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Clinical Pathology in Action > L4 – Gastrointestinal Pathology: helicobscter Pylori > Flashcards

L4 – Gastrointestinal Pathology: helicobscter Pylori Flashcards

1
Q

What is Helicobacter pylori and its prevalence worldwide?

A

H. pylori is a gram-negative, microaerophilic bacterium found in the stomach with a worldwide prevalence of about 50%, rising to 90% in developing countries.

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2
Q

In which morphological forms can H. pylori exist?

A

It can reside in the spiral form and a coccoid, viable but non-culturable form.

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3
Q

Who were the pioneers that identified H. pylori’s role in gastritis?

A

Warren and Marshall identified its role in most cases of gastritis and peptic ulcer disease.

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4
Q

How does H. pylori adapt to the harsh gastric environment?

A

It produces urease, which converts urea to ammonia to neutralise gastric acid, and adheres to the gastric mucosa via specific binding proteins.

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5
Q

What are the primary defence mechanisms of the stomach?

A

The stomach is protected by a mucus layer, an acidic environment that enhances pepsin activity, and epithelial cell regeneration.

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6
Q

How does H. pylori overcome the stomach’s protective mechanisms?

A

By migrating to less acidic regions and neutralising acid with ammonia produced by urease activity.

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7
Q

What role do virulence factors like VacA and CagA play in gastric pathology?

A

VacA induces vacuolisation and epithelial cell death, while CagA disrupts cell–cell adhesion and elicits a strong inflammatory response.

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8
Q

What chronic conditions can result from H. pylori infection?

A

Chronic gastritis, intestinal metaplasia, MALT lymphoma, and ultimately gastric adenocarcinoma.

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9
Q

What are common clinical manifestations of H. pylori-related disease?

A

Symptoms include dyspepsia, abdominal pain, nausea, weight loss, and, in severe cases, gastrointestinal bleeding.

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10
Q

What is Correa’s cascade?

A

It is a stepwise progression from normal gastric mucosa to chronic gastritis, atrophy, intestinal metaplasia, dysplasia, and finally adenocarcinoma.

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11
Q

How are risk factors and protective factors balanced in gastric pathology?

A

Factors such as ethnicity, family history, smoking, and diet increase risk, whereas high fruit, vegetable, and fibre intake are protective.

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12
Q

Why is early detection of precancerous lesions important in gastric pathology?

A

Early detection allows for intervention before the progression to invasive cancer, improving patient prognosis.

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13
Q

How does H. pylori contribute to gastric MALT lymphoma?

A

Chronic infection recruits B and T cells to the gastric mucosa, leading to clonal expansion and eventually lymphoma formation.

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14
Q

What histological features indicate the development of MALT lymphoma?

A

Lymphoepithelial lesions with polyclonal to monoclonal transition, along with chronic inflammatory infiltrates.

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15
Q

What is the significance of MALT lymphoma in the context of H. pylori infection?

A

Eradication of H. pylori can lead to regression of MALT lymphoma, highlighting the infection’s causal role.

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16
Q

What extragastric manifestations can be associated with H. pylori infection?

A

Paraneoplastic syndromes, such as migratory thrombophlebitis and Leser-Trélat sign, may occur.

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17
Q

How does H. pylori-induced gastritis differ from autoimmune gastritis histologically?

A

H. pylori gastritis shows active inflammation with neutrophils, while autoimmune gastritis is characterised by lymphocytic infiltrates and glandular atrophy.

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18
Q

What is the clinical role of urease testing in diagnosing H. pylori infection?

A

Urease tests (rapid urease test, urea breath test) detect the enzyme produced by H. pylori, aiding in non-invasive diagnosis.

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19
Q

How do endoscopic findings assist in the diagnosis of H. pylori-associated pathology?

A

Findings such as mucosal nodularity, erythema, and ulcerations suggest H. pylori infection and warrant biopsy.

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20
Q

What impact does H. pylori eradication have on precancerous gastric lesions?

A

Eradication can result in regression or stabilisation of lesions like intestinal metaplasia, reducing cancer risk.

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21
Q

How do dietary factors modify the risk of H. pylori-induced gastric cancer?

A

Diets high in salt and low in antioxidants can exacerbate mucosal injury and inflammation, promoting carcinogenesis.

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22
Q

What changes occur in the gastric microenvironment during chronic H. pylori infection?

A

Chronic infection leads to altered acid secretion, cytokine release, and mucosal damage that favour neoplastic transformation.

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23
Q

How does the ABC classification of gastritis assist clinicians?

A

It categorises gastritis by aetiology (autoimmune, bacterial, chemical) and helps direct appropriate management strategies.

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24
Q

What is the significance of intestinal metaplasia in the context of H. pylori gastritis?

A

Intestinal metaplasia is a precancerous change that increases the risk for developing gastric adenocarcinoma.

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25
What is Helicobacter pylori and its prevalence worldwide?
H. pylori is a gram-negative, microaerophilic bacterium found in the stomach with a worldwide prevalence of about 50%, rising to 90% in developing countries.
26
In which morphological forms can H. pylori exist?
It can reside in the spiral form and a coccoid, viable but non-culturable form.
27
Who were the pioneers that identified H. pylori’s role in gastritis?
Warren and Marshall identified its role in most cases of gastritis and peptic ulcer disease.
28
How does H. pylori adapt to the harsh gastric environment?
It produces urease, which converts urea to ammonia to neutralise gastric acid, and adheres to the gastric mucosa via specific binding proteins.
29
What are the primary defence mechanisms of the stomach?
The stomach is protected by a mucus layer, an acidic environment that enhances pepsin activity, and epithelial cell regeneration.
30
How does H. pylori overcome the stomach’s protective mechanisms?
By migrating to less acidic regions and neutralising acid with ammonia produced by urease activity.
31
What role do virulence factors like VacA and CagA play in gastric pathology?
VacA induces vacuolisation and epithelial cell death, while CagA disrupts cell–cell adhesion and elicits a strong inflammatory response.
32
What chronic conditions can result from H. pylori infection?
Chronic gastritis, intestinal metaplasia, MALT lymphoma, and ultimately gastric adenocarcinoma.
33
What are common clinical manifestations of H. pylori-related disease?
Symptoms include dyspepsia, abdominal pain, nausea, weight loss, and, in severe cases, gastrointestinal bleeding.
34
What is Correa’s cascade?
It is a stepwise progression from normal gastric mucosa to chronic gastritis, atrophy, intestinal metaplasia, dysplasia, and finally adenocarcinoma.
35
How are risk factors and protective factors balanced in gastric pathology?
Factors such as ethnicity, family history, smoking, and diet increase risk, whereas high fruit, vegetable, and fibre intake are protective.
36
Why is early detection of precancerous lesions important in gastric pathology?
Early detection allows for intervention before the progression to invasive cancer, improving patient prognosis.
37
How does H. pylori contribute to gastric MALT lymphoma?
Chronic infection recruits B and T cells to the gastric mucosa, leading to clonal expansion and eventually lymphoma formation.
38
What histological features indicate the development of MALT lymphoma?
Lymphoepithelial lesions with polyclonal to monoclonal transition, along with chronic inflammatory infiltrates.
39
What is the significance of MALT lymphoma in the context of H. pylori infection?
Eradication of H. pylori can lead to regression of MALT lymphoma, highlighting the infection’s causal role.
40
What extragastric manifestations can be associated with H. pylori infection?
Paraneoplastic syndromes, such as migratory thrombophlebitis and Leser-Trélat sign, may occur.
41
How does H. pylori-induced gastritis differ from autoimmune gastritis histologically?
H. pylori gastritis shows active inflammation with neutrophils, while autoimmune gastritis is characterised by lymphocytic infiltrates and glandular atrophy.
42
What is the clinical role of urease testing in diagnosing H. pylori infection?
Urease tests (rapid urease test, urea breath test) detect the enzyme produced by H. pylori, aiding in non-invasive diagnosis.
43
How do endoscopic findings assist in the diagnosis of H. pylori-associated pathology?
Findings such as mucosal nodularity, erythema, and ulcerations suggest H. pylori infection and warrant biopsy.
44
What impact does H. pylori eradication have on precancerous gastric lesions?
Eradication can result in regression or stabilisation of lesions like intestinal metaplasia, reducing cancer risk.
45
How do dietary factors modify the risk of H. pylori-induced gastric cancer?
Diets high in salt and low in antioxidants can exacerbate mucosal injury and inflammation, promoting carcinogenesis.
46
What changes occur in the gastric microenvironment during chronic H. pylori infection?
Chronic infection leads to altered acid secretion, cytokine release, and mucosal damage that favour neoplastic transformation.
47
How does the ABC classification of gastritis assist clinicians?
It categorises gastritis by aetiology (autoimmune, bacterial, chemical) and helps direct appropriate management strategies.
48
What is the significance of intestinal metaplasia in the context of H. pylori gastritis?
Intestinal metaplasia is a precancerous change that increases the risk for developing gastric adenocarcinoma.
49
What are the main types of gastric adenocarcinoma?
The two main subtypes are intestinal and diffuse adenocarcinoma.
50
How does intestinal-type adenocarcinoma develop?
It arises from areas of intestinal metaplasia and is associated with chronic irritation from H. pylori infection, gastric ulcers, and dietary factors.
51
What characterises diffuse-type gastric adenocarcinoma?
It presents as poorly cohesive, infiltrating cells that disrupt normal gastric architecture, often linked to E-cadherin gene mutations.
52
What are key risk factors for gastric cancer?
Age, male gender, family history, smoking, and dietary habits are significant risk factors.
53
What symptoms might indicate gastric cancer?
Dyspepsia, weight loss, and anemia should raise suspicion for malignancy.
54
How do surveillance programs help in gastric cancer prevention?
Early detection in high-risk populations improves outcomes by enabling timely intervention.
55
What are the main treatment strategies for gastric cancer?
Surgical intervention is key for localized disease, while chemotherapy and targeted therapies play a role in more advanced cases.
56
Why is understanding gastric pathology important for patient outcomes?
Recognizing the links between infection, inflammation, and cancer allows for better screening, prevention, and treatment strategies.
57
What is colorectal adenocarcinoma?
Colorectal adenocarcinoma is a malignant epithelial tumour of the large bowel
58
What is the role of the large bowel in the digestive system?
The large bowel is involved with water absorption from the fecal material and consolidating the stools
59
Where are the majority of colorectal adenocarcinomas found in the large bowel?
The majority of colorectal adenocarcinomas are found on the left side of the large bowel, including the descending colon, sigmoid colon, and rectum
60
What is the significance of tumour location in the large bowel?
Tumours on the right side of the bowel can grow larger before causing symptoms due to the larger size and more fluid stools, whereas tumours on the left side cause symptoms earlier due to obstruction
61
What is the first test for bowel cancer screening?
The first test for bowel cancer screening is looking for blood traces in stools
62
What is the structure of the bowel wall?
The bowel wall consists of the mucosa, submucosa, and muscularis layers.
63
What are the risk factors for colorectal cancer?
Risk factors for colorectal cancer include older age, obesity, physical inactivity, alcohol consumption, and dietary factors such as low fiber and high red meat intake.
64
What are adenomatous polyps?
Adenomatous polyps are benign epithelial tumors of the bowel that can be predisposing factors for colorectal cancer.
65
What is the adenoma-carcinoma sequence?
The adenoma-carcinoma sequence describes the progression from benign adenomatous polyps to malignant adenocarcinoma.
66
What is the significance of the APC gene in colorectal cancer?
The APC gene is involved in the chromosomal instability pathway and is a key factor in the development of both familial and sporadic colorectal cancer.
67
What is Lynch syndrome?
Lynch syndrome is a hereditary condition associated with a higher risk of colorectal cancer and other cancers due to mutations in mismatch repair genes.
68
What are serrated adenomas?
Serrated adenomas are a type of polyp that can be subtle and are associated with a different pathway of neoplasia.
69
What is the TNM system in cancer staging?
The TNM system is used in cancer staging to describe the size and spread of the tumor, lymph node involvement, and metastasis.
70
What role does immunotherapy play in cancer treatment?
Immunotherapy is a treatment option for cancer that involves supporting the immune system to fight cancer, but it has certain risks and side effects.

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