Gynaecological Oncology Flashcards

1
Q

CERVICAL CANCER

  1. where does it develop
  2. how long does it take to develop from precursor cells?
A
  1. Develop at transition zone between squamous and columna epithelium
  2. Takes on average 10 yrs to develop from high grade precursor to invasive cancer
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2
Q

CERVICAL CANCER

  1. how common is it worldwide
  2. how common is it in the UK
A
  1. Second commonest malignancy in females after breast carcinoma worldwide
  2. In the UK it is the third most common gynaecological malignancy after ovarian and endometrial carcinoma
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3
Q

CERVICAL CANCER

  1. when was the screening programme introduced
  2. how has incidence changed over time
  3. risk factors
A
  1. 1988
  2. halved in last 20yrs
  3. HPV (early first sexual experience, multiple partners, non barrier contraceptive) / COCP / high parity / smoking / immunosuppression
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4
Q

CERVICAL CANCER

presentation

A
  • 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)
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5
Q

CERVICAL CANCER

histological types

A
  • 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
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6
Q

CERVICAL CANCER

examination findings

A
  • 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
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7
Q

CERVICAL CANCER

histology

A
  • Punch biopsy

* Small diagnostic loop biopsy at colposcopy

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8
Q

CERVICAL CANCER

further investigation

A
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
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9
Q

CERVICAL CANCER

1. staging system

A

FIGO

0-IV

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10
Q

CERVICAL CANCER

treatment

A
  • 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.
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11
Q

CERVICAL CANCER
treatment for
1. stage Ia1
2. stage Ia2 and Ib1

A
  1. local excision or total abdominal hysterectomy

2. lymphadenectomy and wertheim’s hysterectomy if -ve LN

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12
Q

CERVICAL CANCER
treatment for
1. stage Ib 2 and early IIa
2. > stage Ib2

A
  1. chemoradiotherapy, consider lymphadenopathy and wetherims hysterectomy in selected LN -ve cases
  2. combination chemoradiotherapy
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13
Q

CERVICAL CANCER
treatment for
stage IVb

A

?chemo and pelvic radiotherapy if responsive

? best supportive care +/- palliative radiotherap to control symptoms

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14
Q

HPV VACCINATION PROGRAMME

  1. who gets it
  2. describe the vaccine
A
  1. Girls and boys aged 12-13. Ideally given before becoming sexually active
  2. 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
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15
Q

what gynaecological cancer has the leading cause of death in the UK

A

Ovarian

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16
Q

OVARIAN CANCER

  1. what type are 90% of ovarian cancers
  2. what stage do 75% present at
  3. what are the genes involved?
A
  1. epithelial ovarian cancer
  2. FIGO stage III and above
  3. BRCA1 and BRCA2 and Lynch II syndrome (HNPCC)
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17
Q

OVARIAN CANCER

what investigations are used in surveillance of ovarian cancer?

A

CA125 and TVS/USS

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18
Q

OVARIAN CANCER

aetiology

A
  • 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
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19
Q

OVARIAN CANCER

what factors relating to ovulation increase risk of ovarian cancer?

A

increase risk if multiple ovulations, decreased If ovulation suppressed, nulliparity increases risk, early menarche/late menopause increase risk, COCP decrease risk, pregnancy decrease risk

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20
Q

OVARIAN CANCER

when should patients be referred for clinical genetics counselling?

A

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

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21
Q

OVARIAN CANCER

presentation

A
  • 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
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22
Q

OVARIAN CANCER

investigation

A
  • 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
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23
Q

OVARIAN CANCER

management of ascites and pleural effusion?

A
  • Diagnose – cytology, microbiology, biochem

* Symptom control – drainage, pig tail drain, aseptic technique, use LA

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24
Q

OVARIAN CANCER

surgical treatment

A
  • 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
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25
Q

OVARIAN CANCER

describe chemotherapy and follow up?

A
  • 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
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26
Q

UTERINE CANCER

  1. most common presentation
  2. genetic association
  3. who should receive endometrial sampling?
A
  1. Most commonly presents with post menopausal bleeding. 1 in 10 women with PMB will have endometrial cancer or endometrial hyperplasia
  2. HNPCC - lynch syndrome
  3. recommended for women >45 years with abnormal bleed
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27
Q

UTERINE CANCER

  1. role of trans vaginal USS in diagnosis
  2. risk of progression to cancer for patients with endometrial hyperplasia?
A
  1. <4mm endometrial thickness in postmenopausal women (very low risk 96% NPV)- no need for endometrial sampling
  2. risk of progression to cancer (simple-1% / simple with atypia – 8% / complex – 3.5% / complex with atypia- 30%)
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28
Q
OVARIAN CANCER
FIGO classification stage 1 
1. extent
2. types
3. 5 year survival
A
  1. limited to ovaries
  2. 1a - one ovary / 1b - both ovaries / 1c - ruptured capsule, tumour on owarian surface, positive peritoneal washings
  3. 75-90%
29
Q
OVARIAN CANCER
FIGO classification stage II
1. extent
2. types
3. 5 year survival
A
  1. limited to pelvis
  2. IIa - uterus or tubes / IIb - other pelvic structures / IIc - positive peritoneal washings
  3. 45-60%
30
Q
OVARIAN CANCER
FIGO classification stage III
1. extent
2. types
3. 5 year survival
A
  1. limited to abdomen
  2. IIIa - microscopic metastases / IIIb - macroscopic metastases <2cm / IIIc - macroscopic metastases >2cm
  3. 30-40%
31
Q

OVARIAN CANCER
FIGO classification stage IV
1. extent
2. 5 year survival

A
  1. distant metastases outside abdomen cavity

2. <20%

32
Q

VAGINAL CANCER

  1. how common is it
  2. how do most arise
  3. what type of carcinoma is most common
A
  1. Primary vaginal cancers are rare(1% of gynaecological cancer).
  2. Most vaginal cancers are metastatic from either uterus or vulva.
  3. Predominantly squamous cell carcinoma and commonly HPV related.
33
Q

VAGINAL CANCER

  1. what type is seen in younger women
  2. what is sarcoma botryoides
  3. predisposing factors
A
  1. Vaginal clear cell adenocarcinoma occurs in younger women with DES exposure in utero
  2. rare tumor in young girls with multicystic grape like form
  3. pelvic radiotherapy and long term inflammation due to vaginal pessary or procidentia
34
Q

VAGINAL CANCER

clear cell adenocarcinoma

A
  • Occur in younger women
  • Associated with DES exposure in utero
  • Aim to preserve reproductive function
  • Stage 1 tumours treated with wide local xcision
  • Radiotherapy in advanced stage
35
Q

VAGINAL CANCER

embryonal rhabdomyosarcoma

A
  • Rare
  • Multicystic grape like form
  • Derived from rhabdomyoblasts
  • Presents in infancy
  • Cervical rhabdomyosarcoma can occur in teenagers and uterine rhabdomyosaroma can occur in post menopausal
  • Grape like mass arising from vagina
  • Treatment – preserve fertility and vaginal function – excised followed by chemo / neoadjuvant chemo for larger tumours to reduce size prior to surgery
  • Survival rates 90%
36
Q

VAGINAL CANCER
FIGO stage 0
1. extent of disease
2. 5 yr survival

A
  1. intraepithelial neoplasia

2. 95%

37
Q

VAGINAL CANCER
FIGO stage I
1. extent of disease
2. 5 yr survival

A
  1. tumour limited to vaginal wall

2. 67%

38
Q

VAGINAL CANCER
FIGO stage II
1. extent of disease
2. 5 yr survival

A
  1. limited to vagina and subvaginal tissue but not extending to pelvic sidewall
  2. <39%
39
Q

VAGINAL CANCER
FIGO stage III
1. extent of disease
2. 5 yr survival

A
  1. tumour spread to pelvic sidewall

2. 33%

40
Q
VAGINAL CANCER
FIGO stage IV
1. extent of disease
2. 5 yr survival
3. types
A
  1. tumour spread beyond true pelvis and/or into bladder/bowel mucosa
  2. <19%
  3. IVa - tumour spread to bladder/bowel or directly invading beyond true pelvis / IVb - distant metastases
41
Q

VULVAL CANCER

  1. what type are 90% of vulval cancers
  2. what is the median age of presentation
  3. how does it present
A
  1. squamous cell cancers and 5% is melanoma.
  2. 74
  3. lump, pain ,irritation or bleeding.
42
Q

VULVAR CANCER

  1. precursors
  2. association
A
  1. VIN( vulval intra-epithelial neoplasia ), Lichen sclerosus , Pagets disease (adenocarcinoma)
  2. Associated with persistent infection with HPV in 90% of cases
43
Q

VULVAR CANCER

  1. aetiology
  2. presentation
A
  1. Background of lichen sclerosusor VIN
  2. Vulval cancers commonly present with lump, pain, irritation or bleeding
    May be obvious ulcer
    Older women may delay presentation du to embarrasement
    Referral to secondary care may be delayed if there isn’t high index of suspsion
44
Q

VULVAR CANCER

investigation

A
  • History – vulval symptoms, treatmets, pmh, performacen status
  • Clinical examination – palpable groin LN, size and location of lesion, general medical condition. May be too painful to examine unless under GA
  • Haematological – FBC, U&E, LFT
  • Imaging – CXR
  • Anaesthetic review – usually old and frail so regional anaesthetic may be favourable
  • Histology – biopsy. Small – excised and large – wedge biopsy
45
Q

VULVAR CANCER

surgical treatment

A
  • Both curitive and palliation
  • > 1mm invasion – groin lymphadenectomy
  • Lateral disease can have ipsilateral LN dissection – if +ve LN, bilateral groin LN dissection needed
  • Central disease requires bilateral groin LN dissections
  • Wide local excision of vulval lesion and LN dissection through separate incisions along inguinal ligament
  • Occasionally plastic surgical reconstruction required
  • Complications – wound breakdown and infection, lymphocysts, lymphoedema, DVT/PE
46
Q

VULVAR CANCER

radiotherapy +/- chemotherapy

A
  • Before surgery -shrink primary to reduced morbidity of surgery
  • Used after surery if positive groin LNs to prevent regional recurrence – external beam radiotherapy to treat potentially positive pelvic LN
47
Q

VULVAR CANCER
FIGO stage 0
1. extent of disease

A

intraepithelial neoplasia

48
Q

VULVAR CANCER
FIGO stage I
1. extent of disease
2. types

A
  1. tumour limited to vulva or perineum <2cm diameter (-ve lymph nodes)
  2. 1a- <1mm depth / 1b - >1mm depth of invasion
49
Q

VULVAR CANCER
FIGO stage II
1. extent of disease

A

tumour of any size with spread to adjacent perineal structures with -ve lymph nodes

50
Q

VULVAR CANCER
FIGO stage III
1. extent of disease
2. types

A
  1. tumour any size with or without extension to adjacent perineal structures
  2. IIIa / IIIb / IIIc
51
Q

VULVAR CANCER
FIGO stage IVa
1. extent of disease

A

tumour spread to upper urethra, bladder, bowel, pelvic bones, and/ or fixed/ ulcerated inguinal lymph nodes

52
Q

VULVAR CANCER
FIGO stage IVb
1. extent of disease

A

distant metastases and/or +ve pelvic lymph nodes

53
Q

ENDOMETRIAL CANCER

aetiology

A
  • Post menopausal women
  • Incidence rising
  • Presence of unopposed oestrogen eg HRT, tamoxifen, oestrogen producing tumous, PCOS
54
Q

ENDOMETRIAL CANCER

risk factors

A

obesity, reduced endogenous progesterone production, nulliparity, PCOS, early menarche/ late menopause, genetic predisposition – HNPCC

55
Q

ENDOMETRIAL CANCER

protective factors

A

parity, COCP

56
Q

ENDOMETRIAL CANCER

histology

A
  • Endometrial hyperplasia – premalignant condtion and may have coincidental cancer in 50% of women
  • Adenocarcinoma – endometrial adenocarcinoma-87%, adenosquamous carcinoma -6%, clear cell or papillary serous carcinoma – 6%, MMMT – 1%
57
Q

ENDOMETRIAL CANCER

grading

A
G1 = well differentiated 
G2 = moderately differentiated 
G3 = poorly differentiated or high risk cell type
58
Q

ENDOMETRIAL CANCER

presentation

A
  • PMB
  • Younger women – menstrual disturbance
  • 1% picked up on cervical smears
59
Q

ENDOMETRIAL CANCER

history

A

presenting symptoms, menstrual history, parity, comorbidities, drug history (COCP, HRT, tamoxifen, antihypertensives, oral hypoglycaemics,family history)

60
Q

ENDOMETRIAL CANCER

examination

A
  • Rule out other causes of bleeding (vulval, vaginal, cervical pathology) with examination
  • Bimanual examination – uterine size, mobility, adnexal masses
61
Q

ENDOMETRIAL CANCER

  1. haematological investigations
  2. imaging
  3. biopsy
A
  1. FBC, U&E, LFT
  2. TVUSS, CT chest/abdomen/pelvis. – G3 disease for preoperative staging as increase risk of disease outside of uterus, MRI pelvis – local extent of tumour and presence of grossly involved pelvic lymph nodes, CXR
  3. Endometrial sampling if ET >4mm or persistent bleeding in woman with ET <4mm
    Hysteroscopy - LA as outpatient or GA as inpatient
62
Q

ENDOMETRIAL CANCER

treatment

A
  • Surgery – TAH and BSO and pelvic washings – via transverse or midline incision / laparascopic hysterectomy is gaining populatiry
  • Pelvic lyphadenectomy – role in low grade early disease controversial
  • Adjuvant radiotherapy- limited to vault brachytherapy. If intermediate risk – ERBT with or without vault brachytherapy boost for high risk (G3 stage IB) or localy advanced disease. Role of adjuvant chemo in addition to ERBT in high risk disease
  • PORTEC and ASTEC trials
  • Hormonal – high dose progesterone for advanced and recurrent disease. Largely aiming for palliation of symptoms
  • Palliative radiotherapy – ERBT given at lower risk and in few fractions to control local symptoms
63
Q

ENDOMETRIAL CANCER
FIGO stage I
1. extent of disease
2. 5 yr survival

A
  1. limited to uterine body (Ia / Ib)

2. 85%

64
Q

ENDOMETRIAL CANCER
FIGO stage II
1. extent of disease
2. 5 yr survival

A
  1. Tumour limited to uterine body and cervix

2. 75%

65
Q

ENDOMETRIAL CANCER
FIGO stage III
1. extent of disease
2. 5 yr survival

A
  1. extension to uterine serosa, peritoneal cavity, and or lymph nodes
  2. 45%
66
Q

ENDOMETRIAL CANCER
FIGO stage IV
1. extent of disease
2. 5 yr survival

A
  1. extension beyond true pelvis and/or involvement of bladder/bowel mucosa (IVa/IVb)
  2. 25%
67
Q

general risk factors for cancer?

A
  • Increasing age
  • Nulliparity (ovarian and uterine)
  • Obesity (ovarian and uterine)
  • HRT>10 years (ovarian)
  • Genetics (ovarian and uterine)
  • Early menarche and late menopause (uterine and ovarian)
  • Unopposed oestrogen action (uterine)
  • Smoking (cervical)
  • Multiple sexual partners (cervical)
  • Early age at intercourse (cervical)
68
Q

prevention strategies for cancer

A

30-50% of cancers can be prevented by avoiding risk factors and implementin existing evidence based prevetion strategies (HPV vaccination)

69
Q

early detection of gynaecological cancer

A

Early diagnosis- Awareness and accessing care
• clinical evaluation, diagnosis and staging
• Access to treatment
Screening- Visual inspection with acetic acid (VIA) for cervical cancer in low-income settings
• HPV testing for cervical cancer
• PAP cytology test for cervical cancer in middle- and highincome setting