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RANZCOG -Gynaecology 2024 Edward > Gynae oncology > Flashcards

Gynae oncology Flashcards

1
Q

Cervical Glandular Intraepithelial Neoplasia (adenocarcinoma):
-Incidence
-Risk factors
-Management

A

Incidence:
0.15% of all smears AIS.
15-20% of cervical invasive cancers
Ratio of CGIN to CIN 1:50
Risk factors:
Increased estrogen exposure, HPV 16 and 18 (50% HVP 18)
Management:
All CGIN need referral to colposcopy
Colposcopy:
1. Type 3 Cone Bx to 25mm +/- D&C.
2. If evidence of cancer GONC ref.
3. If clear margins = treatment completed. Cytology + HPV + colp in 6/12 and cytology + HPV in 12 months in primary care then if clear back to 5yrly.
4. If

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2
Q

Cervical Intraepithelial Neoplasia
-Incidence
-Pathophysiology
-Risk factors
-Natural History

A

Pathophysiology:
-Incidence: 80% of women will acquire HPV (Sexually transmitted)
-Oncogenic HPV (ds DNA virus) Viral oncogenes E6 and E7 are over expressed. Stops cell replication suppression
-Affects Transformation zone
-HPV 16&18 cause 70%. 31,33,35,39,45,51,56,58 main types
-80% will clear virus in 1-2 yrs. 10-20% have viral DNA integration into host genome.
Risk factors: Smoking, HIV, Immunosupression, Sexual activity, COC
Natural History:
-CIN 1 70-90% regresses within 2 yrs
-CIN 2 - 50% regresses within 2yrs - 5% progresses to cancer
-CIN 3 30% progression to cancer over 10yrs

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3
Q

What are the different smear results for cervical screening?

A

LSIL - low grade squamous intraepithelial lesion
ASC-US Abnormal squamous cells of undetermined significance
HSIL - high grade squamous intraepithelial lesion
ASC-H Abnormal squamous cells - cannot exclude high grade squamous lesion
AGC - atypical glandular cells
AIS - Adenocarinoma in situ
SCC Squamous cell carcinoma

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4
Q

Squamous columnar junction and transformation zone of the cervix
-Describe what it is
-Describe how it comes about
-Describe types of TZ

A

The endocervix is lined with glandular epithelium. The ectocervix is lined with squamous epithelium. The SCJ is where the 2 cells types meet. The original SCJ begins in the endocervix. It migrates to the ectocervix. Here the migrated columnar cells are converted to metaplastic squamous cells under the influence of vaginal acid and a new SJC between the columnar and metaplastic squamous cells is formed. The cells in between the two SJC becomes the TZ.

Type I - Can see all the TZ
Type 2 - TZ has endocervical component but can see
Type 3 - TZ has endocervical component which can’t see

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5
Q

What are the 10 principles of screening

A
  1. Is an important health problem
  2. There is an available treatment
  3. There are appropriate dx and treatment facilities
  4. There is a latent phase of the disease
  5. There is a test / examination for the disease
  6. The test should be acceptable to the population
  7. The natural Hx of the disease should be well understood
  8. There should be an agreed policy on who to treat
  9. The total cost of finding a case should be balanced with overall medical expenditure
  10. Case finding should be a continuous process
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6
Q

Describe the management of ASC-US or LSIL at colposcopy (3)

A
  1. Guidelines do not recommend treatment of CIN/LSIL
  2. Repeat an HPV at 12 months
    -If negative return to 5yrly screening
    -If HPV +ve do cytology. If cytology is negative or LSIL repeat HPV with LBC in 12/12
    -If HPV 16 or 18 detected then colp
    -If HPV other and HSIL then colp
  3. If HPV + and HSIL/ASC-H on cyto. But LSIL on histo offer diagnostic excision on TZ
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7
Q

Describe management of HSIL on histology

A
  1. Treatment of a histological dx of CIN2/3 is recommended
  2. Test of cure with HPV + LBC co test should be undertaken at 6months
    -If HPV and cyto negative repeat in 12 months.
    -If HPV+ repeat colp regardless of LBC findings
    -If HPV-ve but LBC = LSIL then repeat in 12 months
    -If HPV -ve but LBC = HSIL then colp
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8
Q

Describe cervical screening management in immunocompromised ppl (HIV / Organ transplant)

A
  1. Should undergo annual smears
  2. Refer to Colposcopy for all abnormalities
  3. Consider same management in ppl with immunsuppresent meds or bone marrow transplants
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9
Q

Describe cervical screening if had hysterectomy

A
  1. If subtotal - screening is as per ppl with Cervix
  2. If Total hysterectomy:
    -Normal screening in 5yrs prior - no vault smears
    -No screening in 5yrs prior - 1 x normal vault smear
    -Not returned to 3 yrly screening - 2 x vault smears 12 months apart
    -LSIL in hysterectomy specimen - 2 x vault smears
    -HSIL in hysterectomy specimen - 2 x vault smears + HPV at 6 months and 12 months then 3 yrly vault smears
  3. Hysterectomy for cervical cancer - 3yrly vault smears
  4. Immunocompromised - 3 yrl vault smears
  5. DES exposure - annual vault smears
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10
Q

Describe cervical screening in DES exposed ppl

A

Ppl exposed in utero have increased risk of clear cell adenocarinoma or vagina and cervix
1. Annual smears and colposcopic examination of cervix and vagina

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11
Q

How should endometrial cells on smear be managed

A
  1. If premenopausal and asymptomatic - no further assessment
  2. If post menopausal consider endometrial sampling
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12
Q

What is the age range for cervical screening in Australia and NZ

A
  1. Australia - 25-75yr every 5yrs
  2. NZ 20-69 every 3 yrs
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13
Q

What is the incidence of cervical cancer in pregnancy?

A

Invasive cancer - 1:10 000 (15/100 000)
70% of cervical cancer dx in pregnancy is stage 1
5% of pregnancy women develop abnormal cervical cytology
No evidence the natural hx of cervical cancer is altered by pregnancy

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14
Q

When should smears be done for pregnant women

A
  1. If up to date and normal smears then do 3 mnths postpartum
  2. Do smear in pregnancy if:
    -Never had smear
    -Overdue smear
    -Abnormal smear history and due for a smear
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15
Q

Describe differences seen in cytological specimens in pregnancy

A
  1. Difficult to interpret smears in pregnancy
  2. Hormonal changes cause:
    -Hyperplasia
    -Reactive atypia of squamous and glandular cells
    -Aris-Stella reaction with large multi nuclei cells
    -Cytotrophoblasts and Syncytiotrophoblasts can be seen
    -Increased number of inflammatory cells
    -Exaggerated squamous metaplasia
    -Increased vascular changes
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16
Q

Colposcopy in pregnant people
-When should it be done
-What should be done
-Who should do it

A

-Colposcopy should be done for the same indications as for non-pregnant women. It is safe
-Do a Bx ONLY if invasion is suspected on colposcopy.
-If High grade lesion repeat colp at 20-30/40 and then 6 weeks post partum
-Bx is more complicated - bigger Bx, increased bleeding, risk of pregnancy loss
- Colposcopy should be done by an expert colposcopist
-Pregnancy should be recorded on the lab form for pathologist

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17
Q

Describe timing of treatment of cervical cancer in pregnancy

A
  1. Only treat is invasive cancer is suspected at colposcopy
  2. HSIL progression in pregnancy is low
  3. If stage > 1A1 and <20 weeks treat without delay
  4. If stage 1A1-1B2 (contained in cervix) and >20 weeks can delay until fetal maturity
  5. If higher stage then 1B2 and > 20 weeks treat without delay
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18
Q

Describe management of cervical cancer in pregnancy.

A
  1. Stage with MRI/CXR +/- Pelvic LN dissection (No CT PET to look for + nodes)
  2. If Stage 1A1 - treat with cone Bx
  3. If Stage 1A2 - 1B1 - Large cone / simple trachelectomy
  4. If Stage 1B2 consider rad hyst after delivery
    -can do neoadjuvant chemo while awaiting maturity
  5. If > Stage II treat without delay with chemoradiation.
    -If viable deliver and treat
    -If non-viable terminate and treat
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19
Q

What is the mode of delivery for pregnant women with cervical cancer?

A

If CIN2/3 can do vaginal delivery
Always a CS if Stage >1B1 +/- hysterectomy
- increased risk of mets and haemorrhage with VB

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20
Q

Describe CIN1 characteristics on colposcopy

A
  1. Mosaicism of blood vessels - fine pattern. Looks like paving
  2. Fine looped capillaries
  3. Snow white to bright white acetowhite changes.
  4. Acetowhite changes slow to appear
  5. Acteowhite boarder irregular and throughout ectocervix
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21
Q

Describe CIN2 and 3 characeristics on colposcopy

A
  1. Coarse mosaic pattern of blood vessels
  2. Coarse punctation of blood vessels (blood vessels seen end on)
  3. Sharp boarder
  4. Rapid appearance of acetowhitening
  5. Cuffed crypts
  6. Boarders of lesion raised / prominent
  7. Location near new SJC
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22
Q

Describe the stains and how they work for colposcopy

A
  1. Acteowhite - applied first
    -Abnormal cells with increased protein levels change to white
  2. Iodine - applied second - optional
    -Abnormal cells don’t take up iodine due to low glycogen content
    -Colomnar cells don’t take up iodine
    -Good to further deliniate acetowhite changes
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23
Q

What are the treatment options for CIN

A
  1. Ablation
    -Cryotherapy, laser, cold coagulation, diathermy, thermal ablation
  2. LLETZ
  3. Cone Biopsy
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24
Q

What are the parameters which need to be met for ablation treatment of CIN (4)

A

-Satisfactory colp assessment
-Histology is confirmed
-No cancer or glandular lesion
-Whole lesion is visualised

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25
Q

Describe LLETZ procedure for CIN
-When done
-How done
-Success rates

A
  1. Done for CIN2/3
  2. Uses monopolar diathermy
  3. Depth depends on type of TZ
    -Aim depth 7-10mm
  4. Can do under LA
  5. Success rate 90-98%
  6. Increased failure in HIV 55% (Cone Bx better choice)
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26
Q

Describe cone biopsy for CIN
-when done
-success rates

A
  1. Done when upper limit of TZ not visualised
  2. Where lesion involves glandular changes
  3. Where early invasive cancer is suspected 1A1
  4. 90-94% effective
  5. Up to 32% failure to cure
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27
Q

What are the long term complications of CIN treatment

A
  1. PPROM, PTB, Low BW
    -Highest risk with CKC>Laser cone>LLETZ>Ablation
    -LLETZ >10mm
  2. Cervical stenosis
    -1% with laser
    -1-3% with cone bx
    -Impacts further colp assessments
    -Increases risk labour dystocia RR 3.17 for CS
    -Haematometra/pyometra/subfertility
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28
Q

What is the definition of a borderline ovarian tumour

A

Ovarian tumour which shows:
1. NO stromal invasion
2. Epithelial stratification
3. Cellular atypia
4. Increase mitotic activity
5. Nuclear pleomorphism

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29
Q

Describe the epidemiology of borderline ovarian tumours
-Types and incidence of these
-Demographics of women affected
-Stage at diagnosis
-Risk of progression to invasive cancer

A
  1. Serous - 45-60% (70%). Mucinous 30-50% (11%)
    -Also seromucinous, endometriod, clear cell and Brenners - 5-10%
  2. 15-20% of all epithelial ovarian neoplasms
  3. 33% in women <40yr
  4. Most diagnosed at stage 1 (75%)
  5. 2% risk of progression to low grade serous
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30
Q

What are the USS features of borderline ovarian tumours?

A
  1. Multiloculated (40% of mucinous 30% of serous)
  2. Solid cystic components (40% of mucinous, 78% of serous)
  3. Internal papillations (40% of mucinous, 78% of serous)
  4. Thickened septa
  5. Bilateral - 50% serous are bilateral
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31
Q

What tumour markers are useful in the dx of borderline ovarian tumours

A
  1. Ca125 is not useful
    -Elevated in 20-35% of stage 1 serous
    -Elevated in 15-20% of mucinous
    -Elevated in 80-90% of advanced serous tumours
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32
Q

Describe the management of borderline tumours

A

Management is with surgery:
1. If not for fertility - TAH + BSO + Washings + Omentectomy + peritoneal bx
2. If for fertility - USO or if bilateral tumours - cystectomy / bilateral partial oophorectomies + washings + omental bx
3. If mucinous tumour consider appendectomy
4. Can be done laparoscopically
5. If recurrence treat surgically
No evidence adjuvant therapy is useful unless invasive implants - overall response is low.
-Studies suggest CT doesn’t change time to recurrence
FU: No evidence to suggest any modality of use for FU
-Can consider 6 monthly USS.
-Do if micropapillary pattern seen or intraepithelial implants
-Recommended FU until complete radical surgery undertaken

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33
Q

What is the recurrence rates of borderline tumours following:
1. Cystectomy
2. USO
3. If have non fertility sparing surgery
4. If have fertility sparing surgery

A
  1. Cystectomy - 25%
  2. USO 15%
  3. NFS - 5% (BSO)
  4. FSS 10-20% (up to 40% in literature)
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34
Q

What are the survival rates for borderline ovarian tumours

A

Stage 1 - 99% at 5yrs
Stage 2 - 98% at 5 yrs
Stage 3 - 96% at 5 yrs
Stage 4 - 77% at 5 yrs

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35
Q

What are the factors that affect prognosis of borderline tumours?
1. Serous
2. Mucinous

A
  1. Serous
    -Management with cystectomy = increased risk of recurrence but survival unchanged
    -Micropapillary architecture
    - implants - 66% at 7yrs
    -Microinvasion
    -Grade not significant
  2. Mucinous
    -Extra ovarian tumours
    -Pseudomyxoma peritoneii
    -Implants
    -Invasive foci within tumour - Intraepithelial carcinoma
    -Grade
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36
Q

What are the features of Micropapillary serous tumours

A

-Present in 10-15% of serous borderline tumours
-Tumour contains cribiform and filiform formations
-Likely to have invasive implants
-Likely to be bilateral
-Has higher recurrent rates and mortality rates
-Can progress to low grade serous cancers
-Not often chemosensitive

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37
Q

Describe the staging for ovarian/fallopian/peritoneal cancers

A

Staging is the same for all ovarian/fallopian/peritoneal cancers
Staging is surgical
Stage 1: Confined to ovaries or fallopian tube
-1a - 1 ovary or tube
-1b - both ovaries or tubes
-1c - surgical spill (1c1) / pre-operative rupture (1c2) / + washings (1c3)
Stage 2: Both ovaries with pelvic extensions or peritoneal cancer
-2a - Extension and / or implants on uterus / tubes / ovaries
-2b - Extension to other pelvic intraperitoneal tissues
Stage 3: Spread outside of pelvis or to retroperitoneum LN
-3a - positive retroperitoneal LN
-3b - Macroscopic peritoneal involvement <2cm
-3c - Macroscopic peritoneal involvement >2cm
Stage 4: Distant mets excluding peritoneal mets
-4a - Pleural effusion with positive cyto
-4b - Distant extra abdominal mets including inguinal LN

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38
Q

Describe the epidemiology of epithelial ovarian carcinoma
-Incidence
-Most common age
-Risk factors and protective factors

A
  1. Most common type of malignant ovarian tumour - 90%
  2. Lifetime risk 1.4% (1:70) / ~2%
  3. Most common in women over 50yrs
    -At least 30% of ovarian masses in women >50 - malignant
  4. Risk factors: Older age, nulliparity, early menarche, late menopause, endometriosis, smoking, obesity
    -Genetics
    - BRAC 1 - 40% BRAC 2 - 20% HNPCC - 7% (25% of ovarian cancers)
    - 5% if one 1st degree, 7% if two 1st degree relatives
  5. Protective factors: COC - 50% reduction if >5yr use, pregnancy - 50% reduction if >3 children, lactation, Salpinectomy, hysterectomy
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39
Q

What are the five types of epithelial ovarian cancers

A
  1. High grade serous
  2. Low grade serous
  3. Endometriod carcinoma
  4. Clear cell carcinoma
  5. Mucinous Carcinoma
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40
Q

Describe high grade serous carcinoma
-Prevalence
-Peak age
-Prognosis
-Pathology

A
  1. Most common type of epithelial tumour. 70-80%
  2. Peak age 45-65yrs
  3. Most Dx at stage 3 or 4. Poor prognosis - 20% with +LN. Majority relapse
  4. Pathology:
    -up to 20cm, smooth or papillary projections, cystic or multiloculated.
    -Associated with BRAC 1/2
    -Cytology: marked cytological atypia with high mitotic rate. Comes from STIC lesions
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41
Q

Describe low grade serous epithelial tumour
-Prevalence
-Prognosis
-Pathology

A
  1. Uncommon - 5%
  2. Most Dx at advanced stage - poor prognosis. Slow growing and indolent. Insensitive to CT. Majority relapse
  3. Pathology:
    -Similar to HGSC. Less haemorrhage and necrosis.
    -May originate from fallopian tube
    Cytology - psamomma bodies. Uniform nuclear size and less mitotic activity
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42
Q

Describe endometriod ovarian carcinoma
-Prevalence
-Peak age
-Prognosis
-Pathology

A
  1. 10% of all EOC
  2. Common in 30-40yrs
  3. Earlier dx so better prognosis. Chemosensitive
  4. Pathology:
    -Associated with endometriosis
    -Associated with endometrial carcinoma - 15-20%
    -Associated with Lynch syndrome
    -Usually unilateral, solid or cystic, can have chocolate cyst components
    Cytology: Low grade
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43
Q

Describe Clear cell epithelial ovarian cancer
-Prevalence
-Peak age
-Prognosis
-Pathology

A
  1. 5-10% of all EOC
  2. Perimenopausal women
  3. Presents early (stage 1 or 2) - good prognosis. Not chemosensitive
  4. Pathology:
    -Associated with endometriosis, VTE and paraneoplastic hypercalcemia
    -Average size 15cm, thick walled, uniloculated, yellow fluid
    -Associated with Lynch syndrome
    Cytology: Hobnail appearance
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44
Q

Describe mucinous Carcinoma - epithelial ovarian
-Prevalence
-Peak age
-Prognosis
-Pathology

A
  1. 3-4% of EOC
  2. Perimenopausal age group
  3. Good prognosis - most dx at stage 1
  4. Pathology:
    -Mostly from GI tumour mets
    -Likely arise from borderline mucinous tumours
    -8-20cm, unilateral, solid/cystic, confined to ovary
    -Produce ca19-9
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45
Q

Describe mature cystic teratomas
-Prevalence
-Peak age
-Pathology
-Complications

A
  1. Most common benign tumour of women of reproductive age 20-30’s
    -Account for 95% of all teratomas
  2. Pathology:
    -Arises from germ cells - contains cells from all 3 layers
    -Bilateral in 10-15% of women
    -Fast growth
    -Malignant transformation in 0.2-2% - Increased if Age >50, size >10cm
  3. Torsion is common, if rupture can cause chemical peritonitis
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46
Q

Describe serous cystadenoma
-Prevalence
-Pathology

A
  1. Second most common benign ovarian neoplasm in reproductive age women
  2. Pathology
    -Thin walled, uni/multiloculated
    -12-23% bilateral
    -5-20cm in size
    Cytology: lined with epithelia simillar to fallopian tube
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47
Q

Describe mucinous cystadenomas
-Prevalence
-Pathology

A
  1. 3rd most common benign ovarian neoplasm in reproductive age women
    2.Pathology
    -More likely to be multiloculated cf serous
    -Bilateral 5% of cases
    -Grow larger than serous cystadenomas
    -Lined with mucin producing cells
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48
Q

Describe RMI
-Components
-Sensitivity and specificity

A

RMI = Risk of Malignancy index = Ca125 x M x U
1. Ca125 (less accurate in premenopausal women, can be neg in stage 1)
2. USS findings (U) - 1 point for each - multilocular cysts / solid areas/ bilateral lesions/ascites / mets
=1 if 1 point = 3 if 2-5 points
3. Menopausal state (premenopausal = 1, post menopausal = 3)
A score over 200 = malignancy
-Sensitivity 78%
-Specificity 87%

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49
Q

What is the role of screening for ovarian cancer

A
  1. No role for screening with ca125, USS or pelvic exam
    -Low sens and spec
    -High likelihood of false positives
    -No Survival benefit
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50
Q

What is the treatment for epithelial ovarian cancer

A
  1. Staging laparotomy with hysterectomy, BSO, omentectomy, pelvic and para aortic LN dissection, appendectomy if mucinous, washings.
  2. Chemotherapy
    -Type depends on stage.
    -Combination CT - platinum (carbplatin / cisplatin) and taxane based (Paclitaxel / docetaxel)
    Stage 1a/1b Grade 1-2 - no adjuvant CT
    Stage 1a/1b Grade 3, 1c or 2
    -Adjuvant platinum based CT 3-6 rounds
    Stage 3 and 4
    -Cytoreduction surgery and combination CT
    -Either first or as interval debulking
    -Platinum and taxane bases 6 rounds
    -+/- maintenance Bevacizumab (VEGF inhibitor. Adds 3-4months survival) or PARP inhibitors for those with BRCA
  3. If desiring fertility - USO + annual FU
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51
Q

How should epithelial ovarian cancer be followed up?

A

Follow-up every 3 months for 2 yrs then 6 months for 3 yrs then annually.
PET scan is the most useful for looking at recurrence of disease

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52
Q

How should recurrent epithelial ovarian cancer be managed

A

Most stage 3 and 4 will recur - average time 16 months.
Recurrence should be sx based no survival benefit with imaging or Ca125 monitoring
1. If recurrence less than 6 months = platinum resistant
-consider non-platinum CT
2. If recurrence more than 6 moths = platinum sensitive
-Consider more platinum CT + non-platinum CT
-Consider Bevacizumab
3. Consider secondary cytoreductive surgery
4. If BRCA consider PARP inhibitor

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53
Q

What is the prognosis of Epithelial ovarian cancer by stage
-5yrs survival %
-Prognostic factors

A

Prognostic factors: younger age, better ECOG, lower amount of initial disease, lower grade tumours
Stage 1 - 89%
Stage 2 - 71%
Stage 3 - 41%
Stage 4 - 20%

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54
Q

Describe ovarian germ cell tumours
1. Types
2. Epidemiology

A

Types:
1. Teratoma (Mature - benign, Immature - malignant)
2. Dysgerminomas
3. Yolk sac tumours
4. Mixed germ cell tumours
5. Embryonal Carcinoma
6. Choriocarcinoma
7. Polyembryoma
Epidemiology
-25% of all ovarian tumours
-5% of all malignant tumours
-Mostly in 15-30yr olds

55
Q

Describe Immature teratomas
-Prevalence
-Peak age
-Tumor markers

A
  1. <1% of ovarian teratomas. 35% of malignant germ cell tumours
  2. Most common in women <20yrs
  3. Tumour markers: AFP, LDH, E2
56
Q

Describe dysgerminomas
-Prevalence
-Peak age
-Tumour markers
-Pathology

A
  1. 2% of all ovarian neoplasms. 33% of all malignant germ cell tumours
  2. <20yrs but any age
  3. LDH, HCG, E2
  4. Grossly lobulated, firm, cream coloured.
    Cytology: Fried egg appearence
57
Q

Describe yolk sac tumours
-Prevalence
-Peak age
-Tumour markers
-Pathology

A
  1. 15-20% of malignant germ cell tumours
  2. Young women - 23 median age
  3. AFP and LDH
  4. Invaginated papillary bodies, Schiller duval bodies. Rapid growth and aggressive intraperitoneal dissemination
58
Q

Describe mixed germ cell tumours
-Prevalence
-Tumour markers
-Pathology

A
  1. 5% of malignant germ cell tumours
  2. HCG, AFP, LDH
  3. Consist of 2 or more types of germ cell - mostly dysgerminoma and yolk sac
59
Q

Describe Embryonal Carcinoma - Ovarian germ cell tumour
-Prevalence
-Peak age
-Tumour markers
-Pathology

A
  1. 4% of malignant germ cell tumours
  2. Common in young women (15yr median age)
  3. HCG AFP
  4. Very aggressive, multinucleated giant cells
60
Q

Describe choriocarcinoma of the ovary
-Prevalence
-Tumour markers
-Pathology

A
  1. 2% of malignant germ cell tumours
  2. HCG
  3. Very aggressive, can cause irregular uterine bleeding,
61
Q

Describe polyembryonal germ cell tumours
-Prevalence
-Tumour markers

A
  1. Very rare
  2. HCG AFP
  3. Very aggressive
62
Q

Describe the management of Ovarian germ cell tumours

A
  1. Surgery - dx with histology, staging, treatment
    -Omental bx, peritoneal cytology, limited cytoreduction
    -Can be fertility sparing
    -Cytoreductive surgery improves survival. LN dissection doesn’t
  2. Adjuvant CT unless:
    - Stage 1a
    -Stage 1-2 immature teratoma or dysgerminoma
    GCT are very sensitive to CT
    -Reduces risk of recurrence
63
Q

Describe sexcord stromal tumours of the ovary
-Types
-Epidemiology
-Pathology

A

Types:
1. Sexcord cells - sertoli, Granulosa
2. Stromal cells - Leydig, Fibromas, thecomas
3. Mixed - sertoli-Leydig
2. 4% 0f ovarian neoplasms. 8% of malignant neoplasms
Average age 50
4. Usually low grade, can produce estrogen so see endometrial hyperplasia

64
Q

Describe ovarian fibromas (SCST)
-Prevalence
-Tumour markers
-Pathology

A
  1. Most common SCST. 4% of ovarian neoplasms. Mostly in post menopausal women
  2. ca125
  3. Firm and white, Seen in Meigs syndrome, usually unilateral. Benign
65
Q

Describe ovarian thecomas (SCST)
-Epidemiology
-Pathology

A
  1. Mostly in post menopausal women
  2. Large >40cm, unilateral, benign
    Can produce estrogen ass with endometrial hyperplasia and carcinoma in 15-25%
66
Q

Describe granulosa cells tumours
-Prevalence
-Tumour markers
-Pathology

A
  1. Most common malignant SCST - 90%. Median age 50
  2. Inhibin, AMH, ca125
  3. Malignant, can produce estrogen - hyperplasia and carcinoma, virilization possible but rare.
    Histology: coffee bean nucleii, Exner bodies
67
Q

Describe Sertoli cell tumours (SCST)
-Prevalence
-Pathology

A
  1. Rare, seen in all ages but usually reproductive
  2. Unilateral and solid, virilization sx, can have estrogen sx. Can be benign or malignant. Most are benign
68
Q

Describe sertoli-Leydig cell tumours (SCST)
-Prevalence
-Tumour markers
-Pathology

A
  1. Rare. Peak age 20-30yrs.
  2. AFP, inhibin, ca125
  3. Virilization traits predominate. Can be benign or malignant. Most are benign
69
Q

Describe the management of ovarian SCST

A
  1. Surgery
    -Staging same as EOC
    -Doesn’t require LN dissection
    -Can do cystectomy if fertility sparing.
    -Consider hysterectomy in thecomas-Avoid spill. Increases stage
  2. Chemotherapy
    -Adjuvant CT with Stage 2 or more
    -Platinum based
70
Q

What are the mechanisms of ovarian cancer spread

A
  1. Transperitoneal/transcoelomic
    -to peritoneal surfaces on diaphram/bowel/omentum
  2. Lymphatic spread
    -utero-ovarian, infundibulopelvic and round ligament pathways
    -To external and internal illiac, common illiac lateral sacral and para-aortic nodes
  3. Haematogenous
    -to liver and lung
71
Q

Describe the stages of cervical cancer and management

A

Stage 1A- confined to the cervix <5mm
-Stage 1A1 - <3mm invasion - Cone/LLETZ / Simple Hyst
-Stage 1A2 - 3-5mm invasion - Cone / trachelectomy + PLND or Rad hyst + PLND
Stage 1B >5mm invasion
-Stage 1B1 - Invasion <2cm Rad hyst + PLND / Trachelectomy + PLND
-Stage 1B2 - Invasion 2-4cm Rad hyst + PLND or RT
-Stage 1B3 - Invasion >4cm CRT (Surgery possible/ not recommended)
Stage 2 - Tumour outside cervix but doesn’t involve pelvic sidewall or lower 1/3 of vagina
Stage 2A1 - Tumour upper 2/3rds vagina not parametirum - <4cm - CRT
Stage 2A2 - Tumour upper 2/3rd vagina. Not parametrium >4cm - CRT (Surgery possible/ not recommended)
Stage 2B - Parametrial involvement but not pelvic wall - CRT
Stage 3- Tumour extends to lower 1/3 vag or pelvic side wall or hydronephrosis or pelvic / para aortic LN (CONFINED TO PELVIS)
-Stage 3A - to lower 1/3 of vag - CRT + EBRT
-Stage 3B - to pelvic side wall +/- hydronephrosis
-Stage 3C1 - to pelvic LN - CCRT + ERBT
-Stage 3C2 - to para aortic LN - CCRT + ERBT
Stage 4 - Tumour extends beyond true pelvis or involves bladder/ rectal mucosa - CT +/- RT =?- Bevacizumba
-Stage 4A - spread to adjacent pelvic structures
-Stage 4B - spread to distant pelvic structures

72
Q

Describe the epidemiology of cervical cancer
-Incidence / prevalence
-Aetiology
-Risk factors

A
  1. 3rd most common gynae cancer, 4th most common cancer in women
    Incidence: 1:160 (1:90 in unscreened population)
  2. 99.7% due to HPV
    - Types16 and 18 = 70%
    - Types 31, 33, 35, 39, 45, 52 and 58 = 19%
    -Smoking and immune suppression modify HPV clearance
  3. Risk factors
    -Sexual activity - early onset, multiple partners, STI,
    -Social factors - smoking, Low SES, poor nutrition
    -Genetic predisposition
    -Gynae hx - COC, DES daughter, HIV, VAIN/VIN
73
Q

Describe the route of spread of cervical cancer

A
  1. Direct
    - caudally to vagina
    -Laterally to parametrium
    -Anteriorly to bladder
    -Posteriorly to bowel
  2. Lymphatic
    -External iliac - 43%
    -Obturator - 26%
    -Parametrial - 21%
    -Para aortic in late stages
  3. Haematogenous
    -Lung liver and bone
74
Q

Describe the investigations for staging cervical cancer

A

Staging of cervical cancer is clinical
1. EUA to assess extension into vagina / rectum / bladder and parametrial invasion
-Cystoscopy and sigmoidoscopy if Sx
2. Can do imaging if resources allow to aid in staging but not required
-MRI best for tumour size
-CT PET for Mets
-CXR and USS to assess chest and renal tract involvement in resource limited settings

75
Q

What is the 5yrs survival for cervical cancer by stage?

A

Carcinoma in-situ - 100%
Stage 1 - 85%
Stage 2 - 65%
Stage 3 - 35%
Stage 4 - 7%
Stage 4B - median time for survival - 7months

76
Q

What are the types of cervical cancer

A
  1. Squamous cell carcinoma - 70-80%
  2. Adenocarcinoma - 15-20%
  3. Others 6%
    -Melanomas
    -Sarcomas
    -Lymphomas
    -Small cell carcinoma
77
Q

Describe surgical treatment for cervical cancer
1. For each stage
2. If fertility desired
3. Associated risks

A

Stage 1A1 to 1B2 can undergo surgery with curative intent
Stage 1A1
- If fertility desired Cone / LLETZ. No PLND required
- Better outcome for fertility cf. trachelectomy.
- If fertility not desired simple hysterectomy
- Risk of recurrence, + margins, further management
Stage 1A2
- If fertility = Cone (1A2) / trachelectomy + PLND (if LVSI +)
- Risks - of trachelectomy = PTL, CS to deliver, dysmenorrhoea.
- Fertility not desired - Simple / Rad hyst + PLND / SLNB if low risk
Stage 1B1, 1B2, IIA1 (Surgery preferred)
-Rad hyst + PLND
-Can do trachelectomy+ PLND for 1a2-1b1
-Can do CRT Ib2 and IIa1 - similar outcomes
Stage >=1B3 - CRT
-Can do surgery for stage 1B3 and 2A1 but 80% need CRT as well. Prefer CRT

78
Q

Describe treatment for non-surgical cervical cancer by stage
-Type of treatment
-Duration

A

Stages 1A to 2A - Radiation if surgery contra-indicated. Same outcome for survival and local control
Stage 1B3 and 2A2
-EBRT + weekly cisplatin 5-6 weeks
-Followed by Vaginal Brachy
Stage 2B - 4A - If curative
-Weekly cisplatin + EBRT over 5-6 weeks
-Vaginal brachy
If palliative
-EBRT less grey

79
Q

When should adjuvant CRT be offered for post-op cervical cancer

A
  1. CRT if high risk
    -Positive margins, Positive LN, parametrial spread
  2. RT if intermediate risk
    -2 or more of the following: >4cm tumour size, LVSI, deep stromal invasion
  3. Low risk - no adjuvant treatment
80
Q

Describe the follow-up for cervical cancer patients

A
  1. 3 monthly for first 2 yrs
  2. 6 monthly for next 3 yrs
  3. Annually for life
81
Q

How should recurrence be managed in cervical cancer?
-prognosis
-Site of recurrence
-Incidence in first 3yrs
-Treatment

A
  1. If recurs in first 3yrs - poor prognosis
  2. Local recurrence most common then para aortic LN
  3. 75% recurrences occur in first 3 yrs
  4. If had surgery as primary treatment - CRT or pelvic exenteration if curative intent.
82
Q

Describe the stages of vaginal cancer and the corresponding treatment

A

General:
-Clinically staged - same as cervical cancer
-Imaging doesn’t impact staging
Stage 1: Tumour confined to vagina
-1A1 - <2cm
-1B - >2cm
Upper vagina - Rad hyst + vaginectomy + PLND
Lower vagina - WLE + LND
Stage 2: Tumour invades parametrium but not pelvic side walls - CRT: EBRT + Vaginal brachy+ Cisplatin
2a <2cm 2b > 2cm
Stage 3: Tumour extends to pelvic side wall or lower 1/3 or vag or blocks flow of urine - CRT: EBRT + Cisplatin
Stage 4: 4a Invades bladder or rectal mucosa or 4b extends beyond true pelvis - Palliatative - CRT

83
Q

Describe vaginal cancer
-Incidence
-Types
-Cause

A
  1. Rare. 1-2% of gynaecological cancers
    Only 10-20% are primary most are from cx or vulval spread
    Mean age 60yrs
  2. Types
    Primary 20%
    -Squamous cell carcinoma - 90%
    -Adenocarcinoma - 8-10%
    -Lymphoma, sarcoma, melanoma - rare
    Secondary mets 80%
  3. Most associated with HPV 16 & 18
84
Q

What is DES and what are the complications to mothers, daughters and sons? (RANZCOG Guideline)

A
  1. DES is a synthetic estrogen prescribed to improve pregnancy outcomes between 1940-1980. Didn’t work
  2. DES Mothers - Increased risk breast cancer - 1.27
  3. DES Daughter
    - Breast cancer RR 1.81
    -Clear cell adenocarcinoma of vagina and Cx - RR 40.0
    - Infertility - RR 2.4
    - HSIL and VAIN RR - 2.28
    -Still birth, early pregnancy loss PTD, ectopic pregnancy, -Structural cx 25-33% and uterine abnormalities 69%
  4. DES son - testicular abnormality but no increase in cancer of infertility
85
Q

What are the recommendations for management of DES exposed people?
1. DES Mothers
2. DES Daughters
3. DES Sons
4. 3rd gen exposed

A
  1. Reg health checks and breast screening
  2. Lifetime annual gynae checks. Reg breast screening
  3. Document testicular abnormalities
  4. Screening in accordance to nat screening programmes
86
Q

Describe ca125
-Marker in what cancer
-When to use
-What causes raised values

A
  1. Marker for epithelial ovarian cancer
    -50% raised in early EOC
    -80% raised in late EOC
  2. Use in complex cysts for premenopausal women
    Use in any ovarian cyst in post menopausal women
    Most reliable in post menopausal women
    -Sensitivity 70-90%, specificity 80-100% in post meno
  3. Also raised in:
    -Fibroids, endometriosis, infection, pregnancy, menstruation, endometrial cancer
    -Cirrhosis, pleuritis/pericarditis, ascities, breast/lung/pancreatic cancer
87
Q

What cancers are predominantly associated with:
1. CEA
2. Ca19-9
3. LDH
4. AFP
5. tHCG
6. Inhibin

A
  1. Colon cancer.
  2. Pancreatic cancer
  3. Dysgerminoma
  4. Yolk sac tumour
  5. Choriocarcinoma
  6. Granulosa cell tumour
88
Q

Describe uterine sarcomas
-Incidence
-Risk factors (2)
-Types (3)

A
  1. 1% of all genital tract malignancies. 3-7% of all uterine cancers
  2. Prolonged Tamoxifen, Radiation
  3. -Carcinomsarcoma’s - 50%
    -Leimyosarcoma - 30%
    -Endometrial stromal sarcoma - 15%
89
Q

Describe leiomyosarcomas
-Aetiology
-Age group
-Factors suggestive of leiomyosarcoma (5)
-Prognosis factors (3)
-Treatment

A
  1. Arise from leiomyoma 1-2:1000. Can be de novo
  2. Usually >40yrs
  3. Fast growing in post-menopausal women, >10cm, poor response to GnRH agonists, weight loss, pyrexia of unknown origin
  4. Staging - most important, tumour size, mitotic index
  5. -Surgical - TAH + debulking +/- oophorectomy
    -Adjuvant chemo if Stage 3 or more. Response rate 17-36%
90
Q

Describe endometrial stromal sarcoma - Low grade
-Peak age
-Risk factors (3)
-Prognosis at 5 yrs
-Treatment

A
  1. 40-55 yrs. Usually post menopausal
  2. Estrogen exposure, PCOS, tamoxifen
  3. Good if stage 1&2 90%. Stage 3 or more 50%
  4. TAH + BSO (Hormone responsive). No role for LN dissection
    -Consider hormone therapy
    -Adjuvant chemo
91
Q

Describe endometrial stromal sarcoma - High grade
-Peak age
-Presentation
-Treatment

A
  1. Mean age 50
  2. Usually seen in intracavity polypoid masses with necrosis
  3. TAH + BSO +/- Adjuvant CRT
92
Q

Describe endometrial stromal sarcoma - Undifferentiated
-Peak age
-Prognosis
-Treatment

A
  1. Mean age 60yrs
  2. Highly aggressive and late stage diagnosis (60%)
  3. TAH + BSO + Adjuvant RT
93
Q

Describe carcinosarcoma
-Peak age
-Histological appearance
-Prognosis
-Treatment

A

-Mean age 70 yrs
-Mixed malignant appearing epithelial and mesenchymal elements
-Highly aggressive. 5yrs survival 30%
-TAH + BSO + PLND + Adjuvant CRT

94
Q

Describe the staging for vulval cancer and corresponding treatment

A

Staging is surgical. Based on site, LN and Mets
Stage 1: Confined to vulva
-Stage 1A - <2cm size and <1mm depth - WLE + LND (Ipslateral if >2cm from midline or small tumour)
-Stage 1B - >2cm size or >1mm depth - WLE + LND (Ipslateral if >2cm from midline or small tumour)
Stage 2: Extension to lower 1/3 of adjacent structures - vagina, urethra, anus. LN -ve (Don’t need RT)
Stage 3: + inguinofemoral nodes +/-extension to upper part of adjacent structures
Stage 3A - 1 or 2 nodes <5mm or upper 2/3rd involvement
Stage 3B - 2 or 3 nodes >5mm
Stage 3C - Extracapsular spread
Stage 4 - distant mets or pelvic bone involement or ulcerated LN
Stage 4A - Pelvic bones or ulcerated LN
Stage 4B - distant Mets

95
Q

Describe vulval cancer
-Incidence
-Types (7)
-Modes of spread
-Risk factors

A
  1. Rare.4% of all gynaecological malignancies
  2. -SCC - 80% (75-90%)
    -Keratinizing SCC (dVIN related - older women)
    -Warty basaloid SCC (HPV related 16,18,31,33 - younger women)
    -Melanomas - 5%
    -BBC
    -Pagets disease of the vulva -Adenocarinoma
    -Batholin gland carcinoma
    -Verrucous carcinoma
  3. Direct spread, Lymphatics - superficial and deep inguinal LN to internal and external iliacs. Haematogenous spread rare
  4. HIV, HPV, Smoking, VIN, Vulval dermatoses, age, Cervical cancer
96
Q

What are the investigations for vulval cancer

A
  1. Colposcopy - check cervix and vagina
  2. Biopsy
  3. CXR
  4. CT or pelvic MRI to assess LN. Can do FNA or CT PET for LN also
97
Q

Describe endometrial hyperplasia without atypia
-Histological findings (4)
-Risk of progression
-Management

A
  1. Histology
    -Irregular proliferation of endomtrial glands with cystic dilation and luminal out pouching
    -Increased gland to stroma ratio>50%
    -Increased mitotic activity
    -NO increased nuclear atypia
  2. Risk of progression
    -Concurrence with endometrial carcinoma <1%
    -Progression to invasive carcinoma - <5% in 20 yrs.
    -RR 1.01
    -Spontaneous regression 70-80%
  3. Management
    -Address reversible risk factors - HRT, wt, DM
    -Can observe if: No AUB, reversible risk factors
    -Progesterone therapy - increases regression to 90%
    First line - Mirena
    Second line Continuous PO Progesterone at least 6mnths (low dose 10-20mg PO OD)
    -Low risk 2 x negative bx every 6 months then DC
    -High risk 2 x neg Bx every 6 months then annual surveillance
    -Consider surgical (TH + /- BSO management if:
    -Persistence of EH following 12/12 treatment
    -Progression to atypia
    -Ongoing AUB
    -Declines surveillance
    -If recurrence
98
Q

Describe Endometrial hyperplasia with atypia
-Histology
-Progression
-Management - with / without fertility sparing

A
  1. Histology (4)
    -Diffuse proliferation of endometrial glands
    -Increased gland to stroma ratio >50%
    -Nuclear atypia - enlarged, chromatin clumping, hyperchromisia
    -Increased mitotic activity
  2. Risk of progression
    - 25-60% of concurrent endometrial carcinoma
    -30% risk of progression over 20yrs
    -RR 14-45
    -4% concurrent ovarian cancer
  3. Management if not for fertility
    -Maximise reversible risk factors
    -Review histology at MDM
    -Offer TH +/- BSO (Laparoscopic approach best)
    -BSO if post menopausal
  4. Management if for fertility
    -Rule out co-existent cancer - TVUSS/ca125/MRI/ Hysteroscopy D&C
    -Counsel about risks
    -Review Histology at MDM
    -Progesterone management - Mirena first line, PO second line (High dose 100mg - 600mg OD)
    -Manage reversible risk factors
    -FU with 2 x neg Bx at 3 months and 6 months
    -Recommend disease regression on at least 1 bx before seeking pregnancy
    -Refer to fertility
    -Continue 6-12 monthly bx until hysterectomy
    -Offer hysterectomy when family complete
    -Offer hysterectomy if adenocarcinoma or persistence
99
Q

What are the risk factors for endometrial hyperplasia

A

Menstrual factors: Early menarche, late menopause, nulliparity, PCOS
Iatrogenic factors: Tamoxifen RR 2, HRT RR 2-10
Comorbidities: DM (RR2) Obesity (RR 1.5-7)
Genetic factors: Lynch (20-50% lifetime risk) Cowden syndrome (13-19%)
Other: Oestrogen secreting tumour

100
Q

What are the protective factors against endometrial hyperplasia (4)

A
  1. COC
  2. LNG IUS
  3. Physical activity
  4. Smoking
101
Q

When should endometrial hyperplasia be assessed for (6)

A
  1. PMB
  2. AUB >45yrs
  3. AUB <45 with risk factors
  4. Premenopausal with oligo
  5. Endometrial cells on smear if post menopausal
  6. Screening high risk women - lynch syndrome
102
Q

Describe the normal ET in relation to endometrial cancer
-Probability of endometrial cancer if ET 3-4mm
-Cut off for ET in PMB
-Normal ET in premenopausal women
-proliferative stage
-Secretory phase

A
  1. <1%
  2. > 4mm
  3. 4-8mm
  4. 8-14mm
103
Q

What is the sensitivity of a pipelle for endometrial hyperplasia

A

90%

104
Q

Compare LNG-IUS with PO Progesterone for management of endometrial hyperplasia (7)

A
  1. LNG- IUS = faster time to regression
  2. LNG-IUS = better adherence
  3. LNG-IUS less recurrence
  4. High dose noriethsterone contraindications same as COC
  5. LNG-IUS achieves higher dose of progesterone at endometrium
  6. LNG-IUS = less likely to require hysterectomy at FU
  7. LNG-IUS = also contraception
105
Q

Comment of tamoxifen in regards to endometrial hyperplasia
-Effects on endometrium
-Risk of developing endometrial cancer in PM women
-Cumulative risk of endometrial cancer at:
-5yrs
-5-14yrs
-Management (5 points)

A
  1. Benign cystic hyperplasia, polyps, atypical hyperplasia, endometrial cancer
  2. 4.01. Risk of developing atypical lesions at 2 yrs.
  3. 1.6 and 3.1%
  4. Management
    -Unclear if LNG-IUS should be placed for prevention - not recommended
    -Advise women to report AUB
    -Don’t investigate aSx women
    -If atypical hyperplasia d/w oncologist about changing meds
    -If incidental aSx polyp noted on TVUSS treat as if symptomatic
106
Q

Describe the staging for endometrial cancer

A

Staging is surgical
Stage 1: confined to the uterus
-1a1 - non aggressive (endometrial carcinoma grade 1&2 all others aggressive) histo confined to the endometrium / polyp
-1a2 - non aggressive histo <50% myometrium. No LVSI
-1a3 - Low grade endometrial carcinomas limited to uterus or ovary
Stage 1B - >50% myometrial invasion, non aggressive, no LVSI
Stage 2: Confined to uterus and cervix
-2a invasion of cervical stroma - non aggressive type
-2b substantial LVSI of non aggressive histo type
-2c aggressive histo types with any myometrial involvement
Stage 3: Local spread
Stage 3A: to uterine serosa or adnexa
Stage 3B: to vagina / parametrium / pelvic peritoneum
Stage 3C: To PLN or paraaortic LN
Stage 4: Distant disease
Stage 4A: Invasion of bladder or bowel mucosa
Stage 4B: Abdominal peritoneal mets beyond the pelvis
Stage4C: Distant mets

107
Q

Describe endometrial cancer:
1. Incidence
2. Most common stage at presentation
3. Average age
4. Risk factors (5 groups)
5. Protective factors
6. Prognostic factors

A

1: 6th most common cancer overall. Most common gynae malignancy in high income countries
-Life time risk 3%
2: Stage 1A (75%). 10% of women with PMB
3. 60-65yrs
4. Same as Endometrial hyperplasia
-Unopposed estrogen
-Mestural factors
-Anovulation causes
-Famillial syndromes
-Tamoxifen RR 2-3
5. COC, Progesterone, smoking, physical activity, multiparity
6. Prognostic factors
-LVSI
-Molecular typing
-Grade/stage
-Aggressive histological cell types

108
Q

How does endometrial cancer spread?

A
  1. Direct:
  2. Lymphatic
    -PLN - internal and external iliacs, obturators
    -Inguinal and para aortic (rare)
  3. Haematological
  4. Most common to vagina, ovaries, lungs
109
Q

What are the investigations for endometrial cancer

A
  1. TVUSS to assess endometrial thickness
    -<4mm risk of cancer 0.5%
    ->10mm risk of malignancy 10-20%
  2. Endometrial Bx
    -Pipelle false neg 10-15%
    -Curettage - much lower false negative
  3. Grade 1&2 = MRI + CXR
  4. Grade 3 or more CT CAP
110
Q

What is the treatment for endometrial cancer?
-Stage 1a
-Stage 1b
-Stage 2
-Stage 3

A
  1. TH + BSO - no need PLND as only 5% risk of +LN
    -Laparoscopic if Stage 1 is gold standard
  2. TH + BSO + PLND (PLND guides adjuvant therapy doesn’t increase survival just by doing)
    -high risk disease
    -Radiological + nodes
    -SNB (sens 96%) suggests + nodes in frozen section
  3. Adjuvant radiotherapy
    -Reduces local recurrence but not survival
    Intermediate/Intermediate/high risk - VBT / EBRT if no nodal staging
    -High risk: EBRT
    -Stage III: CRT
  4. Adjuvant CT or neoadjuvant CT - carboplatin and paciltaxel
    -If stage III and 4
  5. Consider RT for palliative Sx control
  6. Women who cannot undergo surgery should have Uterine brachy +/- EBRT
111
Q

Discuss conservative (non-operative) management of Endometrial cancer
-Who should be considered
-What are the cancer characteristics
-What is the management
-What is the response rate

A
  1. Fertility preservation, non operative candidates
  2. Cancer characteristics
    -Grade 1
    -Minimal myometrial invasion
    -Hormone receptor positive ER/PR
  3. LNG IUS or PO provera
  4. Response rate 50-95%. Recurrence rate 66%
112
Q

Discuss follow-up and recurrence in endometrial cancer
-What are the rates of recurrence
-How should recurrence be managed
-Does FU impact outcome

A
  1. Rates:
    -Increased rate of recurrence cf other cancers
    -75% of recurrence symptomatic
    -85% of recurrence in first 2 yrs
    -40% of recurrence is local.
  2. Management of recurrence
    -If vaginal - brachy
    -If pelvic - EBRT
    -If advance CT
  3. No evidence that routine FU improves survival cf investigating those with sx only. If no RT then consider yrly spec to assess vaginal recurrence
113
Q

Discuss Lynch syndrome
-Cause
-Life time risk of endometrial, ovarian and colorectal cancer
-Management
-Criteria

A
  1. Cause
    -DNA mismatch repair genes
    -Inherited in autosomal dominant fashion
    -Also called HNPCC
    -2 hit theory with gene mutations causing errors of cell regulation and DNA repair
  2. Epidemiology
    -Responsible for 3-6% of endometrial cancers
    -Life time risk of endometrial cancer = 40-60%
    -Life time risk of ovarian cancer 10-12%
    -Life time risk of colorectal cancer - 10-37%
  3. Management
  4. Genetic counselling and screening if meeting Amsterdam criteria
  5. Hysterectomy post child bearing years - at 40 or 50
  6. Offer COC or progesterone for endometrial protection in young women
  7. Consider BSO at time of hysterectomy for selected patient. Given HRT if BSO
  8. No need for surveillance from ovarian cancer perspective
  9. Colonoscopy every 1-2 yrs for colorectal surveillance
  10. No evidence to support Bx or TVUSS for endometrial cancer surveillance but many guidelines suggest from age 30-35yrs
  11. Criteria
    Based on Amsterdam criteria
    -3 members affected with colorectal / uterine / renal / small bowel ca
    -Seen in 2 consecutive generations
    -1 has to be in someone under 50 when had cancer
114
Q

Discuss BRCA1&2
-Cause
-Lifetime risk of ovarian and breast cancer
-Management

A
  1. Cause
    -BRCA1&2 are tumour suppressor genes. Mutations in these genes means deregulation of tumour supressing actions
    -Inherited in autosomal dominant fashion
    -BRCA1 chromosome 17, BRCA2 Chromosome 13
  2. Epidemiology
    -Makes up 10-15% of ovarian cancers
    -Lifetime risk for BRCA1Ovarian = 40%, Breast = 60%
    -Lifetime risk for BRCA2 Ovarian = 20%, Breast = 40%
  3. Management
    -Genetic screening and counselling for those who meet criteria
    -Breast:
    - bilateral mastectomy <40yrs
    - Screening from age 30 with MRI +/- USS +/- MMG annually (modality depends on age)
    -Ovarian:
    -Counsel on risks - surgical menopause
    -Offer COC continuous until BSO
    -RRSO from age 40 BRCA1 or when family complete. From 50 if
    BRCA 2
    -Do omental Bx and washing too. Do laparoscopically
    -Reduces risk of ovarian cancer by 96% and breast cancer
    by 50%
    -Offer HRT till 50. No increased risk in breast cancer if no
    personal Hx.
    -Avoid if E sensitive endometrial cancer or personal Hx of breast cancer
    -No role for USS or ca125 for surveillance
115
Q

Name three rare familial syndromes associated with gynae cancers

A
  1. Cowden syndrome
    -Autosomal dominant
    -Lifetime risk 30%
  2. Peutz-Jeghers Syndrome
    - Autosomal dominant
    -Increases ovarian and cervical cancer
  3. Li Fraumeni Syndrome
    -Increased risk ovarian cancer
116
Q

Discuss gestational trophoblastic disease / GTN
-Definition
-Types
-Epidemiology

A
  1. Definition:
    -Tumours of placental tissue origin
    -Can be benign (partial and complete mole)
    -Can be malignant
    -GTN = GTD requiring chemotherapy or excisional treatment because of persistently HCG or mets
  2. Types
    -Benign - partial mole, complete mole
    -Gestational trophoblastic neoplasms
    -Invasive mole
    -Choriocarcinoma
    -Placental site trophoblastic tumour
    - Epitheiloid trophoblastic tumour
  3. Epidemiology
    -Incidence of GTD - 1:200-1:1000
    -Higher in Asian women
    -Higher at extremes of reproductive age
    -GTN develops from:
  4. Hydatiform mole 60%
  5. Miscarriage / termination 30%
  6. Normal birth or ectopic 10%
    -Risk of repeat molar 1:70
117
Q

Describe hydatiform moles
-Types
-Genetics
-Chance of persitence requiring chemotherapy

A
  1. Partial mole. Triploidy with egg being fertilised by >1 sperm. Malignant transformation 0.5-4%
  2. Complete mole. No genetic material from mother.
    -1 sperm fertilise then replicate 75%
    -2 sperm fertilise 25%
    Malignant transformation 15-25%
118
Q

When should GTD be managed as GTN? (4)

A
  1. Rise of HCG >10% over 2 weeks
  2. Plateau or <10% drop in HCG over 3 weeks
  3. HCG still + at 6 months
  4. HCG >20,000 at 4 weeks
119
Q

How should gestational trophoblastic neoplasm be managed?
-Baseline assessment
-Chemo types
-FU advise

A
  1. Refer to MDT - med onc and GONC
  2. Baseline tHCG, FBC, LTF, TFT, Coags, Rh status.
  3. Baseline CXR, Pelvic USS, CT CAP/MRI brain if brain mets suspected.
  4. Assess risk with FIGO/WHO risk assessment score to determine type of chemotherapy
    -<7 = low risk
    - Methotrexate and folonic acid
    - Continue until HCG normal then further 3 cycles
    ->=7 = high risk - Methotrexate, Etopioside, Actinomycin
  5. Offer hysterectomy if confined to uterus
    -Only management for PSTT and ETT as chemo resistant
    -May still need chemo (50% reduction)
  6. Avoid pregnancy for 1 yr following chemotherapy
    -All forms contraception ok. Avoid IUD for 6/12
  7. Alert GP and woman that risk of mole in next pregnancy 1:70 needs early HCG, early imaging and HCG 6/52 PP
  8. FU with monthly HCG:
    -If low risk for 12/12
    -If high risk for 2 yrs
    - If PSTT or ETT for 5 yrs
120
Q

What is the prognosis for GTN following chemotherapy

A
  1. Low risk = 100% cure rate
  2. High risk = 85% cure rate
121
Q

Describe gestational choriocarcinoma

A
  1. Origin:
    -25-50% from complete mole
    -25-50% from normal term pregnancy
    -25% non-molar miscarriage
  2. Tumour crosses placenta so new born needs urinary HCG
122
Q

Describe placental site trophoblastic tumour

A

-Very rare
-May present may yrs following molar or non-molar pregnancy
-Can present with nephrotic syndrome or hyperprolactinemia
-Usually confined to uterus
-Manage with hysterectomy
-Chemotherapy resistant

123
Q

Describe Epithelioid Trophoblastic tumour

A

-Most often follows normal pregnancy
-HCG levels are lower
-Less aggressive that choriocarcinoma
-Manage with hysterectomy as chemotherapy resistant

124
Q

When should cervical smears be done post hysterectomy (5)

A
  1. Sub total hysterectomy for benign reason
  2. Total hyst for benign reasons with no cervical screening in the preceding 5yrs
  3. People not on the 3yrsly cycle need 2 x neg vault smears 12 months apart
  4. Total hyst with LSIL in the histology - 2 x neg vault smears 2 months apart
  5. People with previous HSIL who have not achieved a test of cure. Annual testing until test of cure then 3 yrly
125
Q

Discuss the PLCO trial (Effect of screening on Ovarian cancer mortality
-Aim (1)
-Study type (3)
-Primary outcomes (1)
-Secondary outcomes (2)

A
  1. Aim
    -To evaluate the effect of screening for ovarian cancer on mortality
  2. Study type
    -RCT screening yrly Ca125 6yrs and TVUSS 4yrs vs usual care. Not blinded
    -Women aged 55-74 in USA from general pop
    -FU for 13 yrs
  3. Primary outcome
    -Mortality from ovarian cancer
  4. Secondary outcomes
    -Ovarian cancer incidence
    -Complications from screening
126
Q

Discuss the PLCO trial (Effect of screening on Ovarian cancer mortality
-Number in study
-Outcomes

A
  1. Number in study
    -78 000 randomised appro 39 000 / arm
  2. Outcomes
    -No difference in rate of diagnosis of ovarian cancer between groups 6% vs 5%
    -No difference in deaths from Ovarian cancer in each group
    -15% serious complication rate in women with false positive results from screening
    -No difference in stage at diagnosis between groups
127
Q

Discuss TLH vs TAH for disease free survival in Endometrial cancer stage I (LACE trial)
-Aim (1)
-Study design (3)
-Primary outcomes (1)
-Secondary outcomes (4)

A
  1. Aim
    -To determine whether TLH is equivalent to TAH for treatment of women with endometrial cancer
  2. Study design
    -Multinational RCT. unblinded
    -Randomised women with stage 1 endometrial cancer to TAH vs TLH
    -FU 4.5 yrs
  3. Primary outcomes
    -Disease free survival
  4. Secondary outcomes
    -Disease recurrence
    -Overall survival
    -QoL
    -Morbidity
128
Q

Discuss TLH vs TAH for disease free survival in Endometrial cancer stage I (LACE trial)
-Number included in the trial (2)
-Results (4)

A
  1. Numbers included in the trial
    n = 750 (350 TAH; 400 TLH)
  2. Outcomes
    -Disease free survival favoured TLH 81.3 vs 81.6%. Supports equivalence
    -No difference in recurrence between groups
    -No difference in overall survival
    -Improved QoL in the TLH group
129
Q

Discuss treatment of Vulval cancer
-Early cancers
-Advanced cancers
-Surgery is contra-indicated

A
  1. Early cancers - confined to vulvar
    -WLE + LND
    -If <4cm and >2cm from midline can do ipsilateral nodes
    -If <2cm from midline, >4cm, + ipsilateral nodes = do bilateral nodes
    -Can consider SNB on specific patients
    -EBRT if extracapsular spread or 2+ positive LN
  2. Advanced cancers - extend beyond vulvar or bulky + LN
    -WLE + LND / Pelvic excenoration
    -If LN -ve don’t need RT
    -If LN +ve then RT +/- CT
    -If ulcerated LN then RT +/- resection
  3. Surgery is contra-indicated
    -CRT
130
Q

Discuss molecular grouping in endometrial cancer (7)

A
  1. New way of looking at endometrial cancers instead of morphological factors
  2. Looks at molecular profiling
  3. 4 groups based on molecular profiling (POLE, p53abN, MMRd, NSMP)
  4. Correlates well with prognosis
  5. Better interobserver reliability cf with morphological classification
  6. Most useful for looking at prognosis of grade 3 endometrial cancers (endometrial carcinoma grade 3 and all other cell type cancers)
  7. POLEmut - best prognosis, p53abN, NSMP in ER -ve = bad prognosis. MMRd and NSMP = intermediate prognosis
131
Q

Discuss the HPV screening pathway

A
  1. HPV taken from 25-69yrs for HR HPV
  2. If HPV 16 or 18 detected then reflexive cytology and colp
  3. If HPV other detected then reflexive cytology if HSIL then colp if neg or LSIL then repeat in 1 yr. If persistent HPV other but LSIL or less then repeat in another yr unless >50 in which case refer to colp
  4. If HPV negative then repeat in 5yrs or 3 yrs if immunocompromised
    5.
132
Q

What are the screening requirements for cervical screening.
-Age range
-When to do (2)
-Requirements before existing the program (2)

A
  1. Age range: 25-69
  2. When to do
    -HPV every 5 yrs
    -HPV every 3 yrs if immunocompromised
  3. Requirements before existing
    -HPV is negative
    -If 70-74 without good screening before age 70 should have HPV negative before leaving screening.
133
Q

Compare HPV to cytology in terms of sensitivity and specificity (2)

A
  1. HPV has a greater sensitivity for CIN2
  2. LBC has a greater specificity for CIN 2
    -HPV therefore is the first test and cytology is a second step test

RANZCOG -Gynaecology 2024 Edward (11 decks)

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