects proton pump regulation?
- Parietal cells produce hydrogen ions via the proton pumps
- There are various systems that regulate this
- The main regulators are the cholinergic system and the histaminergic system in the stomach
- Parietal cells are influenced by a number of external inputs, and cells within the fundus
- E.g. cells in the stomach fundus release somatostatin -> reduced parietal cell activity
- Cells in the stomach fundus release gastrin à increased parietal cell activity
If a patient presenting with epigastric pain and a burning sensation tests negative for carbon-urea and stool antigen but NSAID use is positive what is done?
- The second most common cause of peptic ulcers is prolonged NSAID usage
How can NSAIDs cause peptic ulcers?
- NSAID can be directly cytotoxic and reduce mucus production
- Up to here, the NSAID has a similar mechanism to H. pylori (breakdown of barrier -> epithelia exposure)
- Exposing epithelia to the acidic environment can lead to damage of stomach tissue and ulceration
- NSAIDs may increase the likelihood of bleeding (acts as an anti-platelet agent as well). H. pylori does not have this effect
- This can worsen the symptoms and propagate the whole process
How is an ulcer caused by NSAIDs treated?
- Removal of NSAID drugs – you can’t always do this (e.g. in individuals with other co-morbidities)
- Proton Pump Inhibitor or histamine H2 receptor antagonist (Ranitidine) – 4-8 weeks
- H2 receptor stimulation increases acid secretion due to increased activity of the proton pump
- An antagonist can be used to treat NSAID-induced peptic ulcers
- The H2 receptor is also located on the parietal cell
- So omeprazole and ranitidine work together to inhibit proton pump activity
…
In all peptic ulcers, regardless of the aetiology, proton pumps inhibitors are always prescribed.
Explain the underlying pathology of peptic ulcers
- Inhibition of protective mucus
- Destruction of gastric epithelia
- Increased acid production
