Cancers of the Genital Tracts Flashcards

1
Q

Aetiology of vulva cancer. (5)

A

Uncommon, mostly in older women.
Caused in pre-menopausal women by HPV causing vulval intraepithelial neoplasia (precursor to squamous cell carcinoma.
Caused in post-menopausal women by chronic inflammation ie lichen sclerosusor. Causing squamous cell hyperplasia.

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2
Q

Pathophysiology of vulval cancer. (3)

A

Mostly squamous cell carcinoma (90%) but can be melanoma or basal cell carcinoma. Can spread locally to other organs or lymph nodes.

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3
Q

Detection and treatment of vulval cancer. (2)

A

Lumps/ulcers/lesions can be detected by the woman, or in examinations.
Curative surgery would include removing primary tumour and local nodes.

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4
Q

Pathophysiology of cervical cancer. (3)

A

Squamous cell cercinoma (80%) but some are adenocarcinomas. Appear in the transition zone which is the metaplasia between simple columnar and striatified squamous.

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5
Q

Aetiology of cervical cancer. (4)

A

HPV causing proliferation in the transition zone, or cervical intraepithelial neoplasia. Can spread to local nodes, local organs (causing fistulae), or be widespread.

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6
Q

Risk factors for CIN or carcinoma. (5)

A

Increased HPV risk, smoking, multiple births, early first pregnancy or sex, immunosuppresion.

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7
Q

Explain why the HPV vaccination is controversial. (3)

A

Men can still get oral and anal cancer that is related to HPV but they don’t get the vaccine, which wipes out the herd immunity effects.

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8
Q

Detection of cervical cancer. (4)

A

Cervical screening detects abnormal cells and premalignant lesions.
25-49: every 3 years
50-64: every 5 years
65+: if abnormalities indicated.

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9
Q

Aetiology of endometrial cancer. (4)

A

Predisposed by endometrial hyperplasia caused by excessive oestrogen.
Endogenous - obesity (fat turns androgen to oestrogens)
Exogenous - oestrogen only HRT, tamoxifen.
Irregular - polycystic ovarian syndrome.

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10
Q

Presentation of endometrial cancer (2)

A

Intermenstrual bleeding, postmenopausal bleeding.

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11
Q

Pathophysiology of endometrial cancer. (2)

A

Commonly endometrioid adenocarcinoma or serous carcinoma.

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12
Q

Management of endometrial cancer. (3)

A

Hysterectomy +- salpingooophrectory +- lymph nodes.

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13
Q

Pathophysiology of leiomyomata. (3)

A

Benign myometrial cancer, well differentiated, pale.

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14
Q

Presentation of leiomyomata (4)

A

Can be asymptomatic, but can cause pelvic pain, heavy periods (increased SA), urinary frequency (bladder compression).

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15
Q

Pathophysiology of leiomyosarcoma (2)

A

Malignant tumours of the myometrium, poorly differentiated, often with lung mets.

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16
Q

Presentations of ovarian cancer. (6)

A

Often vague symptoms.
Abdominal pain, distension, urinary or GI symptoms, hormonal disturbances.
Ca-125 is a tumour marker used in diagnosis.
Some assocaited with BRCA1/2 mutations.

17
Q

Describe three types of epithelial ovarian tumour of the ovary. (9)

A

Serous - pleomorphic cells, often with spcalcified Psammoma bodies. Often spread to peritoneal surface
Mucinous - atypical cells secreting mucin creating white blobs in cells.
Endometrioid - glands resembling endometrium that may arise in endometriosis.

18
Q

Describe types of germ cell tumours of the ovary. (4)

A

Yolk sac
Embryonal carcinoma
Choriocarcinoma
Teratoma

19
Q

Describe stroma cell tumours of the ovary. (4)

A

Granulosa cell
Thecoma
Fibroma
Sertoli and Leydig cells (yes even in ovary’

20
Q

Describe the 3 types of teratoma found in the ovary. (11)

A

Mature (dermoid cyst) - contains fully differentiates tissue from all germ layers. Often contains skin or hair. Benign.
Immature - immature embryonal tissue, malignant.
Monodermal - one fully differentiated tissue type, most commonly thyroid. Benign but can cause hyperthyroidism.

21
Q

Describe the presentations of the different types of stroma tumour. (8)

A

Theca and granulosa cell tumours can produce excess oestrogen leading to precocious puberty, breast cancer, endometrial hyperplasia and carcinoma.
Sertoli and Leydig cell tumours can produce excess testosterone leading to prevention of female puberty (if prepubescent), sterility, amenorrhoea, breast atrophy, hirsuitism.

22
Q

Risk factor for all testicular cancers. (1)

A

Cryptorchidism (undescended testicle). Can make cancer in both.

23
Q

Presentation for testicular cancer. (2)

A

Mass +- pain.

24
Q

Diagnosis of testicular cancer (2)

A

USS, tumour markers.

25
Q

Explain why biopsy of testicular masses is rare. (2)

A

Benign tumours are really rare, and with a malignant one, if you biopsy it, you give a really high risk of seeding to the other testicle or scrotum or somewhere else.

26
Q

Describe common tumour markers for germ cell tumours. (2)

A
Beta hCG - choriocarcinoma
Alpha fetoprotein (AFP) - yolk sac tumours.
27
Q

What other sort of cancer can ovaries have in them? (2)

A

Mets from somewhere else: breast, GI, other gynae.

28
Q

Describe seminomas. (6)

A

Type of germ cell tumour. Peak age is 40-50, often remains confined to testes for a long time, but can met to nodes. Further spread is rare. Associated with a rise in hCG.

29
Q

Describe the types of non-seminomatous germ cell tumours. (10)

A

Yolk sac tumours - occurs in young children with a good prognosis, all release AFP as a tumour marker.
Embryonal carcinomas, choriocarcinomas and mixed NSGCTs occur in young adults. Chorio have raised hCG, mixed can have raised hCG and AFP.
Teratoma occur in men of all ages. If postpubertal they’re malignant.

30
Q

Metastatic potential of NSGCTs. (2)

A

Tend to metastasise early (before primary tumour palpable) through lymphatics and blood vessels.

31
Q

Management of testicular tumours. (3)

A

Radical orchiectomy.
Seminomas also with radiotherapy.
NSGCTs also with chemotherapy.

32
Q

Types of non-germ cell tumours. (2)

A

Sertoli and Leydig cell

Mets