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Medsci 203 > Chronic Inflammation and Carcinogenesis > Flashcards

Chronic Inflammation and Carcinogenesis Flashcards

1
Q

A 4 step guide for a microbe to cause an infection would be:

A
  1. colonise the host
  2. evade host defenses
  3. proliferate
  4. cause damage
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2
Q

Name the 6 mechanisms of damage

A
  1. exotoxins
  2. degradative enzymes
  3. acute inflammatory damage
  4. post-infection autoimmune damage
  5. chronic inflammatory damage
  6. carcinogenesis
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3
Q

Describe what Peptic Ulcer Disease is and the symptoms one can expect from it

A

Peptic ulcer disease is a condition in which there is a break in the lining of the stomach or small intestine

Symptoms include:

  • upper abdominal pain
  • belching
  • vomiting
  • weight loss
  • bleeding
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4
Q

For a long time, peptic ulcer disease was treated for with ________.

A

antacids

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5
Q

H. pylori has been estimated to have infected __% of the world’s population

A

50%

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6
Q

Days-weeks after infection wit H. pylori can result in:

A

Superficial active gastritis

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7
Q

Months-years after infection wit H. pylori (if left untreated) can result in:

A

Chronic active gastritis

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8
Q

Decades (earlier) after infection wit H. pylori can result in: (3)

A

Antral gastritis, pangastritis, chronic active gastritis

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9
Q

Decades (later) after infection wit H. pylori can result in: (3)

A

Duodenal gastric metaplasia, atrophy intestinal metaplasia, chronic active gastritis

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10
Q

Final stage effects of infection with H. pylori include: (3)

A

duodenal ulcer, gastric cancer/ulcer, MALT lymphoma

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11
Q

Describe the motility of H. pylori and how it is achieved, as well as why this is significant.

A

A flagellum allows H. pylori to swim rapidly to the mucous layer of the stomach following ingestion in order to survive

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12
Q

Describe the shape of H. pylori and why this is significant.

A

H. pylori is helical in shape, which combnined with ‘screw-like’ movement, allows it to penetrate the stomach’s mucous layer.

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13
Q

How does H. pylori counterract stomach acid?

A

H. pylori uses urease to produce a ‘cloud’ of ammonia in order to neutralise acid.

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14
Q

What does H. pylori do when it reaches the mucous layer of the stomach?

A

It crosses the mucous layer of the stomach by causing it to de-gel by raising the pH

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15
Q

What does H. pylori do once it crosses the mucous layer of the stomach?

A

It attaches to the gastric epithelium via Lewis b carbohydrate receptor with BabA adhesin

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16
Q

___ is poorly recognised by TLR4, resulting in low levels of ____ production.

A

LPS is poorly recognised by TLR4, resulting in low levels of cytokine production.

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17
Q

Flagellum subunits are poorly recognised by ____, resulting in low levels of ____ production.

A

Flagellum subunits are poorly recognised by TLR5, resulting in low levels of cytokine production.

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18
Q

Vacuolating toxin A (VacA) inhibits: (3)

A
  1. phagosomal maturation
  2. T/B cell proliferation
  3. iNOS generation
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19
Q

H. pylori is coated with ______ and ______ in order to mimic the host

A

H. pylori is coated with plasminogen and cholesterol in order to mimic the host

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20
Q

Chronic infection + inflammation results in a loss of _____ of cells in the inflamed area

A

function

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21
Q

What is an ulcer, and what are the 3 types of ulcers?

A

An ulcer is a lesion found on the mucous membrane.

  1. Peptic ulcer - in lining of stomach or duodenum, where hydrochloric acid and pepsin are present
  2. Gastric ulcer - in stomach
  3. Duodenal ulcer - in duodenum
22
Q

List the order of the sections of the stomach, starting from the end of the esophagus to the beginning of the small intestine (9)

A
  1. esophagus
  2. cardia
  3. cardial notch
  4. fundus
  5. body
  6. pyloric antrum
  7. pyloric canal
  8. pylorus
  9. duodenum
23
Q

Describe the process of stomach acid production (4)

A
  1. See food/think of food
  2. G (gamma) cells produce gastrin
  3. ECL cells produce histamine
  4. Parietal cells produce acid
24
Q

What is the purpose of somatostatin cells?

A

Acts to inhibit the function of G cells to halt production of more acid via negative inhibition

25
Q

How would H. pylori infection of the antrum affect the function of the stomach?

A

Inflammation leads to loss of function of somatostatin cells which relieves inhibition of G cells, causing increased gastrin and thus acid production.

Excess acid leaks into the duodenum, which causes inflammation of the duodenum, resulting in duodenal ulcers and acid hypersecretion.

26
Q

How would H. pylori infection of the corpus of the stomach affect its function?

A

Inflammation results in loss of parietal cells. As parietal cells are required to make acid, acid production becomes halted.

This results in the development of intestinal-like cells within the stomach, leading to further inflammation and resulting in gastric ulcers and hyposecretion.

27
Q

H. pylori exposure is c______.

A

carcinogenic.

28
Q

Low acid production results in _____ which becomes ____ ______, finally leading to _____ _____.

A

Low acid production results in pangastritis which becomes atrophic gastritis, finally leading to gastric cancer.

29
Q

High acid production results in _____-______ _____ which ultimately becomes ____ ____ ______.

A

High acid production results in antral-predominant gastritis which ultimately becomes peptic ulcer disease.

30
Q

What is the cag pathogenicity island?

A

A >30kb region of genetic material that houses 28 virulence genes - mostly codes for type 4 secretion system (T4SS) which allows bacteria to secrete proteins into host cells - in particular CagA

31
Q

cagA is a ____ secreted from bacteria

A

protein

32
Q

Disease symptoms following the absence of vacA are:

A

Unchanged proportion for mild gastris, slightly decreased other symptoms with the exception of carcinoid which increased.

33
Q

Disease symptoms following the absence of cag are:

A

Absence of all severe disease symptoms , leaving only mild gastritis

34
Q

_____ is important in causing various forms of severe diseases associated with heliobacter pylori

A

cag

35
Q

H. pylori cagA is ______ in the gastric cell

A

phosphorylated

36
Q

CagA-P stimulates phosphorylation cascades - list the 4 resulting effects

A
  1. Apoptosis - especially neutrophils
  2. Morphological change - barrier disruption
  3. Cytokine production - inflammation
  4. Cell proliferation
37
Q

CagA promotes the release of _____ from mitochondria

A

reactive oxygen species (ROS)

38
Q

What is the function of urease in H. pylori?

A

Neutralises gastric acid, gastric mucosal injury via ammonia

39
Q

Name an exotoxin and its function when it comes to H. pylori

A

vacuolating toxin (vacA) - causes gastric mucosal injury

40
Q

Name 3 secretory enzymes which play a role in H. pylori infection

A

mucinase, protease, lipase - gastric mucosal injury

41
Q

What is the function of lipopolysaccharides on H. pylori?

A

Helps to adhere to host cells, inflammation

42
Q

What function do outer proteins serve on H. pylori?

A

Help to adhere to host cells

43
Q

What is T4SS?

A

A pill like structure for the injection of effectors

44
Q

Give an example of an effector in H. pylori infection, and its functions

A

cagA - actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition

45
Q

The initial test for H. pylori is:

A

The breath/sniff test - if stinky = infected lol

46
Q

What is the first-line therapy for H. pylory infection?

A

One-week “triple therapy” - proton pump inhibitor such as omeprazole + antibiotics such as clarithromycin and amoxicillin

47
Q

Acid hypersecretion –> ____ ulcers

A

Acid hypersecretion –> duodenal ulcers

48
Q

Acid hyposecretion –> ____ ulcers

A

Acid hyposecretion –> gastric ulcers

49
Q

Acid ____secretion –> gastric ulcers

A

Acid hyposecretion –> gastric ulcers

50
Q

Acid ____secretion –> duodenal ulcers

A

Acid hypersecretion –> duodenal ulcers

Medsci 203 (10 decks)

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