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Year 4 - Reproductive Health > 1.06 - Gynaecological Oncology > Flashcards

1.06 - Gynaecological Oncology Flashcards

1
Q

What is cervical ectropion?

A

The presence of everted endocervical columnar epithelium on the ectocervix.

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2
Q

Pathophysiology of cervical ectropion.

A

High levels of oestrogen causes eversion of endocervical columnar epithelium onto the ectocervix.

The columnar epithelium is mucus-secreting, which can cause increased vaginal discharge.

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3
Q

Risk factors for cervical ectropion.

A

High levels of oestrogen:
- use of COCP
- pregnancy
- adolescence
- menstruating age

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4
Q

Cervical ectropion is a pre-malignant condition.

True or false?

A

False - cervical ectropion is physiological.

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5
Q

Clinical features of cervical ectropion.

A

Often asymptomatic finding of speculum examination.

It can occasionally present with:
- post-coital bleeding
- intermenstrual bleeding
- excessive discharge (non-purulent)

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6
Q

Differential diagnose for cervical ectropion.

A
  • cervical cancer
  • cervical intraepithelial neoplasia
  • cervicitis
  • pregnancy
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7
Q

How should cervical ectropion be investigated?

A
  • pregnancy test
  • triple swabs if signs of infection
  • cervical smear (exclude cervical intraepithelial neoplasia).
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8
Q

Management of cervical ectropion.

A

Normal variant, and does not require treatment unless symptomatic.

First line treatment is to stop any oestrogen containing medications (e.g. COCP).

If symptoms persist, cryotherapy or electrocautery ablation can be performed.

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9
Q

What are cervical polyps?

A

Benign growths protruding from the inner surface of the cervix, which can rarely undergo malignant change.

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10
Q

Causes of cervical polyps.

A

Hyperplasia of the columnar epithelium of the cervix:
- chronic inflammation
- abnormal response to oestrogen
- localised congestion of cervical vasculature

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11
Q

Clinical features of cervical polyps.

A

Asymptomatic - found on routine cervical screening.

If symptomatic:
- abnormal vaginal bleeding
- vaginal discharge
- infertility

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12
Q

Speculum findings of cervical polyps.

A

Polypoid growths projecting through the external os.

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13
Q

Differential diagnoses for cervical polyps.

A
  • endometrial polyp
  • cervical ectropion
  • cervical cancer
  • STIs
  • fibroids
  • endometritis
  • pregnancy related bleeding

In post menopausal women, always exclude endometrial carcinoma.

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14
Q

Investigations of cervical polyps.

A
  • triple swabs if suggestion of infection
  • cervical smear to exclude cervical intraepithelial neoplasia

Note in 1/4 of women with cervical polyps, endometrial polyps coexist. If bleeding continues following removal, an ultrasound scan should be arranged to assess the endometrial cavity.

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15
Q

How should cervical polyps be managed?

A

Remove them whenever identified using polypectomy forceps, as there is a small risk of malignant transformation.

Any excised polyps should be sent for histological examination to exclude malignancy.

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16
Q

Complications of polypectomy.

A
  • infection
  • haemorrhage
  • uterine perforation
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17
Q

What is the cause of cervical cancer?

A

The persistent infection (>2 years) with high-risk (oncogenic) human papillomavirus (hrHPV).

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18
Q

What is the pre-cancerous change in the cervix that preceed cervical cancer?

A

Cervical intraepithelial neoplasia (CIN)

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19
Q

Risk factors for cervical cancer.

A
  • HPV 16 and 18
  • early first sexual experience
  • multiple sexual partners
  • smoking
  • immunosuppression with HIV
  • COCP
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20
Q

Describe the national HPV vaccination programme.

A

All school children are offered the HPV vaccine, normally between the ages of 11-13.

This protects them against contracting HPV trains 6, 11 (prevent genital warts) and 16,18 (prevent CIN and cervical, vulval, vaginal and anal cancers).

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21
Q

Describe the national HPV screening programme.

A

Cervical screening is available to women and people with a cervix aged 25-64.

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22
Q

What is the cervical cancer screening process?

A

A speculum is inserted and a brush is rotated against the transformation zone of the cervix. The brush is then sent off to the laboratory for testing:

  • HPV screening
  • liquid based cytology
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23
Q

What are the next steps for the following results of the cervical screening programme?

a) hrHPV negative

b) hrHPV positive (normal smear)

c) hrPV positive (abnormal smear)

d) inadequate smear

A

a) routine screening

b) repeat smear in 12 months

c) colposcopy

d) repeat smear within 3 months - colposcopy if remains inadequate

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24
Q

What is colposcopy?

A

Required to diagnose and stage CIN.

Clinician stains the cervix with acetic acid, making abnormal areas turn white (acetowhitening - the more abnormal the areas, the whiter it becomes).

Iodine stain is used to look for abnormal cells - areas of CIN will remain unstained.

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25
Q

How is CIN diagnosed?

A

Biopsy of areas of acetowhitening on colposcopy for staging.

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26
Q

What is the prognosis of CIN 1?

A

60% regresses spontaneously.

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27
Q

How should CIN be managed?

A

CIN 1 - no treatment necessary.

CIN 2/3 - large loop excision of the transformation zone (LLETZ biopsy).

Other options include cone biopsy if abnormal area extends in the cervical canal, or cryotherapy.

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28
Q

Can a pregnant lady be take part in the cervical screening programme?

A

No - screening should be delayed for pregnant individuals until 12 weeks post-partum.

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29
Q

What is the most common type of cervical cancer?

A

Squamous cell carcinoma (~70%).

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30
Q

Pathophysiology of cervical cancer.

A

Persistent hrHPV infection causes CIN, which progresses to cervical cancer over the course of 10-20 years.

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31
Q

What is HPV and how does it cause cancer?

A

Sexually transmitted virus, which can usually be cleared by the immune system within 2 years.

Oncogenic HPV strains can cause persistent infection, producing proteins to inhibit the p53 tumour suppressor protein. This allows for uncontrolled cell division, and can go on to cause pre-malignant and malignant changes.

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32
Q

Clinical features of cervical cancer.

A
  • abnormal vaginal bleeding
  • vaginal discharge (blood-stained & foul smelling)
  • dyspareunia
  • pelvic pain
  • weight loss

NB often asymptomatic, and only detected through routine screening.

33
Q

How should suspected cervical cancer be examined?

A

Speculum examination: assess for evidence of bleeding, discharge and ulceration.

Bimanual examination: assess for pelvic masses.

GI examination: assess for hydronephrosis, hepatomegaly, rectal bleeding, mass on PR.

34
Q

Differentials for cervical cancer.

A
  • cervical ectropion
  • CIN
  • cervical polyps
  • endometrial cancer
  • STIs
  • pregnancy related bleeding
35
Q

In women presenting with symptoms suggestive of cervical cancer, the initial investigation depends on age:

a) pre-menopausal

b) post-menopausal

A

a) test for chlamydia trachomatis infection. If positive, treat infection. If negative, or symptoms persist beyond treatment, refer for colposcopy and biopsy.

b) urgent colposcopy and biopsy.

36
Q

If cervical cancer is confirmed via colposcopy and biopsy, what further investigations may be required?

A
  • CT CAP (?mets)
  • MRI pelvis / PET (staging)
  • EUA with further biopsy
37
Q

What staging system is used for cervical cancer?

A

FIGO staging.

38
Q

What are the surgical management options for cervical cancer?

a) Stage 1a

b) Stage 1b/2a

c) Stage 4a or recurrent disease

A

a) radical trachelectomy if fertility-preservation is a priority (removal of cervix and upper vagina). Otherwise, a laparoscopic hysterectomy with pelvic lymphadenectomy.

b) Radical hysterectomy plus lymphadenectomy.

c) anterior/posterior/total pelvic extenteration.

39
Q

What are the chemotherapy management options for cervical cancer?

A

Cisplatin-based therapy given before treatment by surgery or radiotherapy (neoadjuvent chemotherapy), or after treatment (adjuvent chemotherapy).

It is also the mainstay of treatment in the palliative setting.

40
Q

What are the radiotherapy management options for cervical cancer?

A

Stage 1b to 3 - offered in conjunction with chemotherapy over a 5-8 week course (chemoradiation therapy).

NOTE there is no survival benefit for additional hysterectomy.

41
Q

What is the most common form of endometrial cancer?

A

Adenocarcinoma.

42
Q

What is the pathophysiology of endometrial cancer?

A

Unopposed oestrogen stimulates the endometrium, predisposing to malignancy.

43
Q

Risk factors for endometrial cancer.

A

Prolonged exposure to unopposed oestrogen:
- obesity*
- early menarche / late menopause
- low parity
- PCOS
- HRT (oestrogen alone)
- tamoxifen use

Genetic conditions that predispose to endometrial cancer include HNPCC and BRCA1/BRCA2.

*approximately 40% of endometrial cancer cases are linked to obesity.

44
Q

What is the link between obesity and increased levels of unopposed oestrogen?

A

The greater the amount of subcutaneous fat, the faster the rate of peripheral aromatisation of androgens to oestrogens.

45
Q

Clinical features of endometrial cancer (history).

A

POSTMENOPAUSAL BLEEDING.

  • clear / white vaginal discharge
  • abnormal cervical smears

NB although rare, in premenopausal women symptoms include irregular bleeding or intermenstrual bleeding.

46
Q

Clinical features of endometrial cancer (examination).

A

Abdominal examination: abdominal or pelvic masses.

Speculum examination: vulval/vaginal atrophy; cervical lesions.

Bimanual examination: assess size and axis of uterus prior to endometrial sampling.

47
Q

Differential diagnoses for post-menopausal bleeding.

A
  • endometrial cancer
  • vulval atrophy
  • vulval pre-malignant or malignant conditions
  • cervical polyps
  • cervical cancer
  • endometrial hyperplasia
  • endometrial atrophy
48
Q

How should endometrial cancer be investigated?

A

First line: transvaginal ultrasound scan.

If endometrial thickness >4mm = endometrial biopsy.

If case is high risk, may elect for hysteroscopy with biopsy.

49
Q

What staging system is used for endometrial cancer?

A

FIGO staging

50
Q

How should endometrial hyperplasia be treated?

a) hyperplasia without atypia

b) atypical hyperplasia

A

a) progesterones (e.g. IUS) and surveillance biopsies.

b) total abdominal hysterectomy + bilateral salingo-oophorectomy.

51
Q

How should endometrial carcinoma be managed?

a) Stage 1

b) Stage 2

c) Stage 3

d) Stage 4

A

a) Total hysterectomy and bilateral sapingo-oophorectomy.

b) Radical hysterectomy (surrounding vaginal tissue also removed alongside supporting ligaments of the uterus) + lymphadenectomy.

c) Maximal de-bulking surgery + chemoradiotherapy

d) Maximal de-bulking surgery + low dose radiotherapy / high dose oral progesterones (palliative).

52
Q

What are the risk factors for ovarian cancer?

A

Surface epithelial irritation during ovulation - the more ovulations that take place, the increased risk of developing malignancy:

  • nulliparity
  • early menarche / late menopause
  • HRT (oestrogen only)
  • smoking
  • obesity

BRCA1/BRCA2 and HNPCC are hereditary associations.

53
Q

What is the Risk of Malignancy Index (RMI)?

A

The risk stratification tool used in patients with suspected ovarian cancer.

RMI = U x M x CA125

54
Q

Clinical features of ovarian cancer (history).

A
  • bloating
  • change in bowel habit / urinary frequency
  • weight loss
  • IBS
  • bleeding per vagina
55
Q

Clinical features of ovarian cancer (examination).

A
  • abdominal mass in pelvis
  • ascites
  • pelvic discharge / bleeding
  • adnexal masses
  • cervical excitation
56
Q

How should suspected ovarian cancer be investigated?

A
  • pelvic ultrasound for pelvic masses
  • CA125

Calculate RMI. If ovarian cancer is confirmed, CXR and CT AP can be taken for staging.

57
Q

How should ovarian cancer be managed?

A

Staging laparotomy with attempt to debulk the tumour.

Adjuvent chemotherapy recommended, unless early and low-grade disease.

Follow up involving monitoring of CA125 every 5 years.

58
Q

What is a Bartholin cyst?

A

A fluid-filled sac within one of the Bartholin’s glands of the vagina, caused by a build-up of mucus secretions and blockage of the duct.

The cyst itself can become infected, and develop into an abscess.

59
Q

Risk factors of Bartholin’s cysts.

A
  • personal history of Bartholin’s cysts
  • sexually active
  • history of vulval surgery
  • nulliparous
60
Q

Clinical features of Bartholin’s cysts (history).

A
  • asymptomatic
  • vulvar pain
  • superficial dyspareunia

The cysts can undergo spontaneous rupture, after which the patient typically experiences a sudden relief of pain.

NB Bartholin’s abscess present with an acute onset of pain, and/or difficulty passing urine.

61
Q

Clinical features of Bartholin’s cysts (examination).

A

Unilateral labial mass.

Bartholin’s cyst - soft, fluctuant and non-tender.

Bartholin’s abscess - tense and hard, with surrounding cellulitis.

62
Q

Differential diagnoses for a mass in the vulval region.

A
  • Bartholin’s cyst
  • fibroma
  • vulval cancer
63
Q

How are Bartholin’s cysts investigated?

A

Usually a clinical diagnosis, with no further investigation required.

If woman is aged >40 years, cyst biopsy performed to exclude vulval carcinoma.

If indications of STI, screen and treat.

64
Q

How can small Bartholin’s cysts be managed?

A

If small and asymptomatic, no treatment is required.

Warm baths can be recommended, as they may stimulate spontaneous rupture.

65
Q

How can large / irritable Bartholin’s cysts be managed?

A

Word Catheter - an incision made into the cyst, and a catheter inserted for drainage.

Marsupialisation - vertical incision made into the cyst, allowing for spontaneous draining of the cavity.

66
Q

What is Lichen sclerosus?

A

Chronic inflammatory skin disease of the anogenital region in women, peaking in prepubescent girls and post-menopausal women.

67
Q

What are the causes of Lichen sclerosus?

A

Autoimmune aetiology causing high titre of antibodies to extracellular matrix protein 1.

Main risk factors are:
- family history
- other autoimmune disorders

68
Q

Clinical features of Lichen sclerosus (history).

A
  • itching
  • pain
  • dyspareunia
69
Q

Clinical features of Lichen sclerosus (examination).

A

White atrophic patches on skin in anogenital regions.

Evidence of adhesions or scarring:
- clitoral hood fusion
- fusion of labia minor to labia majora
- posterior fusion resulting in loss of vaginal opening

70
Q

Investigations of Lichen sclerosus.

A

Clinical diagnosis so no further investigations are necessary, unless clinical uncertainty (biopsy).

71
Q

How should Lichen sclerosus be managed?

A

Topical steroids, such as clobetasol propionate.

Once daily at night for 4 weeks > alternate nights for 4 weeks > twice weekly for 4 weeks.

Patients with Lichen sclerosus should be followed-up, as there is a 5% lifetime risk of squamous cell carcinoma.

72
Q

What is the main type of vulval carcinoma?

A

Squamous cell carcinoma

73
Q

Risk factors for vulval carcinoma.

A
  • hrHPV infection
  • multiple sexual partners
  • early age of sexual intercourse
  • Lichen sclerosus
  • Lichen planus
74
Q

Presentation of vulval carcinoma.

A
  • itching
  • burning
  • soreness
  • bleeding
  • pain
  • lump
75
Q

How can vulval carcinoma be diagnosed?

A

Diagnosis is made via Keye’s punch biopsy under local anaesthetic.

It is important to take the biopsy from the edge of the lesion to include a portion of the adjacent normal epithelium.

76
Q

How is vulval cancer staged?

A

FIGO staging.

77
Q

How should early vulval cancer be treated (stage 1 and 2)?

A

Resection of the primary tumour with disease-free surgical margins and appropriate groin lymphadenectomy.

78
Q

What are the complications of groin lymphadenectomy?

A
  • wound dehiscence
  • infection
  • lymphoedema
  • immobility
  • prolonged hospitalisation
79
Q

How should advanced vulval cancer be treated (stage 3 and 4)?

A

Radical vulvectomy with bilateral resection of inguinofemoral lymph nodes.

Year 4 - Reproductive Health (12 decks)

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