Gynae oncology Flashcards
Endometrial cancer aetiology & pathophysiology
Most common form - adenocarcinoma
- caused by unopposed oestrogen
Progesterone is produced by the corpus luteum after ovulation → where women have experienced a longer period of anovulation → predisposed to malignancy
Unopposed oestrogen → endometrial hyperplasia → can predispose to atypia, a precancerous state
Endometrial cancer risk factors
Anovulation
- early menarche and/or late menopause
- low parity
- PCOS
- HRT with oestrogen alone
- tamoxifen use
Age - between 65 and 75 years old
Obesity
Hereditary - lynch syndrome
Endometrial cancer clinical features
Postmenopausal bleeding
Clear/white vaginal discharge
Abnormal cervical smears
Abdominal pain/weight loss
O/E - abdominal/pelvic masses, vulval/vaginal atrophy, cervical lesions, assess size & axis of the uterus prior to endometrial sampling
Endometrial cancer ix
Transvaginal USS
- endometrial thickness > 4mm → endometrial biopsy (pipelle biopsy)
- high risk → hysteroscopy with biopsy
MRI/CT for staging
Baseline bloods prior to intervention
Endometrial cancer FIGO staging
Stage I - carcinoma confined to within uterine body
Stage II - carcinoma may extend to cervix but is not beyond the uterus
Stage III - carcinoma extends beyond uterus but is confined to the pelvis
Stage IV - carcinoma involves bladder or bowel, or has metastasised to distant sites
Endometrial hyperplasia mx
Hyperplasia without atypia - can be treated with progestogens; surveillance biopsies should be performed to identify any progression
Atypical hyperplasia - TAH & BSO
Endometrial carcinoma mx
Stage I - TAH & BSO
Stage II - radical hysterectomy & assessment and removal of pelvic lymph nodes
Stage III - maximal de-bulking surgery
Stage IV - maximal de-bulking surgery; palliative approach may be preferred
Frequent follow up required up to 5 years post-op due to recurrence
Ovarian cancer pathophysiology
Believed to be derived from surface epithelial irritation during ovulation
More ovulations that take place, the increased risk of developing malignancy
Ovarian cancer risk factors
Nulliparity
Early menarche
Late menopause
HRT containing oestrogen only
Smoking
Obesity
Ovarian cancer protective factors
Multiparity
Combined contraceptive methods
Breastfeeding
Ovarian cancer genetic mutations
BRCA1&2 - mutations increase the risk of breast & ovarian cancers; prophylactic BSO can be performed, but does not completely eradicate risk of developing malignancy
Hereditary nonpolyposis colorectal cancer (lynch II syndrome)
Ovarian cancer risk of malignancy index
Tool used in practice to determine the likelihood that ovarian masses are malignant
CA125, menopausal status & ultrasound score
Patients with a RMI >250 should be referred to a specialist gynaecologist
Ovarian cancer clinical features
Incidental & asymptomatic
Chronic pain
PV bleeding
Bloating
Change in bowel habit & urinary frequency
Weight loss
IBS
Ovarian cancer ix
Basic bloods - FBC, U&Es, LFT & albumin
CA125
Abdominal & pelvic USS
Confirmed cancer → staging CAP
Ovarian cancer mx
Surgery - staging laparotomy for those with a high RMI with attempt to debulk the tumour
Adjuvant chemotherapy
Follow-up for 5 years
Cervical cancer aetiology & pathophysiology
Majority are SCCs
Usually develop as a progression from CIN, occurs over the course of 10-20 years
Invasive cervical cancer occurs when the basement membrane has been breached; most common sites of metastasis are lung, liver, bone & bowel
Vast majority are caused by persistent HPV - high risk serotypes are 16 & 18
Cervical cancer risk factors
HPV
Smoking
Other STIs
Long term (> 8 years) COCP use
Immunodeficiency
Cervical cancer clinical features
Abnormal vaginal bleeding
Vaginal discharge (blood-stained, foul-smelling)
Dyspareunia
Pelvic pain
Weight loss
Often asymptomatic
Advanced disease - loin pain, rectal bleeding, radiculopathy, haematuria
O/E - bleeding, discharge, ulceration, pelvic masses, hydronephrosis, hepatomegaly, rectal bleeding, mass on PR
Cervical cancer ix
Pre-menopausal - test for chlamydia trachomatis infection
- if negative → colposcopy and biopsy performed
Post-menopausal - urgent colposcopy and biopsy
Confirmed diagnosis:
- basic blood tests - FBC, LFTs, U&Es
- CT CAP
- further staging scans - MRI pelvis, PET
- +/- examination under anaesthesia with further biopsies
Cervical cancer mx
MDT input
Surgery:
- stage 1a - radical trachelectomy if fertility-preservation priority otherwise hysterectomy with pelvic lymphadenectomy
- stage 1b/2a - radical hysterectomy
- stage 4a/recurrent disease - anterior/posterior/total pelvic extenteration
Radiotherapy:
- stage 1b to 3 - conjunction with chemo (chemoradiation gold standard)
Chemotherapy: often cisplatin-based, neoadjuvant or adjuvant, also mainstay of palliative care
Follow-up: every 4 months for first 2 years & every 6-12 months for subsequent 3 years
Vulval cancer clinical features
Pruritis
Burning
Soreness
Bleeding
Pain
Lump
Most are SCCs & occur on the labia majora, other sites include the clitoris and perineum
Vulval cancer diagnosis
Keye’s punch biopsy
Performed under local anaesthetic
Vulval cancer mx
Surgery gold standard treatment
Early disease - complete resection of primary tumour & appropriate groin lymphadenectomy
Advanced disease - radical vulvectomy with resection of bilateral inguinofemoral lymph nodes
Cervical screening age range
Available to women and people with a cervix aged 25-64
25-49 years: 3 yearly screening
50-64 years: 5 yearly screening
Cervical screening process
Speculum inserted & brush is rotated against the transformation zone of the cervix
Brush head is sent off to the lab for testing:
- HPV screening: testing for HPV first is more sensitive & accurate
- LBC: looks for dyskaryosis
Cervical screening results
hrHPV negative → routine screening
hrHPV positive & normal smear → repeat smear in 12 months
hrHPV positive & abnormal smear → colposcopy
Inadequate smear → repeat smear within 3 months → if remains inadequate → colposcopy
