S11) Cancers of the Reproductive Tracts Flashcards Preview

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Flashcards in S11) Cancers of the Reproductive Tracts Deck (59)
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1

Where can gynaecological tumours arise?

- Vulva

- Cervix (neck of uterus)

- Endometrium (lining of uterus)

- Myometrium (body of uterus)

- Ovary 

2

What are the clinical features of vulval tumours?

- Uncommon 

- Approx. 2/3rds occur > 60 years of age

- Usually squamous cell carcinoma 

3

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

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 

4

What is vulvar intraepithelial neoplasia?

- Vulvar intraepithelial neoplasia involves atypical squamous cells within the epidermis (no invasion)

- It is an in situ precursor of vulval squamous cell carcinoma 

5

How does vulval squamous cell carcinoma spread?

- Spreads initially to inguinal, pelvic, iliac and para-aortic lymph nodes

- Thereafter spreads to lungs and liver 

6

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

How does an HPV infection lead to these conditions?

⇒ 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

7

What are the risk factors for CIN and cervical carcinoma?

 

- Early first sexual intercourse

- Early first marriage/pregnancy

- Multiple births

- Sexual promiscuity

- Immunosuppression (cannot clear HPV infection)

8

Why is cervical screening successful?

- 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 

9

What does cervical screening involve?

- 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

10

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

What sort of abnormalities could be seen? 

- Increased nuclear:cytoplasmic

- Irregular nuclear outlines

- Hyperchromatic nuclei

11

What are the advantages of vaccinating men against HPV too?

- Reduce risk of oral and penile cancer

- Reduce risk of transmission of HPV

- Protect girls who cannot be vaccinated (herd immunity)

12

What is Cervical Intraepithelial Neoplasia?

- 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)

13

What is the treatment for CIN?

- CIN I – follow-up or cryotherapy

- CIN II & CIN III – superficial excision (LLETZ – large loop excision of transformation zone) 

14

What are the different types of invasive cervical carcinomas?

- 80% – squamous cell carcinomas

- 15% – adenocarcinomas (also caused by high risk HPVs) 

15

Which age group is usually affected by invasive cervical carcinoma?

Average age = 45 years 

16

What do invasive cervical carcinomas look like?

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

17

Identify the three ways in which invasive cervical carcinomas spread

Locally to para-cervical soft tissues, bladder, ureters, rectum, vagina

- Lymphatic system to para-cervical, pelvic, para-aortic nodes

- Distally 

18

How does cervical carcinoma present?

- Screening abnormality

- Postcoital, intermenstrual or postmenopausal vaginal bleeding 

19

How are cervical carcinomas treated?

- Microinvasive carcinomas: cervical cone excision

- Invasive carcinomas: hysterectomy, lymph node dissection and radiation and chemotherapy (if advanced)

20

Describe the structure and location of the endometrium

Location: lines internal cavity of uterus

- Structure: glands are within a cellular stroma 

21

Why is endometrial hyperplasia a frequent precursor to endometrial carcinoma? 

- Increased gland:stroma ratio

- Associated with prolonged oestrogenic stimulation:

I. Annovulation

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

III. Exogenous oestrogen

22

What are the clinical features of endometrial adenocarcinoma?

Most common invasive cancer of the female genital tract

- Usual age: 55-75 years

- Presents with irregular or postmenopausal vaginal bleeding 

23

What do endometrial adenocarcinomas look like?

Polypoid or infiltrative 

24

Identify the two types of endometrial adenocarcinoma

- Endometrioid endometrial adenocarcinoma

- Serous carcinoma

25

What are the clinical features of endometrioid endometrial adenocarcinoma?

- 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

How do endometrioid endometrial adenocarcinoma look? 

27

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

Poorly differentiated

- Aggressive

- Exfoliates, travels through oviducts and implants on peritoneal surfaces 

28

What is the commonest tumour of the myometrium?

- Leiomyoma – benign tumour of myometrium (fibroid) 

- Probably most common tumour in women 

29

What are the clinical features of a leiomyoma?

- Often multiple

- Range from tiny → massive

- Asymptomatic or heavy/painful periods, urinary frequency, infertility 

- Malignant transformation rare

30

What does a uterine leiomyoma look like?

- Well circumscribed, round, firm and whitish in colour

- Bundles of smooth muscle (resembles normal myometrium)

31

Describe the clinical features of the malignant tumour of the myometrium

Uterine leiomyosarcoma: 

- Uncommon

- 40-60 years

- Doesn’t arise from leiomyomas

-  Metastasises to lungs 

32

What are the clinical features of ovarian tumours?

- 80% are benign – 20-45 years

- 20% are malignant  – 45-65 years

- Many are bilateral 

33

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

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

34

How do ovarian tumours present?

- 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

What are the clinical features of malignant ovarian tumours?

- Approx 50% spread to other ovary

- Metastasise to regional nodes and elsewhere

- Some associated with BRCA mutations

36

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

Serum CA-125

37

How do we classify ovarian tumours?

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

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

- Serous

- Mucinous

- Endometrioid 

39

How can one classify ovarian epithelial tumours?

- Benign

- Borderline

- Malignant 

40

What are the risk factors for ovarian epithelial tumours?

- Nulliparity / low parity

- Oral contraceptive pill (protective)

- Heritable mutations e.g. BRCA1 and BRCA2

- Smoking

- Endometriosis 

41

How do serous ovarian tumours present?

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

42

How do mucinous ovarian tumours present?

- Large, cystic masses – can be >25kg

- Filled with sticky, thick fluid

- Usually benign/borderline 

43

What is pseudomyxoma peritonei?

- 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

How do endometrioid ovarian tumours present?

- Contain tubular glands resembling endometrial glands

- Can arise in endometriosis (15-20%)

- Associated with endometrial endometrioid adenocarcinoma (15-30%)

45

What are the clinical features of germ cell ovarian tumours?

- Most are teratomas

- Usually benign 

46

Identify some malignant germ cell ovarian tumours

- Dysgerminoma (resembles seminoma of testes)

- Yolk sac tumour

- Choriocarcinoma

- Embryonal carcinoma 

47

Identify and describe the three types of ovarian teratomas

Mature (benign) – most common

- Immature (malignant) – rare, composed of tissues that resemble immature foetal tissue

- Monodermal (highly specialised) 

48

What are the clinical features of ovarian mature teratomas?

- 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

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

Describe its clinical features

Benign

- Composed entirely of mature thyroid tissue

- May be functional and cause hyperthyroidism 

50

Describe the clinical basis of ovarian sex cord-stromal tumours 

- 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

What are the clinical features of granulosa cell tumours?

- 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

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

- 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

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

Identify the structures involved

 

- Uterus

- Fallopian tubes

- Contralateral ovary

- Pelvic peritoneum 

54

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

Identify some other tumours which metastasise to the ovaries

- GI tumours (colon, stomach, biliary tract, pancreas, appendix)

- Breast tumour

- Krukenberg tumour

55

What is a Krukenberg tumour?

- A Krukenberg tumour is a metastatic gastrointestinal tumour within the ovaries

- It is often bilateral and usually from stomach 

56

Identify three tumours which occur in the testes

- Germ cell tumours 

- Sex cord-stromal tumours

- Lymphomas 

57

What are the two different types of germ cell tumours?

- Seminomas

- Non-seminomatous germ cell tumours (NSGCTs)

58

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

- Sertoli cell tumours

- Leydig cell tumours

59

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

- Yolk sac tumours

- Embryonal carcinomas

- Choriocarcinomas

- Teratomas