Endometrial Cancer Flashcards
Stage I (A & B)
Tumor confined to the corpus utero
A:No or less than half myometrial invasion
B:invasion equal to or more than half of the myometrium
Stage II
Tumor invades cervical stroma but does not extend beyond the uterus
Endocervical glandular involvement is stage I
Stage 3 (I, II, III)
Local and/or regional spread of tumor
A:tumor invades the series and/or adnexae
B: vaginal and//or parametrial involvement
C: Mets to pelvic or parasitic lymph node
C1 positive pelvic nodes
C2 positive para-aortic lymph nodes with or withiout positive pelvic node
Stage 4 (A &B)
Tumor invades bladder and/or bowel mucosa and/or distant Mets
A: bladder and or bowel invasion
B: distant Mets, including intra-abdominal metastasis and/or inguinal lymph nodes
Pathophysiology of endometrial hyperplasia
Unopposed oestrogen stimulates endometrial cell growth by binding to estrogen receptors in the nuclei of endometrial cells
Risk factors for endometrial hyperplasia
BMI
Anovulation
Estrogen-secreting ovarian Rumours (granulosa cell tumours
Drug-induced endometrial stimulation (tamoxifen)
?immunosuppression
2 groups of endometrial hyperplasia
- Hyperplasia without atypia
2. Atypical hyperplasia
Risk of EH w/o atypia progressing to endo Ca
5% over 20 years
Majority will regress spontaneously during follow up
Treatment with progestogens has a higher disease regression rate
Progestogen treatment indications in EH w/o atypia
Women who fail to regrew following observation alone
Symptomatic women with AUB
First line medical treatment of EH without atypia
Continuous oral (10mg daily) or mirena (Mirena preferred) for 6 months
Follow up after treatment of EH
Endometrial biopsy after 6 months
6 monthly intervals
Need two negative samples before can discharge
If obese, still should have yearly biopsy after two negative 6 monthly
Mirena usually left in situ
Oral progestogens only used for 6 months
If EH persists for 12 months despite treatment, what to do
Chance of disease regression low
Therefore, proceed to hysterectomy as cancer risk higher
When is surgical mama garment appropriate for women with endometrial hyperplasia?
- progression to atypical hyperplasia occurs during f/u
- no histological regression of hyperplasia despite 12 months of treatment
- there is relapse of EH after completing progestogen tx
- there is persistence of bleeding symptoms
- woman declines to undergo surveillance or comply with medical treatment
When to take ovaries in EH without atypia
Postmenopausal women
What should the initial management of atypical hyperplasia be?
Total hysterectomy
With BSO if post menopausal
How should women with atypical hyperplasia who wish to preserve their fertility or who are not suitable for surgery be managed?
- counsel around underlying risk of malignancy
- investigations should aim to rule out invasive EC or co-existing ovarian cancer
- MDM review
- Mirena 1st line, oral progestogens second
- once fertility no longer required, offer hysterectomy again in view of high risk of disease relapse
How should women with atypical hyperplasia not undergoing hysterectomy be followed up?
3 monthly pipelles until two negative
Then every 6-12 months until hysterectomy
How should endometrial hyperplasia be managed in women wishing to conceive?
Disease regression on one sample prior to trying
Refer to fertility specialist
ART to be considered as birth rate higher and may prevent relapse compared to natural conception
Prior to ART, should have regression of EH as associated with higher preg rates
HRT and EH
- need progestogen component if have uterus
- report any vaginal bleeding
- if have EH and taking HRT, need mirena or progestogen
What is the risk of deveoping EH on adjuvant treatment for breast cancer
Increased risk with tamoxifen Aromatase inhibitors (anastrazole, exemestane and letrozole) not known to increase risk
Incidence of endometrial hyperplasia
28:100000
Peak age of endometrial ca incidence
60-79
Risk factors for endometrial ca
Older age Late menopause (over age 52) Nulliparity Obesity Oestrogen only HRT PCOS DIabetes Insufficient physical activity Family hx lynch syndrome
Protective factors against endometrial ca
Cigarette smoking
COC
Coffee intake
Exercise
Percentage of endometrial ca that is preventable
34%
Percentage of women with PMB that have cancer
10%
Percentage of polyps associated with endometrial hyperplasia
10%
Simple hyperplasia histo
Cystic and branching patterns
Complex hyperplasia
Crowded or closely opposed glands
Atypical histo
Nuclear atypia and hyperplasia
Type I endometrial cancers
Endometriod
Typically low grade
Good prognosis
Oestrogen-driven pathway
Type II endometrial cancers
Typically serous
May also be clear cell, mucinous, squamous, and sarcoma
Not oestrogen driven
Precursor lesion:serous endometrial intraepithelial carcinoma (p53 mutation)
Prognostic factors for endometrial cancer
Cell type Grade Degree of myometrial invasion Lymphovascular space invasion Positive peritoneal washings Age of patient DNA aneuploidy Mets
When can use RT in endometrial ca
Adjuvant RT to treat pelvic nodes and vault
Stage 2 w/ cervical involvement
Stage 3 disease or higher
Palliative RT for stage IV
Palliative RT for recurrence (local)
Primary curative tx in those unfit for surg
Risk of nodal disease in Stage II disease
14-10%
With recurrence, risk of mortality, local recurrence and distant recurrence
33% mort w/in 5 years
50% local
29% distant
Types of uterine sarcomas
Carcinosarcomas
Leiomyosaromas
Endometrial stromal sarcomas
Percentage of concomitant carcinoma in patients undergoing hysterectomy
22-43%
Percentage of EH withOUT atypia that spontaneously resolve
80%
Regression rates of EH with atypia and mirena
Up to 86% (meta-analysis)
False negative rate of pipeline
10-15%
Recurrence timeframe
75% w/in 1 year
85% wi/in 2 years