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Reproduction > 11.2 Tumours Of The Reproductive Tract > Flashcards

11.2 Tumours Of The Reproductive Tract Flashcards

1
Q

Where might HPV cause tumours?

A

Vulva

Cervix

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2
Q

What precursor conditions of the reproductive tract may develop on to invasive cancers?

A

Human Papilloma virus
Endometriosis / endometrial hyperplasia
Vulval interepithelial neoplasia (VIN)
Cervical intraepithelial neoplasia (CIN)

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3
Q

What is a tumour?

A

Any clinically detectable lump or swelling

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4
Q

What is a neoplasm?

A

An abnormal growth of cells that persists after the initial stimulus is removed

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5
Q

What is a malignant neoplasm?

A

An abnormal growth of cells that persists after the initial stimulus is removed and invades surrounding tissue with potential to spread to distant sites

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6
Q

What are metastasis?

A

Malignant neoplasm that has spread to a distant site

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7
Q

What is dysplasia?

A

A potentially pre-neoplastic alteration where cells show disordered organization and abnormal appearances. May be reversible

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8
Q

How common are vulval cancers?

A

Uncommon - 3% of all female cancers

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9
Q

What is the most common cancer of the vulva?

A

Squamous cell carcinoma

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10
Q

What cancers can be found at the vulva?

A

Squamous Cell Carcinoma
Basal Cell Carcinoma
Melanoma
Soft tissue tumours

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11
Q

How might a vulval ulcer present?

A

Lumps
Ulceration
Skin changes (pigmentation/sensation/pain)

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12
Q

What are the 2 normal layers of the skin?

A

Epidermis
Dermis
Subcutis

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13
Q

What are the layers of the epidermis?

A 
Stratum Corneum
Stratum granulosum
Stratum spinosum
Stratum basale 
Basement membrane
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14
Q

Skin cells are a labile cell population, what does this mean?

A

Labile cells are cells that multiply constantly throughout life. These cels are only alive for a short period of time

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15
Q

What happens as skin cells mature?

A

They ascend up the epidermal layers from the stratum basale to the stratum Corneum.
Nuclei get smaller, cytoplasm increases. At top we get variable levels of keratinisation

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16
Q

What happens to the skin in squamous cell carcinoma?

A

Lose all architecture of the skin. Cant differentiate between dermis and epidermis. Cell look atypical with varying nuclei and lack of maturation.
SCC produces keratin (pink) , seen as whirls/pearls of spherical keratin production

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17
Q

What is VIN?

A

Vulval intraepithelial neoplasia is an in situ precursor of vulval squamous cell carcinoma.
Atypical cells in situ, no invasion through basement membrane. May or may not develop into squamous cell carcinoma

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18
Q

How do atypical cells look?

A

Loss of maturation down the epithelial layer.

Nuclei look large, and different from surrounding cells. Larger amount of cytoplasm

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19
Q

Are VIN and vulval SCC related to HPV?

A

Yes - 30% of cases. Usually HPV 16. In younger patients (60s not 80s). Risk factors are the same as per cervical carcinoma

No -70%. Usually associated with longstanding inflammatory conditions (e.g. lichen sclerosus. Peak age of onset = 80s

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20
Q

What is lichen sclerosis?

A

A long-term skin condition, usually affecting post-menopausal women. Causes itching and white patches of skin of genitalia

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21
Q

How does vulval cancer spread?

A

Direct extension
Lymph nodes
Distant metastases.

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22
Q

Where does vulval cancer spread to via direct extension?

A

Anus
Vagina
Bladder

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23
Q

Where does vulval cancer spread to via lymph nodes?

A

Inguinal
Iliac
Para-aortic

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24
Q

Where does vulval cancer spread to via distant metastases?

A

Lungs

Liver

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25
Q

Before mensuration, what are the 2 parts of the cervix?

A

Ectocervix

Endocervix

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26
Q

What is the ectocervix?

A

Part communicating with the vagina. Has a low pH. Covered in stratified squamous epithelium

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27
Q

What is the endocervix?

A

Not in contact with vagina, more distal towards uterus. Has simple columnar epithelium

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28
Q

Why might a cervical ectropion develop during menstration?

A

During mensuration, oestrogen causes anatomical change to cervix - everts. Simple columnar epithelial now exposed to the low pH of the vagina. Endocervix cannot not cope with this acidic environment and become inflammed. Causes a cervical ectropion.

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29
Q

What is a cervical ectropion?

A

When cells of the endocervix develop outside their normal region and are exposed to a low pH. Froms a red and inflammed patch of columnar epithelium. Results in metaplasia

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30
Q

What is the transformational zone?

A

An area of the cervix where stratified squamous epithelium meets columnar epithelium

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31
Q

Why is the transitional zone a common place for cervical cancer?

A

As after menstruation, the columnar cells descend and can undergo metaplasia to from stratified squamous epithelium. Metaplasia increases risk of dysplasia. Dysplasia can progress to become neoplasia

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32
Q

What is the human papilloma virus?

A

A DNA virus. Is sexually transmitted. Low risk and high risk subtypes.

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33
Q

What are low risk HPV subtypes and how do they often present?

A

HPV 6 and HPV 11

Often cause warts on skin, mouth, genitalia

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34
Q

What are high risk HPV subtypes and how do they present?

A

HPV 16 and HPV 18

Can lead to cancer, especially in cervical transformational zone (preferentially infect here)

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35
Q

Describe how high risk HPV can result in cervical cancer

A
  • preferentially infect the cervical transformational zone
  • high risk HPV produce viral proteins (E6 + E7)
  • E6 and E7 proteins inactivate tumour suppressor genes (p53 and retinoblastoma gene)
  • uncontrolled cellular proliferation due to inactivation of tumour suppression genes
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36
Q

What is cervical intraepithelial neoplasia?

A

CIN is in situ dysplasia of the cervical epithelium. Does not break through the basement membrane. Caused by HPV infection.
Divided into 3 different types ( CIN 1/2/3)

37
Q

What determines whether CIN is type 1/2/3?

A

Thickness of cervical epithelium that is displaying abnormal cellular features
CIN 1 = bottom third only
CIN 2 = bottom 2 thirds
CIN = full thickness

38
Q

What happens if the abnormal cells from CIN break through basement membrane?

A

Progressed to invasive squamous cell carcinoma

39
Q

What is a mitotic figure?

A

A cell undergoing division on a slide. Too many/abnormal location may indicate pathology

40
Q

What is the stroma?

A

Supporting connective tissue under the epithelium that contains glands and blood vessels.

41
Q

What are the risk factors for CIN and cervical carcinoma?

A
  • Increased risk of exposure to HPV (Sexual partner with HPV / Multiple partners)
  • Early age of first intercourse
  • Early first pregnancy
  • Multiple births
  • Smoking
  • Low socio-economic status
  • Immunosuppression ( not able to fight HPV infection )
42
Q

What is the treatment of cervical intraepithelial neoplasia?

A 
CIN1
• Often regresses spontaneously
• Follow up cervical smear in 1 year 
CIN 2 & 3
Needs treatment:
• Colposcopy +/- Large Loop Excision of Transformation zone (LLETZ)
43
Q

Describe the cervical cancer screening programme?

A 
Very successful
• Aged 25 – 49 = every 3 years 
• Aged 50 – 64 = every 5 years 
• Over 65 – only if recent
abnormality 
Brush used to scrape cells from transformation zone: Tested for HPV If positive – cells looked at under microscope
44
Q

How might a cells from a cervical cancer screening test present if positive?

A

Large nucleus
Pleomorphism
Irregular nucleur outlines

45
Q

How do we protect against cervical/vulval/oral and anal cancers?

A

Vaccination against HPV = Gardasil
• Recombinant vaccination
• Against HPV (subtypes 6/11/16/18)
• Given aged 12-13

46
Q

What are the different types of invasive cervical cancer?

A

Squamous cell carcinoma (most common)

Adenocarcinoma

47
Q

How does invasive cervical cancer present?

A

Bleeding - Post coital, Inter menstrual, Post menopausal)
Palpable abdominal mass
Picked up on screening occasionally.

48
Q

How are invasive cervical cancers staged?

A

TNM

Figo system

49
Q

How is advanced invasive cervical cancer treated?

A

Hysterectomy
Lymph Node Dissection
+/- Chemoradiotherapy

50
Q

Describe the structure of the endometrium

A

Consists of single layer of columnar epithelium on the stroma. Within the stroma are tubular glands and spiral arteries.

51
Q

What is endometrial hyperplasia?

A

An increased number of cells in the endometrium. Increased gland:stroma ratio. Thickened endometrium >7mm. Can be a precursor to endometrial cancer.

52
Q

How is endometrial hyperplasia investigated?

A

Ultrasound look at thickness of endometrium. If greater than 7mm then a biopsy taken. Histological diagnosis

53
Q

How does endometrial hyperplasia present?

A

Inter-menstrual/post- menopausal bleeding

54
Q

What causes endometrial hyperplasia?

A

excessive oestrogen.
Endogenous
- Obesity (adiposcytes convert androgens into oestrogens)
- Early menarche/late menopause ( increased lifetime amount)
- Oestrogen secreting tumours
Exogenous
- Unopposed oestrogen hormone replacement therapy (HRT)
- Tamoxifen ( treatment for breast cancer )
Irregular Cycle
- Polycystic Ovary Syndrome

55
Q

What risk factors are associated with Tamoxifen?

A

Drugs used to oestrogen receptor positive breast cancer. Blocks oestrogen receptors in the breast but stimulates oestrogen receptors in the endometrium. Can increase the risk of endometrial cancer

56
Q

How does endometrial cancer typically present?

A

Bleeding (Post menopausal/Inter menstrual)

Palpable Mass

57
Q

What are common cancers of the endometrium?

A 
Endometriosis adenocarcinoma (most common)
Serous adenocarcinoma
58
Q

What is endometriosis adenocarcinoma?

A

Type of endometrial cancer. Resembles normal endometrial glands but glands are growing into each other. Cells appear atypical. Commonly arises from hyperplasia

59
Q

What is serous adenocarcinoma?

A

A type of endometrial cancer. More aggressive, less common. Poorly differentiated cells, dont resemble normal endometrial glands.

60
Q

Why is it important to differentiate endometrioid adenocarcinoma from serous adenocarcinoma?

A

As the spread of cancer is very different

61
Q

How does endometrioid adenocarcinoma spread?

A

Direct invasion. Into myometrium and then into local regions/surrounding organs

62
Q

How does serous adenocarcinoma spread?

A

Exfoliates - cells break off from main tumour.
Travels through Fallopian tubes
Deposits on peritoneal surface (Transcoelomic spread - across serous cavities)

63
Q

What features are identifiable in serous adenocarcinoma?

A

Associated with collections of calcium - dark circular bodies (Psammoma bodies)

64
Q

How is endometrial cancer managed?

A

Hysterectomy
Bilateral salpingo- oophorectomy
+/- lymph node dissection
+/- chemo radiotherapy

65
Q

What is a leiomyoma?

A

Benign tumour of the myometrium

A.k.a fibroid

66
Q

How does a leiomyoma appear?

A

Pale, homogenous, well circumscribed mass

67
Q

How does leiomyoma present?

A 
Depends on size
Asymptomatic
 Pelvic pain 
Heavy periods 
Urinary frequency (bladder compression if big)
68
Q

How do leiomyomas appear microscopically?

A

Whorled, intersecting fascicles of benign smooth muscle cells

69
Q

What is a leiomyosarcoma?

A

Malignant tumour of smoothie muscle in myometrium. Atypical cells. Can metastasis to lung.

70
Q

How does ovarian cancer present?

A 
Early symptoms
-Vague and non-specific
-Delayed diagnosis
Later symptoms
-Abdominal pain
-Abdominal distension
-Urinary symptoms
-Gastrointestinal symptoms
-Hormonal disturbances
71
Q

What can be used to help diagnose ovarian cancer?

A

Ca -125 - Serum marker (diagnosis/monitoring recurrence)

BRCA1/2 - Tumour suppressor genes. Associated with high grade serous cancers. Prophylactic salpingo-oophrectomy

72
Q

What type of cancers can occur in the ovary?

A

Lined by epithelium - Epithelial tumours
Contains germ cells - Germ cell tumours
Contains stromal cells - Sex cord stromal tumours
Is also a site for metastatic spread

73
Q

How do ovarian cystic tumours present?

A

Cystic masses containing fluid

74
Q

What are the cost common subtypes of ovarian epithelial tumours?

A

Adenocarcinomas (Serous, Mucinous, Endometrioid)

Can all be benign, borderline, malignant

75
Q

How does an ovarian serous adenoma present on microscopy?

A

Highly atypical cells
Psammoma bodies (calcium collection)
Tumour deposits in peritoneum
- spread via transcoelomic spread into peritoneum from ovaries

76
Q

How does ovarian mucinous adenocarcinoma present on microscopy?

A

Atypical epithelial cells

Cells with big empty open cells, look similar to goblet cells. These cells secrete mucin

77
Q

How does ovarian endometrioid adenocarcinoma present on microscopy?

A

Glands resembling endometrium

May arise in endometriosis. May have synchronous endometrial endometrioid adenocarcinoma

78
Q

What is the most common germ cell tumour?

A

Teratoma ( mature/immature/monoderm )

79
Q

What is a mature teratoma?

A

A dermoid cyst. Benign. Contain fully mature, differentiated tissue from all germ cell layers. Can be bilateral. Often contains skin + hair structures

80
Q

Where do sex cord stromal tumours occur?

A

In the ovarian stroma

81
Q

What are the effects of theca and granulosa cell tumours?

A

Produce Oestrogen
Patient pre-puberty? - Precocious puberty
Patient post-puberty? - Breast cancer, Endometrial hyperplasia, Endometrial carcinoma

82
Q

What are the effects of sertoli/leydig cell tumours?

A 
Produce testosterone 
Patient pre-puberty? Prevents normal female pubertal changes 
Patient post-puberty?
Infertility
Amenorrhoea
Hirsuitism
Male pattern baldness
Breast atrophy
83
Q

Where are common sites of cancers that metastases to the ovary?

A

Breast cancer
GI cancers
Krukenberg tumour
Other gynae tumours

84
Q

What is a risk factor of testicular cancer?

A

Cryptorchidism (undescended testicle)

85
Q

How does testicular cancer present?

A

Mass +/- pain

86
Q

What investigations can be done for testicular cancer?

A

Scans (USS)

Tumour markers - useful in germ cell testicular tumours

87
Q

What are tumour markers of testicular cancer?

A

Beta hCG - produced in a choricarcinoma

Alpha fetoprotein - present in yolk sac tumours but also produced in liver cancer

88
Q

What are the subtypes of testicular tumours?

A
  1. Germ cell
    - seminomatous (seminoma/spermatocytic seminoma)
    - non-seminomatous
  2. Non-germ cell
    - sex cord stromal
    - other (lymphoma/metastases - rare)
89
Q

What is the causative agents of vulval squamous carcinoma?

A

Pre-menopausal women: HPV (VIN)

Post-menopausal women: long-standing dermatomes , lichen sclerosus, squamous hyperplasia.

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