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Year 4 Oncology > Gynaecological Cancer > Flashcards

Gynaecological Cancer Flashcards

1
Q

After how long does HRT increase the risk of ovarian cancer

A

5 years

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2
Q

What type of gynaecological cancer may present with bloating, urinary frequency and urgency

A

Ovarian

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3
Q

What is the gold standard investigation to diagnose endometrial cancer?

A

Hysteroscopy with biopsy

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4
Q

What dermatological condition increases the risk of vuval cancer?

A

Lichen sclerosis

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5
Q

Tumour marker for ovarian cancer?

A

Cancer antigen 125

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6
Q

Raised B HCG and AFP suggest what

A

Germ cell type ovarian cancer

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7
Q

Where does vulval cancer most commonly present r

A

Labia majora

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8
Q

What extend of cervical dyskaryosis should be referred for colposcopy, without waiting for HPV testing on the cervical sample?

A

Moderate to severe

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9
Q

Cervical smears should be delayed until how long after birth, miscarriages and terminations.

A

3 months

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10
Q

What differential can mimic ovarian cancer, causing abdominal discomfort, IMB and raised Ca-125

A

PID

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11
Q

How does ovarian cancer spread?

A

Ovarian cancer initially spreads by local invasion

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12
Q

Risk malignancy index (RMI) prognosis in ovarian cancer is based on what?

A

US findings
CA 125
Menopausal status

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13
Q

Risk factors for endometrial cancer

A

obesity

nulliparity

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

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14
Q

Unfortunately, the uptake of cervical screening amongst lesbian women is around 10 times worse than the general female population, sometimes as a consequence of incorrect advice from healthcare professionals. Why do women who have only ever had sexual relations with women still require cervical smears?

A

HPV, the causative agent of cervical cancer, can be transmitted during genital contact or oral sex. Lesbian and bisexual women should therefore have cervical screening as normal.

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15
Q

Who is offered cervical screening in England and how often?

A

25-49 years: 3-yearly screening

50-64 years: 5-yearly screening

cervical screening cannot be offered to women over 64 (unlike breast screening, where patients can self-refer once past screening age)

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16
Q

When does the NHS advise the best time to take a cervical smear is?

A

Mid cycle

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17
Q

When may a women want to opt out of cervical screening?

A

If she has never been sexually active (including oral sex)

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18
Q

Cervical cancer screening: if sample is hrHPV +ve + cytologically abnormal, what should be done?

A

colposcopy

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19
Q

‘M rules’ for ovarian cysts

A

M rules - cyst is likely malignant and requires biopsy:

Irregular, solid tumour.

Ascites.

At least 4 papillary structures.

Irregular multilocular solid tumour with largest diameter ≥100 mm.

Very strong blood flow.

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20
Q

The first step in the investigation of possible endometrial cancer is what?

A

The first step in the investigation of possible endometrial cancer is to perform a trans-vaginal ultrasound scan to measure the endometrial thickness

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21
Q

What are the common types of cervical cancer?

A

80% of cervical cancers are squamous cell carcinoma.

Adenocarcinoma is the next most common type.

Very rarely there are other types, such as small cell cancer.

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22
Q

What virus is commonly associated with cervical cancer?

A

Cervical cancer is strongly associated with human papillomavirus. Children aged 12 – 13 years are vaccinated against certain strains of HPV to reduce the risk of cervical cancer.

Types 16 and 18 responsible for 70% - these are covered by vaccine

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23
Q

What cancers can HPV cause?

A

The most common cause of cervical cancer is infection with human papillomavirus (HPV).

HPV is also associated with anal, vulval, vaginal, penis, mouth and throat cancers. HPV is primarily a sexually transmitted infection.

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24
Q

How does HPV cause cervical cancer?

A

P53 and pRb are tumour suppressor genes inhibited by proteins produced by HPV, therefore promoting the development of cancer

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25
Q

Which proteins does HPV produce and which gene do they suppress?

A

E6 protein inhibits p53
E7 protein inhibits pRb

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26
Q

Risk factors for cervical cancer

A

Increased risk of catching HPV

Later detection of precancerous and cancerous changes (non-engagement with screening)

Other risk factors:
Smoking

HIV (patients with HIV are offered yearly smear tests)

Combined contraceptive pill use for more than five years

Increased number of full-term pregnancies

Family history

Exposure to diethylstilbestrol during fetal development (this was previously used to prevent miscarriages before 1971)

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27
Q

Factors associated with increased risk of catching HPV?

A

Early sexual activity

Increased number of sexual partners

Sexual partners who have had more partners

Not using condoms

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28
Q

Presentation of cervical cancer

A

Cervical cancer may be detected during cervical smears in otherwise asymptomatic women.

The presenting symptoms that should make you consider cervical cancer as a differential are:

Abnormal vaginal bleeding (intermenstrual, postcoital or post-menopausal bleeding)

Vaginal discharge

Pelvic pain

Dyspareunia (pain or discomfort with sex)

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29
Q

Where there is an abnormal appearance of the cervix suggestive of cancer, an urgent cancer referral for colposcopy should be made to assess further.

What appearances that may suggest cervical cancer?

A

Ulceration
Inflammation
Bleeding
Visible tumour

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30
Q

Colposcopy vs smear test description of abnormalities

A

Colposcopy- dysplasia
Smear test cytology - dyskaryosis

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31
Q

Where is CIN diagnosed?

A

Colposcopy

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32
Q

CIN I

A

mild dysplasia

affecting 1/3 the thickness of the epithelial layer

likely to return to normal without treatment

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33
Q

CIN II

A

moderate dysplasia

affecting 2/3 the thickness of the epithelial layer

likely to progress to cancer if untreated

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34
Q

CIN III

A

severe dysplasia, very likely to progress to cancer if untreated

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35
Q

What CIN stage is sometimes called cervical carcinoma in situ

A

CIN III is sometimes called cervical carcinoma in situ

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36
Q

What does a cervical smear consist of?

A

The test consists of a speculum examination and collection of cells from the cervix using a small brush.

The cells are deposited from the brush into a preservation fluid.

This fluid is transported to a lab where the cells are examined under a microscope for precancerous changes (dyskaryosis).

This way of transporting the cells is called liquid-based cytology.

Cytology is only performed when smear is positive for HPV

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37
Q

Notable exceptions to routine cervical screening program?

A

Women with HIV are screened annually

Women over 65 may request a smear if they have not had one since aged 50

Women with previous CIN may require additional tests (e.g. test of cure after treatment)

Certain groups of immunocompromised women may have additional screening (e.g. women on dialysis, cytotoxic drugs or undergoing an organ transplant)

Pregnant women due a routine smear should wait until 12 weeks post-partum

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38
Q

Possible Cytology results following a cervical smear?

A

Inadequate

Normal

Borderline changes

Low-grade dyskaryosis

High-grade dyskaryosis (moderate)

High-grade dyskaryosis (severe)

Possible invasive squamous cell carcinoma

Possible glandular neoplasia

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39
Q

What infections may be reported in a smear result?

A

HPV

Infections such as bacterial vaginosis, candidiasis and trichomoniasis may be identified and reported on the smear result.

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40
Q

Management of smear results based on PHE guidelines?

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

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41
Q

What does colposcopy involve?

A

A specialist performs colposcopy. 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.

Acetic acid 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.

Schiller’s iodine test 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.

A punch biopsy or large loop excision of the transformational zone can be performed during the colposcopy procedure to get a tissue sample.

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42
Q

What is an LLETZ and what does it involve?

A

A large loop excision of the transformation zone (LLETZ) procedure is also called a loop biopsy. It can be performed with a local anaesthetic during a colposcopy procedure.

It involves using a loop of wire with electrical current (diathermy) to remove abnormal epithelial tissue on the cervix.

The electrical current cauterises the tissue and stops bleeding.

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43
Q

What should you advise women undergoing a LLETZ?

A

Bleeding and abnormal discharge can occur for several weeks following a LLETZ procedure. This varies between women.

Intercourse and tampon use should be avoided after the procedure to reduce the risk of infection.

Depending on the depth of the tissue removed from the cervix, the procedure may increase the risk of preterm labour.

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44
Q

What is a cone biopsy and when is it used in cervical cancer/CIN?

A

A cone biopsy is a treatment for cervical intraepithelial neoplasia (CIN) and very early-stage cervical cancer.

It involves a general anaesthetic.

The surgeon removes a cone-shaped piece of the cervix using a scalpel.

This sample is sent for histology to assess for malignancy.

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45
Q

What are the main risks of a cone biopsy?

A

Pain

Bleeding

Infection

Scar formation with stenosis of the cervix

Increased risk of miscarriage and premature labour

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46
Q

What staging system is used to grade cervical cancer?

A

FIGO, stages 1-4

(FIGO: Federation of Gynaecology and Obstetrics)

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47
Q

FIGO stage 1 cervical cancer

A

Cervical cancer confined to the cervix

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48
Q

FIGO stage 2 cervical cancer

A

Cervical cancer invading the uterus or upper 2/3 of vagina

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49
Q

FIGO stage 3 cervical cancer

A

Cervical cancer invading the pelvic wall or lower 1/3 of the vagina

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50
Q

Management of Cervical intraepithelial neoplasia and early-stage 1A cervical cancer?

A

LLETZ or cone biopsy

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51
Q

Management of cervical cancer Stage 1B – 2A

A

Radical hysterectomy and removal of local lymph nodes with chemotherapy and radiotherapy

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52
Q

Management of stage 2B-4A cervical cancer?

A

Chemotherapy and radiotherapy

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53
Q

Management of stage 4B cervical cancer

A

Management may involve a combination of surgery, radiotherapy, chemotherapy and palliative care

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54
Q

Why is the cervical screening program so important?

A

The 5-year survival drops significantly with more advanced cervical cancer, from around 98% with stage 1A to around 15% with stage 4. Early detection makes a significant difference, which is one reason the screening program is so valuable and important.

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55
Q

What major surgery may be used to treat advanced cervical cancer?

A

Pelvic exenteration is an operation that may be used in advanced cervical cancer.

It involves removing most or all of the pelvic organs, including the vagina, cervix, uterus, fallopian tubes, ovaries, bladder and rectum. It is a vast operation and has significant implications on quality of life.

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56
Q

What is the monoclonal antibody which may be used in combination with chemo therapies in the treatment of metastatic or recurrent cervical cancer, and how does it work?

A

Bevacizumab (Avastin) is a monoclonal antibody that may be used in combination with other chemotherapies in the treatment of metastatic or recurrent cervical cancer. It is also used in several other types of cancer. It targets vascular endothelial growth factor A (VEGF-A), which is responsible for the development of new blood vessels.

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57
Q

Which strains of HPV does the Gardasil vaccine protect against?

A

Strains 6, 11, 16 and 18:

Strains 6 and 11 cause genital warts
Strains 16 and 18 cause cervical cancer

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58
Q

What type of cancer are ~80% of endometrial cancers?

A

Adenocarcinoma

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59
Q

On which hormone do endometrial cancers depend on?

A

Oestrogen

60
Q

Any woman presenting with postmenopausal bleeding has what until proven otherwise?

A

Endometrial cancer

61
Q

What is endometrial hyperplasia and what subtypes exist?

A

Endometrial hyperplasia is a precancerous condition involving thickening of the endometrium.

The risk factors, presentation and investigations of endometrial hyperplasia are similar to endometrial cancer. Most cases of endometrial hyperplasia will return to normal over time. Less than 5% go on to become endometrial cancer.

There are two types of endometrial hyperplasia to be aware of:

Hyperplasia without atypia
Atypical hyperplasia

62
Q

How can endometrial hyperplasia be treated?

A

Endometrial hyperplasia may be treated by a specialist using progestogens, with either:

Intrauterine system (e.g. Mirena coil)

Continuous oral progestogens (e.g. medroxyprogesterone or levonorgestrel)

63
Q

What is unopposed oestrogen and what is the relevance in relation to endometrial cancer?

A

Unopposed oestrogen refers to oestrogen without progesterone.

Unopposed oestrogen stimulates the endometrial cells and increases the risk of endometrial hyperplasia and cancer.

The risk endometrial cancer is associated with the amount of unopposed oestrogen the endometrium is exposed to during the patient’s life.

64
Q

Situations that increase exposure of unopposed oestrogen?

A

Increased age

Earlier onset of menstruation

Late menopause

Oestrogen only hormone replacement therapy

No or fewer pregnancies

Obesity

Polycystic ovarian syndrome

Tamoxifen

65
Q

Why does PCOS increase the risk of cervical cancer?

A

Polycystic ovarian syndrome leads to increased exposure to unopposed oestrogen due to a lack of ovulation.

Usually, when ovulation occurs, a corpus luteum is formed in the ovaries from the ruptured follicle that released the egg.

It is this corpus luteum that produces progesterone, providing endometrial protection during the luteal phase of the menstrual cycle (the second half of the menstrual cycle).

Women with polycystic ovarian syndrome are less likely to ovulate and form a corpus luteum.

Without developing a corpus luteum during the menstrual cycle, progesterone is not produced, and the endometrial lining has more exposure to unopposed oestrogen

66
Q

What should women with PCOS have one of to provide endometrial protection.

A

The combined contraceptive pill
An intrauterine system (e.g. Mirena coil)
Cyclical progestogens to induce a withdrawal bleed.

67
Q

How does obesity increase the risk of endometrial cancer?

A

Obesity is a crucial risk factor because adipose tissue (fat) is a source of oestrogen.

Adipose tissue is the primary source of oestrogen in postmenopausal women.

Adipose tissue contains aromatase, which is an enzyme that converts androgens such as testosterone into oestrogen.

Androgens are produced mainly by the adrenal glands. In women with more adipose tissue, and therefore more aromatase enzyme, more of these androgens are converted to oestrogen.

This extra oestrogen is unopposed in women that are not ovulating (e.g. PCOS or postmenopause), because there is no corpus luteum to produce progesterone.

68
Q

Although Tamoxifen is used to treat oestrogen sensitive breast cancers it increases the risk of endometrial cancer - why?

A

Tamoxifen has an anti-oestrogenic effect on breast tissue, but an oestrogenic effect on the endometrium. This increase the risk of endometrial cancer.

69
Q

Risk factors for endometrial cancer that are not related to unopposed oestrogen?

A

Type 2 diabetes
Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome

70
Q

How is T2DM thought to increase the risk of endometrial cancer?

A

Type 2 diabetes may increase the risk of endometrial cancer due to the increased production of insulin. Insulin may stimulate the endometrial cells and increase the risk of endometrial hyperplasia and cancer. PCOS is also associated with insulin resistance and increased insulin production. Insulin resistance further adds to the risk of endometrial cancer in women with PCOS.

71
Q

What factors are protective against endometrial cancer?

A

Combined contraceptive pill
Mirena coil
Increased pregnancies
Cigarette smoking

72
Q

In what type of cancer is smoking considered a protective factor and why?

A

Smoking appears to be protective against endometrial cancer in postmenopausal women by being anti-oestrogenic. Interestingly, it is not protective against other oestrogen dependent cancers, such as breast cancer (where it increases the risk).

Smoking may have anti-oestrogenic effects in several ways:

Oestrogen may be metabolised differently in smokers
Smokers tend to be leaner, meaning they have less adipose tissue and aromatase enzyme
Smoking destroys oocytes (eggs), resulting in an earlier menopause

73
Q

How can endometrial cancer present?

A

PMB
Postcoital bleeding
Intermenstrual bleeding
Unusually heavy menstrual bleeding
Abnormal vaginal discharge
Haematuria
Anaemia
Raised platelet count

74
Q

Endometrial cancer referral criteria?

A

The referral criteria for a 2-week-wait urgent cancer referral for endometrial cancer is:

Postmenopausal bleeding (more than 12 months after the last menstrual period)

NICE also recommends referral for a transvaginal ultrasound in women over 55 years with:

Unexplained vaginal discharge
Visible haematuria plus raised platelets, anaemia or elevated glucose levels

75
Q

How is ?endometrial cancer investigated?

A

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

Hysteroscopy with endometrial biopsy

76
Q

When might you exclude a diagnosis of endometrial cancer following investigations?

A

Depending on local guidelines, a normal transvaginal ultrasound (endometrial thickness < 4mm) and normal pipelle biopsy are sufficient to demonstrate a very low risk of endometrial cancer and discharge the patient.

77
Q

What is a pipelle biopsy and how might it be used?

A

A pipelle biopsy can be taken in the outpatient clinic. It involves a speculum examination and inserting a thin tube (pipelle) through the cervix into the uterus. This small tube fills with a sample of endometrial tissue that can be examined for signs of endometrial hyperplasia or cancer. Pipelle biopsy is a quicker and less invasive alternative to hysteroscopy for excluding cancer in lower-risk women.

78
Q

FIGO stage 4 cervical cancer

A

Invades the bladder, rectum or beyond the pelvis

79
Q

FIGO stage 1 endometrial cancer

A

Confined to the uterus

80
Q

FIGO stage 2 endometrial cancer

A

Invades cervix

81
Q

FIGO stage 3 endometrial cancer

A

Invades the ovaries, fallopian tubes, vagina or lymph nodes

82
Q

FIGO stage 4 endometrial cancer

A

Invades bladder, rectum or beyond the pelvis

83
Q

Management of endometrial cancer

A

The usual treatment for stage 1 and 2 endometrial cancer is a total abdominal hysterectomy with bilateral salpingo-oophorectomy, also known as a TAH and BSO (removal of uterus, cervix and adnexa).

Other treatment options depending on the individual presentation include:

A radical hysterectomy involves also removing the pelvic lymph nodes, surrounding tissues and top of the vagina
Radiotherapy
Chemotherapy
Progesterone may be used as a hormonal treatment to slow the progression of the cancer

84
Q

Why do many patients with ovarian cancer have a poor prognosis?

A

Ovarian cancer often presents late due to the non-specific symptoms, resulting in a worse prognosis. More than 70% of patients with ovarian cancer present after it has spread beyond the pelvis.

85
Q

Types of ovarian cancer

A

Epithelial cell tumour
Dermoid cyst/germ cell tumour
Sex cord-stromal tumours
Metastasis

86
Q

Subtypes of epithelial cell ovarian tumours

A

Serous tumours (the most common)

Endometrioid carcinomas

Clear cell tumours

Mucinous tumours

Undifferentiated tumours

87
Q

What cause of pelvic pain are germ cell tumours/dermoid cysts consist of?

A

They are particularly associated with ovarian torsion.

88
Q

What markers may be raised in a germ cell tumour of the ovary?

A

Germ cell tumours may cause raised alpha-fetoprotein (α-FP) and human chorionic gonadotrophin (hCG) and LDH

89
Q

What are sex cord-stromal ovarian tumour and what subtypes exist? Let

A

These are rare tumours, that can be benign or malignant. They arise from the stroma (connective tissue) or sex cords (embryonic structures associated with the follicles). There are several types, including Sertoli–Leydig cell tumours and granulosa cell tumours.

90
Q

What is a Krukenberg tumour and what does it look like on histology?

A

A Krukenberg tumour refers to a metastasis in the ovary, usually from a gastrointestinal tract cancer, particularly the stomach. Krukenberg tumours have characteristic “signet-ring” cells on histology, which look like signet rings on under a microscopy.

91
Q

Risk factors for ovarian cancer

A

Age (peaks age 60)

BRCA1 and BRCA2 genes (consider the family history)

Increased number of ovulations (early onset of menarche, late onset of period, nuliparity)

Obesity

Smoking

Hormone replacement therapy

Recurrent use of clomifene

92
Q

Protective factors against ovarian cancer?

A

Having a higher number of lifetime ovulations increases the risk of ovarian cancer. Factors that stop ovulation or reduce the number of lifetime ovulations, reduce the risk:

Combined contraceptive pill
Breastfeeding
Pregnancy (parity)

Later onset of periods (menarche)
Early menopause

93
Q

How might ovarian cancer present?

A

Abdominal bloating

Early satiety (feeling full after eating)

Change in bowelhabits

Loss of appetite

Pelvic pain (/lower back/abdominal/hip/gorin)

Urinary symptoms (frequency / urgency)

Weight loss

Abdominal or pelvic mass

Ascites

94
Q

How might an ovarian mass cause hip or groin pain?

A

An ovarian mass may press on the obturator nerve and cause referred hip or groin pain. The obturator nerve passes along the inside of the pelvic, lateral to the ovaries, where an ovarian mass can compress it.

95
Q

When should you refer directly on a 2-week-wait referral for suspected ovarian cancer?

A

Refer directly on a 2-week-wait referral if a physical examination reveals:

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

Urgently refer any woman with ascites and/or an unexplained pelvic/abdominal mass.

96
Q

Carry out further investigations before referral in women presenting with symptoms of possible ovarian cancer, starting with a CA125 blood test. This is particularly important in women over 50 years presenting with what?

A

New symptoms of IBS / change in bowel habit

Abdominal bloating

Early satiety

Pelvic/abdominal pain

Urinary frequency or urgency

Weight loss

97
Q

Initial investigations for ovarian cancer?

A

CA125 blood test (>35 IU/mL is significant)
Pelvic ultrasound

98
Q

What CA125 is significant?

A

> 35 IU/mL

99
Q

The risk of malignancy index (RMI) estimates the risk of an ovarian mass being malignant, taking account of which three things?

A

Menopausal status (1 for premenopausal, 3 for post)

Ultrasound findings (0-3, depending on n/o abnormalities identified)

CA125 level

ultrasound score x menopausal score x Ca-125 level.

100
Q

Following CA125 and pelvic USS how would you further investigate ?ovarian cancer

A

CT scan to establish the diagnosis and stage the cancer

Histology (tissue sample) using a CT guided biopsy, laparoscopy or laparotomy

Paracentesis (ascitic tap) can be used to test the ascitic fluid for cancer cells

AFP and beta-hCG for younger women who may have germ cell cancers

101
Q

Women under 40 years with a complex ovarian mass require what additional investigation?

A

Alpha-fetoprotein (α-FP)
Human chorionic gonadotropin (HCG)
Lactate dehydrogenase (LDH)

102
Q

What non-malignant condition may cause a raised CA125

A

Endometriosis

Fibroids

Adenomyosis

Pelvic infection

Liver disease

Pregnancy

103
Q

FIGO stage 1 ovarian cancer

A

Confined to the ovary

104
Q

FIGO stage 2 ovarian cancer

A

Spread past the ovary but inside the pelvis

105
Q

FIGO stage 3 ovarian cancer

A

Spread past the pelvis but inside the abdomen

106
Q

FIGO stage 4 ovarian cancer

A

Spread outside the abdomen (distant metastasis

107
Q

How is ovarian cancer managed?

A

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

108
Q

More common subtypes of vulval cancer

A

Around 90% are squamous cell carcinomas. Less commonly, they can be malignant melanomas.

109
Q

Risk factors for vulval cancwe

A

Advanced age (particularly over 75 years)

Immunosuppression

Human papillomavirus (HPV) infection

Lichen sclerosus (Around 5% of women with lichen sclerosus get vulval cancer)

110
Q

What is Vulval intraepithelial neoplasia (VIN)

A

A premalignant condition affecting the squamous epithelium of the skin that can precede vulval cancer. VIN is similar to the premalignant condition that comes before cervical cancer (cervical intraepithelial neoplasia).

111
Q

What is a high grade squamous intraepithelial lesion associated with an who does it typically occur in?

A

High grade squamous intraepithelial lesion is a type of VIN associated with HPV infection that typically occurs in younger women aged 35 – 50 years.

112
Q

What is differentiate VIN associated with and who does it occur in

A

Differentiated VIN is an alternative type of VIN associated with lichen sclerosus and typically occurs in older women (aged 50 – 60 years).

113
Q

Diagnosis and management of VIN?

A

A biopsy is required to diagnose VIN. A specialist will coordinate management. Treatment options include:

Watch and wait with close followup
Wide local excision (surgery) to remove the lesion
Imiquimod cream
Laser ablation

114
Q

How might vulval cancer present?

A

Vulval lump
Ulceration
Bleeding
Pain
Itching
Lymphadenopathy in the groin

Vulval cancer may be an incidental finding in older women, for example, during catheterisation in a patient with dementia

115
Q

Where does vulval cancer most commonly affect and what appearance would it have?

A

Labia majora

Irregular mass
Fungating lesion
Ulceration
Bleeding

116
Q

Diagnosis of vulval cancer?

A

Suspected vulval cancer should be referred on a 2-week-wait urgent cancer referral.

Establishing the diagnosis and staging involves:

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

117
Q

How is vulval cancer staged?

A

FIGO

118
Q

How is vulval cancer managed?

A

Management depends on the stage, and may involve:

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

119
Q

Follow up after treatment of CIN II

A

Women who have been treated for CIN II should be offered cervical screening at 6 months through cervical screening and a HPV test of cure.

120
Q

What type of ovarian tumour is associated with endometrial hyperplasia?

A

Granulosa cell tumours

Atypical hyperplasia of the endometrium is classified as a premalignant condition which develops due to overstimulation of the endometrium by oestrogen. Sex cord stromal tumours (Thecomas, Fibromas, Sertoli cell and granulosa cell tumours) are associated with an increased production of hormones. The sub-type Granulosa cell tumours are associated with the development of endometrial hyperplasia.

121
Q

Management of ovarian cancers stages 2-4?

A

Ovarian cancers which are stage 2-4, are treated primarily by surgical excision of the tumour. This may be accompanied by chemotherapy.

122
Q

Management of ovarian cancer

A

The standard treatment for everyone with ovarian cancer is a ‘staging laparotomy’, which involves:
> Midline laparotomy
> Hysterectomy
> Bilateral salpingo-oophrectomy
> Omenectomy
> Lymph node sampling (para-aortic/pelvic nodes)
> Peritoneal washing (saline solution injected into peritoneal cavity and then removed for cytology)

If early disease surgery can include removal of the uterus, ovaries, Fallopian tubes and infracolic omentectomy

In advanced disease debulking surgery can be performed.

Chemotherapy is recommended for everyone except low-grade stage Ia and Ib.

Stage III and IV cancers may additionally get neoadjuvant chemotherapy.

Intraperitoneal chemotherapy may be performed at the time of operation

123
Q

Why might smears be inadequate

A

Failure to sample the full 360 degrees of the cervical circumference.

Presence of blood on the smear

Cervical inflammation

Age related atrophic changes

124
Q

Any 50-year-old patient who has always had negative smears is now screened at 5-yearly intervals rather than 3-yearly - why?

A

Lower risk

CIN usually develops for the first time in patients under the age of 50 yrs

125
Q

Lletz biopsy

A

A Lletz biopsy (or Large Loop Excision of the Transformation Zone (LLETZ)), by definition, aims to remove the full circumference of the transformation zone.

It also aims to remove all of the CIN lesion.

It is usually performed under local anaesthetic. General anaesthetic is only used for patients who cannot tolerate the outpatient procedure.

It is a diathermy procedure.

It can be performed by a specialist nurse.

126
Q

Lletz complications

A

may cause cervical stenosis

It may cause cervical incompetence

It may cause pyometra

It may make smear follow up difficult

127
Q

Ovarian cancer staging - tumour confined to the ovary?

A

Stage 1

128
Q

Ovarian cancer staging - tumour outside ovary?

A

Stage 2

129
Q

Ovarian cancer staging - tumour outside pelvis but within the abdomen?

A

Stage 3

130
Q

Ovarian cancer staging - tumour with distance metastasis?

A

Stage 4

131
Q

HPV infected endocervical cells may undergo changes results in the development of what cell types?

A

koilocytes

132
Q

Characteristics of koilocytes?

A

enlarged nucleus

irregular nuclear membrane contour

the nucleus stains darker than

normal (hyperchromasia)
a perinuclear halo may be seen

133
Q

Where do epithelial ovarian tumours originiate from?

A

Originate from the epithelium which lines the fimbria of the fallopian tubes or the ovaries

134
Q

What is a key macroscopic feature of an epithelial ovarian tumour?

A

Epithelial tumours are partially cystic, and the cysts can contain fluid

135
Q

Metastatic spread in epithelial ovarian cell tumour?

A

Typically involves peritoneal cavity

Seeding particularly affects:
The bladder
Paracolic gutters
Diaphragm

136
Q

Where do germ cell tumours orignate from?

A

Germ cells int eh embryonic gonad?

137
Q

Growth and spread of ovarian germ cell tumours?

A

These tumours typically grow rapidly and spread predominantly via the lymphatic route

138
Q

How does the prevenance of germ cell tumour differ from other types of ovarian tumour?

A

Germ cell tumours most commonly arise in young women, which is atypical for most cases of ovarian cancer

139
Q

Tumour markers for germ cell ovarian tumours?

A

Alpha-fetoprotein (AFP)

(Sometimes) beta human chorionic gonadotrophin (B-HCG).

140
Q

Where do sex cord stromal ovarian tumours originate from?

A

Originate from connective tissue

141
Q

Epithelial vs sex cord ovarian tumour

A

Epithelial
- most common
- originate from epithelium lining the fimbria of the fallopian tubes or the ovaries
- the initial metastatic spread typically involves the peritoneal cavity, with seeding particularly affecting the bladder, paracolic gutters and the diaphragm

Sex cord stromal tumours
- originate from connective tissues
- rare, less than 5%
- malignant but less agressive

142
Q

What is a Krukenberg tumour?

A

Additionally, ovarian cancer can be secondary to another cancer elsewhere, which has metastasised to the ovary.

A Krukenberg tumour refers to a “signet ring” sub-type of tumour, typically gastrointestinal in origin, which has metastasised to the ovary.

143
Q

Why can ascites occur in late ovarian cancer?

A

Cancer can produce vascular growths

Which increase vessel permeability

144
Q

Ovarian cancer - differentials

A

Differentials include other causes of abdominal discomfort such as gastrointestinal conditions (e.g. irritable bowel syndrome).

Other causes of masses: fibroids, ovarian cysts and other cancers (e.g. bladder, endometrial)

145
Q

Substages of ovarian cancer: Stage I

A

Stage I (limited to the ovaries):

Stage IA: limited to one ovary, the capsule is intact

Stage IB: limited to both ovaries, capsules intact.

Stage IC: tumour limited to one or both ovaries with any of the following:
- capsule ruptured
- tumour on ovarian surface
- malignant cells in ascites or peritoneal washings

146
Q

Substages of ovarian cancer: Stage II

A

Stage II involving one or both ovaries with pelvic extension and/or implants:

Stage IIA: extension and/or implants on the uterus and/or Fallopian tubes.
No malignant cells in ascites or peritoneal washings

Stage IIB: extension to and/or implants on other pelvic tissues.
No malignant cells in ascites or peritoneal washings

Stage IIC: pelvic extension and/or implants (Stage IIA or Stage IIB) with malignant cells in ascites or peritoneal washings.

147
Q

Substages of ovarian cancer: Stage III

A

Stage IIIA: microscopic peritoneal metastasis beyond pelvis (no macroscopic tumour)

Stage IIIB: macroscopic peritoneal metastasis beyond pelvis <2 cm

Stage IIIC: peritoneal metastasis beyond pelvis >2 cm and/or regional lymph node metastasis.

Year 4 Oncology (15 decks)

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