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Reproductive Health (Y4) > 6- Gynaecological oncology > Flashcards

6- Gynaecological oncology Flashcards

1
Q

gynae cancers

A

from most common to leat
- endometrial/ uterus
- ovary
- cervix
- vulva
- vaginal

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2
Q

endometrial cancer background

A
  • Commonest
  • Rare before 35 and rare after 80
  • More common in postmenopausal
  • Common in western world
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3
Q

types of endometrial cancer

A

o Premalignant stage: Endometrial hyperplasia
o Endometrial carcinoma (adenocarcinoma)
o Sarcoma

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4
Q

endometrial hyperplasia

A

Pre-malignant condition of endometrial cancer caused by excess oestrogen without progesterone
e.g.
- early period/ late menopause
- tamoxifen
- obesity
- HRT unopposed with oestrogen
- diabetes

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5
Q

types of endometrial hyperplasia

A

o Hyperplasia without atypia
o Atypical hyperplasia- more likely to become cancer

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6
Q

presentation of endometrial hyperplasia

A

heavy bleeding

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7
Q

management of endometrial hyperplasia

A
  • Mirena
  • Continuous oral progestogens
  • Hysterectomy: for high risk endoplasia with atypia
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8
Q

where does endometrial hyperplasia metastasise to

A
  • Rare at presentation of type 1 cancers
  • Intraperitoneal, lung, bone, brain
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9
Q

causes/ rf for endometrial cancer

A
  • Obesity- adipose is source of oestrogen
  • Early menarche/ late meno
  • Nulliparity
  • PCOS- increased exposure to unopposed oestrogen due to lack of ovulation (due to less likely to ovulate and form CL, which produces progesterone)
  • Unopposed oestrogen e.g. tamoxifen
  • Previous breast or ovarian cancer (BRCA ½)
  • Endometrial polyps
  • Diabetes- due to increased production of insulin in T2
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10
Q

protective factors for endometrial cancer

A
  • Continuous combined HRT
  • COCP/ mirena
  • Multiparety
  • Smoking- antiestrogenic
  • Coffee/ Tea
  • Healthy lifestyle/ PT
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11
Q

presentation of endometrial cancer

A
  • Post menopausal bleeding
  • PCB/ intermenstrual bleeding
  • Abnormal discharge
  • Haematuria
  • Anaemia
  • Raised platelet count
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12
Q

staging of endometrial cancer

A

FIGO

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13
Q

investigations for women presenting with prolonged/ heavy bleeding (especially if postmenopausal)

A

one stop post menopausal bleeding clinic
- H and E
- FBC
- Transvaginal ultrasound for endometrial thickness (normal is less than 4mm post-menopause)
- Pipelle biopsy, which is highly sensitive for endometrial cancer making it useful for excluding cancer (quicker and less invasive than hysteroscopy)
- Hysteroscopy with endometrial biopsy

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14
Q

once endometrial cancer is diagnosed what investigations should happen

A
  • FBC, U and E, LFT
  • CT CAP
  • MRI pelvis
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15
Q

management of endometrial cancer depends on

A
  • Stage
  • Age
  • Fitness
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16
Q

management of endometrial cancer

A

Preferred treatment: Surgical
Surgical treatment 80% of patients have primary surgery
- Hysterectomy PLUS bilateral salpingo-oophorectomy, peritoneal washings
- Laparoscopic / Open

Non Surgical Alternatives
- Progestagens
- Primary Radiotherapy

Adjuvant Radiotherapy if high risk of recurrence
- External beam
- Brachytherapy

Advanced disease/inoperable disease/unfit for surgery
- Chemotherapy
- Radiotherapy
- Hormones
- Palliative Care

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17
Q

ovarian cancer background

A
  • 2nd commonest gynae cance
  • Incidence rising
  • Peak age 70-74
  • No pre-malignant stage
    o THEREFORE NO SCREENING PROGRAMME
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18
Q

where does ovarian cancer metastasise to

A

peritoneal

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19
Q

causes of ovarian cancer

A
  • Obesity
  • Nulliparity
  • Early men/ late men
  • Unopposed oestrogen
  • Family history
  • BRCA1/2
  • Endometriosis
  • Clomifene recurrent use
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20
Q

protective factors agains ovarian cancer

A
  • COCP
  • Pregnancy
  • Breastfeeding
  • Hysterectomy
  • Oophorectomy
  • Sterilisation
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21
Q

presentation of ovarian cancer

A

late due to non specific
- Abdominal swelling and ascites
- Pelvic mass
- Pain
- Anorexia
- N and V
- Weight loss
- Vaginal bleeding
- Bowel symptoms
- Hip/groin pain- mass pressing on obturator nerve

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22
Q

investigations for ovarian cancer

A
  • H and E
  • US
  • FBC and U&E
  • Tumour marker
    o CA125 >35 IU/mL
    o AFP/LDH/ HCG (<40 years)
  • Pelvic US
  • Surgical exploration
  • Histopathology
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23
Q

how to stage ovarian cancer

A
  • CXR
  • CT to assess peritoneal, omental and retroperitoneal disease
  • Cytology of ascitic tap (paracentesis)
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24
Q

types of ovarian cancer - broad

A
  • Benign tumour
  • Borderline tumour
  • Malignant
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25
Q

ovarian cancer can originate from a number of cell lines

A

Epithelial
- serous
- mucinous
- endometriod
- clear
- cell

Germ cell
- teratoma
- yolk sac
- choriocarcinoma
- dysgerminoma

Stroma/sex cord
- granulosa cell
- sertoli-leydig cell

Miscellaenous and metastatic
- primary lymphoma
- metastases
- krukenberg tumour

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26
Q

most common types of ovarian cancer

A

Epithelial
o Serous
o Mucinous-
Germ cells
o Teratoma (dermoid)

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27
Q

krugenberg tumour

A

Krugenberg tumour- metastasis in ovary usually from GI cancer- signet ring cells

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28
Q

staging of ovarian cancer

A
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29
Q

management of ovarian cancer: epithelial cancer

A
  • Surgery + chemotherapy
  • Staging laparotomy, TAH PLUS BSO and debulking
  • Platinum (Cisplatin, carboplatin) and Taxane (paclitaxel)
  • In women of reproductive age, where the tumour is confined to one ovary, oophorectomy only may be considered
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30
Q

management of ovarian cancer: non-epithelial tumours

A

often occur in young women and can be extremely chemo-sensitive (e.g. germ cell). Often treated with combination of ‘conservative’ surgery and chemo

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31
Q

management of ovarian cancer: recurrent disease

A

palliative chemo

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32
Q

causes of high CA125

A

CA125 is a tumour marker for epithelial cell ovarian cancer. It is not very specific, and there are many non-malignant causes of a raised CA125:
* Endometriosis
* Fibroids
* Adenomyosis
* Pelvic infection
* Liver disease
* Pregnancy

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33
Q

risk of malignancy index

A
34
Q

cervical cancer background

A
  • 3rd most common gynae in England
  • More common in developing
  • Bimodal age distribution
  • Low socioecomic groups
35
Q

types of cervical cancer

A
  • 2/3 squamous cell carcinoma
    -15% adenocarcinoma
36
Q

50% with cervical cancer have nerve had a

A

smear

37
Q

ovarian cancer risk factors

A
  • HPV
  • Young age at first intercourse
  • Multiple partners
  • Exposure
  • Smoking
  • COCP
  • Immunosuppression/ HIV
  • Non compliance with cervical screening
38
Q

protective factos for cervical cancer

A
  • HPV vaccine
  • Cervical screening compliance
39
Q

presentation of cervical cancer

A
  • Post coital bleeding
  • PMH
  • IMB
  • Dyspareunia
  • Blood stained vaginal discharge
  • In advanced
    o Fistulae
    o Renal failure
    o Nervous foot pain
    o Lower limb oedema
40
Q

human papilloma virus

A
  • Most women will be infected at some time
  • HPV infection is common in late teens and early twenties
  • Infection lasts on average 8 months
  • Prevalence 5% by age 50
    o Immunological clearance of virus
    o Reduced opportunities for re-infection
  • HPV is an accepted necessary (but not sufficient) cause of cervical cancer
  • Cervical cancer could be viewed as a rare complication of a common infection
  • A vaccine can reasonably be expected to prevent most cases of cervical carcinoma
  • Biggest implication is in developing nations
41
Q

oncogenic HPV

A

16 and 18

42
Q

wart/ low-risk HPV

A

6 and 11

43
Q

pathophysiology of HPV and cervical cancer

A

HPV (esp subtypes 16 & 18): produce proteins (E6&7) which suppress the products of ‘p53’ tumour suppressor gene in keratinocytes

44
Q

presentation of HPV

A
  • Asymptomatic
  • Can be cleared or persist or cause CIN
45
Q

CIN

A

cervical intraepithelial neoplasia

46
Q

cervical intraepithelial neoplasia

A

is a grading system for the level of dysplasia (premalignant change) in the cells of the cervix. CIN is diagnosed at colposcopy (not with cervical screening). The grades are:
* CIN I: mild dysplasia, affecting 1/3 the thickness of the epithelial layer, likely to return to normal without treatment
* CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated
* CIN III: severe dysplasia, very likely to progress to cancer if untreated

47
Q

progonosis of CIN

A

CIN III is sometimes called cervical carcinoma in situ.
* Asymptomatic and pre-malignany
* Can regress, persist or progress to cancer
* Best Estimates
* 60% CIN1 regress spontaneously
* 30% of CIN3 progress to invasion over 5-10 years

48
Q

management of CIN

A
  • see and treat concept
  • excisional: LLETZ or cold knife cone
  • destructive: cryocautery, diaethermy
49
Q

LLETZ

A

large loop excision of the transformation zone (LLETZ). LLETZ is often done at the same time as colposcopy.

50
Q

staging of cervical cancer

A

screening is very importnant due to less advanced cancers have a much better prognosis

51
Q

management of cervical cancer

A
  1. Microinvasive carcinoma: can be more conservative. If fertility is an issue, then cone biopsy can be used. Once family is complete, hysterectomy is appropriate.
  2. Clinical Lesions (1b - 2a): Wertheim’s radical hysterectomy or chemoradiotherapy (survival same)
  3. Clinical lesions beyond stage 2a: Chemoradiotherapy
  4. Postoperative radiotherapy: with lymph node involvement
  5. Recurrent disease: Radiotherapy, chemotherapy, monoclonal antibody (bevacizumab) exenteration (removal of most pelvic organs), palliative care
52
Q

complications of treatment

A
53
Q

cervical screening starts at

A
  • Starts at 25 years old
  • Every 3 years from 25-50
  • 5 years from 50-65
  • After 65 selected patients only
54
Q

what happens during a smear

A
  • Speculum examination
  • Cells collected from cervix (transformation zone) and exfoliated morphology examined
  • Samples initially tested for high risk HPB and then Liquid based cytology- UK
55
Q

classification of smear results

A
  • Normal
  • Inadequate
  • Borderline- HPV test
  • Mild Dyskaryosis- HPV test
  • Moderate Dyskaryosis- coloscopy
  • Severe Dyskaryosis- coloscopy
  • Possible Invasion
56
Q

management of smear results

A
  • Inadequate sample – repeat the smear after at least three months
  • HPV negative – continue routine screening
  • HPV positive with normal cytology – repeat the HPV test after 12 months
  • HPV positive with abnormal cytology – refer for colposcopy
57
Q

coloscopy

A

It involves inserting a speculum and using equipment (a colposcope) to magnify the cervix. This allows the epithelial lining of the cervix to be examined in detail. During colposcopy, stains such as acetic acid and iodine solution can be used to differentiate abnormal areas.

58
Q

coloscopy and acetic acid

A
  • Causes abnormal cells to appear white. This appearance is described as acetowhite. This occurs in cells with an increased nuclear to cytoplasmic ratio (more nuclear material), such as cervical intraepithelial neoplasia and cervical cancer cells.
59
Q

coloscopy and schiller iodine test

A
  • Involves using an iodine solution to stain the cells of the cervix. Iodine will stain healthy cells a brown colour. Abnormal areas will not stain.
60
Q

biopsy and cervical cancer summary

A

Large loop excision of transformational zoen (LLETZ)
- Under local anaesthetic during colposcopy
- Loop of wire with electrical current (diathermy) used tor emove abnormal tissue
- Risk of infection and preterm labour

Punch biopsy

Cone biopsy for CIN
- For high risk CIN or for low grade cervical cancer - under general
- Surgeon removes a cone-shaped piece of the cervix using a scalpel (pain, bleeding, infection, stenosis of cervix)

61
Q

HPV vaccine

A

Vaccination
* Gardasil: 6,11,16,18
* Cervarix:16 & 18
* NHS Programme
* 3 injections over 6 months
* Ideally prior to SI
* 5 years protection
* Still need smears (HPV 31, 45 & others)

62
Q

HPV Vaccination

A
  • Gardasil: 6,11,16,18
  • Cervarix:16 & 18
  • NHS Programme
  • 3 injections over 6 months
  • Ideally prior to SI
  • 5 years protection
  • Still need smears (HPV 31, 45 & others)
63
Q

vulval cancer

A
  • Very rare
  • Elderly patients
  • Usually SCC
  • Caused by HPV and chronic skin disease
  • premalignant condition - VIN
64
Q

Vulvar intrapetihelial neoplasia (VIN)

A
  • Involves squamous epithelium
  • Can resolve spontaneously
  • Can progress to vulval cancer
65
Q

presentation of VIN

A
  • Can be asymptomatic
  • Can present with itching/burning/pain
66
Q

treatment of VIN

A
  • Conservative: Antihistamine
  • Medical: Imiquimod
  • Surgical: Excision
67
Q

risk factors for vulval/ vaginal cancer

A
  • HPV
  • Herpes simples virus type 2
  • Smoking
  • Immunosuppression
  • Chronic vulvar irritation
  • Conditions such as Lichen sclerosis
68
Q

Vulval cancer may present with symptoms of:

A
  • Vulval lump
  • Ulceration
  • Bleeding
  • Pain
  • Itching
  • Lymphadenopathy in the groin

Vulval cancer most frequently affects the labia majora, giving an appearance of:
* Irregular mass
* Fungating lesion
* Ulceration
* Bleeding

69
Q

investigation 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)
70
Q

lichen sclerosis

A

Lichen sclerosus is a chronic inflammatory skin condition that presents with patches of shiny, “porcelain-white” skin. It commonly affects the labia, perineum and perianal skin in women. It can affect other areas, such as the axilla and thighs. It can also affect men, typically on the foreskin and glans of the penis.

71
Q

pathophysiology of lichen sclerosis

A

Lichen sclerosus is thought to be an autoimmune condition. It is associated with other autoimmune diseases, such as type 1 diabetes, alopecia, hypothyroid and vitiligo.

72
Q

pathophysiology of lichen sclerosis

A

Lichen sclerosus is thought to be an autoimmune condition. It is associated with other autoimmune diseases, such as type 1 diabetes, alopecia, hypothyroid and vitiligo.

73
Q

diagnosis of lichen sclerosus

A

usually made clinically, based on the history and examination findings.

Where there is doubt, a vulval biopsy can confirm the diagnosis.

74
Q

typical presentation of lichen sclerosis

A

The typical presentation in your exams is a woman aged 45 – 60 years complaining of vulval itching and skin changes in the vulva. The condition may be asymptomatic, or present with several symptoms:

  • Itching
  • Soreness and pain possibly worse at night
  • Skin tightness
  • Painful sex (superficial dyspareunia)
  • Erosions
  • Fissures
    The **Koebner phenomenon **refers to when the signs and symptoms are made worse by friction to the skin. This occurs with lichen sclerosus. It can be made worse by tight underwear that rubs the skin, urinary incontinence and scratching.
75
Q

appearanc eof lichen sclerosis

A

“Porcelain-white” in colour
Shiny
Tight
Thin
Slightly raised
There may be papules or plaques

76
Q

management of lichen sclerosis

A

cannot be cured but can be symptom controlled
- potent topical steroids e.g. clobetasol propionate 0.05% (dermovate)
- emollients

77
Q

cervical ectropion

A

normal physiological condition due to increased expsorue to oestrogen

78
Q

cervical ectropion aetiology and pathophysiology

A

The cervix is the lower portion of the uterus. It is composed of two regions; the ectocervix and the endocervical canal.

1) Endocervical canal (endocervix) – the more proximal, and ‘inner’ part of the cervix. It is lined by a mucus-secreting simple columnar epithelium.
2) Ectocervix– the part of cervix that projects into the vagina. It is normally lined by stratified squamous non-keratinised epithelium.

A cervical ectropion is the presence of everted endocervical columnar epithelium on the ectocervix. This change is thought to be induced by high levels of oestrogen, and does not represent metaplasia.

79
Q

why increased vaginal discharge in cervical ectropion

A

The columnar epithelium contains mucus-secreting glands, and thus some individuals with cervical ectropion experience increased vaginal discharge. It may also give rise to post-coital bleeding, as the fine blood vessels present within the epithelium are easily broken during intercourse.

80
Q

RF for cervical ectropion

A
  • Use of the combined oral contraceptive pill
  • Pregnancy
  • Adolescence
  • Menstruating age (it is uncommon in post-menopausal women)
81
Q

presentation of cervical ectropion

A
  • post-coital bleeding
  • discharge
  • IMB

On speculum examination, the everted columnar epithelium has a reddish appearance – usually arranged in a ring around the external os.

82
Q

managament of cervical ectropion

A

normal variant and does not require treatment unless ysmptomatic

First line- stop oestrogen containing medication e.g. COCP

Second line; ablation by electrocautery

Reproductive Health (Y4) (34 decks)

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