H Pylori Cards Flashcards
What are three common causes of duodenal ulcers?
H Pylori, NSAIDS, steroids
What % of gastric cancers are associated with H Pylori?
70%; this makes H Pylori a WHO Type 1 definitive carcinogen
What two types of cancer are associated with H. Pylori?
Gastric adenocarcinoma and gastric lymphoma (MALT lymphoma)
Where and under what conditions does H Pylori grow?
H pylori grows in the antral and pyloric regions of the stomach; grows slowly in low O2
What are the outcomes of H Pylori infection?
85% simple gastritis; 10-15% progress to peptic ulcer (usually duodenal); 1% progress to gastric cancer
How is H Pylor infection usually acquired?
Within famillies or close contacts; often in childhood (90% by age 10)
What is the environmental reservoir for H Pylori?
There is no environmental reservoir; strains follow human migration
What are the protective benefits of H Pylori infection?
Possibly decreased esophageal carcinoma, childhood asthma, and TB
How does H Pylori colonize the stomach?
H Pylori colonizes mucus (NOT the lumen), penetrates it via chemotaxis and acid excretion, then attaches to intercellular junctions of epithelial cells.
Where does H Pylori grow and replicate?
Epithelial surface of gastric epithelium, attached at the intercellular junctions
How does H Pylori protect against stomach acid exposure?
H Pylori secretes urease, which hydrolyzes urea into CO2 (released/absorbed) and NH3 which buffers the stomach’s acidic pH
What is the histological findings of gastritis?
Inflammation in interstitial spaces between mucinous glands. 100% of people with H. Pylori infection develop histological gastritis.
How does H Pylori evade the innate immune system? (4 ways)
- LPS is 100x less bioactive, avoiding recognition TLR-4. 2. Molecular mimicry of blood group O-antigens. 3. Membrane-sheathed flagella protects from TLR-5 recognition. 4. Induces expansion of Tregs
Which cells does H Pylori likely infect to cause gastric cancer?
It likely infects stem cells or other progenitor cells; intestinal lining is too short-lived to be cancer-inducing
What are three modifiable risk factors for gastric cancer?
High salt diet, low iron, smoking
What does the H Pylori virulence factor CagA do?
Disrupts cell polarity at intercellular junctions allowing H pylori to acquire nutrients; increased iron uptake by epithelium; inhibit apoptosis/stimulate proliferation; increase pro-inflammatory signals (which may lead to chronic inflammation/cancer)
How does H Pylori CagA enter the cell?
A Type 4 Secretion System, or “molecular microsyringe,” injects a set of 30+ genes into the epithelium
What are the two main H Pylori virulence factors?
CagA and VacA
What does the H Pylori virulence factor VacA do?
VacA is a toxin that causes “vacuolation” or accumulation of vesicles within the epithelium. Role in pathogenesis remains unclear, but VacA is associated with increased risk of peptic ulcers and gastric cancer.
How do duodenal ulcers modify the risk of gastric cancer?
Duodenal ulcers (with high acid secretion) actually lower the risk of gastric cancer (marked by low acid secretion/achlorhydria)
What is the precursor condition to gastric cancer?
Atrophic gastritis (gastritis where gastric glands are lost and replaced by fibrous/intestinal epithelium)
What is the currently recommended way to screen/treat H Pylori infection?
Screen adults that have symptoms of gastritis; treat adults with symptoms of an ulcer.
Describe the shape and gram stain of H Pylori
Gram negative; spiral or curved shape
Why would you treat an asymptomatic H Pylori infection?
Reduce the risk of gastric cancer in patients with first-degree relatives who have had gastric cancer
