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[AMS] Reproductive System > S11) Cancers of the Reproductive Tracts > Flashcards

S11) Cancers of the Reproductive Tracts Flashcards

1
Q

Where can gynaecological tumours arise?

A
  • Vulva
  • Cervix (neck of uterus)
  • Endometrium (lining of uterus)
  • Myometrium (body of uterus)
  • Ovary
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2
Q

What are the clinical features of vulval tumours?

A
  • Uncommon
  • Approx. 2/3rds occur > 60 years of age
  • Usually squamous cell carcinoma
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3
Q

How many vulval squamous neoplastic lesions are related to HPV infection?

A
  • 30% HPV-related (6th decade) – risk factors the same as for cervical carcinoma
  • 70% HPV-related (8th decade) – often occur in longstanding inflammatory and hyperplastic conditions of the vulva e.g. lichen sclerosis
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4
Q

What is vulvar intraepithelial neoplasia?

A
  • Vulvar intraepithelial neoplasia involves atypical squamous cells within the epidermis (no invasion)
  • It is an in situ precursor of vulval squamous cell carcinoma
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5
Q

How does vulval squamous cell carcinoma spread?

A
  • Spreads initially to inguinal, pelvic, iliac and para-aortic lymph nodes
  • Thereafter spreads to lungs and liver
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6
Q

Almost all cases of CIN and cervical carcinoma are related to high risk HPVs.

How does an HPV infection lead to these conditions?

A

⇒ Infects immature metaplastic squamous cells in transformation zone

⇒ Produces viral proteins E6 & E7 which interfere with activity of TSGs to cause inability to repair damaged DNA and increase cell proliferation

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7
Q

What are the risk factors for CIN and cervical carcinoma?

A
  • Early first sexual intercourse
  • Early first marriage/pregnancy
  • Multiple births
  • Sexual promiscuity
  • Immunosuppression (cannot clear HPV infection)
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8
Q

Why is cervical screening successful?

A
  • Cervix accessible to visual examination (colposcopy) and sampling
  • Slow progression from precursor lesions → invasive cancers (years)
  • Pap test detects precursor lesions and low stage cancers
  • Allows early diagnosis and curative therapy
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9
Q

What does cervical screening involve?

A
  • Cells from the transformation zone are scraped off
  • Cells are stained with Pap stain
  • Cells are examined microscopically
  • Cervical cells can be tested for HPV DNA
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10
Q

In cervical screening, abnormalities are referred for colposcopy and biopsy.

What sort of abnormalities could be seen?

A
  • Increased nuclear:cytoplasmic
  • Irregular nuclear outlines
  • Hyperchromatic nuclei
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11
Q

What are the advantages of vaccinating men against HPV too?

A
  • Reduce risk of oral and penile cancer
  • Reduce risk of transmission of HPV
  • Protect girls who cannot be vaccinated (herd immunity)
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12
Q

What is Cervical Intraepithelial Neoplasia?

A
  • CIN is a dysplasia of squamous cells within the cervical epithelium, induced by infection with high risk HPVs
  • Three stages: CN I mostly regresses spontaneously, some progress to CN II (in situ carcinoma) and 10% may progress to an invasive carcinoma (CN III – 2-10 years)
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13
Q

What is the treatment for CIN?

A
  • CIN I – follow-up or cryotherapy
  • CIN II & CIN III – superficial excision (LLETZ – large loop excision of transformation zone)
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14
Q

What are the different types of invasive cervical carcinomas?

A
  • 80% – squamous cell carcinomas
  • 15% – adenocarcinomas (also caused by high risk HPVs)
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15
Q

Which age group is usually affected by invasive cervical carcinoma?

A

Average age = 45 years

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16
Q

What do invasive cervical carcinomas look like?

A

Exophytic (external) or infiltrative (stromal invasion through basement membrane)

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17
Q

Identify the three ways in which invasive cervical carcinomas spread

A
  • Locally to para-cervical soft tissues, bladder, ureters, rectum, vagina
  • Lymphatic system to para-cervical, pelvic, para-aortic nodes
  • Distally
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18
Q

How does cervical carcinoma present?

A
  • Screening abnormality
  • Postcoital, intermenstrual or postmenopausal vaginal bleeding
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19
Q

How are cervical carcinomas treated?

A
  • Microinvasive carcinomas: cervical cone excision
  • Invasive carcinomas: hysterectomy, lymph node dissection and radiation and chemotherapy (if advanced)
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20
Q

Describe the structure and location of the endometrium

A
  • Location: lines internal cavity of uterus
  • Structure: glands are within a cellular stroma
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21
Q

Why is endometrial hyperplasia a frequent precursor to endometrial carcinoma?

A
  • Increased gland:stroma ratio
  • Associated with prolonged oestrogenic stimulation:

I. Annovulation

II. Increased oestrogen from endogenous sources (e.g. adipose tissue)

III. Exogenous oestrogen

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22
Q

What are the clinical features of endometrial adenocarcinoma?

A
  • Most common invasive cancer of the female genital tract
  • Usual age: 55-75 years
  • Presents with irregular or postmenopausal vaginal bleeding
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23
Q

What do endometrial adenocarcinomas look like?

A

Polypoid or infiltrative

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24
Q

Identify the two types of endometrial adenocarcinoma

A
  • Endometrioid endometrial adenocarcinoma
  • Serous carcinoma
25
Q

What are the clinical features of endometrioid endometrial adenocarcinoma?

A
  • More common
  • Mimics proliferative glands
  • Arises due to endometrial hyperplasia
  • Spreads by myometrial invasion to local lymph nodes and distant sites
  • Associated with unopposed oestrogen and obesity
26
Q

How do endometrioid endometrial adenocarcinoma look?

A
27
Q

What are the clinical features of serous carcinoma (endometrial adenocarcinoma)?

A
  • Poorly differentiated
  • Aggressive
  • Exfoliates, travels through oviducts and implants on peritoneal surfaces
28
Q

What is the commonest tumour of the myometrium?

A
  • Leiomyoma – benign tumour of myometrium (fibroid)
  • Probably most common tumour in women
29
Q

What are the clinical features of a leiomyoma?

A
  • Often multiple
  • Range from tiny → massive
  • Asymptomatic or heavy/painful periods, urinary frequency, infertility
  • Malignant transformation rare
30
Q

What does a uterine leiomyoma look like?

A
  • Well circumscribed, round, firm and whitish in colour
  • Bundles of smooth muscle (resembles normal myometrium)
31
Q

Describe the clinical features of the malignant tumour of the myometrium

A

Uterine leiomyosarcoma:

  • Uncommon
  • 40-60 years
  • Doesn’t arise from leiomyomas
  • Metastasises to lungs
32
Q

What are the clinical features of ovarian tumours?

A
  • 80% are benign – 20-45 years
  • 20% are malignant – 45-65 years
  • Many are bilateral
33
Q

Why do ovarian cancers have such a poor prognosis (70% 1 year survival)?

A

Ovarian cancers have often spread beyond the ovary by the time of presentation and therefore the prognosis is often poor

34
Q

How do ovarian tumours present?

A
  • Most non-functional – produce symptoms when large, invasive or metastasise
  • Mass effects – abdominal pain and distension (GI & urinary symptoms)
  • Ascites
  • Hormonal problems – menstrual disturbances and inappropriate sex hormones
35
Q

What are the clinical features of malignant ovarian tumours?

A
  • Approx 50% spread to other ovary
  • Metastasise to regional nodes and elsewhere
  • Some associated with BRCA mutations
36
Q

Which tumour marker is used in the diagnosis and monitoring of ovarian carcinoma recurrence and progression?

A

Serum CA-125

37
Q

How do we classify ovarian tumours?

A

Dependent on the tissue from which they have arisen:

  • Müllerian epithelium (including endometriosis)
  • Germ cells (pluripotent)
  • Sex cord-stromal cells (form the endocrine apparatus of the ovary)
  • Metastases
38
Q

What are the three main histological types of ovarian epithelial tumours?

A
  • Serous
  • Mucinous
  • Endometrioid
39
Q

How can one classify ovarian epithelial tumours?

A
  • Benign
  • Borderline
  • Malignant
40
Q

What are the risk factors for ovarian epithelial tumours?

A
  • Nulliparity / low parity
  • Oral contraceptive pill (protective)
  • Heritable mutations e.g. BRCA1 and BRCA2
  • Smoking
  • Endometriosis
41
Q

How do serous ovarian tumours present?

A

Often spread to peritoneal surfaces and omentum, therefore commonly associated with ascites

42
Q

How do mucinous ovarian tumours present?

A
  • Large, cystic masses – can be >25kg
  • Filled with sticky, thick fluid
  • Usually benign/borderline
43
Q

What is pseudomyxoma peritonei?

A
  • Pseudomyxoma peritonei is a condition caused by cancer cells (mucinous adenocarcinoma) which produce extensive mucinous ascites due to epithelial implants on peritoneal surfaces
  • There’s frequent involvement of ovaries which can cause intestinal obstruction
44
Q

How do endometrioid ovarian tumours present?

A
  • Contain tubular glands resembling endometrial glands
  • Can arise in endometriosis (15-20%)
  • Associated with endometrial endometrioid adenocarcinoma (15-30%)
45
Q

What are the clinical features of germ cell ovarian tumours?

A
  • Most are teratomas
  • Usually benign
46
Q

Identify some malignant germ cell ovarian tumours

A
  • Dysgerminoma (resembles seminoma of testes)
  • Yolk sac tumour
  • Choriocarcinoma
  • Embryonal carcinoma
47
Q

Identify and describe the three types of ovarian teratomas

A
  • Mature (benign) – most common
  • Immature (malignant) – rare, composed of tissues that resemble immature foetal tissue
  • Monodermal (highly specialised)
48
Q

What are the clinical features of ovarian mature teratomas?

A
  • Most are cystic
  • Almost always contain skin-like structures, usually contains hair, sebaceous material and tooth structures
  • Usually occur in young women
  • 10-15% bilateral
49
Q

The most common types of monodermal ovarian teratomas is the struma ovarii.

Describe its clinical features

A
  • Benign
  • Composed entirely of mature thyroid tissue
  • May be functional and cause hyperthyroidism
50
Q

Describe the clinical basis of ovarian sex cord-stromal tumours

A
  • Derived from ovarian stroma (which is derived from sex cords)
  • Sex cord produces Sertoli & Leydig cells (testes) and granulosa and theca cells (ovaries)
  • Tumours resembling all of these four cell types can be found in the ovary and can be feminising or masculinising
51
Q

What are the clinical features of granulosa cell tumours?

A
  • Most occur in post-menopausal women
  • May produce large amounts of oestrogen → precocious puberty in pre-pubertal girls
  • Associated with endometrial hyperplasia, endometrial carcinoma and breast disease in adults
52
Q

What are the clinical features of ovarian Sertoli-Leydig cell tumours?

A
  • Blocks normal female sexual development (in children – functional)
  • Causes defeminisation and masculinisation (in women – functional): breast atrophy, amenorrhoea, sterility, hair loss
  • Peak incidence in teens/ twenties
53
Q

Metastases to the ovaries are most commonly due to Mϋllerian tumours.

Identify the structures involved

A
  • Uterus
  • Fallopian tubes
  • Contralateral ovary
  • Pelvic peritoneum
54
Q

Metastases to the ovaries are most commonly due to Mϋllerian tumours.

Identify some other tumours which metastasise to the ovaries

A
  • GI tumours (colon, stomach, biliary tract, pancreas, appendix)
  • Breast tumour
  • Krukenberg tumour
55
Q

What is a Krukenberg tumour?

A
  • A Krukenberg tumour is a metastatic gastrointestinal tumour within the ovaries
  • It is often bilateral and usually from stomach
56
Q

Identify three tumours which occur in the testes

A
  • Germ cell tumours
  • Sex cord-stromal tumours
  • Lymphomas
57
Q

What are the two different types of germ cell tumours?

A
  • Seminomas
  • Non-seminomatous germ cell tumours (NSGCTs)
58
Q

What are the two types of sex cord-stromal tumours?

A
  • Sertoli cell tumours
  • Leydig cell tumours
59
Q

Identify four types of non-seminomatous germ cell tumours (NSGCTs)

A
  • Yolk sac tumours
  • Embryonal carcinomas
  • Choriocarcinomas
  • Teratomas

[AMS] Reproductive System (21 decks)

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