Flashcards in PEPTIC ULCERS Deck (21)
What is a peptic ulcer?
A peptic ulcer in an open sore of the mucosa of the stomach or duodenum.
Where in the abdomen do people with peptic ulcers most often experience pain?
When do patients with a gastric ulcer experience pain?
Shortly after eating
When do patients with a duodenal ulcer experience pain?
May start a couple of hours after eating and will recede after eating food.
What are the complications of a peptic ulcer?
Vomiting dark brown blood (coffee ground)
Perforation of stomach wall
Peritonitis --> Sepsis
Increased risk of malignancy
What are the factors that are normally well balanced which contribute towards the development of a peptic ulcer when they fall out of balance?
Gastric acid and pepsin secretion
Mucus defense barrier
What are the risk factors for developing a peptic ulcer?
H. pylori infection (70% of gastric ulcers)
NSAIDs, such as aspirin.
Zollinger-Ellison syndrome (hypergastrinaemia)
How do NSAIDs lead to the development of a peptic ulcer?
Inhibit prostaglandin production through inhibition of cyclo-oxygenase.
This prevents production of prostaglanding H2 (from arachodinic acid) which is a precursor for (among others) prostaglandin E2.
Prostaglandin E2 is an inhibitor of H2 mediated gastric acid secretion.
How does H. pylori infection lead to the development of a peptic ulcer?
The H pyloria bacteria go through the mucus lining to penetrate the epithelial lining.
The ammonia produced by the bacteria to regulate pH is toxic to the epithelial cells. The damage and the ensuing inflammation allows the stomach acid and the pepsin to overwhelm the protective mechanisms and the ulcer develops.
How would someone with a peptic ulcer typically present?
Dull, gnawing ache epigastric pain
Pain after eating (gastric ulcer)
Pain 2 hours after eating, that is relieved by further eating (duodenal ulcer)
How do we diagnose a patient with peptic ulcers?
Endoscopy with biopsy
What is the more invasive way in which we diagnose whether the patient's peptic ulcer was a result of H. pylori infection?
CLO test (Rapid urease test):
Biopsy is taken from the antrum of the stomach and placed into a medium containing urea and an indicator such as phenol red. An increase in pH as a result of production of ammonia by H. pylori urease changes colour from yellow to red.
Histology of biopsy
Culture from biopsy also used
In which patients might you want to take a biopsy from the fundus or body of the stomach, when carrying out the CLO test (assessing the presence of H. pylori)?
Patients on therapy with proton pump inhibitors.
Evidence to suggest that the H. pylori moves proximal in these patients.
What is the less invasive way in which we diagnose whether the patient's peptic ulcer was a result of H. pylori infection?
Urea breath test:
Patient drinks a solution enriched with 13C-labelled urea.
The amounts of 13C-CO2 product from the urease is measured in the breath.
What are the treatment options for someone diagnosed with a peptic ulcer?
Ulcers associated with H. pylori:
Antibiotics (amoxicillin, clarithromycin and metronidazole)
Ulcers not associated with H. pylori:
Proton pump inhibitors (omeprazole)
H2 blockers (renitidine)
Where are most peptic ulcers founds?
75% are duodenal
What are the factors that contribute to the maintenance of the mucosal defense barrier which prevents the formation of peptic ulcers?
Surface mucus secretion
Bicarbonate secretion into mucus
Mucosal blood flow
Apical surface membrane transport
Epithelial regenerative capacity
Elaboration of prostaglandins
What type of bacteria is H. pylori?
Spiral shaped gram negative
What are the antibiotics used to eradicate H. pylori in someone with acute gastritis?
Combination of amoxicillin, clarithromycin and metronidazole
2 times a day for 7 days
What might you be able to do for a patient with peptic ulcers where the taking of NSAIDs is still clinically desirable (eg severe rheumatoid arthritis)?
Use lowest dose of NSAID
Misoprostol is a synthetic prostaglandin analogue with mucosal protective properties
Concomitant use of PPI and NSAIDs
Switch NSAID to cox-2 inhibitor (increased risk of adverse cardiovascular side effects)