Gynaecological Oncology Flashcards
CERVICAL CANCER
- where does it develop
- how long does it take to develop from precursor cells?
- Develop at transition zone between squamous and columna epithelium
- Takes on average 10 yrs to develop from high grade precursor to invasive cancer
CERVICAL CANCER
- how common is it worldwide
- how common is it in the UK
- Second commonest malignancy in females after breast carcinoma worldwide
- In the UK it is the third most common gynaecological malignancy after ovarian and endometrial carcinoma
CERVICAL CANCER
- when was the screening programme introduced
- how has incidence changed over time
- risk factors
- 1988
- halved in last 20yrs
- HPV (early first sexual experience, multiple partners, non barrier contraceptive) / COCP / high parity / smoking / immunosuppression
CERVICAL CANCER
presentation
- Cervical smear suggestive but need biopsy
- Incidental at treatment for pre-invasice disease
- PCB
- Post menopausal bleeding
- Rarer which suggests advanced disease – heavy bleeding PV, ureteric obstruction, weight loss, bowel disturbance, fistula (vesicovaginal)
CERVICAL CANCER
histological types
- Squamous cell carcinoma – 85-90%
- Adenocarcinoma – 10-15%
- Neuroendocrine tumour - <1% (originates from argyrophil cells in cervix, may present with carcinoid syndrome, median survival <2yrs)
- Clear cell carcinoma - <1% (<25yrs secondary to DES exposure in utero) / (>45yrs not associated with DES), treat as per adenocarcinoma but prognosis is worse)
- Glassy cell carcinoma («1% - median age 35yrs, presents with bleeding – often normal smear history, similar prognosis to adenocarcinoma)
- Sarcoma botryoides of the cervic («1%) – type ofembryonal rhabdomyosarcoma, median age 14yrs (5months-45yrs), local excision with or withour chemotherapy
- Lymphoma of cervix – no need for surgical excision, responds well to combination chemotherapy
CERVICAL CANCER
examination findings
- Vaginal and bimanual examination – roughened hard cervix with or without loss of fornices and fixed cervix, if there is extension of disease
- Colposcopy- irregular cervical surface, abnormal vessels, dense aceto-white changes
CERVICAL CANCER
histology
- Punch biopsy
* Small diagnostic loop biopsy at colposcopy
CERVICAL CANCER
further investigation
if cancer confirmed on biopsy • U&E, LFT, FBC • CT abdomen and pelvis • MRI pelvis • Examination under anaesthetic – bimanul vaginal examination, less often performed now as MRI, insert fiducial markers
CERVICAL CANCER
1. staging system
FIGO
0-IV
CERVICAL CANCER
treatment
- Dependent on stage and age
- Age associated with increased stage at presentation
- Laparoscopic surgery – can be performed as a separate procedure to wetheims hysterectomy to allow for formal paraffin-embedded histology of LN rather than frozen section
- Fertility sparing surgery – young women / eg radical trachelectomy for early stage disease (1a2 and early stage 1b1). Vaginal procedure involving removal of cervix and paracervial tissue to internal os with cerclage suture at internal os.
CERVICAL CANCER
treatment for
1. stage Ia1
2. stage Ia2 and Ib1
- local excision or total abdominal hysterectomy
2. lymphadenectomy and wertheim’s hysterectomy if -ve LN
CERVICAL CANCER
treatment for
1. stage Ib 2 and early IIa
2. > stage Ib2
- chemoradiotherapy, consider lymphadenopathy and wetherims hysterectomy in selected LN -ve cases
- combination chemoradiotherapy
CERVICAL CANCER
treatment for
stage IVb
?chemo and pelvic radiotherapy if responsive
? best supportive care +/- palliative radiotherap to control symptoms
HPV VACCINATION PROGRAMME
- who gets it
- describe the vaccine
- Girls and boys aged 12-13. Ideally given before becoming sexually active
- Gardasil quadrivalent vaccine (covers HPV types 16. 18, 6, 11) and also protects against genital warts
Safe sex practices and use of condoms
Protection with immunisation maintained for 10 years
15 high risk HPV known and so HPV vaccination does not prevent all cervical cancers
what gynaecological cancer has the leading cause of death in the UK
Ovarian
OVARIAN CANCER
- what type are 90% of ovarian cancers
- what stage do 75% present at
- what are the genes involved?
- epithelial ovarian cancer
- FIGO stage III and above
- BRCA1 and BRCA2 and Lynch II syndrome (HNPCC)
OVARIAN CANCER
what investigations are used in surveillance of ovarian cancer?
CA125 and TVS/USS
OVARIAN CANCER
aetiology
- Irritation of ovarian surface epithelium by damage during ovulation
- BRCA mutations – increase risk of ovarian and breast cancer
- HNPCC (lynch II syndrome) – rarer than BRCA, lifetime risk 12%, prophylactic hysterectomy and BSO
- Screening – blood sample, BRCA1 and 2
OVARIAN CANCER
what factors relating to ovulation increase risk of ovarian cancer?
increase risk if multiple ovulations, decreased If ovulation suppressed, nulliparity increases risk, early menarche/late menopause increase risk, COCP decrease risk, pregnancy decrease risk
OVARIAN CANCER
when should patients be referred for clinical genetics counselling?
2 (breast/ovary cancer) in 1st/2nd degree relative, Three 1st and 2nd degree relatives with breast, ovary, colorectal, stomach, endometrial cancers, 2 1st/2nd degree relatives one with ovarian cancer any age and one with breast cancer <50, 2 1st/2nd degree relatives with ovarian cancer at any age
OVARIAN CANCER
presentation
- Vague, common symptoms which can be misinterpreted as other conditions eg IBS, diverticular disease, middle aged spread
- 50% present to a specialty other than gynae
- Common symptoms – abdominal distension, increased girth, urinary symptoms, change in bowel habit, abnormal vaginal bleeding, detection of pelvic mass
OVARIAN CANCER
investigation
- History – symptoms, risk factors, comorbidities, fanily history
- Clinical examination – mass, ascites, omental mass, pleural effusion, supraclavicular lymph nodes
- Haematological tests – FBC, U&E, LFTs / tumour markers (CA125, / carcinoembryonic antigen -CEA – raised in colorectal, normal in ovarian / CA19.9 – raised in mucinous tumours / AFP, hCG, LDH, inhibin, oestradol
- Imaging – USS if CA125 raised / CXR – pleural effusion or lung metastases / CT abnomen or pelvis – omental caking, peritoneal implants, liver metastases, para-aortic LN
OVARIAN CANCER
management of ascites and pleural effusion?
- Diagnose – cytology, microbiology, biochem
* Symptom control – drainage, pig tail drain, aseptic technique, use LA
OVARIAN CANCER
surgical treatment
- High RMI – staging laparotomy through midline incision
- Laparotomy to remove as much tumour as possible
- Achievement of optimal debulking is positive prognostic factor
- Full stage 1a cancers important as it affects whether adjuvant chemotherapy is required
- Stage IIIc or IV – may benefit from neoadjuvant chemotherapy prior to debulking
OVARIAN CANCER
describe chemotherapy and follow up?
- Recommended for all patients who are low risk early stage disease.
- In advance disease (II and greater) – platinum agents are better than carboplatin
- 6 cycles of carboplatin with or without paclitaxel every 3 weeks
- IIIc / IV – neoadjuvant chemotherapy – 3 cycles
- Investigations before chemo – CT, creatinine clearance, CrEDTA, histological diagnosis
UTERINE CANCER
- most common presentation
- genetic association
- who should receive endometrial sampling?
- Most commonly presents with post menopausal bleeding. 1 in 10 women with PMB will have endometrial cancer or endometrial hyperplasia
- HNPCC - lynch syndrome
- recommended for women >45 years with abnormal bleed
UTERINE CANCER
- role of trans vaginal USS in diagnosis
- risk of progression to cancer for patients with endometrial hyperplasia?
- <4mm endometrial thickness in postmenopausal women (very low risk 96% NPV)- no need for endometrial sampling
- risk of progression to cancer (simple-1% / simple with atypia – 8% / complex – 3.5% / complex with atypia- 30%)