Gynaecological malignancy Flashcards
Pathophysiology of vulval cancer
- Majority are SCC but can be adenocarcinoma
- Warty type - a/w HPV
- Keratinising type - a/w lichen sclerosus in elderly women
Usually spreads to the inguinal + femoral LNs, followed by the pelvic LN + haematogenous
How may vulval cancer present?
- Pruritic raised lesion that may ulcerate + bleed
- Occasionally affects mucus membrane causing a hyper pigmented ulcerated lesion
- Most on labia majora
Management of vulval cancer
- Stage IA: WLE + u/l groin node dissection
* >Stage 1: radical vulvectomy + b/l groin lymphadenectomy +/- radiotherapy, usually palliative
What are the types of vulval intraepithelial neoplasia and how do you manage it?
Loss of the epithelial architecture
- Squamous VIN:
- Usual VIN: affects 30-50yos, a/w smoking + HPV. Asymptomatic/itch/pain/dysuria/ulcer, white/pink/pigmented plaques/papules. 3-4% become invasive
- Differentiated VIN: postmenopausal, a/w squamous hyperplasia/lichen sclerosus/lichen simplex chronicus, precursor to HPV-negative keratinising SCC
*Non-squamous VIN: Paget’s disease - papule lesions of various colours, rare
M: biopsy, search for neoplasia of the vagina or cervix, treat with imiquimod cream, laser or superficial excision
Vaginal intraepithelial neoplasia
Usually a/w cervical lesions, asymptomatic + superficial changes until develops into carcinoma
Vaginal adenosis
Columnar epithelium replaces squamous - usually this reverts but can become adenocarcinoma
Vaginal carcinoma
- Usually SCC but can be adenocarcinoma, in UK usually mets from the cervix or endometrium
- CF: irregular bleeding, offensive discharge, fistulae, exophytic lesion or indurated mass
- Direct + LN spread
- M: palliative radiotherapy unless stage I (surgery)
What is the aim of cervical screening and who is currently invited for it?
Aims to detect non-invasive precursor of cervical cancer (ie CIN) in asymptomatic population, to reduce morbidity mortality. There is a natural history of changes that may be over 10y from early changes to cancer
NHS programme for all women registered with a GP are invited every 3y (age 25-49) and 5y (age 50-64), and >65y if one of their last 3 tests were abnormal
What are the possible outcomes from cervical screening?
Cells taken from transformation zone and now all are tested for HPV- if HPV+ do cytology. Possible results:
- Inadequate sample: not enough cells, cells not seen clearly or infection present. 3 inadeqaute-do colposcopy
- Borderline nuclear change or mild dyskaryosis: if HPV positive colposcopy (as now all are tested for HPV), if negative back to routine recall
- Moderate dyskaryosis CIN II - urgent colposcopy
- Severe dyskaryosis CIN III - carcinoma in situ - urgent colposcopy
- Suspected invasive cancer - urgent colposcopy
- Glandular neoplasia - possible adenocarcinoma
Cervical intraepithelial neoplasia management
- Low grade: cytological + colposcopy surveillance every 6m for a defined period
- Higher grade: excise by scalpel/laser/LLETZ, destroy transformation zone by ablation/cryocautery/coagulation diathermy, cone biopsy if cannot see TZ
Pathophysiology of cervical cancer
- 80% SCC and 20% AC, most occur in the transformation zone where columnar becomes squamous epithelium
- RF: CIN, HPV infection (types 16+18 and 33), HIV, smoking, lower socio-economic status, immunosuppression, early age of 1st intercourse
How is cervical cancer staged?
I: IA microscopic, I cervix only
II: beyond cervix but not to the lower 1/3 vagina or pelvic wall
III: to pelvic wall/lower 1/3 of vagina or causes renal issues like hydronephrosis
IV: beyond pelvis to mucosa of bladder/rectum, IVB-distant spread
How may cervical cancer present if not on screening?
- PCB, dyspareunia, IMB, irregular bleeding, PMB, foul discharge (thin + watery, may have blood)
- Later: ureteric obstruction, renal failure, excruciating pain (bone + nerve), oedema of lower limbs, urinary/bowel sx
- Colposcopy: white cells, small blood vessels below epithelium, don’t stain brown with Lugoli’s iodine, early cancer is raised/ulcerated/friable, more advanced often fixed/friable/warty
How is cervical cancer managed and what is the prognosis like?
- Early stage (IA/I): LLETZ, local excision or hysterectomy if completed family
- Later: surgery (usually radical hysterectomy + LN dissection, may keep ovaries), radiotherapy, platinum-based chemo
Stage I 5y survival 85% but stage IV 10%
What factors increase the risk of endometrial adenocarcinoma?
- Hereditary syndromes e.g. HNPCC
- High oestrogen levels: obesity, exogenous (e.g. HRT without progesterone), endogenous (e.g. granulosa cell tumours), Tamoxifen (acts as unopposed oestrogen - hyperplasia), nulliparity, late menopause, PCOS, DM
- Endometrial hyperplasia itself
How may endometrial adenocarcinoma present?
- PMB - endometrial cancer until proven otherwise
- Irregular bleeding or HMB
- Pyometria - uterus infection with purulent discharge
Endometrial cancer path
- Type I - endometroid adenocarcinoma - the majority, a/w hyperoestrogenic states
- Type II - other types eg clear cell, more aggressive
*Spread: myometrium, cervix, pelvic + para-aortic LN
How would you investigate suspected endometrial adenocarcinoma?
- TV USS: <5mm endometrium v low risk, unreliable pre-menopause as thickness varies over the menstrual cycle
- Endometrial aspirate (pipelle)
- Hysteroscopy: pass through internal Os into uterus, visualise + take biopsies, can have with GA if cannot tolerate. Complications are small but include uterus perforation and pelvic infection
How is endometrial adenocarcinoma staged and managed?
Stage I-myometrium (good prognosis), stage II to cervix but not outside uterus, III local/regional spread, IV bladder/bowel/distant mets
- TAH + BSO
- Monitor CA-125
- Adjuvant radiotherapy to reduce pelvic recurrence
- Chemo
What are the non-epithelial uterine cancers? (3% of uterine cancers)
- Stromal sarcomas - a/w adenomyosis and endometriosis, p/w discharge + bleeding
- Mixed Mullerian tumours (carcinosarcomas) - from epithelium + stroma, have early spread
- Leiomyosarcomas - may arise in a pre-existing fibroid, rapidly-growing ‘fibroid’ but often asymptomatic
What are the features of ovarian lesions?
- OFTEN ASYMPTOMATIC
- Symptoms: abdo enlargement, ascites, pressure on bladder/rectum, torsion (pain, vomiting), ruptured cyst (pain, haemorrhage), disturbed menstrual cycle from hormones, bloating, reduced appetite
- Signs: abdo distension, central dullness with resonant flanks, gross ascites, may be palpable on VE, usually non-tender, benign tumours are usually freely-mobile
What are functional ovarian cysts?
They occur during menstrual life
- Follicular cysts: commonest, walls of granulosa cells and contain clear fluid + sex steroids, they can cause endometrial hyperplasia and HMB, usually only last around 2 months
- Lutein cysts: granulosa type (cysts of corpus luteum, can cause amenorrhoea or pain) and theca type (high hCG so seen in hydatidiform mole, rupture - haemorrhage)
- Physiological cysts in early pregnancy are common and resolve from T2, reassure, are the corpus luteum
Serous cystadenomas
Common type of benign cyst, often b/l, may become malignant (psammoma bodies seen-calcium collection). May be so large that they fill the peritoneal cavity and often replace the normal ovary
Mucinous cystadenomas
Common type of benign cyst, often become very big, fluid contains mucin, secretory, less likely to become malignant than serous type
Mucinous ystadenocarcinoma: if ruptures may implant in the PC causing pseudomyxoma peritonii (tho mucin tumour of appendix more common cause)
