Flashcards in H. Pylori Deck (23):
What is H. pylori?
A gram negative rod found on the luminal surface of gastric epithelium. Its prominent flagella facilitate its penetration into the mucous layer of the stomach
Why can H. pylori exist in the highly acidic stomach?
it produces urease which converts the urea present in gastric juices to ammonia and CO2. This increases the pH of the stomach
Name the 3 gastric diseases H.pylori has been found to be a cofactor in
1. duodenal and gastric ulcers
2. gastric cancer
3. MALT lymphoma
What changes in the stomach are associated with duodenal ulcer in patients with H. pylori?
- Antral predominant diffuse gastritis
- increased acid
- increased gastrin
What changes in the stomach are associated with gastric ulcers or gastric cancer caused by H. pylori?
- Corpus predominant multifocal atrophic gastritis
- decreased acid
- increased gastrin
What bacterial virulence factors of H. pylori are associated with carcinogenesis?
- cagA and vac A genes are associated with increased carcinogenesis
- cagA causes neutrophil recruitment and inflammation
What % of those infected with H. pylori develop gastric cancer?
only 1-3% however, 95% of patients burg gastric cancer have H. pylori
What % of patients with H. pylori have PUD?
- 90% of duodenal ulcers are associated with H. pylori
- 70-80% of gastric ulcers
Why is H. pylori eradication important in PUD?
- improves healing of ulcers
- reduces rebreeding rates (if GIB as presentation)
- 95-98% of duodenal ulcers heal with H. pylori treatment vs. 85-95% with acid suppression alone
- 85% of gastric ulcers vs 60% with acid suppression alone
What extra-GI diseases are associated with H. pylori?
idiopathic iron deficiency anaemia
How does H. pylori cause gastric and duodenal ulcers?
1. depletion of astral D cell somatostatin
2. increased gastrin secretion by G cells and histamine secretion by ECL cells (lack of negative feedback from somatostatin)
3. increased gastrin and histamine stimulates acid release by gastric parietal cells
4. increased acid leads to metaplasia and ulcer formation
What different tests can be done to detect H. pylori?
Serology - HP specific IgG
HP stool Ag
C13 urea breath test
Rapid urease - CLO test
What are the pros and cons of HP serology?
sens/spec only 80-85%
unreliable in low prevalence areas
cannot use to test for eradication post treatment as IgG levels persist for 6-12 months
What are the pros and cons of the HP stool Ag test?
sens, spec good - 94% and 91% respectively
affected by PPI, H2 antagonists and ABs - must withheld for 2-4 weeks
What are the pros and cons of the C13 urea breath test?
most reliable non-invasive test
- sens and spec 98%
affected by PPI, H2 antagonists and ABs - withheld for 2-4 weeks
What is the CLO test, what are its pros and cons?
biopsy placed in urea containing medium
urease from H. pylori converts urea -> ammonia and medium changes colour
sens spec 90-95% - improved with multiple biopsies
What is the standard initial treatment for H. pylori?
Triple therapy for 10 days
* Metronidazole if penicillin allergic
What is the standard treatment for triple therapy failure?
this is first line therapy in high Clarithromycin resistance areas (>15%)
What is the main reason for treatment failure with triple therapy?
Clarithromycin +/- Metronidazole resistance
Who should be tested for H. pylori?
Patients with dyspepsia
FH of stomach cancer
high risk ethnic groups for gastric cancer
- japanese, Chinese, Korean, Russians
Long-term NSAID/Aspirin use
partners of treatment failures
Who should be tested after treatment to ensure eradication?
- H. pylori associated ulcer
- persistent dyspepsia after treatment
- H. pylori associated MALT
- post resection for early gastric cancer
What is MALT?
Low grade B cell lymphoma strongly associated with H. pylori infection
- HP virulence genes play little role (compared to gastric cancer)