Gynaecological Tumours Flashcards

1
Q

How common are vulval tumours and who do they affect the most?

A

Uncommon (approx 3% of female genital cancers)

2/3rds in women over 60

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2
Q

What are the types of vulval tumours?

A

Squamous cell carcinoma - most common
Extramammary Paget’s disease
Basal cell carcinoma
Malignant melanoma

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3
Q

Risk factors for vulval squamous cell carcinoma?

A

Same for cervical carcinomas:

  • HPV
  • intercourse
  • early marriage
  • early first pregnancy
  • multiple births
  • many partners
  • promiscuous partner
  • long term use of OCP
  • partner with carcinoma of the penis
  • low socio-economic class
  • smoking
  • immunosuppression
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4
Q

What are the usual causes of squamous cell carcinoma of the vulva in older and younger women?

A

70s - long standing inflammatory and hyperplastic conditions of the vulva eg lichen sclerosis

50s - usually HPV and risk factors same as cervical carcinoma

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5
Q

What is the precursor to squamous neoplastic lesions of the vulva?

A

Vulvar intraepithelial neoplasia (VIN)

-atypical squamous cells within the epidermis (no invasion)

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6
Q

Which lymph nodes does vulval squamous cell carcinoma spread to?

Where else?

A

Inguinal, pelvic, iliac and para-aortic lymph node

Lungs and liver

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7
Q

Survival if a lesion of vulval squamous cell carcinoma is less than 2cm?
Following which procedures?

A

90% 5 year survival

Vulvectomy and lymphadenectomy

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8
Q

Where includes gynaecological tumours?

A
Cervix
Endometrium
Myometrium
Ovary
Vulva
Tumours of gestation
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9
Q

What are the two important viruses causing cervical carcinoma?

A

HPV 16

HPV 18

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10
Q

How do the viruses cause squamous cell carcinoma?

A

Infect immature metaplastic squamous cells in the transformation zone
Produce viral proteins which interfere with activity of tumour suppressor genes - inability to repair damaged DNA and increase proliferation of cells

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11
Q

Risk factors for CIN and cervical carcinoma?

A
Sexual intercourse
Early first marriage
Early first pregnancy
Multiple births
Many partners
Promiscuous partner
Long term use of OCP
Partner with carcinoma of penis
Low socio-economic class
Smoking
Immunosuppression
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12
Q

Why is cervical screening so successful?

A

Cervix accessible to visual examination and sampling
Slow progression from precursor lesions to invasive cancers
Pap test detects precursor lesions and low stage cancers
Allows early diagnosis and curative therapy

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13
Q

How is the cervical screening done?

A

Cells from transformation zone are scraped off, stained with Papanicolaou stain and examined microscopically

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14
Q

When is cervical screening done?

A

Starts age 25
Every three years until 50
Every 5 years from 50-65

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15
Q

What happens if the result of cervical screening is abnormal?

A

Referred for colposcopy (visualisation of cervix) and biopsy

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16
Q

For how many years does the vaccine against HPV protect for?

A

Up to 10 years

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17
Q

What is cervical intraepithelial neoplasia?

A

Dysplasia of squamous cells within the cervical epithelium, induced by infection with high risk HPVs

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18
Q

What is dysplasia?

A

Enlargement of an organ/tissue by the proliferation of cells of an abnormal type - early stage in development of cancer

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19
Q

What are the CIN stages?

What is the outcome of each one?

A

CIN I - most regress spontaneously and a small % progress to..
CIN II
CIN III - carcinoma in situ - 10% progress to invasive carcinoma in 2-10 years, 30% regress

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20
Q

How long does it take to go from CIN I to CIN III

A

7 years

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21
Q

What is the management of each CIN stage?

A

CIN I - follow-up or cryotherapy

CIN II and III - superficial excision

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22
Q

Average age of presentation of cervical carcinoma?

A

45

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23
Q

What are the most common types of cervical carcinomas?

A

80% squamous cell carcinoma

15% adenocarcinoma

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24
Q

Where can cervical carcinoma spread to?

A

Para-cervical soft tissues, bladder, ureters, rectum, vagina

Lymph nodes - para-cervical, pelvic, para-aortic
Distally

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25
Q

How does cervical carcinoma usually present?

A

Screening abnormality

Postcoital, intermenstrual or postmenopausal vaginal bleeding

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26
Q

Treatment of cervical carcinoma?

A

Microinvasive - cervical cone excision - 100% survival

Invasive - hysterectomy, lymph node dissection, radiation and chemotherapy - 62% 10 year survival

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27
Q

What is the endometrium made up of?

A

Glands with a cellular stroma

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28
Q

What is the frequent precursor to endometrial carcinoma?

A

Endometrial hyperplasia

-increased gland to stroma ratio

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29
Q

What is endometrial hyperplasia associated with?

A

Annovulation
Increased oestrogen from endogenous sources eg adipose tissue
Exogenous oestrogen

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30
Q

How is endometrial carcinoma treated?

A

If complex and atypical, hysterectomy

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31
Q

What age does endometrial adenocarcinoma affect?

A

55-75, unusual before 40

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32
Q

Usual presentation of endometrial adenocarcinoma?

A

Irregular or postmenopausal vaginal bleeding

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33
Q

How common is endometrial adenocarcinoma?

A

Very common - most common invasive cancer of female genital tract
75% 10 year survival

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34
Q

What can endometrial carcinoma be classed as?

A

Polypoid or infiltrative

35
Q

What are the two most common types of endometrial adenocarcinoma?

A

Endometrioid endometrial adenocarcinoma
-associated with unopposed oestrigen and obesity

Serous carinoma

36
Q

Give pathophysiology of endometrioid endometrial adenocarcinoma and how it spreads

A

Mimics proliferative glands
Arises in setting of endometrial hyperplasia

Spreads by myometrial invasion and direct extension to adjacent structures - local lymph nodes and distal sites

37
Q

Features of serous endometrial adenocarcinoma carcinoma?

A

Poorly differentiated, aggressive, worse prognosis

38
Q

How does serous endometrial adenocarcinoma spread?

A

Exfoliates
Travels through Fallopian tubes
Implants on peritoneal surfaces and grows

39
Q

What are fibroids?

A

Uterine leiomyoma
Benign tumour of myometrium (uterine smooth muscle)
Often multiple
Range from tiny to massive

40
Q

Symptoms of fibroids?

A

Asymptomatic
Heavy/painful periods
Urinary frequency due to bladder compression
Infertility

41
Q

What does uterine leiomyoma look like?

A

Well circumscribed, round, firm, whitish, well differentiated
Bundles of smooth muscle - resembles normal myometrium

42
Q

How common is leiomyosarcoma and who does it affect?

A

40-60 years

Uncommon

43
Q

Where do uterine leiomyosarcomas usually metastasise to?

A

Lungs

-highly malignant

44
Q

Are most ovarian tumours benign or malignant?

A

80% are benign

45
Q

When do most benign ovarian tumours occur?

When do most malignant tumours occur?

A

Benign: 20-45 years
Malignant: 45-65 years

46
Q

Why is prognosis of ovarian tumours poor?

A

Usually spread beyond the ovary by the time of presentation - few symptoms

47
Q

When do non-functional (don’t produce hormones) ovarian tumours usually give symptoms?

What symptoms do they produce?

A

When they become large, invade adjacent structures and metastasise

Abdominal pain
Abdominal distension
Urinary and GI symptoms
Ascites due to malignant spread through peritoneum

48
Q

What hormonal problems can ovarian tumours cause?

A

Menstrual disturbances

Inappropriate sex hormones

49
Q

Where do most malignant ovarian tumours spread to?

A

Regional nodes
Liver and lungs
50% to other ovary

50
Q

What is used to diagnose and monitor disease recurrence of ovarian cancer?

A

CA-125

Possible future screening test

51
Q

What are the general classifications of ovarian tumours?

A
Müllerian epithelium (including endometriosis)
Germ cells (pluripotent)
Sex-cord stromal cells (form the endocrine apparatus of the ovary)
Metastases to the ovary
52
Q

What are the three main histological types of ovarian Muüllerian epithelial tumours?
What can each be classified as?

A

Serous
Mucinous
Endometrioid

Benign, borderline or malignant

53
Q

Risk factors for ovarian epithelial tumours?

A

Nulliparity or low parity
Heritable mutations eg BRCA1&2
Smoking
Endometriosis

OCP protective (fewer ovulations)

54
Q

Why are serous Mullerian epithelial ovarian tumours commonly associated with ascites?

A

Often spread to peritoneal surfaces and omentum

55
Q

What do mucinous ovarian tumours usually look like?

A

Large, cystic masses
Filled with sticky, thick, mucinous fluid
Usually benign or borderline

56
Q

Give features of Mullerian epithelial endometrioid ovarian tumours

A

Contain tubular glands resembling endometrial glands
Can arise in endometriosis
Sometimes have associated endometrial endometrioid adenocarcinoma, probably arising separately

57
Q

What are the types of germ cell ovarian tumours?

A

Most are teratomas - benign
Other types are malignant
-non-gestational choriocarcinoma (aggressive and often fatal, produces human chorionic gonadotropin)
-yolk sac (produces alpha-fetoprotein)

58
Q

Three groups of ovarian teratomas?

A

Mature (benign) - most common

Immature (malignant) - rare, composed of tissues resembling immature fetal tissue)

Monodermal (highly specialised - one cell type)

59
Q

Who do ovarian teratomas usually occur in?

A

Young women usually

60
Q

What do teratomas often contain?

A
Cystic
-hair
-sebaceous material
-teeth
AKA dermoid cysts as they often have skin-like structures

Also tissue from other germ layers

  • cartilage
  • bone
  • thyroid
  • neural tissue
61
Q

Common types of monodermal ovarian tumours?

A

Struma ovarii

  • benign
  • composed of mature thyroid tissue
  • hyperthyroidism

Carcinoid

  • malignant
  • can be function producing 5HT (serotonin) and can cause carcinoid syndrome
62
Q

Where are ovarian sex-cord stromal tumours derived from?

A

Ovarian stroma derived from sex cords of the embryonic gonad

63
Q

What do sex cords normally give rise to?

A

Sertoli and Leydig cells in testes

Granulosa and theca cells in the ovaries

64
Q

What can sex cord stromal tumours cause?

A

Feminising if from granulosa/theca cell

Masculinising if from Leydig cells

65
Q

Who do granulosa cell tumours usually occur in?

A

Post-menopausal women

66
Q

What are the signs and symptoms of granulosa cell tumours?

A

Produce lots of oestrogen

  • precocious puberty in pre-pubertal girls
  • adults - associated with endometrial hyperplasia, endometrial carcinoma, breast disease
67
Q

What problems can Sertoli-Leydig cell tumours produce?

A
In children - block normal female sexual development
Women - defeminisation and masculisation
-breast atrophy
-amenorrhoea
-sterility
-hair loss
-hirsutism with male hair distribution
-clitoral hypertrophy
-voice changes
68
Q

When is the peak incidence of Sertoli-Leydig cell tumours?

A

Teens/twenties

69
Q

Where do metastases to the ovaries usually come from?

A

Mullerian tumours

  • uterus
  • Fallopian tubes
  • contralateral ovary
  • pelvic peritoneum

Sometimes GI

  • colon
  • stomach
  • biliary tract
  • pancreas
  • appendix

Breast

Krukenberg tumour - drops down from stomach

70
Q

What is gestational trophoblastic disease?

A

Tumours and tumour-like conditions which show proliferation of placental tissue

71
Q

Types of gestational trophoblastic disease?

A
Hydatidiform mole (growing mass of tissue in the uterus due to abnormal conception)
Invasive mole (tumorous growth associated with gestation)
Choriocarcinoma
72
Q

What is a hydatidiform mole?

A

Cystic swellings of chorionic villi and trophoblastic proliferation

73
Q

Presentation of a hydatidiform mole?

A

Diagnosed in early pregnancy with ultrasound scan

Miscarriage

74
Q

Highest risk group of hydatidiform mole?

A

Extremes of repro life

  • teens
  • 40-50 years
75
Q

Types of hydatidiform mole?

A

complete

partial

76
Q

What do hydatidiform moles look like?

A

Friable mass of thin-walled, translucent, grape-like structures = swollen oedematous villi

77
Q

How is a hydatidiform mole treated?

A

Curettage followed by HCG monitoring - if HCG doesn’t fall, may indicate an invasive mole (rarely happens)

78
Q

What is an invasive mole?

A

Mole that penetrates or perforates uterine wall

Locally destructive - can cause uterine rupture requiring hysterectomy

79
Q

Symptoms and signs of an invasive mole?

A

Vaginal bleeding and uterine enlargement

Persistently elevated HCG

80
Q

How is an invasive mole treated?

A

Chemotherapy

81
Q

What is a gestational choriocarcinoma?

A

Malignant neoplasm of trophoblastic cells derived from previously normal or abnormal pregnancy, with no villi present
Rapidly invasive, metastasises widely but responds well to chemo

82
Q

How can non-gestational choriocarcinomas arise?

A

From germ cells in the ovary or in the mediastinum

83
Q

How does gestational choriocarcinoma present?

A

Vaginal spotting

High HCG levels

84
Q

How is gestational choriocarcinoma treated?

A

Uterine excavation and chemotherapy

-high cure rate