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RANZCOG Written Exam > GONC > Flashcards

GONC Flashcards

1
Q

Name the 4 molecular subtypes in endometrial carcinoma that guide risk category and management

A

1.POLL
2. P53
3. MMRd (mismatch repair deficiency)
4. NSMP (non-specific molecular profile)

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2
Q

name the histological subtypes of endometrial carcinoma (7)

A

1) endometrioid carcinoma (low - non aggressive type) and high grade - agressive)
Aggressive subtype
2) serous carcinoma
3) clear cell carcinoma
4) mixed carcinoma
5) undifferentiated carcinoma
6)carcinosarcoma
7) other -> mesonephric, GI mucinous like

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3
Q

What is the prognostic effect of P53 mutations on high grade endometrioid carcinoma

A

Poor prognosis - modifies stage if stage 1-II

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4
Q

What is the prognostic effect of POLE mutations on high grade endometrioid carcinoma

A

Good prognosis - modifies stage if I - II

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5
Q

What is the prognostic effect of Non-specific molecular profile (NSMP) and MMRd mutations on high grade endometrioid carcinoma?

A

intermediate prognosis - does not alter stage

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6
Q

What is the most important prognostic factor for high grade endometroid carcinoma?

A

Molecular subtype

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7
Q

How is endometrial carcinoma staged?

A

Surgico -Histopathologically

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8
Q

What is involved in surgical staging for endometrial carcinoma?

A

TLH + BSO + washings + sentinal node biopsy
TLH = non inferior to TAH (LACE trial - JAMA 2017)

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9
Q

Describe “grade” in endometrial carcinoma

A

Describes the % solid component on histo architecture -> prognostic indicator
Low grade
- G1 Endometroid <5%
- G2 5-50%
High grade (Grade3) - >50%
Extent of nuclear atypia upgrades G1-2 by 1

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10
Q

List negative prognostic factors for endometrial carcinoma

A
  1. P53 mutation
  2. non endometroid subtype
  3. High (3) Tumour grade
  4. Extent of myometrial invasion >50%
  5. Involvement of serosa
  6. Lymphovascular invasion
  7. lymph node involvement
  8. Medical comorbidites and age
  9. Recurrence
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11
Q

What is the incidence of endometrial Ca

A

2.3 % by age 85 -> incidence increasing as is mortality

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12
Q

List reasons endometrial cancer is increasing in incidence

A

-obesity -> high aromatase activity, increase in conversion androgens -> oestrogen, stimulates endometrium + proinflammatory adipokines
- T2Dm - excess insulin + ILG -> up regulates cell survival and proliferation pathways
-aging pop

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13
Q

What is the negative predictive value of ET<5mm TV for endometrial Ca

A

96%

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14
Q

Commonest subtype Cervical Ca

A

Squamous cell carcinoma (70-80%) - relative incidence declining, adenocarcinoma approx 10%

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15
Q

Complications of cervical cancer

A

Obstructive uropathy

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16
Q

DES associated subtype of Cx Ca

A

clear cell Ca

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17
Q

Mx of stage 1A1 Cx Ca

A

Fertility sparing - Cervical conisation (Lletz, cold knife, laser) IF clear margins and no LVSI
Family complete - hysterectomy (any route)
LVSI pos -> sential node bx or pelvic lympadenecomy + radical hysterectomy
<1% of A1A ca have pos nodes if margins clear.

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18
Q

Treatment for stage 1AII -> 1BII cx ca

A

radical hysterectomy + bs +/- oophorectomy with bilateral pelvic LNanectomy

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19
Q

What is anterior exenteration?

A

removal of Cx Ca and adjacent structures including vagina and bladder

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20
Q

Less common subtype Cx ca

A

adenosquamous (5%) small cell, lymphoma, sarcoma, clear cell, primary melanoma of cx.

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21
Q

Risk factors for Cx Ca

A
  1. Family Hx - first deg relative 80% increased risk of SCC, approx 50% risk of adeno
  2. ?parity + young age at first sexual encounter + birth (SCC only)
    3.OCP -double risk if OCP use 5+ years, risk returns to baseline at 10 y post use
    4.Immunodeficiency
  3. Oncogenic HPV exposure
  4. Smoking
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22
Q

Clinical Syx of Cx Ca

A

-IMB/PCB
abnormal -vaginal discharge
-PMB
- Advanced disease -> back/leg pain (nerve involvement), haematuria (bladder invasion), bowel syx, malaise, LL oedema, renal failure (obstructive uropathy)

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23
Q

What is the purpose of staging ca

A

Defines anatomical extent of disease and differentiate treatment strategies and survival outcomes

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24
Q

How is Cx ca staged?

A

combination 1. clinical -> EUA, colposcopy, endocervical curretage, hysteroscopy +/- cystoscopy + /- proctoscopy
2.Imaging - xray, CT or MRI (preferred)
3.Histopathological

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25
Describe Stage 1 Cx Ca
Ca confined to the cervix (doesn't matter if extends into body of the uterus) 1A1 depth of invasion <3mm 1A2 DOI 3-5mm 1B1 DOI >5mm, lesion <2cm 1B2 Lesion between 2-4cm 1B3 Lesion >4cm
26
Describe Stage 2 Cx Ca
Carcinoma limited to upper 2/3 of vagina and no pelvic sidewall invasion IIA1 Lesion <4cm IIA2 Lesion >4cm IIB parametrial invasion
27
Describe Stage IV Cx Ca
IVA spread to bladder or bowel IVB distant mets
27
Describe Stage 3 Cx Ca
Local invasion of lower third vagina, pelvic sidewall, pelvic or paraaortic nodes or causing obstructive uropathy IIIA - lower this vagina IIIB - pelvic sidewall extension OR hydronephrosis/obsructive uropathy IIIC1 - pelvic nodes IIIC2 - para-aortic nodes
28
In cx adenocarcinoma, why is removing both tubes recommended?
Higher risk of recurrence into adnexae cf SCC
29
Cx ca- Fertility preserving surgery for stage 1B1 and below
radical trachelectomy + cerclage + BL SNL/LND
29
Cx Ca- Management for stage 1B3/IIA2 (tumours >4cm +/- parametrial spead)
Platinum based combined chemo radiotherapy (CCRT) (Radical surgery no survival benefit but more higher morbidity with combined RX -> usually needed as high risk recurrence requiring adjuvant chemo/rads)
30
Cx Ca Stage IIB upwards or recurrence
CCRT OR pelvic exenteration (in medically fit pt)
31
What is the cure rate of Cx of CCRT in Stage IIB + Cx Ca
20-50%, also improves syx inc vaginal discharge and neuropathic pain
32
What is the mortality risk of pelvic exenteration?
2-4%
33
Other Rx bedsides CCRT for stage IVB Cx Ca
platinum doublets (>effect than cisplatin), carboplatin-paclitaxel, bevacuxixumab - anti vegf monor cloncal ab
34
Why do you need to biopsy/remove bilateral LN in Cx cancer?
central structure, drains bilaterally, potential FN if only assessing unilateral nodes
35
What is the route of hysterectomy recommended from Cx cancer mx?
OPEN Minimally invasive approach = worse outcomes/lower disease free survival as per LACC and other trials Association between uterine manipulators and worse outcomes
36
Describe chemo/rads regimen for Cx Cancer
Platinum based chemo + EBR + bradytherapy
37
Imaging modalities for recurrent Cx Ca
MRI, PET
38
Mx of recurrance of Cx Ca
EBRT Exenteration Palliative chemo rads
39
Describe radial trachelectomy
surgical removal of cervix, paracervical tissues and upper vagina, with cerclage at internal os. Lap or vaginal approach.
40
Obstetric outcomes for those with early Cx Ca who undergo fertility preserving surgery (ie radical trachelectomy + LND
42% achieve pregnancy 50% will require ART 25% live birth rate 50% PTB (20% extreme preterm)
41
Follow up for 1A1 Cx Ca
6-12 monthly CST first 1 year, then annually for 9 years.
42
Complications of Rx of Cx Ca
1. Sexual morbidity/Fertility considerations - vaginal stenosis, sexual dysfunction -> dilators, psych support 2. Menopause -> suitable for HRT 3. Lymphodema -> 77% of post Surgery + Rads 4. Bladder + bowel dysfunction 5. Psychological
43
Prognostic indicator for Cx Ca
stage, subtype, tumour bulk, age and performance status of pt *LVSI = poor prognosis (though not included in FIGO stageing)
44
5 year survival of stage 1A1 Cx Ca
95%
45
5 year survival of Stage IVB Cx Ca
14%
46
Highest risk of recurrence in what time frame?
2 years
47
Obstetric complications of cone biopsy
Risk of PTB Risk of mid trimester loss Cervical dystocia -> FTP and CS
48
Vulval Ca incidence
1-4% of gynae ca, incidence rising, morality rate stable More prevalent at older age
49
Name the histopathological subtypes of vulval Ca
SCC (90%) Adenocarcinaom (inc pagets disease of vulva) Basal cell Merkel Cell Sarcoma Melanoma
50
RF for vulval Ca
Differentiated VIN +/- Lichen sclerosis HR HPV, smoking, immunnosuppression
51
Clinical presentation of vulval ca
pruritis Ulcerated lesion with rolled edges
52
53
Prognostic factor for vulval Ca (5)
1. inguinofemoral LN pos -> most sig for 5 year survival 2. FIGO stage 3. Grade 4. Depth of invasion (1-2mm =8% +ve nodes, 3-5mm DOI 30% pos nodes) 5. Age/functional status of person
54
Describe Figo stage 1 vulval Ca
tumour confined to the vulva 1A <2cm and DOI <1mm 1B tumour >2cm or DOI >1cm
55
Describe Figo stage 2 vulval Ca
Tumour of any size extending to lower third of urethra, vagina or anus, neg LN
56
Describe Figo stage 3 vulval Ca
tumour of any size extending to upper part of perineal structures OR pos LN IIIA = local extension to upper 2/3 of structure, OR LN mets <5mm IIIB LN mets >5mm IIIC LN Mets with extracapsular spread
57
Describe Figo stage 4 vulval Ca
tumour fixed to bone, ulcerated nodal mets or distant mets IVA pelvic bone or regional ulcerated or fixed LN IVB distant mets
58
Investigations for Vulval Ca
Vulvoscopy Punch biopsy Imaging to assess for nodal status (usually CT CAP) FNA or core biopsy of nodes PET CT if chemo rads
59
Treatment for 1A vulval Ca
wide local excision - risk of groin mets <1%
60
Treatment for 1B vulval Ca
radical wide local excision, groin LND
61
When in vulval ca would you perform a bilateral groin LND?
midline primary lesion (<1cm clear of midline), or if ipsilateral nodes are positive
62
Complications of LND
wound breakdown, lymphodema, infection, prolonged hospitalisation
63
Indications for adjuvant radiotherapy for vulval Ca (4)
Sentinel LN met <= 2cm (alternative to iliofemoral lND) Extracapsular spread of LN (IIIC) 2 or more pos groin nodes Involved surgical margins
64
Rx for locally advanced vulval Ca
- neo-adjuvant chemo to reduce tumour bulk in locally advanced disease then surgery OR primary chemo/rads for those with locally unresectable disease - chemo (platinum based) for distant mets
65
Special cases - Rx of verrucous carcinoma or BCC of vulva, melanoma
WLE only (LN mets very uncommon). Avoid Rads for verrucous Ca - anplastic transformation. Immunotherapy options for melanoma +MDT mx
66
Ca bartholins gland
Rx as per SCC vulva. Resection may compromise sphincters -> may need defunctioning stoma Chemo rads as usually present at advanced stage
67
Subtypes of Gestational trophoblastic disease (3)
Complete hydatiform mole Partial mole Placental site nodule
68
Subtypes of gestation trophoplastic neoplasia (4)
choriocarcinoma Invasive mole Placental site tumour Epitheloid trophoblast tumour
69
Pathophysiology of partial molar pregnancy
1 set maternal genes (haploid ovum) + 2 sets paternal genes (usually dispermic fertilisation) -> triploid conceptus (90%) 10% tetraploid or mosaic
70
Pathyphys of complete molar pregnancy
diploid - empty egg, mono (80%) or di (20%) spermic -> make a diploid cell with only paternal origin.
71
What is a biparental complete hydatiform mole?
complete mole arising due to genomic imprinting and autosomal recessive mechanisms - associated with genetic mutation of NLRP7 19q
72
RF for molar pregnancy
advanced maternal age Previous mole (2% after 1 prev, 20% after 2) Asian ethnicity Family Hx - suggests possible biparental complete mole autosomal recessive mole
73
Prevalence of complete mole
1:1000 pregnancies
74
Prevalence of partial mole
3:1000
75
In which GTD is P57 expressed?
incomplete molar pregnancies -> complete moles dont have any maternal alleles from which P57 is derived
76
What is the risk of progression to GTN for 1a) partial vs b) complete molar pregnancy
a) partial - 1% b) complete - 15%
77
Why is surgical mx 1st line for GTD?
16% greater risk of gtn, risk of embolising throphblastic tissue High rate of incomplete evacuation May consider at advanced gestation if foetal parts large
78
Risk of twin pregnancy with GTD
diagnostic uncertainty ?viable second twin with cmp vs partial mole Early loss Ptb PET Thyrotoxicosis Risk of progression to GTD
79
Can you use cervical ripening for d&C with molar pregnancy?
yes
80
Ranzcog f/u for pmp and cmp
partial weekly bhcg until 3 neg in a row Complete as above + monthly for 6 months
81
Post pregnancy Mx for someone with PMHx of molar pregnancy
placenta for history, BHCG 6 week PP (though as per RCOG -> 1% risk of GTN for pt with neg BHCG 56 days post evacuation of molar pregnancy)
82
Presentation of GTN
persistent vaginal bleeding (>8 weeks post pregnancy) Syx of mets -> dyspnoea, haemoptysis, neurologival syx, vaginal lesions
83
Describe FIGO anatomical staging for GTN
1= confined to uterus 2= extension to pelvis 3= extension to lungs Stage 4 mets other than lungs
84
what is FIGO scoring for GTN
system to stratify need for multi agent chemo (risk of resistance to MTX regimen along)
85
What is the treatement for GTN with FIGO/who score of <7
IM MTX with rescue folate
86
What is the treatment for GTN with FIGO/who score of >=7
multi drug IV chemo -> EMA-Co
87
What is EMACO
Multi agent chemo for high risk resistance gtm Etopisde Mtx Actinomycin d Cyclophosphamide Oncovin
88
When can pts conceive again after GTN
12 months post BHCG neg/completion of Rx
89
What contraception options suitable for GTN pts
insert IUD after 6-8 weeks (risk of perf/expulsion OCP and other contraception fine immediately
90
Special consideration if placental tissue consistent with GTN?
Urinary BHCG on neonate - can metastasis to baby!
91
prognosis for GTN
cure rate close to 100%, multidose chemo close to menopause can impact fertility and premature menopause
92
What is the rate of future pregnancy in pt with GTN
80% will be able to have further pregnancy
93
Features of placental site or epithelioid trophoblastic tumours
histopath -> no chorionic villi Slower growing - often confined to uterus Lymphatic spread Usually diploid More commonly arise after a non molar pregnancy Lower BHCG
94
Mx of PSTT/ETT
multidrug chemo (often resistance) Surgical Mx - Hysterectomy + Pelvic LND
95

RANZCOG Written Exam (5 decks)

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