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OBG: Oncology and neonatalology > Postmenopausal bleeding > Flashcards

Postmenopausal bleeding Flashcards

1
Q

What is the definition of postmenopausal bleeding?

A

vaginal bleeding occurring after 12 months of amnoerrhoea, in women at the age where the menopause can be expected or women who have experienced premature ovarian failure or premature menopause

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2
Q

What is the most important thing to rule out in cases of postmenopausal bleeding?

A

endometrial malignancy

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3
Q

What is the most common cause of postmenopausal bleeding?

A

vaginal atrophy

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4
Q

What is vaginal atrophy?

A

thinning, drying and inflammation of the walls of the vagina due to a reduction in oestrogen following the menopause

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5
Q

What are 10 causes of postmenopausal bleeding?

A
  1. Vaginal atrophy
  2. HRT
  3. Endometrial hyperplasia
  4. Endometrial cancer
  5. Cervical cancer
  6. Ovarian cancer
  7. Vaginal cancer
  8. Trauma
  9. Vulval cancer
  10. Bleeding disorders
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6
Q

What can occur due to HRT causing PMB?

A

periods or spotting can continue in some women for many months with no pathological cause, or endometrial hyperplasia due to long-term oestrogen therapy may occur

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7
Q

What is a protective factor against endometrial hyperplasia?

A

use of the combined oral contraceptive pill

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8
Q

What proportion of patients with postmenopausal bleeding have endometrial cancer? What proportion of it presents with bleeding?

A

10%; 90% of it presents with PMB

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9
Q

Which type of ovarian cancer is particularly likely to cause postmenopausal bleeding?

A

oestrogen-secreting (theca cell) tumours

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10
Q

What is the management for all causes of postmenopausal bleeding?

A

all women over age of 55 with PMB must be investigation within 2 weeks by ultrasound for endometrial cancer - transvaginal ultrasound best

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11
Q

What are 9 things to ask about in the history for postmenopausal bleeding?

A
  1. Timing of bleeding
  2. Quantity of bleeding
  3. Consistency of bleeding
  4. Full gynaecological history
  5. Full obstetric history
  6. Risk factors for endometrial cancer
  7. Menstrual timeline from menarche to menopause
  8. Full drug history - including HRT
  9. Red flag symptoms for gynae cancer
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12
Q

What examination should be performed for postmenopausal cancer?

A

full vaginal and abdominal examination, looking for any masses or abnormalities within abdomen or felt from within the vagina, as well as speculum visualisation of walls of vagina and cervix

may see blood or discharge

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13
Q

What are 3 immediate tests that can be performed when a woman consults with PMB?

A
  1. Urine dipstick - haematuria or infection
  2. FBC - anaemia, bleeding disorder
  3. Ca-125 blood test
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14
Q

What is the type of ultrasound of choice for women referred on the 2 week cancer pathway who present with PMB?

A

transvaginal ultrasound

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15
Q

What is assessed on ultrasound of the uterus when women are referred on the 2 week pathway for PMB?

A

thickness of the endometrial lining; acceptable depth <5mm (sometimes said to be 4?)

this may miss some pathology so if clinical suspicion high, further testing required

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16
Q

How is a definitive diagnosis of endometrial cancer made?

A
  • endometrial biopsy either during hysteroscopy or by aspiration (pipelle) biopsy as outpatient
  • pipelle biopsy: thin flexible tube inserted into uterus via speculum to remove cells for testing
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17
Q

What imaging for gynaecological cancer may be performed?

A

CT or MRI of uterus, pelvis and abdomen, in secondary care

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18
Q

If a woman presents with PMB and is HRT what should be done?

A

still need to investigate for endometrial cancer with transvaginal ultrasound of endometrial thickness

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19
Q

What is the treatment for vaginal atrophy? 3 aspects

A

topical oestrogens, conservative measures like lubrication for symptoms, HRT

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20
Q

If a bleed is due to the type of HRT that a patient is on (and there is no endometrial hyperplasia/carcinoma) what is a management option?

A

different HRT preparations can be used to try and reduce it

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21
Q

What is the usual management of endometrial hyperplasia?

A

dilatation and curettage to remove excess endometrial tissue

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22
Q

What is the definition of endometrial hyperplasia?

A

abnormal proliferation of endometrium in excess of the normal proliferation that occurs during hte menstrual cycle

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23
Q

What are 4 types of endometrial hyperplasia?

A
  1. Simple
  2. Complex
  3. Simple atypical
  4. Complex atypical
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24
Q

What is the commonest type of endometrial tumour?

A

adenocarcinomas (arising from endometrial glands)

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25
Q

What are 11 risk factors for endometrial carcinoma?

A
  1. Obesity (especially upper body)
  2. Diabetes mellitus
  3. Nulliparity
  4. Late menopause
  5. Unopposed oestrogen therapy
  6. Tamoxifen
  7. Oesotrgen-secreting tumours (granulosa/theca cell ovarian tumours)
  8. Carbohydrate intolerance
  9. PCOS
  10. Personal history of breast or colon cancer
  11. Family history of breast, colon or endometrial cancer
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26
Q

What are 2 factors that decrease the risk of endometrial cancer?

A
  1. Combined oral contraceptive pill
  2. Progestogens
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27
Q

What causes high levels of oestrogen in obesity?

A

aromatisation in body fat of peripheral androgens to oestrogens

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28
Q

What proportion of cases of endometrial cancer are thought to be related to obesity?

A

a third

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29
Q

What is thought to be the relationship of diabetes/hypertension and endometrial cancer?

A

possibly result of increased incidence of obesity in these groups, but role of insulin has been questioned

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30
Q

By what factor does unopposed HRT increase the risk of endometrial cancer?

A

4x (reduced to <1.0x with opposed HRT)

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31
Q

Why is the use of the COCP thought to reduce the risk of endometrial cancer?

A

probably because it administers progestogens throughout the cycle

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32
Q

Why do smokers have a lower incidence of endometrial cancer?

A

they are more likely to reach an earlier menopause

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33
Q

What are 2 broad types of endometrial cancer?

A
  1. Type I: seen around time of menopause or soon after, tumour cells have oestrogen and progesterone receptors
  2. Type II: not related to oestrogen production, seen in older women
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34
Q

How does the prognosis of type I endometrial cancer compare with type II and why?

A

much poorer prognosis for type II; type II progress more rapidly, not associated with hyperplastic or in situ phase whereas type I has premalignant change, slower growth

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35
Q

What is the cardinal symptom of endometrial carcinoma?

A

abnormal uterine bleeding - most commonly postmenopausal

any irregular uterine bleeding in those over 40 (especially if obese/ other risk factors) should be investigated

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36
Q

What are 4 symptoms of endometrial cancer?

A
  1. Postmenopausal bleeding
  2. Irregular uterine bleeding pre-menopause
  3. Vaginal discharge - blood stained, watery or purulent
  4. Can present with abnormal cells on a smear consistent with endometrial origin
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37
Q

What does pain in endometrial cancer usually indicate?

A

metastatic spread - rarely associated with early disease

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38
Q

What is the mode of spread of endometrial cancer?

A

principally direct spread, usually involves myometrium

cervix, fallopian tubes as well as local supporting tissues (parametrium) can also become involved with more locally advanced cases

lymphatic and haematogenous spread may also occur

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39
Q

What are the 4 main methods of investigation for endometrial cancer?

A
  1. Transvaginal ultrasound scanning
  2. Endometrial biopsy
  3. Dilatation and curettage
  4. Hysteroscopy
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40
Q

How is dilatation and curettage for endometrial cancer performed?

A

carried out under general anaesthesia, combined with hysteroscopy

cervix dilated to allow introduction of sharp curette, instrument that scrapes of endometrium for histological analysis

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41
Q

How commonly is dilatation and curettage now performed in suspected endometrial cancer?

A

used to be standard of care but rarely used alone now - combined with hysteroscopy in cases where additional investigations are required

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42
Q

What does hysteroscopy involve to investigate endometrial cancer?

A

visualising inside of uterine cavity directly using a hysteroscope (fine telescope), can be introduced with or without anaesthesia depending on the instrument and the local facilities

biopsy or curettage can be performed as same time

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43
Q

What is the gold standard investigation for endometrial cancer?

A

hysteroscopy with biopsy

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44
Q

What is endometrial hyperplasia?

A

increased number of endometrial cells due to proliferation and this results in a thicker endometrium

terms cystic glandular hyperplasia/simple hyperplasia/glandular hyperplasia/ endometrial hyperplasia are synonymous

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45
Q

What is the binary classification of endometrial hyperplasia?

A

with or without atypia

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46
Q

What might it be difficult to distinguish severe atypia in the hyperplastic state from?

A

well-differentiated carcinoma

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47
Q

What is needed for a diagnosis of endometrial hyperplasia?

A

should be increase in gland-to-stromal ratio

glands may vary in size and shape or may branch abnormally

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48
Q

What is seen on histology in hyperplasia with atypia? 3 things

A
  1. loss of polarity of cells within the glands
  2. increase in nuclear-cytoplasmic ratio
  3. nuclear irregularity with hyperchromatic changes, chromatin clumping and prominent nucleoli
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49
Q

How can benign endometrial lesions be differentiated from those with invasive potentia?

A

atypia - if prseent, likely to become invasive

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50
Q

What proportion of patients with endometrial hyperplasia with atypia will develop carcinoma?

A

10-20% will in 10 years

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51
Q

How is endometrial hyperplasia usually discovered?

A

endometrial biopsy as part of investigation of abnormal uterine bleeding

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52
Q

In which group of patients does simple endometrial hyperplasia typically occur?

A

anovulatory teenagers, and perimenopausal years

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53
Q

What is the treatment of simple endometrial hyperplasia?

A

Progestogens - Mirena IUS often used to manage abnormal uterine bleeding in premenopausal women

54
Q

What is the recommended management for atypical hyperplasia?

A

hysterectomy

55
Q

What is the histological appearance of endometrial carcinoma?

A
  • can have variety of histological appearances depending on if purely glandular or has areas of squamous differentiation (may appear malignant or benign)
  • or whether demonstrates papillary or clear cell pattern
    • latter 2 associated with poorer prognosis
56
Q

Which 2 histological appearances of endometrial carcinoma are associated with a poorer prognosis?

A
  1. papillary
  2. clear cell pattern
57
Q

What is another type of endometrial cancer in addition to the most common, adenocarcinoma?

A

endometrial sarcoma - locally agressive tumour that metastasizes early, genearlly poor prognosis

58
Q

What is the key indicator of prognosis of endometrial cancer?

A

the stage, based on FIGO 2009 scheme (International Federation of Gynaecology and Obstetrics)

59
Q

What are 7 factors which all affect the prognosis of endometrial cancer?

A
  1. Histological type
  2. Histological differentiation
  3. Stage of disease
  4. Myometrial invasion
  5. Peritoneal cytology
  6. Lymph node metastasis
  7. Adnexal metastasis
60
Q

What is the staging system for endometrial cancer?

A

FIGO staging

  • I
    • IA: Tumour confined to the uterus, no or <50% myometrial invasion
    • IB: Tumour confined to the uterus, >50% myometrial invasion
  • II
    • II: Cervical stromal invasion, but not beyond uterus
  • III
    • IIIA: Tumour invades serosa or adnexa
    • IIIB: Vaginal and/or parametrial involvement
    • IIIC1: Pelvic node involvement
    • IIIC2: Para-aortic involvement
  • IV
    • IVA: Tumour invasion bladder and/or bowel mucosa
    • IVB: Distant metastases including abdominal metastases and/or inguinal lymph nodes
61
Q

How are endometrial sarcomas staged?

A

new corpus sarcoma staging system based on criteria used in other soft tissue sarcomas

62
Q

Before management of endometrial carcinoma is performed, what investigation is done first?

A

MRI scan before operating to determine degree of involvement of local tissues and allow assessment of lymph nodes

sometimes CT but MRI better to look at local infiltration

63
Q

What is the mainstay of treatment for endometrial carcinoma?

A

surgical management: hysterectomy and bilateral salpingo-oophorectomy

often performed laparoscopically (reduces length of stay, recovery time etc.)

peritoneal cytology usually also sent

64
Q

Which part of the management of endometrial cancer is there debate about?

A

whether pelvic lymph nodes should be removed - trade off between complications and additional information (positive or negative) that each option brings

certainty of negative lymph nodes can redue/limit adjuvant radiotherapy

65
Q

What is the management of endometrial cancer if it has spread beyond the uterus?

A

individualised treatment, often focused on gaining control of local tumour

surgery if in fallopian tubes followed by adjuvant treatment

if more widespread, should be managed depending on degree and location of spread + condition of patient

66
Q

What is the treatment of endometrial cancer after surgery?

A
  • related to stage of disease
  • radiotherapy may be used as adjuvant (postoperative) if tumour invades myometrium deeply - higher risk of extrauterine disease
  • local radiotherapy to vault of vagina (brachytherapy) may prevent recurrence developing in this area
  • radiotherapy to whole pelvis (external beam radiotherapy) will also prevent local disease recurring but doesn’t improve survival
67
Q

What treatment of endometrial cancer may be used if the patient is medically unfit for major surgery? 2 things

A
  • radiotherapy - but becoming less common as most patients’ comorbidity can be optimised for surger
  • high dose progestogens can be used to slow progression (but less commonly used now
68
Q

If endometrial cancer is very widespread what treatment amy be considered?

A

chemotherapy - cisplatinum and doxorubicin most helpful (controversial effect on response rate)

69
Q

What is the recurrence of edometrial cancer like?

A

for most treated patients, will not recur and prognosis good

70
Q

When and where does recurrence of endometrial cancer typically occur?

A

usually within first 2 years of primary treatment

most commonly in vault of vagina

also in lymph node chains, lungs, bone, liver

71
Q

If recurrence of endometrial cancer occurs at a distance site what is the management and why?

A

should aim to maximise quality of life rather than subject to treatment with high morbidity and slim chance of success

this is because 80% with distant recurrent disease will die wihtin 2 years

72
Q

What are 3 options for management of recurrence of endometrial cancer in the vaginal vault?

A
  • if have not received radiotherapy should be considered for this treatment
  • for the remainder, choice is between hormonal therapy and chemotherapy
    • main hormonal option is high-dose progestogens, which may give a response (slowing disease) in 30%
    • chemotherapy can produce tumour shrinkage in some cases but toxicity is considerable
73
Q

What type of cancer are the vast majority of vulval cancers?

A

squamous cell carcinoma

74
Q

In what age group do most cases of vulval carcinoma occur?

A

over age of 65 years

75
Q

What are 5 risk factors for vulval carcinoma?

A
  1. Age >65years
  2. HPV infection
  3. Vulval intraepithelial neoplasia (VIN)
  4. Immunosuppression
  5. Lichen sclerosus
76
Q

What is the typical presentation of vulval carcinoma?

A

lump or ulcer on labia majora; may be associated with itching, irritation

77
Q

What is lichen sclerosus?

A

inflammatory condition which usually affects the genitalia and is more common in elderly females; leads to atrophy of epidermis with white plaques forming

78
Q

What is the key clinical feature of lichen sclerosus?

A

itch is prominent

79
Q

How is a diagnosis of lichen sclerosus usually made?

A

usually on clinical grounds, but biopsy may be performed if atypical features are present

80
Q

What is the management of lichen sclerosus?

A

topical steroids and emollients

81
Q

What are 4 situations when you should consider biopsy of lichen sclerosus?

A
  1. Suspicion of neoplastic change i.e. persistent area of hyperkeratosis, erosion or erythema, new warty or papular lesions
  2. Disease fails to respond to adequate treatent
  3. Extragenital lichen sclerosus, with features suggesting overlap with morphoea
  4. Pigmented areas in order to exclude abnormal melanocytic proliferation
82
Q

What are the 4 groups that benign ovarian cysts can be divided into?

A
  1. physiological cysts (follicular cysts and corpus luteum cyst)
  2. benign germ cell tumours (dermoid cyst)
  3. benign epithelial tumours (serous cystadenoma, mucinous cystadenoma)
  4. sex cord stromal tumours
83
Q

When should you perform a biopsy on an ovarian cyst?

A

if they are complex i.e. multi-loculated

84
Q

What is the commonest type of ovarian cyst?

A

follicular cysts

85
Q

What are 2 types of physiological ovarian cysts?

A
  1. follicular cysts
  2. corpus luteum cyst
86
Q

What causes a follicular cyst in the ovary?

A

due to non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle

87
Q

What is the usual prognosis for follicular cysts of the ovary?

A

commonly regress after several menstrual cycles

88
Q

What causes a corpus luteum cyst of the ovary?

A

during the menstrual cycle if pregnancy doesn’t occur the corpus luteum usually breaks down and disappears. if this doesn’t occur, the corpus luteum may fill with blood or fluid and form a corpus luteal cyst

89
Q

How are corpus luteum cysts likely to present?

A

more likely to present with intraperitoneal bleeding (than follicular cysts)

90
Q

What is the key type of benign germ cell tumour affecting the ovary to know about?

A

dermoid cyst

91
Q

What is another name for dermoid cysts and what are they?

A

also called mature cystic teratomas

usually lined with epithelial tissue and hence may contain skin appendages, hair and teeth

92
Q

What is the median age of diagnosis of dermoid cysts?

A

30 years old (most common benign ovarian tumour in woman under 30)

93
Q

How commonly are dermoid cysts bilateral?

A

10-20% of cases

94
Q

What is the usual presentation of dermoid cysts?

A

usually asymptomatic; torsion more likely than with other ovarian tumours

95
Q

What are the 2 key ypes of benign epithelial tumours of the ovary?

A
  1. Serous cystadenoma (first most common)
  2. Mucinous cystadenoma (second most common)
96
Q

What are benign epithelial tumours of the ovary?

A

arise from the ovarian surface epithelium

97
Q

What do serous cystadenomas of the ovary bear a resemblane to?

A

the most common type of ovarian cancer - serous carcinoma

98
Q

What proportion of serous cystadenomas of the ovary are bilateral?

A

20%

99
Q

What is the typical morphology of mucinous cystadenomas?

A

typically large, may become massive

100
Q

What is a possible complication of mucinous cystadenomas?

A

if rupture, may cause pseudomyxoma peritonei - presence of mucin in the peritoneal cavity (commonest cause is appendix cancer)

101
Q

How do the cysts of PCOS appear on ultrasound?

A

bulky ovaries with multiple small follicles, fibrotic capsule, smooth surface - ring of pearls sign on TVUSS

102
Q

What are sex cord-stromal tumours?

A

rare ovarian tumours composed of granulosa cells, theca cells, Sertoli cells, Leydig cells, and fibroblasts of stromal origin, singly or in various combinations

103
Q

What are 4 examples of sex cord stromal tumours of the ovary?

A
  1. Fibroma (commonest)
  2. Sertoli-Leydig cell tumour (produce androgens)
  3. Thecoma (produce oestrogens)
  4. Lipoma
104
Q

When would you consider non-conservative management of ovarian cysts?

A

if persists (most resolve spontaneously) or if >5cm

105
Q

What is the prognosis of ovarian cancer usually like and why?

A

poor prognosis due to late diagnosis

106
Q

What is the commonest type of ovarian cancer?

A

90% epithelial in origin, 70-80% od cases due to serous carcinomas

107
Q

What has now been recognised is often the site of what is considered an ‘ovarian’ cancer?

A

distal end of fallopian tube

108
Q

What are 4 risk factors for ovarian cancer?

A
  1. Family history: mutations of the BRCA1 or the BRCA2 gene
  2. Early menarche
  3. Late menopause
  4. Nulliparity (many ovulations)
109
Q

What are 5 clinical features of ovarian cancer?

A
  1. Abdominal distension and bloating
  2. Abdominal and pelvic pain
  3. Urinary symptoms e.g. urgency
  4. Early satiety
  5. Diarrhoea

notoriously vague

110
Q

What is the recommended investigation for suspected ovarian cancer?

A
  • CA-125
    • if raised (>35 IU/ml) then urgent USS of abdomen and pelvis
  • ultrasound
111
Q

What is the normal range for CA125?

A

<35 IU/mL

112
Q

When should you not use CA-125 measurement as screening for ovarian cancer?

A

in asymptomatic women

113
Q

What is the definitive diagnosis for ovarian cancer?

A

diagnostic laparotomy usually

114
Q

What does the management of ovarian cancer usually involve?

A

combination of surgery and platinum-based chemotherapy

115
Q

What is the prognosis of ovarian cancer?

A

80% of women have advanced disease at presentation; 5-year survival is 46% (across all stages)

116
Q

In which age group is vulval intraepithelial neoplasia (VIN) more common?

A

postmenopausal women, but may occur in any age group

117
Q

What has been the trend in VIN in recent years and why is this thought to be?

A

increased; probably reflects changes in sexual practice and increased recognition

118
Q

What proportion of VIN will progress to vulval cancer?

A

up to 9%

119
Q

What is VIN and what is thought to cause it?

A

dysplastic lesion of the squamous epithelium of vulva; as with CIN, associated with persistent infection with HPV in >90% of cases. smoking also associated with it

120
Q

What type of HPV is VIN particularly associated with?

A

HPV 16

121
Q

What symptoms may be associaed with VIN?

A
  • primarily itch, also pain and ulceration
  • over 20% may be asymptomatic
  • lesions may appear raised, hyperkeratotic, and warty or flat and erythematous
  • frequently found at multiple sites on the vulva (50%)
122
Q

How is a diagnosis of VIN made?

A

punch or excision biopsy

123
Q

What condition should also be investigated for if a diagnosis of VIN is made?

A

CIN - should have regular cervical smears as HPV can cause multifocal disease

124
Q

What are 3 aspects of management of vulval intra-epithelial neoplasia?

A
  1. Surveillance - careful follow up, biopsy suspicious lesions
  2. Surgery - excision of painful/rritating lesions can be performed
  3. Immunotherapy - imiquimod can be help with clearance of genital warts
125
Q

What is the mainstay of treatment for vulval cancer?

A

surgery both for curative intent and for palliation

126
Q

What is the cause of most vaginal cancer?

A

most are metastases from either above (cervical cancer or uterine) or below (vulval)

127
Q

What is the comonest true vaginal malignant tumour?

A

squamous cell carcinomas

128
Q

What are 5 predisposing factors for vaginal cancer?

A
  1. Previous hisory of intraepithelial neoplasia
  2. Invasive carcinoma of vulva, vagina, cervix
  3. Pelvic radiotherapy
  4. Long-term inflammation due to vaginal pessary or procidential
  5. Squamous cell carcinoma commonly HPV-related
129
Q

What is the key predisposing factor to the vaginal clear cell adenocarcinoma type of tumour?

A

DES (diethylstilbestrol) exposure in utero - DES was administered to milllions of pregnant women at risk of miscarriage or premature delivery between 1940 and 1971

daughters of these women at risk of this cancer

130
Q

What are the 3 things involved in the risk-malignancy index (RMI) for ovarian cancer?

A

CA-125, USS findings, menopausal status

131
Q

What is the purpose of the risk malignancy status for ovarian cancer?

A

predicts prognosis

132
Q

What are 3 things that can cause a raised CA-125 in addition to ovarian cancer?

A
  1. Endometriosis
  2. Menstruation
  3. Benign ovarian cysts

OBG: Oncology and neonatalology (14 decks)

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