H.pylori And GI Ulceration Flashcards

1
Q

What is the taxonomy order?

A
Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species 
(Then the species have their subspecies/strain)
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2
Q

Types of bacterial morphologies?

A

1) cocci
2) rod/bacilli
3) budding/appendage
4) helical
(Others on slide)

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3
Q

Describe the bacterial cell envelope?

A

Gram positive has a single surrounding cell membrane and a peptidoglycan cell wall on the outside.

Gram negative has 2 membranes: inner (plasma) and outer membranes. Also has a peptidoglycan cell wall in between the membranes.

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4
Q

Explain the process of gram-staining.

A

1) Heat-fixation of bacteria sample to slide (so they don’t rinse out during washing)
2) Adding the primary stain, crystal violet.
3) Adding the mordant, iodine
4) Adding acetone or ethanol (for decolourisation)
5) Counterstain with safranin.

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5
Q

What happens to gram positive and negative bacteria during the gram staining?

A

Gram-positive remains purple even after adding acetone and safranin. Due to thick peptidoglycan layer.
Gram-negative decolourises when acetone is added then turns pink when safranin is added. Due to thin peptidoglycan layer.

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6
Q

What diseases can H.pylori cause?

A

1) Gastric Ulcers
2) Duodenal Ulcers
3) Stomach cancer
4) Mucosa Associated Lymphoid Tissue (MALT) lymphoma

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7
Q

Morphology of H.pylori?

A
  • Helix shape (curved rod)
  • Lophotrichous flagella
  • Gram-negative
  • 3 micrometers long/0.5 micrometers wide
  • Microaerophilic (needs a bit of O2)
  • Needs CO2 for growth
  • Forms biofilms
  • Produces adhesin’s that help it adhere to gastric epithelial
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8
Q

How does H.pylori survive in stomach acid?

A

Produces urease enzymes that raise the local pH from 2 to 6/7. This is because the urease breaks down urea releasing CO2 and ammonia which are both basic.

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9
Q

Where is H.pylori’s most favoured site of infection?

A

The gastric antrum (pyloric antrum of stomach). But it is also present in the mucus that overlies the mucosa.

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10
Q

Symptoms of H.pylori infection?

A

1) acute gastritis
2) nausea
3) flatulence
4) bad breath
5) abdominal pain

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11
Q

Several ways that H.pylori harms the stomach?

A

1) ammonia is toxic to cells
2) proteases, VacA, phospholipases, CagA cause inflammation
3) HcpA (helicobacter cysteine-rich proteins) trigger immune response.

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12
Q

What is vacA?

A

Vacuolating cytotoxin A that increases bacterial (H.pylori) fitness and induces apoptosis.

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13
Q

What are the tests carried out to identify H.pylori infection?

A

1) Urea breath test
2) Serological test
3) Stool antigen test
4) Stool immunoassay and PCR
5) Endoscopy and biopsy

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14
Q

What is chemotaxis?

A

Movement towards a chemical stimulus

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15
Q

How does H.pylori exhibit chemotaxis?

A

It swims to burrow into the mucin gel lining, and moves underneath the neutral pH environment, to reach the epithelial cells. (chemotaxis).
Then produces urease to neutralise acid and adhesin to stick to lipids and carbohydrates on cell membrane.

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16
Q

How does H.pylori cause ulcer formation?

A

1) chemotaxis away from gastric fluid to epithelial cells through the mucus layer.
2) Urease is used to neutralise surrounding gastric acid hence destabilising mucin
3) chemotaxis of other bacteria. they replicate and cause mucus destruction
4) mucous membrane is damaged leading to inflammation. effector molecules and proteases from organism cause inflammation as well.
5) ulcer is formed due to mucosal cell death caused by cytotoxins (VacA) and ammonia.

17
Q

What is cagA?

A

It encodes a major virulence protein associated with ulcers.

18
Q

How does H.pylori lead to cancer?

A

1) normal gastric mucosa
2) 3 stages of gastritis: superficial, chronic, atrophic
3) Intestinal metaplasia (change in nature of tissue)
4) Dysplasia (presence of abnornmal cell types in a tissue)
5) Gastric Adenocarcinoma (cancer formed from glandular structures in epithelial tissue)

19
Q

What two things can chronic gastritic cause?

A

MALT Lymphoma or Gastric/Duodenal ulcers

20
Q

How is H.pylori treated?

A

With 2 antibiotics (e.g. amoxicillin and clarithromycin) and 1 proton pump inhibitor (e.g. pantoprazole)