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Phase 3a topics > gynae cancers > Flashcards

gynae cancers Flashcards

1
Q

Histology cervical cancer

A

squamous cell cancer (80%)
adenocarcinoma (20%)

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2
Q

Biggest risk factor in developing cervical cancer?

A

HPV 16,18 & 33

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3
Q

What virsuses cause genital warts

A

HPV 6 & 11

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4
Q

How does HPV cause cervical cancer?

A

HPV 16 & 18 produces the oncogenes E6 and E7 genes respectively
E6 inhibits the p53 tumour suppressor gene
E7 inhibits RB suppressor gene

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5
Q

screening pathway for cervical cancer

A
  1. Test for high-risk human papillomavirus strains (hrHPV)
    If negative return to normal recall
  2. If positive → cytology
    If cytology negative, retest hrHPV in 12 months
    If hrHPV is then negative return to recall, if hrHPV positive repeat again in 12 months
    If hrHPV is positive at 24 months, cytology is normal refer to colposcopy anway
  3. If cytology positive → colposcopy
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6
Q

If sample is inadequate HPV cervical screening, what do you do?

A

Retest in 3 months
If inadequate again –> colposcopy

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7
Q

Normal recall for cervical screening

A

Age 25 years: first invitation.
Age 25-49 years: screening every 3 years.
Age 50-64 years: screening every 5 years.
Women 65 years of age or older if they have not had a cervical screening test since 50 years of age or a recent cervical cytology sample is abnormal.

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8
Q

cervical screening and pregnancy

A

cervical screening in pregnancy is usually delayed until 3 months postpartum unless missed screening or previous abnormal smears.

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9
Q

women with HIV and cervical screening

A

Cervical cytology at diagnosis.

Cervical cytology should then be offered annually for screening.

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10
Q

What is the test of cure pathway for CIN?

A

Individuals who have been treated for CIN1, CIN2, or CIN3 should be invited 6 months after treatment for a test of cure repeat cervical sample in the community

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11
Q

Management of cervical intraepitlealial neoplasia

A

Large loop excision of the transformation zone (LLETZ)

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12
Q

Cervical cancer stage 1A

A

Confined to cervix, only visible by microscopy and less than 7 mm wide:
A1 = < 3 mm deep
A2 = 3-5 mm deep

Gold standard of treatment is hysterectomy +/- lymph node clearance
Nodal clearance for A2 tumours

For patients wanting to maintain fertility, a cone biopsy with negative margins can be performed

Radical trachelectomy is also an option for A2

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13
Q

Cervical cancer stage 1B

A

Confined to cervix, clinically visible or larger than 7 mm wide:
B1 = < 4 cm diameter
B2 = > 4 cm diameter

Radiotherapy with concurrent chemotherapy is advised
Radiotherapy may either be bachytherapy or external beam radiotherapy
Cisplatin is the commonly used chemotherapeutic agent

For B2 tumours: radical hysterectomy with pelvic lymph node dissection

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14
Q

Stage II and III cervical cancer

A

Stage 2: Extension of tumour beyond cervix but not to the pelvic wall
A = upper two thirds of vagina
B = parametrial involvement

Stage 3: Extension of tumour beyond the cervix and to the pelvic wall
A = lower third of vagina
B = pelvic side wall

NB: Any tumour causing hydronephrosis or a non-functioning kidney is considered stage III

Radiation with concurrent chemotherapy
Radiotherapy may either be bachytherapy or external beam radiotherapy
Cisplatin is the commonly used chemotherapeutic agent

If hydronephrosis, nephrostomy should be considered

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15
Q

Stage IV cervical cancer

A

Extension of tumour beyond the pelvis or involvement of bladder or rectum
A = involvement of bladder or rectum
B = involvement of distant sites outside the pelvis

Radiation and/or chemotherapy is the treatment of choice
Palliative chemotherapy may be best option for stage IVB

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16
Q

What complications is there with LLETZ and cone biopsy

A

pre term labour in future pregnancies

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17
Q

What does FSH do?

A

development of follicle beyond secondary
stimulates granulosa cells to multiply and produce oestrogen
Induces LH receptors on granulosa cells of the dominant follicle

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18
Q

What does oestrogen do?

A

stimulates proliferation of granulosa cells
exerts negative feedback on the secretion of gonadotrophins
works with progesterone to maintain lining in luteal phase

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19
Q

What does LH do?

A

stimulates theca cells to synthesise androgens
the mid-cycle surge in LH causes ovulation

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20
Q

What does progesterone do?

A

Helps to build and maintain endometrial lining
progesterone is produced in large amounts by the corpus luteum to maintain the lining

the drop in progesterone due to degeneration of corpus luteum (due to no hCG) causes endmetrial shedding

21
Q

what are the 4 key follicular stages

A

Primordial follicles
Primary follicles
Secondary follicles
Antral follicles (also known as Graafian follicles)

22
Q

Histology of most endometrail cancers

A

adenocarcinoma

23
Q

risk factors for endometrial cancer

A

obesity
Nulliparity (Nulliparity is a risk factor for endometrial cancer. This is because during pregnancy, the balance of hormones shifts towards progesterone, which is a protective factor.)
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT). The BNF states that the additional risk is eliminated if a progestogen is given continuously
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma

24
Q

2 week wait criteria for ?endometrial cancer

A

Age over 55 with post menopausal bleeding (must be >12 months since last period)

Consider if over 55 and:
Unexplained vaginal discharge
Visible haematuria plus raised platelets, anaemia or elevated glucose levels

25
Q

Investigations for endometrial cancer?

A

Transvaginal ultrasound for endometrial thickness (normal is less than 4mm post-menopause)

Hysteroscopy with endometrial biopsy

Pipelle biopsy, which is highly sensitive for endometrial cancer making it useful for excluding cancer

26
Q

Stages of endometrial cancer?

A

Stage 1: Confined to the uterus
Stage 2: Invades the cervix
Stage 3: Invades the ovaries, fallopian tubes, vagina or lymph nodes
Stage 4: Invades bladder, rectum or beyond the pelvis

27
Q

Managemnet of endometrial cancer

A

total abdominal hysterectomy with bilateral salpingo-oophorectomy, also known as a TAH and BSO (removal of uterus, cervix and adnexa).

progestogen therapy is sometimes used in frail elderly women not consider suitable for surgery

28
Q

how may endometrial hyperplasia present?

A

intermenstrual bleeding

29
Q

What is endometrial hyperplasia ?

types?

A

abnormal proliferation of the endometrium in excess of the normal proliferation that occurs during the menstrual cycle. A minority of patients with endometrial hyperplasia may develop endometrial cancer

types:
hyperprolifertaion without atypia
atypical hyperplasia

30
Q

Management of endometrial hyperplasia?

A

Intrauterine system (e.g. Mirena coil)
Continuous oral progestogens (e.g. medroxyprogesterone or levonorgestrel) and retest in 3 months

If atypia : hysterectomy advised

31
Q

Invetsigations for ovarian cancer?

A

CA-125

If CA-125 is over 35 the do abdo USS

Diagnosis is difficult and usually involves CT for staginh and diagnostic laparotomy

32
Q

Most common ovarian cancer histlogy

A

epithelial cell tumour - serous tumour

33
Q

What are teratomas?

A

germ cell tumours

34
Q

Particular complication with teratomas?

A

ovarian torison

35
Q

Blood tests in teratomas

A

raised alpha-fetoprotein (α-FP)
raised human chorionic gonadotrophin (hCG)

36
Q

Risk factors for ovarian cancer

A

Age (peaks age 60)
BRCA1 and BRCA2 genes (consider the family history)
Increased number of ovulations
Obesity
Smoking
Recurrent use of clomifene

Factors that increase the number of ovulations, increase the risk of ovarian cancer. These include:
Early-onset of periods
Late menopause
No pregnancies

37
Q

2 week wait criteria for ovarian cancer

A

Ascites
Pelvic mass (unless clearly due to fibroids)
Abdominal mass

38
Q

What investigation should women under 40 years with a complex ovarian mass have

A

?teratoma

Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)

39
Q

What can raise CA-125?

A

Endometriosis
Fibroids
Adenomyosis
Pelvic infection
Liver disease
Pregnancy

40
Q

Management ovarian cancer

A

Ovarian cancer will be managed by a specialist gynaecology oncology MDT. It usually involves a combination of surgery and chemotherapy.

41
Q

Management ovarian cancer

A

Ovarian cancer will be managed by a specialist gynaecology oncology MDT. It usually involves a combination of surgery and chemotherapy.

42
Q

Stages of ovarian cancer

A

Stage 1: Confined to the ovary
Stage 2: Spread past the ovary but inside the pelvis
Stage 3: Spread past the pelvis but inside the abdomen
Stage 4: Spread outside the abdomen (distant metastasis)

43
Q

Most common histology vulval cancer

A

squamous cell carcinomas

44
Q

Invetsigations for vulval cancer

A

Biopsy of the lesion
Sentinel node biopsy to demonstrate lymph node spread
Further imaging for staging (e.g. CT abdomen and pelvis)

45
Q

management of lichen sclerosus

A

topical steroids and emollients

46
Q

Presentation of vaginal cancer?

A

abnormal discharge

47
Q

management vulval cancer?

A

Wide local excision to remove the cancer
Groin lymph node dissection
Chemotherapy
Radiotherapy

48
Q

what do theca cells do?

A

stimulated by LH to make androgen which can be converted to oestrogen by granulosa cells

49
Q

what do granulosa cells do?

A

stimulated by FSH to produce estrodiol

Phase 3a topics (39 decks)

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