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HY OBGYN - (edited) > Gynae Cancers- Cervical, Endometrial, Ovarian, Vulval > Flashcards

Gynae Cancers- Cervical, Endometrial, Ovarian, Vulval Flashcards

1
Q

Who does cervical cancer typically affect?

A

Younger women, peaking in reproductive years

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2
Q

What are the common types of cervical cancer?

A
  • Squamous cell carcinoma (80%)
  • Cervical adenocarcinoma (10%)
  • Small cell cancer
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3
Q

What virus is cervical cancer typically associated with?

A

Human papillomavirus- persistent infection (longer than 2 years) with hiigh-risk HPV (hrHPV) causes cervical cancer

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4
Q

When is the HPV vaccine given and to who? What does the HPV vaccine protect against?

A
  • Aged 12-13
  • Ideally given to boys and girls before they become sexually active
  • Current NHS vaccine: Gardasil, protects against HPV strains 6 & 11 (genital warts); and 16 & 18 (cervical cancer)
  • The vaccine is normally given in school
  • Given as 2 doses- girls have the sexond dose between 6-24 months after the first
  • HPV vaccine should also be offered to men who have sex with men < age 45 to protect against anal, throat and penile cancers
  • Injection site reactions are particularly common with HPV vaccines
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5
Q

What is the purpose of smear tests?

A

To screen for precancerous and cancerous changes to the cells of the cervix

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6
Q

What type of cancer is HPV associated with?

A
  • Over 99.7% of cervical cancers
    • HPV testing is now integral to cervical cancer screening
    • Samples are first tested for HPV and only if they are positive is cytology then performed
  • ~ 85% of anal cancers
  • ~ 50% of vulval and vaginal cancers
  • ~ 20-30% of mouth and throat cancers
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7
Q

What strains of HPV are responsible for cervical cancers?

A

Types 16 and 18

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8
Q

What is the treatment for HPV infection?

A

No treatment (most infections resolve within 2 years, some will persist)

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9
Q

What happens to the cervix during a HPV infection?

A

Infected endocervical cells may undergo changes resulting in development of koilocytes- enlarged nucleus, irregular nuclear membrane contous, the nucleus stains darker (hyperchromasia), perinuclear halo may be seen: KOILOCYTOSIS is accepted as pathognomonic (characteristic of a particular disease) of HPV infection

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10
Q

How does HPV cause cancer?

A

HPV produces two proteins E6 and E7 which inhibit tumour supressor genes p53 and pRb respectively

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11
Q

What causes cervical cancer?

A
  • Acquiring HPV infection, particularly types 16 and 18
    • Multiple sexual partners, early sexual activity
    • Low socieoeconomic status
    • Not using condoms
  • Inadequate cervical screening
  • Smoking
  • Co-infection with other STIs such as HSV, chlamydia, gonococcal infections
  • COCP for > 5 years
  • FHx in a 1st degree relatives
  • Increased number of full-term pregnancies
  • Exposure to diethylstilbestrol (DES) during fetal development
    • Used to prevent miscarriage during pregnancy between 1945 and 1970
  • Women who have conditions associated with immunosuppression are at increased risk of acquiring HPV, persistent infection, precancerous lesions, and invasive cervical cancer. This includes women who
    • Have HIV- more likely to develop persistent HPV infections at an earlier stage which develop into cancer sooner
    • Take immunosuppressants, eg if they have had an organ transplant or IBD
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12
Q

What are the risks of catching HPV?

A

The risk of acquiring HPV infection depends on:

  • The number of sexual partners
  • The age at first sexual intercourse
  • The likelihood that the woman’s partner or partners were infected with HPV
  • Whether or not a condom is used
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13
Q

What are the presenting symptoms of cervical cancer?

A

Many women will be asymptomatic.

Consider possibility of cervical cancer in the following non-specific symptoms

  • Intermenstrual bleeding
  • Postcoital bleeding
  • Postmenopausal bleeding
  • Blood-stained vaginal discharge
  • Pelvic pain/dyspareunia
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14
Q

After taking a history suspicious of cervical cancer, what is the next step?

A
  • Examine the cervix with a speculum (during examination swabs can be taken to exclude infection) - assess for evidence of bleeding, discharge & ulceration
  • Bimanual examination- assess for pelvic masses
  • GI examination- assess for hydronephrosis, hepatomegaly, rectal bleeding, PR mass
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15
Q

What appearance on speculum is suggestive of cervical cancer?

A
  • The cervix may appear inflamed or friable and bleed on contact (although the most likely cause for this will be infection with Chlamydia trachomatis)
  • There may be a visible ulcerating or fungating lesion, or a foul-smelling serosanguineous vaginal discharge
  • Visible tumour

Urgent cancer referral for colposcopy should be made to assess further

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16
Q

If a smear test returns normally can that rule out cervical cancer?

A

No

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17
Q

What is cervical interaepithelial neoplasia?

A

Cervical intraepithelial neoplasia (CIN) develops in the transformation zone of the cervix

A grading system for the level of dysplasia (premalignant change) in the cells of the cervix, its diagnosed at colposcopy (not with cervical screening)

  1. CIN I: mild dysplasia, affecting 1/3 the thickness of the epithelial layer, likely to return to normal without treatment
  2. CIN II: moderate dysplasia, affecting 2/3 the thickness of the epithelial layer, likely to progress to cancer if untreated
  3. CIN III: severe dysplasia, very likely to progress to cancer if untreated
  • Cervical cancer usually develops as a progression from CIN- this occurs over 10-20 years
  • Not all cases of CIN progresses to cancer, most spontaneously regress
  • When the basement membrane of the epithelium is breached, invasive cervical cancer occurs- metastases to bone, bowel, liver and lungs
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18
Q

What is the difference between dysplasia found during colposcopy and dyskaryosis on smear results?

A
  • Dyskaryosis: histological term, refers to the change of appearance in cells that cover the surface of the cervix
    • Detected by smear test
    • Earliest stage of malignancy
  • Dysplasia: cytological term, describes the nuclear abnormalities/ abnormal cells within the squamous epithelium of the cervix
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19
Q

Who performs a smear test?

A

A practise nurse

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20
Q

What are cervical smear samples tested for?

A

High-risk HPV before the cells are examined, if the HPV test is negative then the person does not have HPV and the cells are not examined and the smear is considered negative

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21
Q

When is a cervical smear offered to females?

A
  • 24.5 years should receive their first invitation to ensure they can be screened before they are aged 25 years
  • Every 3 years for those ages 25-49
  • Every 5 years for those aged 50-64
  • Woman > 65 should be screened if:
    • A recent cervical sytology is abnormal
    • They have not had cervical screening since the age of 50 and they request one
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22
Q

What are the possible cytology results to the smear test?

A
  • Inadequate
  • Normal
  • Borderline changes
  • Low-grade dyskaryosis
  • High-grade dyskaryosis (moderate)
  • High-grade dyskaryosis (severe)
  • Possible invasive squamous cell carcinoma
  • Possible glandular neoplasia
  • Infections such as BV, candidiasis, trichomoniasis can be identified
  • Actinomyces-like organisms found in women with IUD (coil)- do not require treatment unless symptomatic (eg pelvic pain or abnormal bleeding)- removal of IUD if symptomatic
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23
Q

What are the possible management options of the smear test?

A
  • Inadequate sample – repeat the smear after at least three months
  • hrHPV negative – continue routine screening
  • hrHPV positive- managed depending on cytology results:
    • hrHPV positive with abnormal cytology reported as borderline dyskaryosis or worse - refer for colposcopy
    • hrHPV positive with normal cytology – repeat the HPV test after 12 months
      • If the HPV testing is negative at 12 months, individuals can be safely returning to routine recall
      • Individuals who remain hrHPV positive, cytology normal at 12 months, should have a repeat HPV test in a further 12 months
      • Individuals who become hrHPV negative at 24 months can be safely returned to routine recall
      • If hrHPV positive at 24 months- refer for colposcopy
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24
Q

What does a colposcopy involve? What staining methods are used and what biopsies can be taken?

A

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 - stains such as acetic acid and iodine solution can be used to differentiate abnormal areas

  • Acetic acid: causes abnormal cells to appear white - acetowhite/ Occurs in cells where there is an increased nuclear to cytoplasmic ratio such as CIN & cervical cancer cells
  • Schiller’s iodine test: iodine solution to stain cervix cells, stains healthy cells brown and abnormal cells will not stain
  • Punch biopsy or large loop excision of the transformational zone can be performed during colposcopy to get tissue sample
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25
Q

How is a Large Loop Excision of the Transformation Zone performed? What are some risks/ cautions to tell the patient beforehand?

A

Under local anaesthetic during a colposcopy with a loop diathermy to remove abnormal epithelial tissue on the cervix cauterising the tissue and stopping it from bleeding

  • Bleeding/ abnormal discharge can occur for several weeks
  • Avoid intercourse after procedure to reduce risk of infection
  • May increase risk of pre-term labour depending on the depth of tissue removed from the cervix
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26
Q

When is a cone biopsy done? What are some risks of this procedure?

A

As a treatment for CIN and very early-stage cervical cancer under general anaesthetic

Cone shaped piece of cervix is removed using a scalpel

Sample sent to histology to assess for malignancy

Risks

  • Pain
  • Bleeding
  • Infection
  • Scar formation and cervical stenosis
  • Miscarriage and preterm labour risk increases
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27
Q

What is the international federation of Gynaecology and Obstetrics (FIGO) staging system for cervical cancer?

A

Stage 1: Confined to the cervix

  • A) Identified only microscopically
  • B) Gross lesions, clinically identifiable

Stage 2: Invades the uterus or upper 2/3 of the vagina

  • A) No parametrial involvement.
  • B) Obvious parametrial involvement.

Stage 3: Invades the pelvic wall or lower 1/3 of the vagina

  • A) No extension to sidewall
  • B) Extension to sidewall and/or hydronephrosis

Stage 4: Invades the bladder, bowel, rectum or beyond the pelvis

  • A) Involves bladder/rectum
  • B) Involves distant organs
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28
Q

Broadly how is cervical cancer managed?

A
  • Biopsy
  • BBN: breaking bad news during a specific appointment for this
  • MRI scan: plan rest of treatment
  • Discussion at MDT meeting
  • Decide treatment
    • Cervix responds very well to radiotherapy- often a combination of external beam therapy and intracavity brachytherapy- an acceptable alternative to surgery in early-stage disease
    • Stage 1b to 3: RT offered in conjunction with chemotherapy over a 5-8 course- evidence suggests hysterectomy offers no benefits in terms of survival for these stages so chemoradiation therapy is the gold standard
    • Surgical approaches
      • Radical hysterectomy
      • Radical trachelectomy (increased risk of mid pregnancy loss & pre-term labour)
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29
Q

When is chemotherapy given in cervical cancer patients?

A
  • Chemotherapy in cervical cancer is often cisplatin-based
  • It can be given before treatment by surgery or radiotherapy (known as neoadjuvant chemotherapy), or after treatment (adjuvant chemotherapy)
  • It is also the mainstay of treatment in the palliative setting
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30
Q

What is the usual treatment for cervical intraepithelial neoplasia and early-stage 1A cervical cancer?

A

LLETZ or cone biopsy

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31
Q

What is the treatment for:

Stage 1B – 2A

Stage 2B – 4A

Stage 4B cervical cancer?

A

Stage 1B – 2A: Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy

Stage 2B – 4A: Chemotherapy and radiotherapy

Stage 4B: Management may involve a combination of surgery, radiotherapy, chemotherapy and palliative care

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32
Q

What is the range of 5 year survival depending on stage of cervical cancer?

What follow-up should be arranged for cervical cancer patients following treatment?

A
  • 98% with stage 1A
  • 15% with stage 4

Follow up:

  • Patients should be reviewed by a gynaecologist every 4 months after treatment has been completed for the first 2 years, and every 6-12 months for the subsequent 3 years
  • All follow-ups should involve a physical examination of the vagina and cervix (if they haven’t been removed)
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33
Q

When is pelvic exenteration used?

A

Advanced cervical cancer

Involves removing most or all of pelvic organs- vagina, cervix, fallopian tubes, ovaries, bladder, rectum

Significant implications on QoL

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34
Q

What chemotherapy agent is used in the treatment of metastatic or recurrent cervical cancer?

A

Bevacizumab (avastin) a monoclonal antibody

  • Targets vascular endothelial growth factor A (VEGF-A) which is responsible for the development of new blood vessels

Also used for Wet age-related macular degeneration - where it is injected directly into the patients eye to stop new blood vessels forming on the retina

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35
Q

What is the commonest gynaecological cancer?

A

Endometrial cancer

  • Best prognosis too!
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36
Q

What type of cancer are most endometiral cancers?

A

Adenocarcinoma

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37
Q

What stimulates the growth of endometrial cancer?

A

Oestrogen

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38
Q

What is the most likely diagnosis of a woman with postmenopausal bleeding?

A

Endometrial cancer

39
Q

What are some causes of a thickened endometrium?

A
  • Benign polyp
  • Endometrial cancer
  • Tamoxifen
40
Q

What is endometrial hyperplasia? Types and treatment?

A

Precancerous condition involving thickening of the endometrium, in excess of the normal prolieration that occurs during the menstrual cycle

A minority will develop endometrial cancer- <5%

Types:

  • Without atypia- treated w/ high dose progestogens (oral) or IUD (mirena coil)
  • Atypical hyperplasia- highest risk of progression to malignancy, treated with total abdominal hysterectomy
41
Q

What are the layers of the uterus?

A
  • Peritoneum- a double layered membrane, continuous with the abdominal peritoneum. Also known as the perimetrium
  • Myometrium- thick smooth muscle layer. Cells of this layer undergo hypertrophy and hyperplasia during pregnancy in preparation to expel the fetus at birth
  • Endometrium- inner mucous lining of uterus- 2 parts
    • Deep stratum basalid: changes little throughout the menstrual cycle and is not shed at menstruation
    • Superficial stratum functionalis: Proliferates in response to oestrogens, and becomes secretory in response to progesterone. It is shed during menstruation and regenerates from cells in the stratum basalis layer
42
Q

What are the risk factors of endometrial cancer?

A

Exposure to unopposed oestrogen (stimulates the endometrial cells leading to hyperplasia and cancer)

  • Increased age
  • Earlier menarche
  • Late menopause
  • Unopposed oestrogen (HRT)
  • No or fewer pregnancies
  • Obesity
  • PCOS (lack of ovulation causes increased exposure to unopposed oestrogen)
  • Tamoxifen
  • HNPCC

The COCP and smoking are protective

43
Q

What can be given to women with PCOS for endometrial protection?

A
  • Combined contraceptive pill
  • Intrauterine system
  • Cyclical progesterones to induce a withdrawal bleed
44
Q

Why is obesity a risk factor for endometrial cancer?

A
  • Adipose tissue is a source of oestrogen
  • Adipose tissue contains enzyme aromatase which converts androgens such as testosterone into oestrogen
  • Androgens are produced by the adrenal glands
  • Women with more adipose tissue means more aromatase so more oestrogen formed
  • This extra oestrogen is unopposed in women that are not ovulating (eg PCOS or post menopause) because there is no corpus luteum to produce progesterone
45
Q

How does tamoxifen increase the amount of unopposed oestrogen?

A

Anti-oestrogenic effect on breast tissue but an oestrogenic effect on the endometrium

46
Q

What are some risk factors for endometrial cancer which are not related to unopposed oestrogen?

A
  • Type 2 diabetes
    • Due to increased insulin production, insulin may stimulate the endometrial cells and increase endometrial hyperplasia/ cancer
    • PCOS is also assosicated w/ insulin resistance & increased insulin production - further adding to the cancer risk
  • Hereditary nonpolyposis colorectal cancer or lynch syndrome
47
Q

What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Increased pregnancies
  • Cigarette smoking
48
Q

What oestrogen dependent cancer is smoking not protective against?

A

Breast cancer

49
Q

How does smoking have an antioestrogenic effect?

A
  • Oestrogen may be metabolised differently in smokers
  • Smokers tend to be leaner and so have less adipose tissue and aromatase enzyme
  • Smoking destroys oocytes (eggs) resulting in an earlier menopause
50
Q

What is the main presenting symptom for endometrial cancer?

A

Post-menopausal bleeding is the main one​

  • Post-coital bleeding
  • Intermenstrual bleeding
  • Unusually heavy menstrual bleeding
  • Abnoraml vaginal discharge (unusual features)
  • Haematuria
  • Anaemia
  • Raised platelet count
  • Weight loss, cachexia
  • Secondary abdominal mass
    • Pelvic mass or ascites effects
  • Abdominal distension
  • Abdominal obstruction if intestines involved
  • Asymptomatic
51
Q

When is a 2WW referral needed for suspected endometrial cancer?

A
  • Age > 55 with Postmenopausal bleeding (more than 12 months since last menstrual period)
    • Consider in women < 55
  • Direct access for transvaginal ultrasound scan for women > 55 with:
    • Unexplained symptoms of vaginal discharge who:
      • Are presenting with these symptoms for first time or
      • Have thrombocytosis or
      • Report haematuria or
    • Visible haematuria and:
      • Low haemoglobin levels or
      • Thrombocytosis or
      • High blood glucose levels
52
Q

What are the three investigations for diagnosing and excluding endometrial cancer?

A

First line Ix is trans-vaginal ultrasound- a normal endometrial thickness <4mm has a high negative predictive value

Hysteroscopy wityh endometrial biopsy

Pipelle biopsy which is highly sensitive for endometrial cancer

53
Q

What is a pipelle biopsy?

A

Speculum examination with a thin tube inserted into the uterus through the cervix - tube fills with a sample of endometrial tissue that can be examined for endometrial hyperplasia or cancer

As an alternative nd less invasive alternatve to hysteroscopy for excluding cancer in low risk women

54
Q

What investigations are sufficient to rule out endometrial cancer and dischage a patient?

A
  • Normal transvaginal ultrasound (endometrial thickness < 4mm)
  • Normal pipelle biopsy
55
Q

What is the FIGO staging for 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

56
Q

Broadly describe the treatment for endometrial cancer?

A

Primary surgery if cancer has not spread

Total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH and BSO - removal of cervix, uterus and adnexa)

Stage 2- radical hysterectomy

Send to lab for histology assessment which will decide the rest

  • Additional radiotherapy may be required
  • Vaginal brachytherapy- high dose localised RT

Progesterone may be used to slow the progression of the cancer

57
Q

Why does ovarian cancer often present late?

A

Non-specific symptoms resulting in a worse prognosis (more than 70% of patients with ovarian cancer present after it has spread beyond the pelvis)

Prognosis is 35% compared with endometrial cancer which is 78% survival

58
Q

What are some different types of ovarian cancers?

A
59
Q

What is the most common type of ovarian cancer? And some subsets?

A

Epithelial cell tumours

  • Serous tumours (the most common)
  • Endometrioid carcinoma
  • Clear cell tumour
  • Mucinous tumour
  • Undifferentiated tumour
60
Q

Are dermoid cysts / germ cell tumours benign or malignant?

A

Benign

61
Q

What kind of tumours are dermoid cysts and germ cell tumours?

A

Teratomas (they come from germ cells)

Contain various types of tissue- skin, teeth, hair, bone

Particularly associated w/ ovarian torsion

Rise in AFP and hCG

62
Q

What tumour markers may be raised in germ cell tumours?

A

Alpha-fetoprotein

Human chorionic gonadotrophin

63
Q

Are sex cord-stromal tumours cancerous?

A

Can be benign or malignant

64
Q

What are some types of sex cord-stromal tumours?

A

Sertoli-leydig cell tumours

Granulosa cell tumours

65
Q

What is a krukenberg tumour?

A

Metastasis in the ovary, usually from a gastrointestinal tract cancer particularily the stomach

Signet ring cells on histology

66
Q

What are some risk factors for ovarian cancer?

A
  • Age (peaks at 60)
  • Early menarche
  • Late menopause
  • Nulliparity
  • Infertility
  • Never used COCP
  • BRCA1 and BRCA2 genes (consider the family history), Lynch syndrome
  • Increased number of ovulations
  • Obesity
  • Smoking
  • Recurrent use of clomifene
67
Q

What are the factors which increase the number of ovulations (and thus the risk of ovarian cancer)?

A
  • Early onset of periods
  • Late menopause
  • No pregnancies
68
Q

What are some factors which are protective against ovarian cancer?

A
  • Combined contraceptive pill
  • Breastfeeding
  • Pregnancy
69
Q

How can ovarian cancer present?

A

Abdominal bloating/ persistent abdominal distesion

Early satiety (feeling full after eating)

Loss of appetite

Pelvic or abdominal pain

Urinary symptoms (frequency / urgency)

Weight loss

Abdominal or pelvic mass

Ascites

(have a low threshold for referring older women)

Hip or groin pain if pressing on obturator nerve

70
Q

Why does hip/groin pain occur in ovarian cancer?

A

Due to compression on the obturator nerve (as it passes along the inside of the pelvis, lateral to the ovaries)

71
Q

When should a 2WW referral be made for suspected ovarian cancer?

A
  • Ascites
  • Pelvic mass (unless clearly due to fibroids)
  • Abdo mass
72
Q

What symptoms should prompt further investigations for ovarian cancer (starting with CA125)?

A

Women older than 50 presenting with:

New symptoms of IBS / change in bowel habit

Abdominal bloating

Early satiety

Pelvic pain

Urinary frequency or urgency

Weight loss

73
Q

What are the inital investigations for ovarian cancer in primary or secondary care?

A

CA125 blood test (>35 is significant)

If Ca125 is high, organise ultrasound of abdomen and pelvis

74
Q

What is the risk of malignancy index (RMI) calculating?

A
  • RMI- Risk Malignancy Index
  • Helps determine likelihood malignancy
  • = U x M x CA123
  • U = ultrasound features (0 if no feature, 1 if one feature, 3 if >1 feature (if 2-5 of the following characteristics present- multiocular, solid areas, mets, ascites, bilateral lesions))
  • M = Menopausal status (pre-menopause = 1, post-menopause = 3)
75
Q

What are some other further investigations in secondary care to include?

A
  • CT scan to establish the diagnosis and stage cancer
  • Histology (tissue sample) using a CT guided biopsy, laparoscopy or laparotomy
  • Paracentesis (ascitic tap) - assesses ascitic fluid for cancer cells
  • Diagnosis is difficult and usually involves diagnostic laparotomy
76
Q

What tumour markers are required for a woman under 40 with a complex ovarian mass?

A

α-FP

hCG

77
Q

What cancer is CA125 a marker for & what else can cause it be raised?

A

Epithelial cell ovarian cancer- it is not very specific

there are many other causes of raised ca125 such as endometriosis, fibroids, adenomyosis, pelvic infection, liver disease, pregnancy

78
Q

What are the stages of the FIGO system used for 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)

79
Q

How is ovarian cancer managed?

A

Specialist gynarcology oncology MDT usually involving a combination of surgery and platinum-based chemotherapy

80
Q

Is vulval cancer common?

A

Rare (compared with other gynarcological cancers)

81
Q

What is the most common type of vulval cancers?

A

90% are squamous cell carcinoma (less commonly malignant melanoma)

82
Q

What are some risk factors for vulval cancers?

A
  • Advanced age (over 75)
  • Immunosuppression
  • HPV (human papillomavirus) infection
  • Lichen sclerosus
  • Vulval intraepithelial Neoplasia (VIN)
83
Q

What is lichen sclerosus?

What percent of women with lichen sclerosus get vulval cancer?

A
  • It is an inflammatory condition that usually affects the genitalia and is more common in elderly females
  • Features- white patches that may scar, prominent itch, superficial dysparaenia/ dysuria
  • Mx- topical steroids and emollients
  • 5% develop vulval cancer
84
Q

What is vulval intraepithelial neoplasia?

A

Premalignant condition affecting the squamous epithelium of the skin preceding vulval cancer

85
Q

What is a high grade squamous intraepithelial lesion?

A

Type of VIN associated with HPV infection that typically occurs in younger women aged 35-50 years

86
Q

What is differentiated VIN?

A

Alternative type of VIN associated with lichen sclerosus, typically occuring in older women (aged 50-60 years old)

87
Q

How is VIN diagnosed?

A

A biopsy

88
Q

What are the treatment options for VIN?

A

Watch and wait with close follow up

Wide local excision (surgery) to remove the lesions

Imiquimod cream

Laser ablation

89
Q

How may vulval cancer present?

A

Vulval lump

Ulceration

Bleeding

Pain

Itching

Lymphadenopathy in the groin

90
Q

Where does vulval cancer commonly affect?

A

Labia majora

91
Q

How to establish diagnosis of vulval cancer and stage?

A

Biopsy of the lesion

Sentinel node biopsy to demonstate lymph node spread

Further imaging for staging (CT abdo and pelvis)

92
Q

What is the management of vulval cancer?

A
  • Wide local excision to remove the cancer
  • Groin lymph node dissection
  • Chemotherapy
  • Radiotherapy
93
Q

List 6 causes of post-menopausal bleeding?

A
  1. Most common cause is vaginal atrophy: thinning, drying, and inflammation of the walls of the vagina due to a reduction in oestrogen following the menopause can result in vaginal bleeding
  2. HRT is also a common cause: periods or spotting can continue in some women taking HRT for many months with no pathological cause, or endometrial hyperplasia due to long-term oestrogen therapy may occur, which can also cause bleeding
  3. Endometrial hyperplasia- RF include obesity, unopposed oestrogen use, tamoxifen, PCOS and T2DM
  4. Endometrial cancer: 10% pts with post-menopausal bleeding have endometrial cancer and up to 90% pts with endometrial cancer present with post-menopausal bleeding
  5. Cervical cancer
  6. Ovarian cancer: especially oestrogen-secreting (theca cell) tumours
  7. Vaginal cancer: uncommon but can present with post-menopausal bleeding
  8. Other- trauma, vulval cancer, bleeding disorders

HY OBGYN - (edited) (10 decks)

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