H Pylori Cards Flashcards

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1
Q

What are three common causes of duodenal ulcers?

A

H Pylori, NSAIDS, steroids

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2
Q

What % of gastric cancers are associated with H Pylori?

A

70%; this makes H Pylori a WHO Type 1 definitive carcinogen

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3
Q

What two types of cancer are associated with H. Pylori?

A

Gastric adenocarcinoma and gastric lymphoma (MALT lymphoma)

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4
Q

Where and under what conditions does H Pylori grow?

A

H pylori grows in the antral and pyloric regions of the stomach; grows slowly in low O2

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5
Q

What are the outcomes of H Pylori infection?

A

85% simple gastritis; 10-15% progress to peptic ulcer (usually duodenal); 1% progress to gastric cancer

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6
Q

How is H Pylor infection usually acquired?

A

Within famillies or close contacts; often in childhood (90% by age 10)

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7
Q

What is the environmental reservoir for H Pylori?

A

There is no environmental reservoir; strains follow human migration

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8
Q

What are the protective benefits of H Pylori infection?

A

Possibly decreased esophageal carcinoma, childhood asthma, and TB

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9
Q

How does H Pylori colonize the stomach?

A

H Pylori colonizes mucus (NOT the lumen), penetrates it via chemotaxis and acid excretion, then attaches to intercellular junctions of epithelial cells.

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10
Q

Where does H Pylori grow and replicate?

A

Epithelial surface of gastric epithelium, attached at the intercellular junctions

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11
Q

How does H Pylori protect against stomach acid exposure?

A

H Pylori secretes urease, which hydrolyzes urea into CO2 (released/absorbed) and NH3 which buffers the stomach’s acidic pH

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12
Q

What is the histological findings of gastritis?

A

Inflammation in interstitial spaces between mucinous glands. 100% of people with H. Pylori infection develop histological gastritis.

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13
Q

How does H Pylori evade the innate immune system? (4 ways)

A
  1. 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
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14
Q

Which cells does H Pylori likely infect to cause gastric cancer?

A

It likely infects stem cells or other progenitor cells; intestinal lining is too short-lived to be cancer-inducing

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15
Q

What are three modifiable risk factors for gastric cancer?

A

High salt diet, low iron, smoking

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16
Q

What does the H Pylori virulence factor CagA do?

A

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)

17
Q

How does H Pylori CagA enter the cell?

A

A Type 4 Secretion System, or “molecular microsyringe,” injects a set of 30+ genes into the epithelium

18
Q

What are the two main H Pylori virulence factors?

A

CagA and VacA

19
Q

What does the H Pylori virulence factor VacA do?

A

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.

20
Q

How do duodenal ulcers modify the risk of gastric cancer?

A

Duodenal ulcers (with high acid secretion) actually lower the risk of gastric cancer (marked by low acid secretion/achlorhydria)

21
Q

What is the precursor condition to gastric cancer?

A

Atrophic gastritis (gastritis where gastric glands are lost and replaced by fibrous/intestinal epithelium)

22
Q

What is the currently recommended way to screen/treat H Pylori infection?

A

Screen adults that have symptoms of gastritis; treat adults with symptoms of an ulcer.

23
Q

Describe the shape and gram stain of H Pylori

A

Gram negative; spiral or curved shape

24
Q

Why would you treat an asymptomatic H Pylori infection?

A

Reduce the risk of gastric cancer in patients with first-degree relatives who have had gastric cancer