Vulval CA Flashcards
(46 cards)
1A treatment
excision with definitive margins or less than 1mm of depth
WLE is not necessary
FFDG PET scan is for what
is better than CT for more effetely assessing and detecting inguinofemoral LN involvement compared to CT
good for planning op and LN dissection =/- frozen section
what are the margins for a radical WLE
2cm surgically and 8mm fixed tissue
depth should be to the inferior fascia of the urogenital diagram and if needed 1cm of the urethra can be removed
should you remove both femoral and inguinal LN
yes
when do you do bilateral LN dissection
if tumour os < or = 2 cm from the midline
do both femoral and inguinal LN dissection for sentinel LN dissection
when do you go back and do the contralateral LN
if found positive SLN , also need to go back and remove the enblock dissection of the initial SNL
indication for SNL procedure as per GROINSS V study
- unifocal tumors confined to the vulva
- tumors less than 4cm in diameter
- stromal invasion more than 1mm
- clinically and radiologically negative groin nodes
NEED all 4 points
what do you do if you don’t find a SLN
do full unblock dissection on that side if >2cm from the midline
indication for radiotherapy for Vulval CA
- extra capsular spread
- 2 or more positive nodes on imaging without SLN
- If lesion < or equal to 4cm and SNL met < or equal to 2mm then avoid full enbloc dissection and do radiotherapy
if advanced vulval CA with no suspicious nodes on imaging what to do
do bilateral inguinefemoral lymphadenectomy and if negative don’t need radiotherapy and no need to do pelvic LN
what is the type of CA in bartholins CA
transitional or SCC or adenocarcinoma
there are also adenoid cystic and adenoquamous variants
What do all SCCs show of vulval CAs
show intense p16 expression consistent with presence of HPV
treatment of Bartholins CA is
radical hemivulvectomy and bilateral groin dissection
do radiation of positive margins or perineurial invasion
what is vulval high grade squamous intraepithelial lesion caused by
HVP 16, 33 and 4
is a lower and slower risk of progression to VSCC
what is the median age of diagnosis of vHSIL
49
what is the commonest precursor lesion in the HR-HPV- independent pathway
dVIN
- approx 68% of lesions are already associated with VSCC at diagnosis
main RF for HPV independent precursor lesions
age
LS
what are the high risk HPV vaccine types
6, 11, 16,18
6 and 11 cause genital warts
what. are histopathological features of vHSIL
acanthosis
hyperkeratosis
parakeratosis
signs of reduced cell maturation
vHSIL is HR HVP associated
what are typical features of dVIN
parakeratosis
elongated and anastomizing rete ridges, atypia in the basal cells, abnormal keratinocytes and prominent intracellular bridges
what are HPV independent lesions
dVIN
VAAD- vulvular acanthuses with altered differentiation
DEVIL differentiated exophytic vulval intraepithelial lesion
p 53 wild type verruciform anancthotic
vHSIL what does it demonstrate immunohitochemically
p16 positivity - indicative of HPV status but low expression of p53.6
Is VAAD a precursor lesions
yes to VSCC
VAAD/DEVILs are distinct why?
for the absence of TP53 mutations and presence of PIK3CA mutation
