L6 – Gynaecopathology: Infection-Related Tumours of the Cervix Flashcards

1
Q

What is the primary aetiological agent in cervical epithelial pathology?

A

Human papilloma virus (HPV) is the dominant infectious agent causing cervical neoplastic changes.

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2
Q

How many HPV genotypes are known and which are considered high risk?

A

There are over 300 genotypes; high-risk types (e.g. HPV 16 and 18) account for around 75% of cervical cancers.

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3
Q

Where is HPV most commonly detected in the cervix?

A

HPV typically affects the squamo–columnar junction of the cervix.

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4
Q

How does HPV persist in infected cells?

A

The virus can exist as a circular episome; in cervical cancer, integration into the host DNA disrupts regulatory regions.

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5
Q

What is koilocytosis and what does it indicate?

A

Koilocytosis is perinuclear clearing seen in HPV-infected cells, indicating productive infection.

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6
Q

How does the integration of HPV DNA affect cell regulation?

A

Integration leads to disruption of the E2 gene and overexpression of oncogenes E6 and E7, which inactivate tumour suppressors such as p53.

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7
Q

What does CIN stand for and how is it graded?

A

CIN stands for cervical intraepithelial neoplasia, graded from 1 (mild dysplasia) to 3 (severe dysplasia).

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8
Q

What is the difference between HPV-related and HPV-independent cervical carcinomas?

A

While most cervical cancers are HPV-driven, a significant proportion—especially adenocarcinomas—may be HPV-independent and carry a worse prognosis.

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9
Q

What imaging or cytological features are used to stage cervical carcinoma?

A

Staging involves assessing the extent of invasion, lymph node involvement, and, in some cases, the use of cervical screening programmes.

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10
Q

How does the cervical screening programme contribute to cervical cancer prevention?

A

Regular screening detects pre-neoplastic lesions early, allowing for prompt treatment and reduction in cancer incidence.

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11
Q

What is the clinical importance of distinguishing between CIN and invasive carcinoma?

A

CIN lesions can often be managed conservatively, whereas invasive carcinoma requires more aggressive treatment.

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12
Q

How does early detection via screening influence prognosis?

A

Early detection significantly improves survival rates by allowing treatment before invasion and metastasis occur.

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13
Q

What are common treatments for CIN and cervical carcinoma?

A

Treatments include local excision, cryotherapy for CIN, and for invasive carcinoma, radical hysterectomy with or without radiotherapy.

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14
Q

How is the role of HPV vaccination integrated into cervical cancer prevention?

A

HPV vaccination, along with screening and treatment, forms a triad in global strategies to eliminate cervical cancer.

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15
Q

What is the impact of treatment on the prognosis of cervical carcinoma?

A

Effective treatment can dramatically reduce mortality, particularly when cancers are detected at an early stage.

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16
Q

Why is ongoing research important in HPV-related cervical pathology?

A

It continues to refine screening, diagnostic, and treatment modalities, especially for lesions that are HPV-independent.

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17
Q

What cytological differences are noted between low-grade and high-grade CIN?

A

Low-grade CIN shows mild atypia and koilocytic changes, whereas high-grade CIN displays marked atypia and loss of cellular polarity.

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18
Q

How does disruption of the E2 gene lead to cervical carcinogenesis?

A

Loss of E2 results in uncontrolled expression of E6 and E7, which inactivate tumour suppressor proteins p53 and Rb.

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19
Q

What are the benefits and limitations of HPV DNA testing in cervical screening?

A

It improves sensitivity but may detect transient infections that do not progress to neoplasia.

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20
Q

How does colposcopy enhance the diagnostic accuracy of cervical lesions?

A

It provides magnified visualisation of the cervical epithelium and allows for targeted biopsies.

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21
Q

How do morphological features of cervical adenocarcinoma affect treatment?

A

Adenocarcinoma may be HPV-independent and often requires more extensive surgical management due to its aggressive behaviour.

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22
Q

What impact does the integration status of HPV DNA have on lesion progression?

A

Integrated HPV DNA is more frequently associated with high-grade lesions and a higher risk of progression to invasive carcinoma.

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23
Q

How does quality control in cervical screening programmes affect patient outcomes?

A

Regular, high-quality screening reduces cervical cancer incidence by ensuring early detection and treatment.

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24
Q

What is the significance of persistent HPV infection in cervical pathology?

A

Persistence is a key factor in progression from low-grade lesions to high-grade CIN and invasive carcinoma.

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25
What is the primary function of cervical cancer screening programs?
Cervical cancer screening programs aim to detect precancerous and early-stage cancerous changes, reducing incidence and mortality.
26
How does HPV contribute to cervical cancer development?
HPV infection leads to cellular dysregulation, promoting cervical intraepithelial neoplasia (CIN) and invasive carcinoma.
27
What are the two major epithelial types of the cervix?
The cervix consists of endocervical (glandular) and ectocervical (squamous) epithelium.
28
Where is the transformation zone located, and why is it significant?
The transformation zone is the area where squamous and glandular epithelium meet, a common site for HPV-related changes.
29
How do low-grade and high-grade cervical intraepithelial neoplasia (CIN) differ?
Low-grade CIN lesions often regress spontaneously, whereas high-grade CIN has a higher risk of progressing to cancer.
30
What are the primary histological types of cervical cancer?
The two major types are squamous cell carcinoma and adenocarcinoma.
31
Why is squamous metaplasia important in HPV-related pathology?
Squamous metaplasia is the normal replacement of glandular epithelium with squamous cells but can become dysplastic in HPV infections.
32
What embryological structures contribute to the formation of the female reproductive tract?
The Müllerian ducts give rise to the female reproductive tract, including the uterus, fallopian tubes, and cervix.
33
How can Müllerian duct abnormalities affect reproductive health?
Improper fusion of Müllerian ducts can cause anatomical abnormalities, affecting fertility and increasing pathology risks.
34
What are the clinical signs of cervical cancer?
Common clinical signs of cervical cancer include abnormal vaginal bleeding, pelvic pain, and postcoital spotting.
35
How does adenocarcinoma of the cervix differ from squamous cell carcinoma?
Adenocarcinoma originates from glandular epithelium and may not always be HPV-related, whereas squamous cell carcinoma is strongly linked to HPV.
36
What is the role of HPV vaccination in preventing cervical cancer?
HPV vaccination prevents infection with high-risk strains, reducing the incidence of cervical cancer.
37
Why is postmenopausal bleeding a significant clinical symptom?
Postmenopausal bleeding is a red flag for malignancy and should prompt immediate investigation.
38
How does endometrial carcinoma classification affect prognosis?
Type 1 endometrioid carcinomas are generally slow-growing, while Type 2 serous carcinomas are more aggressive with poorer prognosis.
39
What are the histological features of endometrioid carcinoma versus serous carcinoma?
Endometrioid carcinoma features gland formation similar to normal endometrium, whereas serous carcinoma exhibits highly atypical, aggressive cells.
40
Why is the detection of adenocarcinoma in cervical screening important?
Cervical screening must detect both squamous and glandular lesions to ensure early diagnosis and treatment.
41
How does the implementation of screening and vaccination programs impact cervical cancer rates?
Countries with well-implemented HPV vaccination and screening programs have seen a significant decline in cervical cancer rates.
42
What is the significance of hormonal dysregulation in gynecopathology?
Hormonal imbalances can contribute to gynecological disorders, including endometrial hyperplasia and cancer.
43
How do genetic abnormalities contribute to gynecological cancers?
Genetic mutations, such as those affecting tumor suppressors, can drive the development of gynecological malignancies.
44
Why is understanding cervical histology important in diagnosing cervical neoplasia?
Understanding cervical histology helps differentiate between normal, dysplastic, and malignant changes, guiding diagnosis and treatment.
45
What embryological structure gives rise to the uterus, fallopian tubes, and cervix?
The Müllerian ducts (paramesonephric ducts).
46
What is the significance of mesonephric remnants in female reproductive anatomy?
They are benign remnants but can be mistaken for malignancies if not recognized.
47
Why is fusion of the Müllerian ducts important in uterine development?
Proper fusion is essential for normal uterine anatomy; failure can cause uterine malformations like bicornuate or septate uterus.
48
What anatomical feature increases vulnerability to HPV infection in the cervix?
Areas of squamous metaplasia at the transformation zone are more susceptible to HPV infection.
49
What is squamous metaplasia, and where does it occur in the cervix?
The replacement of glandular epithelium by squamous epithelium, occurring at the cervical transformation zone.
50
Why is the transformation zone of the cervix important in cervical screening?
It is the site where squamous and glandular epithelia meet and where HPV-related lesions often arise.
51
What cytological feature indicates productive HPV infection?
Koilocytosis, seen as a perinuclear clearing around the nucleus.
52
What is the main difference in viral DNA behavior between low-risk and high-risk HPV infections?
Low-risk HPV maintains episomal DNA, while high-risk HPV integrates its DNA into the host genome.
53
Which viral proteins are involved in disrupting host tumor suppressor pathways during high-risk HPV infection?
E6 and E7 viral proteins.
54
How does HPV-mediated disruption of p53 affect cellular behavior?
It inhibits key tumor suppressor pathways, leading to increased cellular proliferation and genomic instability.
55
Why can most low-grade HPV infections regress spontaneously?
Because the immune system can often clear HPV infections before neoplastic progression occurs.
56
What risk factor, besides HPV, increases the likelihood of cervical cancer progression?
Smoking.
57
What cytological changes are seen in low-grade cervical intraepithelial neoplasia (CIN 1)?
Expansion of the basal epithelial layer with koilocytosis in upper layers.
58
How does high-grade CIN differ microscopically from low-grade CIN?
High-grade CIN shows full-thickness atypia and loss of cellular maturation.
59
What histological feature indicates invasion in cervical carcinoma?
Invasion into the cervical stroma and destruction of normal architecture.
60
What is the typical route of lymphatic spread for cervical cancer?
Through pelvic lymph nodes.
61
Why is fertility-preserving surgery sometimes possible for early cervical cancer?
Procedures like LLETZ (large loop excision of the transformation zone) can remove pre-cancerous lesions while preserving the uterus.
62
Why has the HPV vaccination programme been extended to boys in some countries?
To reduce the spread of HPV and prevent HPV-related cancers in males, such as oropharyngeal cancer.
63
What other cancers, besides cervical cancer, are associated with HPV infection?
Penile, anal, vaginal, vulvar, and oropharyngeal cancers.
64
Why is postmenopausal cervical cancer a growing concern despite vaccination programmes?
Older, postmenopausal women were not vaccinated and often have less regular screening.
65
How does the colposcopy procedure assist in diagnosing cervical pre-cancerous changes?
It enables direct visualization of abnormal cervical epithelium for biopsy.
66
What is the advantage of modern liquid-based cytology over traditional PAP smears?
Liquid-based cytology removes debris and blood, making interpretation clearer and more reliable.
67
Why are adenocarcinomas harder to detect with current cervical screening methods?
They may not be HPV-driven and thus evade virus-based screening tests.
68
What is the clinical consequence of HPV-negative cervical adenocarcinomas?
They often present at later stages and carry a worse prognosis due to delayed detection.
69
What anatomical factors make the cervix prone to local tumor spread?
The cervix's close proximity to the bladder, rectum, and pelvic walls facilitates local spread.
70
What are potential complications if cervical tumors invade surrounding structures?
Invasion into bladder or rectum can cause fistulae and complicate surgical management.