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ESA 4 - Reproductive System > Gynaecological Tumours > Flashcards

Gynaecological Tumours Flashcards

1
Q

Where can gynaecological tumours arise?

A 
Vulva
Cervix
Endometrium 
Myometrium
Ovary
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2
Q

What is the transformation zone?

A

Where the endothelium of the cervix undergoes metaplasia from glandular to squamous epithelium

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3
Q

How does the transformation zone differ between older and younger women?

A

In younger women, the transformation zone is further out into the ectocervix

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4
Q

What are almost all cases of CIN and cervical carcinoma related to?

A

High risk HPVs

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5
Q

What are HPVs?

A

DNA viruses

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6
Q

How many types of high risk HPVs are known?

A

15

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7
Q

What are the most important HPVs in the pathogenesis of cervical carcinoma?

A

16 and 18

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8
Q

What % of cases of HPV are related to HPV 16?

A

60%

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9
Q

What % of cases of cervical carcinoma are related to HPV 18?

A

10%

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10
Q

How does HPV lead to the development of CIN or cervical carcinoma?

A

Infect immature metaplastic squamous cells in the transformation zone

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11
Q

What is the result of HPV infecting the immature metaplastic squamous cells in the transformation zone?

A

More common in younger women, as they have more transformation zone available to infect, therefore easier to catch

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12
Q

How does infection with HPV cause CIN?

A

They produce viral proteins E6 and E7

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13
Q

What do viral proteins E6 and E7 do?

A

Interfere with the activity of tumour suppressor proteins (p53 and RB) to cause inability to repair damaged DNA and increased proliferation of cells
Activate telomerase to cause cell immortality

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14
Q

What is true of most genital HPV infections?

A

They are transient and eliminated by the immune response in months

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15
Q

What do the risk factors for CIN and cervical carcinoma relate to?

A

Mostly related to HPV infection

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16
Q

What are the 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 the penis
Low socio-economic class
Smoking
Immunosuppression
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17
Q

Describe the prevalence of cervical cancer worldwide?

A

It is the third most common cancer in women

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18
Q

What has caused the rate of cervical cancer to decrease significantly?

A

Introduction of screening

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19
Q

What makes cervical cancer a good condition for screening?

A

Cervix accessible to visual examination
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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20
Q

How can the cervix be accessed for visual examination?

A

Colposcopy

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21
Q

How long does the progression from precursor lesions to invasive cancers take?

A

Years

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22
Q

What does cervical screening involve?

A

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

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23
Q

Other than Pap staining, how can cervical screens be interpreted?

A

Test for HPV DNA in cervical cells - molecular method of screening

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24
Q

How is testing for HPV DNA in cervical cells often used?

A

To make a judgement when cells are mildly atypical

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25
Q

When do people undergo cervical screening?

A

Starts at age 25
Every 3 years until age 50
Every 5 years 50-65

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26
Q

What happens if abnormalities are found on cervical screening?

A

Sent for colposcopy and biopsy

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27
Q

What HPV vaccine is used in the UK?

A

Gardasil

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28
Q

Who is vaccinated against HPV in the UK?

A

Girls aged 12-13 years

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29
Q

When was the HPV vaccination programme introduced?

A

2008

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30
Q

How long does the HPV vaccination protect for?

A

Up to 10 years

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31
Q

What cancers does the HPV vaccination protect against?

A 
Cervical
Vulval and vaginal 
Genital warts
Oral cancers
Anal cancers
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32
Q

Is screening still required following the HPV vaccine?

A

Yes, because it doesn’t protect against all high risk types

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33
Q

What is the controversy surrounding HPV vaccination?

A

Boys arent vaccinated

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34
Q

Why is it controversial that boys arent vaccinated against HPV?

A

Could protect against penile cancer

Can be paid for privately

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35
Q

What is cervical intraepithelial neoplasia?

A

Dysplasia of squamous cells within the cervical epithelium

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36
Q

What is cervical intraepithelial neoplasia induced by?

A

Infection with high risk HPVs

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37
Q

What are the types of cervical intraepithelial neoplasia?

A

CIN I
CIN II
CIN III

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38
Q

What is the prognosis of CIN?

A

Most regress spontaneously, only a small percentage progresses to CIN II

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39
Q

What is the prognosis of CIN II?

A

A proportion of cases progress to CIN III

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40
Q

What is the prognosis of CIN III?

A

10% progress to invasive carcinoma in 2-10 years

30% regresses

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41
Q

How long does the transition from CIN I to CIN III take?

A

Approx 7 years

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42
Q

What is the treatment for CIN I?

A

Follow up, often biopsy

Cryotherapy

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43
Q

What is the treatment for CIN II and III?

A

Superficial excision (cone, large loop excision of transformation zone)

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44
Q

What does superficial excision in CIN II and III usually include?

A

External os, transformation zone, some ectoderm

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45
Q

What is the average age of onset of invasive cervical carcinoma?

A

45 years

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46
Q

Why does invasive cervical carcinoma have a later age of onset?

A

Takes longer to develop

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47
Q

What % of invasive cervical carcinomas are squamous cell carcinomas?

A

80%

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48
Q

What % of invasive cervical carcinomas are adenocarcinomas?

A

15%

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49
Q

Where are adenocarcinomas of the cervix found?

A

Higher in the transformation zone or endocervical canal

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50
Q

What are the types of invasive cervical carcinoma?

A

Exophytic or infiltrative

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51
Q

How does invasive cervical carcinoma spread?

A

Locally
Lymph nodes
Distally

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52
Q

How does invasive cervical carcinoma spread locally?

A 
Para-cervical soft tissues
Bladder
Ureters
Rectum
Vagina
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53
Q

What lymph nodes does invasive cervical carcinoma spread to?

A

Para-cervical
Pelvic
Para-aortic

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54
Q

How does cervical carcinoma present?

A

Screening abnormality

Postcoital, intermenstural, or postmenopausal vaginal bleeding

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55
Q

How are microinvasive cervical carcinomas treated?

A

Cervical cone excision

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56
Q

What is the 5 year survival of microinvasive cervical carcinomas?

A

100%

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57
Q

How are invasive cervical carcinomas treated?

A

Hysterectomy
Lymph node dissection
If advanced, radiation and chemotherapy

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58
Q

What is the 10 year survival of invasive cervical carcinomas?

A

62%

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59
Q

What is the endometrium?

A

The lining of the cavity of the uterus

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60
Q

How does endometrium appear histologically?

A

Glands with cellular stroma

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61
Q

What is endometrial hyperplasia a frequent precursor to?

A

Endometrial carcinoma

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62
Q

What are the histological features of endometrial hyperplasia?

A

Increased gland to stroma ratio

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63
Q

What is endometrial hyperplasia associated with?

A

Prolonged oestrogenic stimulation

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64
Q

What can cause prolonged oestrogenic stimulation?

A

Anovulation
Increased oestrogen from endogenous sources
Exogenous sources

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65
Q

When is anovulation common?

A

Around the time of the menopause

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66
Q

Where may oestrogen come from endogenously?

A

Adipose tissue

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67
Q

What is the result of oestrogen coming from adipose tissue?

A

Endometrial hyperplasia is more common in obese women

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68
Q

Why does endometrial hyperplasia cause endometrial carcinoma?

A

Because increased cell turnover, so damage to DNA, so increased risk of cancer

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69
Q

How is endometrial hyperplasia treated?

A

Hysterectomy, if complex and atypical

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70
Q

What is the most common invasive cancer of the female genital tract?

A

Endometrial adenocarcinoma

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71
Q

What is the usual age of endometrial adenocarcinoma?

A

55-75 years

Unusual before 40

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72
Q

What is the usual presentation of endometrial adenocarcinoma?

A

Irregular or postmenopausal vaginal bleeding

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73
Q

What is the prognosis of endometrial adenocarcinoma?

A

Early detection and cure possible, so overall 75% 10 year survival

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74
Q

What are the potential appearances of endometrial adenocarcinoma?

A

Polypoid

Infiltrative

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75
Q

What is the most common type of endometrial adenocarcinoma?

A

More common

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76
Q

What is the less common type of endometrial adenocarcinoma?

A

Serous carcinoma

77
Q

How does endometrioid endometrial adenocarcinoma appear histologically

A

Mimics proliferative glands

78
Q

In what setting does endometrioid endometrial adenocancer typically arise?

A

In the setting of endometrial hyperplasia

79
Q

What is endometrioid endometrial adenocarcinoma associated with?

A

Unopposed oestrogen

Obesity

80
Q

Where does endometrioid endometrial adenocarcinoma spread?

A

Adjacent structures
To local lymph nodes
To distant sites

81
Q

How does endometrioid endometrial adenocarcinoma spread to adjacent structures?

A

Myometrial invasion

Direct extension

82
Q

How does serous endometrial adenocarcinoma differ from endometrioid?

A

Poorly differentiated
Aggressive
Worse prognosis

83
Q

How does serous endometrial adenocarcinoma spread?

A

Exfoliates, travels through Fallopian tubes, implants on peritoneal surfaces

84
Q

What is the most common tumour of the myometrium?

A

Leiomyoma (fibroid)

85
Q

What is a fibroid?

A

A benign tumour of the myometrium

86
Q

How many fibroids does a woman typically have?

A

Often multiple

87
Q

What size are fibroids?

A

Range from tiny to massive, filling the pelvis

88
Q

What are the symptoms of fibroids?

A

May be asymptomatic, or can cause heavy/painful periods, urinary frequency (bladder compression), infertility

89
Q

Does malignant transformation occur with fibroids?

A

No

90
Q

What does a uterine fibroid look like?

A

Well circumscribed, round, firm, and whitish in colour

91
Q

What do fibroids look like histologically?

A

Bundles of smooth muscle that resembles normal myometrium

92
Q

What is a uterine leiomyosarcoma?

A

An uncommon malignant tumour of the myometrium

93
Q

What is the peak incidence of uterine leiomyosarcoma?

A

40-60 years

94
Q

What is the prognosis of uterine leiomyosarcoma?

A

Highly malignant, and metastasises to lungs

95
Q

What % of ovarian tumours are benign?

A

Approx 80%

96
Q

When do benign ovarian tumours generally occur?

A

20-45 years (child bearing age)

97
Q

When do malignant ovarian tumours generally occur?

A

45-65 years

98
Q

What % of cancers in women are ovarian cancers?

A

3%

99
Q

What is the prognosis for malignant ovarian cancers?

A

Poor, because many have often spread beyond the ovary by the time of presentation

100
Q

Are ovarian tumours unilateral or bilateral?

A

Many are bilateral (benign and malignant)

101
Q

What is the 1 year survival from ovarian cancer?

A

70%

102
Q

What is the 5 year survival from ovarian cancer?

A

41%

103
Q

What is the 10 year survival from ovarian cancer?

A

38%

104
Q

How do ovarian tumours present?

A

Mass effects

Hormonal problems

105
Q

What is the result of most ovarian tumours being non functional, on the presentation?

A

They only produce symptoms when they become large, invade adjacent structures, or metastasise

106
Q

What are the mass effects of ovarian tumours?

A

Abdominal pain
Abdominal distention
Urinary gastrointestinal symptoms
Ascites

107
Q

What hormonal problems can ovarian tumours present with?

A

Menstrual disturbances

Inappropriate sex hormones

108
Q

What % of malignant ovarian tumorus spread to the other ovary?

A

50%

109
Q

Where do ovarian tumours spread to?

A

Regional nodes and elsewhere, e.g. Liver and lungs

110
Q

What is the cancer marker for ovarian tumours?

A

CA-125

111
Q

How is CA-125 used in ovarian cancer?

A

In diagnosis

Monitor disease recurrence and progression

112
Q

What mutation are some ovarian cancers associated with?

A

BRCA

113
Q

How can carriers of the BRCA mutation be treated?

A

Prophylactic salpinog-oophrectomy

114
Q

What are ovarian tumours classified on the basis of?

A

The tissue from which they have arisen

115
Q

What are the potential classifications of ovarian tumours?

A

Mullieran epithelium (including endometriosis)
Germ cells
Sex cord-stromal cells (from endocrine apparatus of the ovary)
Metatases

116
Q

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

A

Serous
Mucinous
Endometrioid

117
Q

How can all the histological types of ovarian epithelial tumours be classified?

A

Benign
Borderline
Malignant

118
Q

What is true of many ovarian epithelial tumours?

A

Many are cystic

119
Q

What are the risk factors for ovarian epithelial tumours?

A

Nulliparity or low parity
Heritable mutations, e.g. BRCA1 and BRCA2
Smoking
Endometriosis within the ovary

120
Q

Why does nulliparity or low parity increase the risk of ovarian epithelial tumours?

A

With every ovulation, there is a break in the ovary and healing, which predisposes the cell to cancer due to division and repair of cells

121
Q

What is protective against ovarian epithelial tumours?

A

OCP

122
Q

What are serous ovarian tumours commonly associated with?

A

Ascites

123
Q

Why are serous ovarian tumours often associated with ascites?

A

Because they often spread to peritoneal surfaces and omentum

124
Q

What are mucinous ovarian tumours?

A

Often large, cystic masses filled with sticky, thick fluid

125
Q

Are mucinous ovarian tumours benign or malignant?

A

Usually benign or borderline

126
Q

What happens in pseudomyxoma peritonei?

A

Extensive mucinous ascites, with epithelial implants on peritoneal surfaces, and frequent involvement of the ovarise

127
Q

What can pseudomyxoma peritonei cause?

A

Intestinal obstruction

128
Q

What is the most likely primary in pseudomyxoma peritonei?

A

Extra-ovarian, usually appendix

129
Q

How do endometrioid ovarian tumours appear histologically?

A

Tubular glands resembling endometrial glands

130
Q

What % of endometrioid ovarian tumours arise in endometriosis?

A

15-20%

131
Q

What % of endometrioid ovarian tumours have associated endometrial endometrioid adenocarcinoma?

A

15-30%

132
Q

What % of ovarian neoplasms are germ cell ovarian tumours?

A

15-20%

133
Q

Give two types of germ cell ovarian tumours?

A

Teratomas

Non-gestational choriocarcinoma

134
Q

What does a non-gestational choriocarcinoma do?

A

Produces human chorionic gonadotrophin

135
Q

How is non-gestational choriocarcinoma unlike the gestational type?

A

They are aggressive and often fatal

136
Q

What are the groups of ovarian teratomas?

A

Mature (benign)
Immature (malignant)
Monodermal

137
Q

What is the most common type of ovarian teratoma?

A

Mature

138
Q

What are immature ovarian teratomas composed of?

A

Tissues that resemble immature foetal tissue

139
Q

What does a monodermal ovarian carcinoma produce?

A

One kind of highly specialised tissue

140
Q

What are mature ovarian teratomas also known as?

A

Dermoid cysts

141
Q

Why are mature ovarian teratomas also known as dermoid cysts?

A

As they almost always contain skin-like structures

142
Q

Who do ovarian mature teratomas usually occur in?

A

Young women - in their 20s

143
Q

What % of ovarian mature teratomas are bilateral?

A

10-15%

144
Q

What do ovarian mature teratomas usually contain?

A

Hair and sebaceous material, can contain tooth structures

Often tissues from other germ layers - cartilage, bone, thyroid, neural tissue

145
Q

What is the most common type of monodermal ovarian teratomas?

A

Struma ovarii

146
Q

Are struma ovarii benign or malignant?

A

Benign

147
Q

What are struma ovarii composed of?

A

Entirely of mature thyroid tissue

148
Q

How do struma ovarii present?

A

May be functional and cause hyperthyroidism

149
Q

What are ovarian sex cord stromal tumorus derived from?

A

Ovarian stroma, which is derived from sex cords of embryonic gonad

150
Q

What does the sex cord produce?

A

Sertoli and Leydig cells in testes

Granulosa and theca cells in ovaries

151
Q

What kind of cells can be present in ovarian sex cord-stromal tumours?

A

Any of those produced by sex cord

152
Q

What effect can ovarian sex cord stromal tumours have?

A

They can be feminising (granulosa/theca cell tumours) or masculinising (Leydig cell tumours)

153
Q

Who do many granulosa cell tumours occur in?

A

Post-menopausal women

154
Q

What may granulosa cells tumours produce?

A

Large amounts of oestrogen

155
Q

What is the result of the granulosa cell tumours producing a large amount of oestrogen?

A

In pre-pubertal girls, may produce precocious puberty

In adult women, may be associated with endometrial hyperplasia, endometrial carcinoma, and breast disease

156
Q

When is the peak incidence of ovarian sertoli-leydig cell tumours?

A

Teens/twenties

157
Q

What do ovarian Sertoli-Leydig cell tumours cause in children?

A

May block normal female sexual development

158
Q

What do ovarian Sertoli-Leydig cell tumours cause in women?

A

Can cause defeminisation and masculinisation;

  • Breast atrophy
  • Amennorrhea
  • Sterility
  • Hair loss
  • Hisuitism with male hair distribution
  • Clitoral hypertrophy
  • Voice changes
159
Q

What is the most common type of tumour that metastasises to the ovaries?

A

Mullerian tumours

160
Q

Where do Mullerian metastases to the ovaries come from?

A

Uterus
Fallopian tubes
Contralateral ovary
Pelvic peritoneum

161
Q

Other than Mullerian tumours, what other primary sites may metastasise to ovaries?

A

Gastrointestinal tumours - colon, stomach, biliary tract, pancreas, appendix
Breast

162
Q

What is a Krukenberg tumour?

A

A metastatic gastrointestinal tumour within the ovaries

163
Q

Where is the primary of a Krukenberg tumour?

A

Usually from stomach

164
Q

How common are vulval tumours?

A

Uncommon

165
Q

What proportion of vulval tumours occur in women over 60 years of age?

A

Approx 2/3

166
Q

What kind of cancers are vulval tumours?

A

Usually squamous cell carcinoma

167
Q

What % of vulval squamous neoplastic lesions are related to HPV infection?

A

Approx 30%

168
Q

What is the peak age for vulval squamous carcinomas related to HPV infections?

A

6th decade

169
Q

What are the risk factors for vulval squamous cell carcinomas related to HPV infections?

A

Same as for cervical carcinoma

170
Q

What is the peak age for vulval squamous ell carcinomas unrelated to HPV infection?

A

8th decade

171
Q

When do vulval squamous cell carcinomas unrelated to HPV often occur?

A

In longstanding inflammatory and hyperplastic conditions of the vulva, e.g. lichen sclerosis

172
Q

What is VIN (vulvar intraepithelial neoplasia)?

A

Atypical squamous cells within the epidermis (no invasion)

173
Q

What is VIN a precursor to?

A

Vulval squamous cell carcinoma

174
Q

Where does vulval squamous cell carcinoma spread to?

A

Initially to nodes
Lungs
Liver

175
Q

What nodes does vulval squamous cell carcinoma spread to?

A

Inguinal
Pelvic
Iliac
Para-aortic

176
Q

What is the 5 year survival for vulval squamous cell carcinoma lesions less than 2cm?

A

90%, following vulvectomy and lymphadenectomy

177
Q

What is gestational trophoblastic disease?

A

Tumours and tumour like conditions which show proliferation of placental tissue - villous and/or trophoblastic

178
Q

What are the major trophoblastic diseases?

A

Hydatidiform mole (complete and partial)
Invasive mole
Choriocarcinoma

179
Q

What is a hydatidiform mole associated with?

A

Choriocarcinoma

180
Q

What is a hydatidiform mole?

A

Cystic swelling of chorionic villi and trophoblastic proliferation

181
Q

When does a hydatidiform mole occur?

A

When there is an abnormally fertilised ovum - ovum that has lost maternal DNA, or 2 sperm fertilise ovum

182
Q

How is a hydatidiform mole usually diagnosed?

A

In early pregnancy, with USS

Can present with miscarriage

183
Q

What groups are at highest risk of hydatidiform mole?

A

Teenagers, and 40-50 years

184
Q

What are the types of hydatidiform mole?

A

Complete

Partial

185
Q

What does a hydatidiform mole look like histologically?

A

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

186
Q

How is a hydatidiform mole treated?

A

Curettage, followed by hCG monitoring

187
Q

What may be indicated if hCG levels don’t fall following treatment for hydatidiform moles?

A

Invasive mole

188
Q

What is a gestational choriocarcinoma?

A

Malignant neoplasm of trophoblastic cells derived from previous normal or abnormla pregnancy

189
Q

Are villi present with gestational choriocarcinoma?

A

No

ESA 4 - Reproductive System (31 decks)

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