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SA reproductive > 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
  • 3% of all female cancers
  • Approx. 2/3rds occur > 60 years of age
  • Usually squamous cell carcinoma (skin cancer)
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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 into the basement membrane)
  • It is an in situ precursor of vulval squamous cell carcinoma
  • can progress into squamous cell carcinoma
  • large nuclei that look different
  • in rare cases this can be caused by HPV
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5
Q

How does vulval squamous cell carcinoma spread?

A

anus, vagina

  • Spreads initially to inguinal, pelvic, iliac and para-aortic lymph nodes as they are the lymph nodes near by
  • Thereafter spreads to lungs and liver when it gets into blood stream
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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, no breaking through basement membrane

⇒ Produces viral proteins E6 & E7 which interfere with activity of TSGs to cause inability to repair damaged DNA and increase cell proliferation, they inactive tumour suppressor genes p53

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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
  • start at 23yrs
  • 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 as this can cause CIN
  • can sometimes also pick up invasive spumous cell carcinoma
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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, anal 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: depends on how much of the layer has been effected

CN I mostly regresses spontaneously inner ⅓, some progress to CN II ⅔(in situ carcinoma) and 10% may progress to an invasive squamous cell carcinoma (CN III – 2-10 years)

  • here there is no maturation of cells and they look abnormal
  • there is no invasiveness of this however
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13
Q

What is the treatment for CIN?

A
  • CIN I – follow-up or cryotherapy, can regress spontaneously
  • 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

(CIN is an pre curser to invasive squamous cell carcinoma)

  • 80% – squamous cell carcinomas
  • 15% – adenocarcinomas (cancer of glands) (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

- presents with bleeding, post Menstural bleeding

  • Associated with prolonged oestrogenic stimulation
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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 (most common)
  • Serous carcinoma
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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 (cervix, vagina and ovaries)
  • Associated with unopposed oestrogen and obesity
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26
Q

How do endometrioid endometrial adenocarcinoma look?

A
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27
Q

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

A
  • Poorly differentiated
  • Aggressive
  • Exfoliates, cell break off tumour and travels through fallopian tubes and implants on peritoneal surfaces (transolomic spread) across serous cavities
  • semoma bodies are seen which are circles of calcium
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28
Q

What is the commonest tumour of the myometrium?

A
  • Leiomyoma – benign tumour of myometrium (fibroid)
  • pale growth, homogenous, well localised
  • Probably most common tumour in women
  • arranged in fascicles
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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
  • (bare in mind leiomyoma independent of this and doesn’t lead to this condition)

looks like fascicles

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

they present as cysts

  • Serous
  • Mucinous
  • Endometrioid
39
Q

How can one classify ovarian epithelial tumours?

A
  • Benign
  • Borderline - cells start to show atypical but no stromal invasion
  • 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 (cells are producing mucus)
  • 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 (most common place is ovary) (15-20%)
  • Associated with leading into 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)

(more scary it looks aka more differentiated more likely it is benign)

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 (all to do with excess oestrogen)
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 who have already had their period) – 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 (most common)
  • 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

these both produce testosterone

59
Q

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

A
  • Yolk sac tumours
  • Embryonal carcinomas
  • Choriocarcinomas
  • Teratomas
60
Q

invasive squamous cell carcinoma of the vulva presentation

A
  • can no longer distinguish between epidermis and dermis
  • atypical cells seen
  • keratin Is produced (small circles)
  • you will see a spread of random cells inside the normal tissue
61
Q

what are the different linings of the cervix made up of

A
  • ecto cervix in communication with vagina: stratified squamous to protect against acid
  • endo cervix - simple columnar
62
Q

what is an ectropion

A
  • during menustration the simple columnar cells in the end cervix are everted out cervix and are exposed to acidic environment
  • this causes inflammation
  • metaplasia occurs and they turn into stratified squamous cells to adapt
  • can on a rare occasion can progress to become neoplasia but this is reversible
63
Q

2 main types of HPV

A

low risk: 6:11, warts on skin around mouth and genitalia

high risk: 16 and 18 can cause cancer, during metaplasia of cervix cells during menstruation they can become infected with high risk HPV e6 and e7

64
Q

when considering HRT why do you need to know about a historectomy

A
  • HRT can come in two forms:
    1. oestrogen and progesterone
  1. unopposed oestrogen

need to know if they still have a uterus and you just give unopposed oestrogen it puts them at an increased level of oestrogen

this increases their chance of endometrial hyperplasia and potentially cancers

65
Q

what are some causes for increased oestrogen in the body

A

I. Annovulation

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

III. Exogenous oestrogen (hormone replacement therapy)

IIII. Adipocytes convert androgens into oestrogen

IIIII. late menopause or early menarche

IIIII. tumour

IIIIII. tamoxifen drug used to treat Breast cancer but stimulates oestrogen production in endometrium

IIIIIII. PCOS

66
Q

treatment of endometrial adernocarcinoma

A
  • hysterectomy
  • remove both fallopian tubes and ovaries
  • can potentially try chemo
67
Q

BRCA 1 + 2

A
  • tumour suppressor genes
  • in the ovary any mutation of these show high grade serous cancer
  • if you have low levels of these you may need screening
68
Q

features of a benign ovarian epithelial tumour vs malignant

A

macroscopic:

benign:

  • smooth outline

malignant:

  • solid and empty areas
  • complex architecture growing into itself
  • psammoma bodies that can exfoliate and spread into the peritoneum
69
Q

what are psammoma bodies

A

found in ovarian serous adenocarcinoma

they are round collections of calcium

70
Q

what are some tumour markers used for testicular cancer

A

mainly used for germ cell testicular tumours:
- HCG - produced by a choriocarcinoma

  • AFP - in yolk sac tumours (these are also produced in liver cancer)

SA reproductive (22 decks)

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