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(LUSUMA) 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
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

(LUSUMA) Reproductive System (21 decks)

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