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clinical pathology > L5 - Gastrointestinal pathology : how Helicobacter pylori defined gastric pathology > Flashcards

L5 - Gastrointestinal pathology : how Helicobacter pylori defined gastric pathology Flashcards

- Understanding how HP interacts with the host - Recognising the features of HP induced gastritis - Appreciating how the chronic damage induced by HP leads to precancerous lesions - Assessing the different forms of cancers assiciated with HP exposure.

1
Q

What are the major conditions linked to gastric pathology?

A

Abnormal motility, inflammation, infection, and severe conditions like gastric cancer ( becoming more frequent)

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2
Q

How has the understanding of gastric cancer improved in recent years?

A

The use of endoscopy allows earlier detection, leading to less aggressive and more successful treatments.

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3
Q

What type of carcinoma are gastric and oesophageal

A

adenocarcinomas (formed from glandular structures in epithelial tissue)

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4
Q

What is the most common pathogen associated with inflammatory gastric disease?

A

Helicobacter pylori (H. pylori).

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5
Q

What is the estimated prevalence of Helicobacter pylori in the general population?

A

Approximately 50%, with higher levels (up to 90%) in developing countries.

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6
Q

because of H.pyloris being found in at a high abundance in the general population what is the assumption

A

that it forms part of the normal gut microflora

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7
Q

what is the global burden of gastric cancer

A
  • 4th most common malignant disease (~930,000)
  • 2nd most common cause of cancer related death worldwide (~700,000)
  • Falling incidence of distal gastric cancer
  • Increasing incidence of proximal gastric cancer
  • Wide geographical variation
  • ethnic and geographic association (not always clear when one ends and the other starts)
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8
Q

Helicobacter pylori general info

A

gram-negative microaerobic bacterium with a worldwide prevalence.

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9
Q

What are the forms and key features of Helicobacter pylori?

A

Spiral or coccoid form, with flagella that allow mobility along the gastric mucosa.

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10
Q

When was the link between the bacterium and the clinical symptoms associated with gastritis confirmed

A

in the early 80s

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11
Q

How was the link between H. pylori and gastritis established?

A

Warren and Marshall drank H. pylori, developed gastritis, and confirmed its presence via biopsies (+ inflammation) earning them the Nobel Prize.

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12
Q

What are the common conditions caused by H. pylori infection?

A

Gastritis, gastric ulcers, and duodenal ulcers.

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13
Q

How is H. pylori-associated gastritis treated?

A

With antibiotics and proton pump inhibitors to reduce stomach acidity and protect the mucosa ( once you identify the cause of disease and have a valid treatment option, the patient can be cured)

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14
Q

What are the protective mechanisms of the stomach against infection?

A

mucus coating, acidic environment, and specialised cells (e.g., parietal and chief cells).

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15
Q

What is the Cardia

A

the first part of the stomach, which is connected to the esophagus. It contains the cardiac sphincter, which is a thin ring of muscle that helps to prevent stomach contents from going back up into the esophagus.

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16
Q

What type of cells line the esophagus

A

squamous epithelial cells because it has to sustain mechanical trauma

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17
Q

What type of cells line the cardia

A

monostratified glandular epithelium which produce mucus that protect the stomach lining from the corrsive effects of gastric acid

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18
Q

What does H. pylori do to survive in the acidic stomach environment?

A

Uses flagella to penetrate mucus and get ontop of the cell membrane. Here the environment is less acidic.
Releases urease to convert urea into ammonia, neutralising stomach acid.
Adheres closely to the mucosa and disrupts cell junctions.

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19
Q

What are the functions of different stomach regions?

A

Fundus: Produces mucus via foveolar cells.
Body/Corpus: Releases acid (parietal cells) and pepsinogen (chief cells).
Antrum: Produces mucus and gastrin, which regulates acid secretion.

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20
Q

What role does gastrin play in the stomach?

A

It stimulates acid release, which activates pepsinogen into pepsin for digestion.

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21
Q

What is the role of pepsin

A

enzyme which starts the digestive process and allows the digested molecules to be absorbed in the small bowel later on

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22
Q

What is the feedback loop in the stomach

A

Stimulus: Food enters the stomach.
G cells: Release Gastrin
→ Parietal cells: Release HCl
→ Chief cells: Release Pepsinogen
HCl: Activates Pepsinogen → Pepsin
Pepsin: Breaks down proteins → Stimulates G cells (positive feedback)
Negative Feedback:
↑ HCl → Stimulates D cells: Release Somatostatin
Somatostatin: Inhibits Gastrin released

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23
Q

How does H. pylori disrupt the gastric mucosa?

A

It creates a niche by neutralising acid and adhering to cells, damaging junctions and altering the local pH.

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24
Q

Can you recognise Helicobacter pylori when taking a biopsy of the stomach.

A

yes - this allows for immediate diagnosis which isn’t very common in histology (diagnose with almost 100% certainty)

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25
Q

How can anti-acid treatment affect detection of H. pylori?

A

It can make it harder to identify the bacterium and alter results of other tests, like the breath test.

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26
Q

What does a positive breath test for H. pylori indicate?

A

Increased ammonia due to changes in stomach acidity caused by H. pylori.

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27
Q

What test is most reliable for confirming H. pylori?

A

Genetic testing on gastric samples.

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28
Q

Name the exotoxin associated with H. pylori.

A

Vacuolating cytotoxin A (VacA).

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29
Q

What is the effect of VacA?

A

affects the cell structures causing ballooning, degeneration, and immediate cell death, leading to acute gastritis and ulcers.

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30
Q

What cytotoxin is associated with chronic inflammation caused by H. pylori?

A

Cytotoxin-associated gene A (CagA).

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31
Q

How does CagA contribute to disease?

A

It affects cell attachment, induces chronic inflammation, and is linked to adenocarcinoma and mucosa-associated lymphoid tissue (MALT) lymphoma.

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32
Q

What conditions can H. pylori cause?

A

Gastritis, peptic ulcers, adenocarcinoma, and MALT lymphoma.

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33
Q

How does gastritis progress if untreated?

A

Acute gastritis → Chronic gastritis → Atrophic gastritis → Intestinal metaplasia → Dysplasia → gastric Adenocarcinoma.

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34
Q

What happens if a patient is treated at the acute gastritis stage

A

the gut will go back to normal functionality and morphology

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35
Q

At which point does antimicrobial eradication of H.pylori interrupt the cascade

A

up until intestinal metasplasia and SPEM ( acute and chronic gastritis, atrophic gastritis and intestinal metaplasia / spem)

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36
Q

What is functional dyspepsia?

A

a chronic digestive condition that causes stomach pain, bloating, and other symptoms without an obvious cause

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37
Q

What is GERD?

A

Gastroesophageal reflux disease is a digestive condition that occurs when stomach acid flows back up into the esophagus

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38
Q

What is the link between functional dyspepsia / GERD and HP

A

not entirely clear of the role of HP but symptoms improve with eradication HP (valid connection)

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39
Q

how does HP lead to gastritis

A

HP infection causes inflammation of the stomach lining as it damages the mucosal layer. over time acute inflammation can turn into chronic inflammation and the ongoing inflammation can increase the stomachs vulnerability to acid damage ( ulcers and gastric cancer)

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40
Q

How does HP lead to peptic ulcers

A

virulent factors e.g. VacA m1 is possibly associated with an increased risk of peptic ulcer disease

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41
Q

What dietary factors increase susceptibility to H. pylori-related gastritis?

A

High salt, low iron, and high fat diets.

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42
Q

What dietary factors may protect against gastric cancer?

A

Diets rich in fruits, vegetables, and fibre.

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43
Q

What is atrophic gastritis?

A

Loss of gastric glands and reduction of gland-to-stroma ratio, often considered a precancerous lesion

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44
Q

What is intestinal metaplasia?

A

Replacement of gastric epithelium with intestinal-type epithelium.

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45
Q

What does dysplasia indicate in the stomach?

A

Precancerous changes in the mucosa, characterised by disorganised nuclei and loss of maturation.

46
Q

What is the hallmark of adenocarcinoma in gastric pathology?

A

Invasion of glandular-structured tumours into the stroma and mucosa.

47
Q

What do blue inflammatory dots in gastric tissue indicate?

A

Presence of inflammatory cells in gastritis.

48
Q

How can acute and chronic gastritis be differentiated histologically?

A

Acute shows neutrophils; chronic shows lymphocytes and plasma cells ( which release cytokines which can cause more damage to the mucosa)

49
Q

What histological finding is characteristic of intestinal metaplasia?

A

Goblet cells in the stomach mucosa

50
Q

What histological change defines dysplasia?

A

Increased nuclear size, disorganisation, and loss of mucin production.

51
Q

What are the main types of gastritis?

A

Bacterial, autoimmune, and chemical/reactive.

52
Q

What causes autoimmune gastritis?

A

Immune reactions targeting gastric cells.

53
Q

What is reactive gastritis often caused by?

A

Bile reflux or chemical exposure.

54
Q

Name significant risk factors for gastric cancer.

A

H. pylori infection, ethnicity, smoking, and family history, obesity, previous radiation therapy or chemotherapy for other malignancy

55
Q

What regions have higher incidences of gastric cancer?

A

Japan, China, Chile, Northern Italy, Portugal, and Russia.

56
Q

Incidence of gastric cancer in Japanese who move to America

A

Incidence of gastric carcinoma in Japanese Americans was 3-6 times higher than those of US born whites, but the incidence started to decline in second generation immigrants (more than just the ethnic aspect +/- other aspects - multifactorial system)

57
Q

How does socioeconomic status affect gastric cancer risk?

A

Lower socioeconomic status often correlates with delayed diagnosis and treatment.

58
Q

What is being found about the age range for onset of gastric cancer

A

It is being found more and more frequently in younger patients

59
Q

What is the role of obesity in gastric cancer?

A

It is associated with increased risk, though mechanisms are unclear.

60
Q

How are gastric biopsies typically taken?

A

Samples are collected from different stomach regions (fundus, corpus, antrum) to assess damage distribution.

61
Q

What is being looked for when assessing gastric biopsies

A

The extent, quantity and type of inflammation e.g. mild, focal, predominantly lymphocytic and the amount of atrophy with glandular density and possible metaplasia

62
Q

What does increased inflammatory cell infiltration in the stomach indicate?

A

Active gastritis.

63
Q

What are the histological differences between chronic gastritis and atrophic gastritis?

A

Chronic gastritis shows inflammation without gland loss; atrophic gastritis shows gland loss and stromal expansion.

64
Q

What is microsatellite instability associated with?

A

with better prognosis in gastric cancer (better response to treatment, improved survival, smaller number of lymph node metastasis)

65
Q

Where can unusual lymph node metastasis be found in gastric cancer?

A

In the left supraclavicular region.

66
Q

What causes paraneoplastic syndromes in patients with gastric cancers

A

release of hormones that are associated with the tumour

67
Q

What are some clinical manifestations of gastric conditions

A

Abrupt appearance of keratosis, thrombophlebitis, polyartheritis nodosa, trousseau syndrome and Pseudoacalsia

68
Q

what is the appearance of seborrheic keratosis like

A

waxy light tan, brown or black growths that look scaly or as if they were dripped onto the skin by a candle.

69
Q

What causes polyarthritis nodosa

A

vascular inflammatory changes

70
Q

What causes trousseau syndrome

A

acquired blood clotting disorder that results in migratory thrombophlebitis

71
Q

How can gastric cancer be diagnosed early in Japan?

A

Through a screening programme that allows for mucosectomy of intramucosal tumours.

72
Q

What is mucosectomy?

A

The removal of the mucosal layer, used in early-stage gastric cancer treatment to remove the lesion.

73
Q

What is the role of neutrophils in acute gastritis?

A

They are the predominant inflammatory cells in acute inflammation.

74
Q

What inflammatory cells are seen in chronic gastritis?

A

Lymphocytes and plasma cells.

75
Q

What happens during atrophic gastritis?

A

Destruction of glands and possible progression to intestinal metaplasia

76
Q

How can Helicobacter pylori affect the acidic environment of the stomach?

A

By neutralising acidity, allowing the bacterium to survive.

77
Q

What is the function of flagella in Helicobacter pylori?

A

It helps the bacterium move through the mucus layer of the stomach.

78
Q

What is the role of the cytotoxin associated gene A (cagA)?

A

It contributes to chronic inflammation and may lead to more severe outcomes, such as adenocarcinoma.

79
Q

What is the link between Helicobacter pylori and adenocarcinoma?

A

Chronic infection with Helicobacter pylori can lead to persistent inflammation, atrophy, and metaplasia, increasing cancer risk.

80
Q

What is the role of proton pump inhibitors (PPIs) in Helicobacter pylori testing?

A

They can alter test results by affecting stomach acidity.

81
Q

What type of cancer is most commonly associated with Helicobacter pylori infection

A

Gastric adenocarcinoma.

82
Q

What is intestinal metaplasia an early sign of?

A

It is a potential precursor to gastric cancer (it is defined as an increase in cell numbers)

83
Q

How is intestinal metaplasia identified histologically?

A

By the presence of goblet cells, which are normally found in the intestines but not the stomach. (metaplasia is defined by going from one mature native type of cell into another mature type of cell that you don’t expect to see there)

84
Q

What is dysplasia in the context of gastric cancer?

A

Abnormal cell development that may progress to adenocarcinoma (preneoplastic) .

85
Q

How does Helicobacter pylori contribute to chronic gastritis?

A

By triggering a prolonged inflammatory response that can lead to gland destruction.

86
Q

What is the significance of the gland-to-stroma ratio in gastric biopsies?

A

A decreased ratio (decreased number of glands) can indicate atrophy, which is a precursor to cancer.

87
Q

How does Helicobacter pylori cause ulcer formation?

A

By producing toxins that damage the gastric mucosa, leading to ulceration.

88
Q

What type of gastric cancer is associated with familial genetic mutations?

A

Hereditary gastric cancer, which often involves mutations in the E-cadherin gene.

89
Q

What is the primary treatment for early-stage gastric cancer in Japan?

A

Mucosectomy

90
Q

in what region of the stomach do bacterial gastritis tend to be found

A

in the lower component of the stomach

91
Q

What is microsatellite instability

A

A genetic abnormality that is associated with a change in the number of repeated DNA bases in a microsatellite region (repeated sections of non coding DNA)

92
Q

What are clinical manifestations for gastric conditions

A
  • Malaise loss of appetite dyspepsia
  • Pain
    -Nausea
  • Vomit
  • Weight loss
  • Anemia ( hematemesis and / or melena)
93
Q

What are probably the most feared manifestations

A

anemia and weight loss (because if you haven’t significantly changed your diet or exercise regime and anemia indicates bleeding both of which are signs for some chronic condition e.g. adenocarcinoma)

94
Q

what is the survival rate with poor prognosis if advanced

A

less than 20% have a 5 year survival

95
Q

what is the survival rate if prognosis is made early on in gasrtic cancer

A

90% survive 5 years

96
Q

where is early gastric carcinoma confined to

A

the mucosa and submucosa regardless of perigastric lymph nodal mets

97
Q

where is advanced carcinoma

A

infiltrated the muscularis propria

98
Q

What is the first step in the development of MALT lymphoma?

A

The process begins with H. pylori infection, which recruits B and T cells to the gastric mucosa.

99
Q

How do epithelial cells contribute to MALT lymphoma development during chronic H. pylori infection?

A

Chronic infectious stimulation causes epithelial cells to express high levels of HLA-DR and CD80 on their surface, which activate T cells.

100
Q

How do CD4 T cells activate B cells in MALT?

A

Activated CD4 T cells stimulate B cells through CD40L-CD40 interaction, aided by cytokines and chemokines.

101
Q

Why do lymphoepithelial lesions in MALT persist and avoid apoptosis?

A

The interaction among epithelial cells, T cells, and B cells allows these cells to cooperatively survive within the lesions and resist apoptosis.

102
Q

What role do cytokines and chemokines play in MALT development?

A

They facilitate communication between T cells and B cells, supporting their activation and survival.

103
Q

What is thought to be the origin of lymphomas

A

Lymphoepithelial lesions (LELs)

104
Q

What facilitates the transition from polyclonal to monoclonal lesions

A

chronic stimulation with exogenous or autoantigens increasing the frequency of their transformation

105
Q

what kind of MALT lymphomas can progress and become H.pylori independent

A

H.pylori dependent alterations e.g. trisomies 3,12 or 18

106
Q

what will eventually happen to a MALT lymphoma

A

it may transform into a high grade tumour when there is e.g. complete inactivation of tumour suppressor gene P53, homologous deletion of the P16 gene and chromosomal translocation of cMYC and BCL6 ( all associated with MALT lymphoma transformation)

107
Q

what does a MALT lymphoma stand for

A

Mucosa associated lympjoid tissue lymphoma

108
Q

what other types of gastric tumours ( apart from MALT lymphoma) are there

A

tumours of the smooth muscle, fat, gastrointestinal stroma tumour (associated with abnormalities in the tyrosine kinase) and gastric adenocarcinoma diffuse type ( doesn’t make glands )

109
Q

what is gasrtic adenocarcinoma : diffuse type made up of

A

single cells (with a signet ring appearance) and CDH1 E-cadherin mutation that individually infiltrate the gastric wall. They arise directly from gastric foveolar epithelium and have a worse prognosis

110
Q

Gastric carcinomas and familiar or hereditary origin

A
  • 10% of gastric carcinomas show familial clustering
  • 1-3% of gastric carcinomas arise from inherited gastric cancer predisposition syndromes
    (hereditary diffuse gastric carcinoma (HDGC), Familial adenomatous polyposis, hereditary nonpolyposis colorectal carcinoma (or lynch syndrome), Petuz-Jeghers syndrome, Li-fraumeni syndrome and Gasrtic hyperplastic polyposis)
111
Q

Hereditary diffuse gastric carcinoma

A

HDGC is an autosomal dominant disorder with high penetrance, approx 30% of individuals with HDGC have a germline mutation in the tumour suppressor gene E-cadherin or CDH1. the inactivation of the second allele of E-cadherin through mutation, methylation and loss of heterozygosity eventually triggers the development of gastric cancer.

112
Q
A

clinical pathology (5 decks)

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