Gynaecological Tumours Flashcards Preview

ESA 4 - Reproductive System > Gynaecological Tumours > Flashcards

Flashcards in Gynaecological Tumours Deck (189):
1

Where can gynaecological tumours arise?

Vulva
Cervix
Endometrium
Myometrium
Ovary

2

What is the transformation zone?

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

3

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

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

4

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

High risk HPVs

5

What are HPVs?

DNA viruses

6

How many types of high risk HPVs are known?

15

7

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

16 and 18

8

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

60%

9

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

10%

10

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

Infect immature metaplastic squamous cells in the transformation zone

11

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

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

12

How does infection with HPV cause CIN?

They produce viral proteins E6 and E7

13

What do viral proteins E6 and E7 do?

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

14

What is true of most genital HPV infections?

They are transient and eliminated by the immune response in months

15

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

Mostly related to HPV infection

16

What are the risk factors for CIN and cervical carcinoma?

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

17

Describe the prevalence of cervical cancer worldwide?

It is the third most common cancer in women

18

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

Introduction of screening

19

What makes cervical cancer a good condition for screening?

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

20

How can the cervix be accessed for visual examination?

Colposcopy

21

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

Years

22

What does cervical screening involve?

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

23

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

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

24

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

To make a judgement when cells are mildly atypical

25

When do people undergo cervical screening?

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

26

What happens if abnormalities are found on cervical screening?

Sent for colposcopy and biopsy

27

What HPV vaccine is used in the UK?

Gardasil

28

Who is vaccinated against HPV in the UK?

Girls aged 12-13 years

29

When was the HPV vaccination programme introduced?

2008

30

How long does the HPV vaccination protect for?

Up to 10 years

31

What cancers does the HPV vaccination protect against?

Cervical
Vulval and vaginal
Genital warts
Oral cancers
Anal cancers

32

Is screening still required following the HPV vaccine?

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

33

What is the controversy surrounding HPV vaccination?

Boys arent vaccinated

34

Why is it controversial that boys arent vaccinated against HPV?

Could protect against penile cancer
Can be paid for privately

35

What is cervical intraepithelial neoplasia?

Dysplasia of squamous cells within the cervical epithelium

36

What is cervical intraepithelial neoplasia induced by?

Infection with high risk HPVs

37

What are the types of cervical intraepithelial neoplasia?

CIN I
CIN II
CIN III

38

What is the prognosis of CIN?

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

39

What is the prognosis of CIN II?

A proportion of cases progress to CIN III

40

What is the prognosis of CIN III?

10% progress to invasive carcinoma in 2-10 years
30% regresses

41

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

Approx 7 years

42

What is the treatment for CIN I?

Follow up, often biopsy
Cryotherapy

43

What is the treatment for CIN II and III?

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

44

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

External os, transformation zone, some ectoderm

45

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

45 years

46

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

Takes longer to develop

47

What % of invasive cervical carcinomas are squamous cell carcinomas?

80%

48

What % of invasive cervical carcinomas are adenocarcinomas?

15%

49

Where are adenocarcinomas of the cervix found?

Higher in the transformation zone or endocervical canal

50

What are the types of invasive cervical carcinoma?

Exophytic or infiltrative

51

How does invasive cervical carcinoma spread?

Locally
Lymph nodes
Distally

52

How does invasive cervical carcinoma spread locally?

Para-cervical soft tissues
Bladder
Ureters
Rectum
Vagina

53

What lymph nodes does invasive cervical carcinoma spread to?

Para-cervical
Pelvic
Para-aortic

54

How does cervical carcinoma present?

Screening abnormality
Postcoital, intermenstural, or postmenopausal vaginal bleeding

55

How are microinvasive cervical carcinomas treated?

Cervical cone excision

56

What is the 5 year survival of microinvasive cervical carcinomas?

100%

57

How are invasive cervical carcinomas treated?

Hysterectomy
Lymph node dissection
If advanced, radiation and chemotherapy

58

What is the 10 year survival of invasive cervical carcinomas?

62%

59

What is the endometrium?

The lining of the cavity of the uterus

60

How does endometrium appear histologically?

Glands with cellular stroma

61

What is endometrial hyperplasia a frequent precursor to?

Endometrial carcinoma

62

What are the histological features of endometrial hyperplasia?

Increased gland to stroma ratio

63

What is endometrial hyperplasia associated with?

Prolonged oestrogenic stimulation

64

What can cause prolonged oestrogenic stimulation?

Anovulation
Increased oestrogen from endogenous sources
Exogenous sources

65

When is anovulation common?

Around the time of the menopause

66

Where may oestrogen come from endogenously?

Adipose tissue

67

What is the result of oestrogen coming from adipose tissue?

Endometrial hyperplasia is more common in obese women

68

Why does endometrial hyperplasia cause endometrial carcinoma?

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

69

How is endometrial hyperplasia treated?

Hysterectomy, if complex and atypical

70

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

Endometrial adenocarcinoma

71

What is the usual age of endometrial adenocarcinoma?

55-75 years
Unusual before 40

72

What is the usual presentation of endometrial adenocarcinoma?

Irregular or postmenopausal vaginal bleeding

73

What is the prognosis of endometrial adenocarcinoma?

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

74

What are the potential appearances of endometrial adenocarcinoma?

Polypoid
Infiltrative

75

What is the most common type of endometrial adenocarcinoma?

More common

76

What is the less common type of endometrial adenocarcinoma?

Serous carcinoma

77

How does endometrioid endometrial adenocarcinoma appear histologically

Mimics proliferative glands

78

In what setting does endometrioid endometrial adenocancer typically arise?

In the setting of endometrial hyperplasia

79

What is endometrioid endometrial adenocarcinoma associated with?

Unopposed oestrogen
Obesity

80

Where does endometrioid endometrial adenocarcinoma spread?

Adjacent structures
To local lymph nodes
To distant sites

81

How does endometrioid endometrial adenocarcinoma spread to adjacent structures?

Myometrial invasion
Direct extension

82

How does serous endometrial adenocarcinoma differ from endometrioid?

Poorly differentiated
Aggressive
Worse prognosis

83

How does serous endometrial adenocarcinoma spread?

Exfoliates, travels through Fallopian tubes, implants on peritoneal surfaces

84

What is the most common tumour of the myometrium?

Leiomyoma (fibroid)

85

What is a fibroid?

A benign tumour of the myometrium

86

How many fibroids does a woman typically have?

Often multiple

87

What size are fibroids?

Range from tiny to massive, filling the pelvis

88

What are the symptoms of fibroids?

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

89

Does malignant transformation occur with fibroids?

No

90

What does a uterine fibroid look like?

Well circumscribed, round, firm, and whitish in colour

91

What do fibroids look like histologically?

Bundles of smooth muscle that resembles normal myometrium

92

What is a uterine leiomyosarcoma?

An uncommon malignant tumour of the myometrium

93

What is the peak incidence of uterine leiomyosarcoma?

40-60 years

94

What is the prognosis of uterine leiomyosarcoma?

Highly malignant, and metastasises to lungs

95

What % of ovarian tumours are benign?

Approx 80%

96

When do benign ovarian tumours generally occur?

20-45 years (child bearing age)

97

When do malignant ovarian tumours generally occur?

45-65 years

98

What % of cancers in women are ovarian cancers?

3%

99

What is the prognosis for malignant ovarian cancers?

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

100

Are ovarian tumours unilateral or bilateral?

Many are bilateral (benign and malignant)

101

What is the 1 year survival from ovarian cancer?

70%

102

What is the 5 year survival from ovarian cancer?

41%

103

What is the 10 year survival from ovarian cancer?

38%

104

How do ovarian tumours present?

Mass effects
Hormonal problems

105

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

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

106

What are the mass effects of ovarian tumours?

Abdominal pain
Abdominal distention
Urinary gastrointestinal symptoms
Ascites

107

What hormonal problems can ovarian tumours present with?

Menstrual disturbances
Inappropriate sex hormones

108

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

50%

109

Where do ovarian tumours spread to?

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

110

What is the cancer marker for ovarian tumours?

CA-125

111

How is CA-125 used in ovarian cancer?

In diagnosis
Monitor disease recurrence and progression

112

What mutation are some ovarian cancers associated with?

BRCA

113

How can carriers of the BRCA mutation be treated?

Prophylactic salpinog-oophrectomy

114

What are ovarian tumours classified on the basis of?

The tissue from which they have arisen

115

What are the potential classifications of ovarian tumours?

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

116

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

Serous
Mucinous
Endometrioid

117

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

Benign
Borderline
Malignant

118

What is true of many ovarian epithelial tumours?

Many are cystic

119

What are the risk factors for ovarian epithelial tumours?

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

120

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

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

What is protective against ovarian epithelial tumours?

OCP

122

What are serous ovarian tumours commonly associated with?

Ascites

123

Why are serous ovarian tumours often associated with ascites?

Because they often spread to peritoneal surfaces and omentum

124

What are mucinous ovarian tumours?

Often large, cystic masses filled with sticky, thick fluid

125

Are mucinous ovarian tumours benign or malignant?

Usually benign or borderline

126

What happens in pseudomyxoma peritonei?

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

127

What can pseudomyxoma peritonei cause?

Intestinal obstruction

128

What is the most likely primary in pseudomyxoma peritonei?

Extra-ovarian, usually appendix

129

How do endometrioid ovarian tumours appear histologically?

Tubular glands resembling endometrial glands

130

What % of endometrioid ovarian tumours arise in endometriosis?

15-20%

131

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

15-30%

132

What % of ovarian neoplasms are germ cell ovarian tumours?

15-20%

133

Give two types of germ cell ovarian tumours?

Teratomas
Non-gestational choriocarcinoma

134

What does a non-gestational choriocarcinoma do?

Produces human chorionic gonadotrophin

135

How is non-gestational choriocarcinoma unlike the gestational type?

They are aggressive and often fatal

136

What are the groups of ovarian teratomas?

Mature (benign)
Immature (malignant)
Monodermal

137

What is the most common type of ovarian teratoma?

Mature

138

What are immature ovarian teratomas composed of?

Tissues that resemble immature foetal tissue

139

What does a monodermal ovarian carcinoma produce?

One kind of highly specialised tissue

140

What are mature ovarian teratomas also known as?

Dermoid cysts

141

Why are mature ovarian teratomas also known as dermoid cysts?

As they almost always contain skin-like structures

142

Who do ovarian mature teratomas usually occur in?

Young women - in their 20s

143

What % of ovarian mature teratomas are bilateral?

10-15%

144

What do ovarian mature teratomas usually contain?

Hair and sebaceous material, can contain tooth structures
Often tissues from other germ layers - cartilage, bone, thyroid, neural tissue

145

What is the most common type of monodermal ovarian teratomas?

Struma ovarii

146

Are struma ovarii benign or malignant?

Benign

147

What are struma ovarii composed of?

Entirely of mature thyroid tissue

148

How do struma ovarii present?

May be functional and cause hyperthyroidism

149

What are ovarian sex cord stromal tumorus derived from?

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

150

What does the sex cord produce?

Sertoli and Leydig cells in testes
Granulosa and theca cells in ovaries

151

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

Any of those produced by sex cord

152

What effect can ovarian sex cord stromal tumours have?

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

153

Who do many granulosa cell tumours occur in?

Post-menopausal women

154

What may granulosa cells tumours produce?

Large amounts of oestrogen

155

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

In pre-pubertal girls, may produce precocious puberty
In adult women, may be associated with endometrial hyperplasia, endometrial carcinoma, and breast disease

156

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

Teens/twenties

157

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

May block normal female sexual development

158

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

Can cause defeminisation and masculinisation;
- Breast atrophy
- Amennorrhea
- Sterility
- Hair loss
- Hisuitism with male hair distribution
- Clitoral hypertrophy
- Voice changes

159

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

Mullerian tumours

160

Where do Mullerian metastases to the ovaries come from?

Uterus
Fallopian tubes
Contralateral ovary
Pelvic peritoneum

161

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

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

162

What is a Krukenberg tumour?

A metastatic gastrointestinal tumour within the ovaries

163

Where is the primary of a Krukenberg tumour?

Usually from stomach

164

How common are vulval tumours?

Uncommon

165

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

Approx 2/3

166

What kind of cancers are vulval tumours?

Usually squamous cell carcinoma

167

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

Approx 30%

168

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

6th decade

169

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

Same as for cervical carcinoma

170

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

8th decade

171

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

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

172

What is VIN (vulvar intraepithelial neoplasia)?

Atypical squamous cells within the epidermis (no invasion)

173

What is VIN a precursor to?

Vulval squamous cell carcinoma

174

Where does vulval squamous cell carcinoma spread to?

Initially to nodes
Lungs
Liver

175

What nodes does vulval squamous cell carcinoma spread to?

Inguinal
Pelvic
Iliac
Para-aortic

176

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

90%, following vulvectomy and lymphadenectomy

177

What is gestational trophoblastic disease?

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

178

What are the major trophoblastic diseases?

Hydatidiform mole (complete and partial)
Invasive mole
Choriocarcinoma

179

What is a hydatidiform mole associated with?

Choriocarcinoma

180

What is a hydatidiform mole?

Cystic swelling of chorionic villi and trophoblastic proliferation

181

When does a hydatidiform mole occur?

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

182

How is a hydatidiform mole usually diagnosed?

In early pregnancy, with USS
Can present with miscarriage

183

What groups are at highest risk of hydatidiform mole?

Teenagers, and 40-50 years

184

What are the types of hydatidiform mole?

Complete
Partial

185

What does a hydatidiform mole look like histologically?

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

186

How is a hydatidiform mole treated?

Curettage, followed by hCG monitoring

187

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

Invasive mole

188

What is a gestational choriocarcinoma?

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

189

Are villi present with gestational choriocarcinoma?

No