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Gynae > Oncology + Vulval Disorders > Flashcards

Oncology + Vulval Disorders Flashcards

1
Q

What’s the FIGO staging of cervical cancer?

A

1 - Confined to cervix
a. Max depth of invasion <5mm
__1. Stromal invasion <3mm
__2. Stromal invasion 3 to <5mm
b. Max depth 5mm or more
__1. Stromal invasion 5mm to <2cm __2. Stromal invasion 2cm to<4cm
__3. Stromal invasion 4cm andabove

2 - Invaded upper 2/3rd of vagina + no pelvic wall involvement
a. No parametrial involvement
___1. <4cm in greatest dimension
___2. 4cm/more
b. Parametrium involved

3- Lower 1/3rd of vagina involved
a. Lower 1/3rd of vagina only
b. Extension to pelvic side wall +/ hydronephrosis or non-functioning kidney
c . Pelvic +/ paraaortic lymph nodes (irrespective of tumour size)
___1. Pelvic lymph nodes mets
___2. Paraaortic lymph node mets

  1. Tumour extends beyond true pelvis/ has involved bladder/rectum
    a. Spread to adjacent organs
    b. Spread to distant organs
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2
Q

Ultrasound features in keeping with malignancy?

A

M5 rules - MAP IIN

Multilocular solid mass
Ascites
Papillary projections (4 or more)
Irregular solid contour
INcreased vascular flow

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3
Q

What percentage of ovarian neoplasms are dermoid cysts/mature teratomas?

A

40%

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4
Q

What percentage of dermoid cysts contain thyroid tissue/endodermal derivatives?

A

5-20%

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5
Q

What percentage of dermoid cysts:
A. Undergo torsion
B. Rupture spontaneously
C. Are asymptomatic
D. Contain malignant components?

A

A. 3.5-10%
B. <5%
C. 60%
D. 2%

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6
Q

What is a fibrosarcoma?

A

A fibroma with >3 mitoses per 10 high power fields

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7
Q

What is Meigs syndrome?

A

Pelvic mass
Ascites
Right pleural effusion

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8
Q

What percent of malignant ovarian tumours are dysgerminomas?

A

2-5%

Dysgerminomas are the commonest malignant germ cell tumour

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9
Q

What percentage of patients with germ cell tumour present with stage 1 disease?

A

70%

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10
Q

What percentage of patients with sex cord stromal tumour present with stage 1 disease?

A

60-95%

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11
Q

T/F. Dysgerminomas are associated with gonadal dysgenesis?

A

True. Karyotyping should be offered especially in amenorrheic patients

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12
Q

T/F. Dysgerminomas are usually bilateral? What percentage of ovarian dysgerminomas are bilateral?

A

10-15%

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13
Q

Incidence of Endometrial cancer?

A

2/100,000 women per year :<40yrs

40-60/100,000 women per yr: >60yrs

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14
Q

Median age of occurrence of endometrial ca?

A

63 years

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15
Q

In general, what is the survival rate for endometrial cancer at 1 yrs, 5 yrs and 10yrs?

A

1 yr: 90%
5 yrs: 77%
10 yrs: 75%

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16
Q

5 year survival rate for stage 1 vs stage 4 endometrial cancer?

A

85% vs 25%

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17
Q

What is the risk of endometrial cancer in overweight/obese women?

A

2-3 times increased risk

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18
Q

What are the risk factors for endometrial cancer?

A

Age - increased risk over 60yrs
Nulliparity
LMP: irregular menses/amenorrhea/
anovulatory cycles;
menopause- on HRT?
- Tibolone increases risk 80%
- oestrogen only increase 50%
Chronic illness:
*DM - hyperinsulinaemia from insulin resistance increases activity of oestrogen on uterine tissue
*Personal h/o breast ca? On tamoxifen? - triples risk of breast ca
*PCOS - obesity, hyperinsulinaemia
*Obesity/sedentary lifestyle - risk is 2-3 times higher
FHx - breast cancer, colon cancer (hereditary non-papolomatous colon cancer is seen with <5% of endometrial ca)

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19
Q

How many deaths from endometrial cancer are attributed to tamoxifen therapy?

A

2/10,000 women per year!

Remember baseline risk is 2/100,000 (<40yrs) & 40-60/100,000 (>60yrs)

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20
Q

What reduces the risk of endometrial cancer?

A

1.Multiparity - first pregnancy
reduces risk by 30%; 25%
for each successive birth.
– older age at last birth reduces risk
2. COCPs -6% reduction per year
of use (fewer days of unopposed oestrogen exposure).
- risk reduction continues for 20yrs after stopping use
3. More sex hormone binding globular levels - more oestrogen is bound/ less metabolically active oestrogen
4. Physical activity - healthy weight/not obese
5. Aspirin esp in obese women decreases risk 28% meta-analysis

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21
Q

What is the broad FIGO classification/staging of endometrial cancer?

A

Stage 1 confined to corpus uteri
Stage 2 invades cervical stroma but
does not extend beyond the
uterus
Stage 3 local/regional spread
Stage 4 invasion of bladder/bowel/
distant mets

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22
Q

What is the Stage 1 FIGO classification of endometrial cancer?

A

Confined to corpus uteri

1A - no invasion/ <50% myometrial invasion

1B - >50% myometrial invasion

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23
Q

What is the Stage 2 FIGO classification of endometrial cancer?

A

Invasion of cervical stroma but no extension outside uterine corpus

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24
Q

What is the Stage 3 FIGO classification of endometrial cancer?

A

think from top of uterus down

3A - invasion of serosa of corpus +/- adnexa

3B- invasion of vagina +/- parametrium

3C - Lymph node spread
3C1 - Pelvic LN spread
3C2 - paraaortic node spread +/-
PLN spread

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25
Q

What is the Stage 4 FIGO classification of endometrial cancer?

A

4A - invasion of bladder/ bowel mucosa

4B- distant Mets (including inguinal/intraabdominal LNs)

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26
Q

Most common type of endometrial cancer?

A

Endometrioid - 75%

Composed of malignant glandular epithelial elements

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27
Q

Which types of endometrial cancer are more aggressive?

A

Type II category endometrial cancer- aggressive, fast growing, not related to oestrogen.

*Grade III endometrioid
adenocarcinomas
*Papillary serous - 5%-10%
*Clear cell- 1%-5%
*Malignant Mixed Mullerian
tumours/ carcinosarcomas: 1-2%
*Uterine sarcomas- 3%

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28
Q

What are the categories of endometrial cancer?

A

There are two categories of endometrial cancer- dependent on the histology, molecular profile and clinical course.

Type I - slow growing, low-grade (I-II) adenocarcinomas
— related to oestrogen — therefore seen in obese patients with peripheral conversion of androstenedione to oestrone in body fat.
– Diagnosed early and has a favourable prognosis
– 80% of cases

Type II
- more aggressive, fast growing and unrelated to oestrogen.
- Makes up 10% of cases
- Have i) p53 mutations
ii) loss of Heterozygosity at several chromosomal loci
- less favourable prognosis
- presents at an later stage

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29
Q

Aetiology of endometrioid vs clear cell and papillary serous carcinomas?

A

Endometrioid goes thru the pre-malignant phase of atypical hyperplasia.

Clear cell and papillary serous arise from a series of GENETIC mutations

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30
Q

What is the risk of recurrence for endometrial cancer?

A

7-18%

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31
Q

Main stay of treatment for endometrial cancer with multiple or distant recurrences?

A

High dose progesterone therapy.

GnRH analogues may be used in progesterone refractory cases.

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32
Q

How do you manage Stage 1 endometrial cancer?

A

TAH & BSO - Laparoscopic or laparotomy

LND is debatable - may increase morbidity (e.g. lymphoedema) without clear benefit.
- no evidence of benefitnon overall survival or recurrence free survival
—–therefore it is NOT recommended

  • If the patient is not fit for surgery (obesity, cardiac disease…) then treat with:
    External beam RT &/brachytherapy
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33
Q

How do you manage Stage 2 endometrial cancer?

A

TAH & BSO & consider pelvic/paraaortic LND

  • 20% chance of spread to PLN at this stage.
  • if 1) surgical margins are attained & 2)nodes are free of disease = NO need for adjuvant RT
  • If the patient is not fit for surgery (obesity, cardiac disease…) then treat with:
    External beam RT &/brachytherapy
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34
Q

How do you manage Stage 3/4 (intraabdominal disease) endometrial cancer?

A

Stage 3: AIM to cure!!

  • TAH & BSO + maximal surgical debulking
  • pelvic RT and vaginal RT
  • chemo for high grade tumours, especially if PLN disease!
  • Can consider neoadjuvant chemo for large pelvic masses, followed by debulking sx.

Stage 4: If distant mets:
- Palliative hysterectomy
- may be followed by pelvic RT and or chemotherapy (for palliation and to increase the symptom-free interval)

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35
Q

Incidence of lichen sclerosus?

A

1/300 to 1/1000

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36
Q

What systemic disorders are associated with lichen sclerosis or erosive lichen planus?

A

Autoimmune disorders:
Thyroid (Graves)
Alopecia Areata
Type 1 DM
Pernicious anaemia
Vitiligo

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37
Q

Vulvar dystrophy management?

A

Avoid:
- irritants
- tight clothing
- soaps, shampoos, bubble bath
- condoms with spermicide

Use:
- soap substitutes (decrease irritation)
- emollients (maintain and protect skin barrier)

Counsel:
About condition and long term complications

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38
Q

Vulvar dystrophy management?

A

Avoid:
- irritants
- tight clothing
- soaps, shampoos, bubble bath
- condoms with spermicide

Use:
- soap substitutes (decrease irritation)
- emollients (maintain and protect skin barrier)

Counsel:
About condition and long term complications

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39
Q

Differential Diagnosis for vulval dystrophy?

A

There are 9:

  1. Dermatitis
  2. Vulval candidiasis
  3. Atrophic vaginitis
  4. Contact dermatitis
  5. Lichen simplex
  6. Lichen sclerosus or Lichen planus
  7. Dermatoses
  8. Infection
  9. Systemic skin disorder
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40
Q

Discuss the types of vulval intraepithelial neoplasia?

A
  • VIN are premalignant lesions of which there are 2 types:
    Differentiated & Usual type

Differentiated Type
- is rare and seen in older women age 55-85 yrs
- associated with lichen sclerosus
- O/E: Unifocal ulcer or plaque
- May progress to keratinizing squamous carcinoma of the vulva
- This type of VIN is more likely to progress than the usual type

Ususal Type
- more common and seen in women 35-55yrs
- associated with smoking, HPV 16, CIN, VaIN and chronic immunosuppression
- Various presentations:
— mutifocal and multicentric
— papules/plaques/patches
— red/white/pigmented
— erosions/nodules/warts/
hyperkeratosis
- Associated with Warty or Basaloid squamous cell carcinoma of the vulva

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41
Q

What is the aim of management of VIN?

A
  1. relieve symptoms (of intense
    pruritus)
  2. exclude invasive disease
  3. reduce RISK of developing
    invasive disease
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42
Q

Management options for VIN?

A

Surgical and Non-surgical

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43
Q

Outline non-surgical management of VIN?

A
  1. Topical imiquimod cream
    - used 2-3 times/wk
    - has up to 81% clinical &
    histological response rate
    - S/Es: pain, erythema, swelling
    – can cause non-compliance
  2. Cidofovir - gives clinical and
    histological response
  3. Laser ablation - EFFECTIVE
    • Used when:
      - tissue conservation is
      important i.e. at glands &
      hood of clitoris
      - if pt refuses/is unfit for sx
      - failure rate: 40%
      - Not used on hair bearing
      skin because of the
      involvement of skin
      appendages
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44
Q

Outline surgical options for VIN?

A

Local excision and simple/radical vulvectomy

Local excision - provides histological sample for diagnosis.
- same recurrence rates as vulvectomy
- risk lower (but still exists) if margins are disease free;
- has higher response states compared to non-surgical management

** Women should have access to reconstructive surgery**
- as larger/ mutifocal lesions when healed can lead to scarring and tension - w/ subsequent pain and psychosexual morbidity.

Simple/Radical vulvectomy
- NOT recommended
- due to adverse effects on sexual
function & female body image

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45
Q

What percentage of women undergoing excision of VIN have clinically unrecognized invasion?

A

12-17%

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46
Q

Surveillance for VIN

A

Annual
- clinical assessment
- vulcoscopy
- biopsy suspicious lesions
- colposcopy: as 4% of pts will have intraepithelial neoplasia at OTHER lower genital tract sites
- examine cervix, vagina, vulval
and perinatal skin

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47
Q

Risks recurrence for VIN?

A
  • Increased with multifocal/multicentric disease (Usual type).
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48
Q

Risk of invasive cancer after surgical treatment for VIN?

A

4%

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49
Q

Risk of cancer w/in 8 years of diagnosis of VIN?

A

40%

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50
Q

T/F Lichen sclerosus is an autoimmune condition?

A

True. 40% have another autoimmune condition

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51
Q

Age of presentation for lichen sclerosus?

A

Any age (even children!!) but more common in postmenopausal women

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52
Q

Symptoms of lichen sclerosus?

A
  1. Severe pruritus (worse at night)
  2. Uncontrollable scratching with trauma and bleeding to area
  3. Dyspareunia
  4. Pain and or discomfort
  5. Difficulty urinating? ( fusion one labia minora over urethra)
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53
Q

Examination findings of lichen sclerosus?

A
  • Vulva affected in a Figure of 8 configuration
  • Erythema and keratinization of the vulval skin
    • Hyperkeratosis may be present
      as white, thickened skin
  • Atrophic skin that splits easily
  • Lateral fusion and resorbtion of labia minora
  • lateral fusion of clitoral hood and burying of clitoris
  • Medial fusion of labia minora causing:
    • Narrowing of the vaginal introitus
    • Skin bridges at the fourchette
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54
Q

Treatment for lichen sclerosus?

A

Medical with Ultra-potent steroids.

Surgical management/CO2 laser ablation is not recommended. Disease may recur around the scar.

—- Laser may be useful to treat sequelae of scarring due to lichen sclerosus (urinary retention/narrowing of the introitus)

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55
Q

Medical management of lichen sclerosus?

A

Clobetasol pro-pi-onate
- MOST potent topical steroid
- 54-96% have partial/complete
symptom resolution.
- Women <50yrs have higher
response rates

84% relapse within 4 yrs

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56
Q

How is clobetosol propionate prescribed for lichen sclerosus?

A

Varies and no optimal regime has been identified. However,

Common dosing is:
Daily x 1mth
Alternate days x 1mth
Twice weekly x 1mth
Review at 2-3 months

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57
Q

Treatment for steroid resistant lichen sclerosus?

A
  1. Potent topical steroid w/ antifungal/antibacterial agent to treat secondary infection (if that is a concern). E.g. Dermovate
  2. Oral retinoids (aci-tre-tin) for recalcitrant disease may be prescribed by an experienced dermatologist.
  3. UV phototherapy has been shown to have benefit in a small number of cases
  4. Tacrolimus & Pimicrolimus
    - calcineurin inhibitors
    - suppress T lymphocytes response thereby reducing inflammation
    - OFF License use
    - 77% with full/partial response
    - Avoids adverse effects of steroids
    - Max effects after 120-24wks of treatment
    - Do NOT use for >2yrs due to concerns about potential malignancy
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58
Q

F/U for lichen sclerosus?

A

2-3 after treatment to assess response

  • if stable assess ANNUALLY
  • If active disease, assess as clinically required.
  • provide written and verbal information about:
    -the risk of progression to VIN (usual type preceded by lichen sclerosus)
    • malignant change (2-4% lifetime
      risk)
  • Advise to return for review if any change in the appearance/texture of their lesions (e.g. hardening of skin)
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59
Q

Discuss lichen planus

A

(Planus - planet, all over)

  • affects anywhere on body, but usu affects mucosa surfaces (especially oral mucosa)
  • cause unknown. ? Autoimmune
  • Planus = 4 Ps of appearance:
    • Polygonal and flat topped
    • Purple (violaceous)
    • Pruritic
    • Plaques and Papules
      + with a fine, white reticular pattern (Wickham striae)
  • Tends to be EROSIVE in mouth and genital region - and associated with pain rather than pruritus
  • Erosive lichen planus is WELL DEMARCATED, glazed erythema around the introitus
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60
Q

Discuss lichen simplex chronic or
Chronicus vulval dermatitis.

A
  • severe pruritus esp at night
    (Lichen sclerosus has this too)
  • inflammation to labia majora; can spread to inner thighs and mons pubis.
  • may be areas of thickening or lichenification (hyperpigmentation and thickening due to constant scratching)
  • Cause: stress, low iron stores, symptoms can be exacerbated by chemical/contact dermatitis

Treatment:
- avoid soaps and irritants
- use emollients and soap substitutes
- Antihistamines/ antipruritics for pruritus
- topical steroids (moderate/ ultra-potent) may be required to break the itch-acratch cycle

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61
Q

Discuss vulval psoriasis

A
  • Affects vulval skin
  • Vaginal mucosa NOT included
  • O/E: smooth, non-scaly, red/pink discrete lesions
    Exam nails and scalp for psoriasis plaques. Flexor surfaces also.

Treatment:
- emollients
- soap substitutes
- calcipo-tri-ene (vit D cream)
DO NOT is cold tar on genitals!

62
Q

What’s Bechet’s disease?

A
  • Chronic, multisystem disorder.
  • causes recurrent, painful oral and genital ulcers (cervix, vagina and vulva) leaves scars

Tx: Topical/ systemic
immunosuppressants

63
Q

Discuss Paget’s disease of the vulva

A

-Rare
-Occurs in postmenopausal women
-Assoc. with underlying
ADENOcarcinoma
- Main symptom: pruritus
- O/E : ecezematous appearance- lichenification, erythema and excoriations
- check GIT, urinary Tract and breast
- Treatment - excision to exclude adenocarcinoma of skin appendages
- surgical margins hard to obtain due to subclinical disease.

  • Recurrence is common
64
Q

T/F VIN can be treated with laser ablation?

A

True, but only on hairless areas.

In pts who are unfit/refuse sx and those in whom tissue conservation is important (glans and hood of clitoris).

65
Q

Vulval candiasis, discuss.

A

Irritation and soreness to vulva and anus.

Risks: DM, obesity, prolonged
antibiotic use

O/E: inflammation with satellite lesions extending from the labia majora to the inner thighs or mons pubis

Tx: Topical antifungal +/- oral preparations

66
Q

Discuss Vulval Crohn’s disease

A

Vulva may be involved by DIRECT spread from involved bowel OR “metastatic” granulomas.

O/E: vulva is swollen and oedematous; ulcers; draining sinuses, abscesses

Tx: Metronidazole + oral
immunomodulators

67
Q

T/F adenocarcinomas make it 25% of vulval malignancies?

A

False

95% squamous cell
<5% melanomas

Adenocarcinoma is included in the rest

68
Q

Incidence of vaginal/vulvar cancers?

A

<1% of all cancers

8% of gynae cancers

1.7/100,000 women

69
Q

Death rate from vulval cancer

A

Almost same as the incidence:

1.2/100,000 women

70
Q

Age group affected by vulval cancer?

A

70 -80’s

Incidence increases with age and peaks over age 85

71
Q

Lifetime risk of vulval cancer?

A

1/293

72
Q

Risk factors for vulval cancer?

A

-Multifocal disease 5-90%
-Lichen sclerosus 4-7%
-VIN (Differentiated-keratinizing squamous, usual- warty/ basaloid squamous)
-Paget’s disease (adenocarcinoma)
-Melanoma in situ
-HPV 16, 18, 31 - 30-40% association either vulval ca, 80% assoc w/ vin
-Immunosuppression
-Prev cervical ca or CIN
- HSV type 2 (interacts with HPV to cause vulval and other lower genital tract cancers)
- h/o radiotherapy for uterine ca

73
Q

Clinical evaluation of vulval ca?

A

O/E: Vulval exam
1. Tumour size and location(90% have visible tumour)
2.Assess of vagina, urethra, bladder base or anus is involved
3. Palpate for infiltration deep to public and ischial bones
**EUA may be necessary
4. Palpate for groin LNs

Biopsy:
- Biopsy area of transition from normal to malignant tissue
- >1mm depth to asess invasion
- oriented for the pathologist

  • small punch Biopsy under local for elderly patient
  • excisional Biopsy for smallesions where a wide margin of normal tissue can easily be obtained
  • if pt is bleeding/in pain, then biopsy can be done at time of definite sx as a frozen section PRIOR to any radical procedure

Investigations
Cbc, u&e, cxr, ecg
Pap smear (if overdue)
CT CAP if tumour >2cm to detect disease above inguinal ligament

74
Q

FIGO staging of vulval cancer?

A

Remember tumour grows from outside up into vagina/anus/urethra

Stage 1 - localized to vulva and perineum, 2cm or less
A- tumour 2cm or less,
stromal invasion 1mm or less
B- tumour less than 2cm diameter,
>1mm stromal invasion +
neg LNs

Stage 2- tumour of any size extending to lower third vagina/urethra or anus + neg LNs

Stage 3 - tumour of any size +/- extension into adjacent perineal structures with POSITIVE inguinofemoral LNs:
A- 1 node of any size or 2 LNs <5mm
B- 2 or more LNs >5mm, or
3/more LNs <5mm
C- positive LNs w/ extracapsular
spread

Stage 4
A- tumour invades upper urethra/ Bladder mucosa/ rectal mucosa or is fixed to bone and or bilateral regional LN mets

B- distant mets/Pelvic LNs

75
Q

What is the general population’s risk of breast, ovarian and endometrial cancer?

A

Breast 10%
Ovarian - 1.4%
Endometrial - 1.1%

76
Q

What is the risk of breast and invariant cancer in a BRCA 1 positive pt?

A

Breast - 65%
Ovarian - 39%

77
Q

What is the risk of breast and ovarian cancer in a BRCA 2 positive pts?

A

Breast - 45%
Ovarian - 11%

78
Q

What is the incidence of BRCA 1 & 2 mutations in breast and ovarian cancers in families?

A

52 and 32%

79
Q

How are BRCA 1 & 2 mutations inherited?

A

Autosomal dominant

80
Q

Incidence of BRCA mutations in Ashkenazi jews?

A

2%

81
Q

What points in the family history would make u suspect BRCA mutation in the family?

A
  • 3/more relatives with breast/ovarian cancer (clustering).
    • esp if early onset
  • bilateral breast OR bilateral ovarian ca OR breast & ovarian ca in the same woman
  • serous ovarian cancers
82
Q

What cancer surveillance or screening can be done for women with the BRCA mutation?

A

No screening test for ovarian ca.

For breast ca - for Annual MRI for women aged 30-49 years
- compared to mamnogram is more ideal for younger pts at risk of high grade tumours

83
Q

Benefit of prophylactic sx in a pt with a BRCA mutation? What types of prophylactic surgery can be performed for these patients?

A

Allows intervention before the development of cancer.

Types of prophylactic surgeries:
1. Prophylactic BSO
2. Prophylactic mastectomy

Bilateral oophorectomy decreases the risk of ovarian cancer by 50%.

Salpingectomy decreases risk of more aggressive primary peritoneal cancer.
- cancer risk decreases from as high as 40% to 1-2%
- 20 yrs post BSO, residual risk is 4.3%

84
Q

Benefit of prophylactic BSO?

A

Reduced risk of:
1. ovarian ca from 40% to 1-2%
2. primary peritoneal ovarian ca.
3. reduced risk of breast ca by 50%

85
Q

Residual risk of primary peritoneal ca 20yrs post BSO?

A

4.3%

86
Q

What are the risks associated eith prophylactic BSO?

A
  1. Surgical - haemorrhage, damage to surrounding structures
  2. Premature menopause
  3. Psychological distress- loss of
    fertility, early menopause
87
Q

What age should prophylactic surgery be performed for pts with BRCA mutations?

A

BRCA1 - early 30’s as the risk of cancer increases significantly after age 30 yrs.

BRCA2 - early 40’s as risk of cancer increases after age 40yrs.

88
Q

Which other cancers are associated ith BRCA mutations?

A

BRCA 2 is associated with male breast cancer (6%) and prostate cancer

89
Q

What percentage of hereditary ovarian ca is attributable to BRCA1?

A

90%

90
Q

What percentage of hereditary ovarian ca is attributable to BRCA2?

A

5-10%

91
Q

What percentage of ovarian ca is hereditary?

A

5-10%

92
Q

What percentage of hereditary ovarian ca is attributable to BRCA mutations?

A

95% of families with breast AND ovarian ca.

40-50% of families with breast ca only

93
Q

Which hereditary conditions are assoc. With increased risk of ovarian/endometrial/breast cancer?

A

BRCA 1&2 mutations
Lunch syndrome/HNPCC
Peurz-Jeughers

94
Q

What kind of inheritance is associated. With HNPCC/Lynch? What are the associated mutations?

A

Autosomal dominant

Mutations in mismatch repair genes:
MLH1, MSH2 & MSH6

95
Q

What are the risks of ovarian and endometrial cancer assoc. with HNPCC?

A

Risks vary of which genes are affected.

MLH1 - 3.4% ovarian, 27%
endometrial
MSH2 - 10.4% ovarian, 40% endometrial
MSH6 - 71% risk endometrial

96
Q

Is prophylactic sx an option for pts with HNPCC?

A

Yes, if the patient desires it.
-Prophylactic BSO for MLH1 and MSH2 mutations.
-Prophylactic hysterectomy can be done for MSH6 mutations due to the very high risk of endometrial cancer.

97
Q

T/F. HNPCC is assoc. with breast ca?

A

False. They are associated with ovarian and endometrial cancer

98
Q

Cancer surveillance for HNPCC?

A

2 yearly colonoscopy to reduce mortality from colorectal cancer

99
Q

What factors make the prognosis for choriocarcinoma is worse?

A
  1. normal pregancy or spontaneous miscarrage
  2. Blood groups B or AB
  3. Interval between pregnancy and chemo >12mths

*Prognosis is BETTER after:
1. a known molar pregnancy
2. Blood groups O and A
3. Interval between pregnancy and chemo is <4mths

100
Q

In patients with HNPCC, where are the majority jmof colon cancers located?

A

70% are Proximal to the splenic flexure

101
Q

Most common gynae cancer in the developed world?

A

Ovarian cancer, specifical epithelial ovarian

102
Q

List the subtypes of epithelial ovarian cancers.

A

Serous - 68%
Clear cell - 13%
Endometrioid - 9%
Mucinous - 3%
Brenner
Mixed
Undifferentiated

103
Q

What percentage of endometrial cancer is HNPCC associated with?

A

<5%

104
Q

How are families selected for molecular testing for HNPCC?

A

Using the Amsterdam criteria, families most likely to have HNPCC families will fulfill all the criteria:

(Think 3, 2 , 1)

  1. Colorectal ca in at least 3 first degree relatives of each other, where familial adenomatous polyposis coli has been excluded
  2. Colorectal ca in 2 successive generations.
  3. Colorectal ca diagnosed in at least one relative <50yrs
105
Q

By how much does OCPs decrease the risk of endometrial ca?

A

40%

OCPs (progesterones) prevent proliferation of the endometrium.
- use for 12-23mths =40% reduction in risk and use for 10yrs = 60% risk reduction

106
Q

What percentage of women with the BRCA mutation, who undergo prophylactic oophorectomy have occult ovarian tumours?

A

12%

12% of women who have a prophylactic oophorectomy will have occult ovarian tumours noted in histopathology.

107
Q

By how much does prophylactic BSO decrease the risk of ovarian ca?

A

Prophylactic BSO decreases risk of ovarian cancer from up to 40% to 1-2%

108
Q

What size breast tumour is suitable for breast conservation surgery?

A

<2.5cm

109
Q

What is the screening schedule as per the NHS Breast Screening Programme?

A

<50yrs - not offered screening
50 - 71yrs - screening every 3 years

  • Older pts with less breast fat makes a mammogram easier to perform.
110
Q

What are features of a benign breast mass on ultrasound?

A
  1. Smooth and well circumscribed
  2. Hyper/iso/mildly hypoechoic
  3. Thin, exhogenic capsule
  4. Ellipsis shape w/ max diameter in the transverse plane
  5. 3 or fewer gentle lobulations
  6. Absence of malignant findings
111
Q

What is the commonest cause of breast lumps in women 35-50 yrs? Briefly describe this lesion.

A

Breast cyst

  • Fluid accumulation due to obstruction of extralobular terminal ducts OR fibrosis due to intraductal epithelial proliferation.
  • U/S: well-defined oval or round, anechoic structure in a thin wall.
112
Q

Which HPV types are assoc. With VIN?

A

16 MOSTLY
18, 31, 33, 45

They are associated with approx 30-40% of cases.

Hence HPV vaccines that cover 16 and 18 result in sig reduction of VIN in young women.

113
Q

What percentage of women who have vulval ca present with lichen sclerosus?

A

25%

114
Q

What percentage of pts with untreated VIN progress to invasive squamous cell ca (vulval ca)?

A

5%

115
Q

Describe the types and presentation of VIN.

A

Two types: differentiayed and usual

Diffentiated
- rarer
- older pts (55-85)
- some associated with lichen sclerosus
- unifocal ulcer/plaque
- linked to keratinizing squamous cell ca of vulva
- higher risk of progression to ca

Usual type
- younger pts (35-55)
- warts, basaloid, mixed
- assoc with HPV 16, CIN, VaIN, smoking, chronic immunosuppression
- multifocal, multicentric
-varied appearance: red, white/pigmented, plaques/papules/patches
- assoc. With warty or basaloid squamous cell ca

116
Q

T/F. VIN pts are more likely to develop CIN and AIN (anal intraepithelial neoplasia)

A

True

117
Q

In pts with vulval cancer, when can groin node dissection be avoided?

A
  • stage 1A squamous cancer
  • basal cell
  • verrucous tumour
  • melanoma
118
Q

In vulval cancer, what type of groin node dissection done for lateral vs central disease?

A

Lateral disease:
- ipsilateral GND. Contralateral GND is done if the ipsilateral node is positive.

Central disease:
Bilateral GND done via different incisions to reduce morbidity (triple incision technique)

119
Q

What are the complications associated with surgery for vulval ca?

A
  1. Wound infection
  2. Wound dehiscence
  3. DVT & PE
  4. Pressure sores
  5. Introital stenosis
  6. Psychosocial complications
  7. Urinary incontinence
  8. Faecal incontinence
  9. Rectocoele
  10. Lymphoedema
  11. Hernia
120
Q

What is the negative predictive value of sentinel node biopsy in vulval ca?

A

95-100%

121
Q

Which nodes are removed in groin node dissection (in vulval cancer)?

A
  • superficial inguinal nodes AND
  • deep femoral nodes

Higher risk of recurrence with removal of superficial inguinal LND only.

122
Q

Preservation of which structure in groin node dissection in vulval ca will reduce both groin wound and lower limb issues?

A

The long saphenous vein

123
Q

What are the categories of endometrial cancer?

A

Type 1 and 2 based on histopath, molecular profile and clinical course.

Type 1:
- slow growing, low-grade (I-II) adenocarcinoma
- linked to oestrogen and obesity
- 80% of cases if endometrial ca
- usu diagnosed early with good prognosis

Type 2- aggressive, faster growing
- grade III adenocarcinomas
- NOT LINKED to oestrogen
- 10% of cases
- have p53 mutations
- have loss of heterozygosity on several chromosomal loci
- present at later stages
- less favourable prognosis

124
Q

Histological types of endometrial cancer?

A

1.Endometrioid - 75%
– has malignant glandular epithelial elements
— arises from complex hyperplasia
2. Papillary-serous - 5-10%
3. Clear cell - 1-5%
* both papillary and clear cell occur due to a sequence of genetic mutations*
4. Carcinosarcomas (MMMT)- 1-2%
5. Uterine sarcomas - 3%
6. Mucinous - 1%
7. Adenocarcinomas (with squamous differentiation)
8. Adenosquamous (malignant squamous component)
9. Adenocanthoma (benign squamous element)
10. Undifferentiated

125
Q

What percentage of endometrial cancers are inherited?

A

<5%

126
Q

What’s the figo staging of vulval cancer?

A

Stage 1 - vulva +/- perineum, 2cm/less width
1a: no more than 1mm deep, width 2cm/less
1b: >1mm deep or >2cm wide

Stage 2: tumour of any size growing into lower 1/3rd urethra, lower 1/3rd vagina/anus. NEG nodes

Stage 3: any size +/- adjacent perineal structures with POSITIVE inguino/femoral LNs

  • 3a: vulva+/- perineum; growing to anus, lower vagina/urethra PLUS POSITIVE LNS (1 nearby >5mm spread or 2 nearby <5mm each)

-3b: vulva +/- perineum + anus, lower vagina/urethra + POS nearby LNs ( 2/more >5mm or 3/more nearby <5mm)

-3c: positive LNs + extracapsular spread

Stage 4:
4a: Bladder, rectum, upper vagina/urethra, pelvic bone, regional LNs/ LN ulceration

4b: distant mets (lung, bone), pelvic LNs

Stage 4:

127
Q

Risk of endometrial ca in overweight/obese women compared to healthy weight?

A

2-4 times greater risk

128
Q

Lifetime risk of breast ca in UK?

A

11%

129
Q

Most common cancer in pregnancy and puerperoum? Incidence?

A

Breast ca

1 in 3000 (0.03%)

130
Q

Which HPV subtype is associated with adenocarcinoma?

A

HPV 18

131
Q

Detection Rates of endometrial ca with pipelle in postmenopausal women vs premenopausal?

A

99% vs 91% (premenopausal)

132
Q

What is the sensitivity and specificity of pipelle sampling?

A

Sensitivity 81%
Specificity 98%

133
Q

T/F. In endometrial ca, lymphatic spread to para-aortic nodes commonly occur without pelvic node involvement.

A

False. Involvement of para-aortic nodes are less common if pelvic nodes are NOT involved.

134
Q

5 year survival for endometrial cancer?

A

80%

Overall prognosis for endometrial ca is generally good, as most present early (Type 1 endometrial ca!!)
- prognosis varies based on histological subtype, tumour grade, depth of myometrial invasion, presence/absence of lymphovascular space invasion

135
Q

What is the optimal surgery in early stage (Figo stage 1 - 2a) ovarian cancer?

A

Midline laparotomy
Tah + bso
Infracolic omentectomy
Pelvic lymphadenectomy
Biopsies of any peritoneal deposits
Random sampling of pelvic and abdominal peritoneum
Retroperitoneal LN assessment (+/- bilateral sampling of pelvic and para-aortic LNs)
Cytology from ascites/ peritoneal washings

136
Q

What is the risk of malignancy in simple, unilocular, unilateral ovarian cysts <5cm in diameter? Management?

A

<1%

Premenopausal- should resolve in 3 menstrual cycles.
- if 5-7cm, yearly u/s followup.

Postmenopausal:
Manage conservatively with f/u scan in 4mths for cysts 2-5cm

137
Q

Management of a simple ovarian cyst >7mm?

A

Consider MRI as u/s may not be able to fully evaluate the cyst.

Ovarian cysts that persist or increase in size are unlikely to be functional and SURGICAL management is indicated.
- no consensus of max diameter for sx but most studies use 6cm as the ULN for conservative management.

138
Q

What are the NHS recommendations for f/u after treatment for low grade and high grade disease?

A

Low grade/CIN 1:
Papsmear/cytology at 6, 12 and 24mths post treatment. If all negative = return to routine/low risk f/u.

High grade/CIN 2/ 3:
- papsmeae/cytology at 6 and 12 months then yearly for the next 9 years = all normal = return to routine/high risk f/u

139
Q

Lifetime increase in risk of breast ca after CTPA?

A

13.6%

140
Q

What are borderline ovarian tumours?

A
  • a Heterogenous group of tumours seen in younger patients
  • have higher proliferative activity than benign tumours but are NOT invasive

Protective factors:
- older patients (common in young)
- multiparity
- lactation

  • Unlike invasive ovarian cancer OCPs are NOT protective
  • diagnosis usu made after sx for a presumed benign lesion.

Management: Surgical staging
- conservative management may be considered with patients with fertility desires.

141
Q

8 week pregnant pt with a prev pap smear showing mild dyskaryosis. She is due for a repeat. What do u recommend?

A

Do not delay the test and repeat mid trimester (unless there is a clinical contraindication).

  • if she had a previously normal pap smear, then it could have been deferred to after pregnancy.
142
Q

What is the risk of contralateral LN involvement for lateral vulval tumours

A

<1%

In these cases the contralateral LN is resected via a separate incision (triple incision technique)

Median tumours = bilateral groin node dissection

  • both superficial inguinal and deep femoral nodes are resected.
143
Q

What are the recommendations for surgical management for borderline ovarian tumours?

A
  • conservative management for women who wish to preserve fertility
  • tah +bso+ infracolic omentectomy
  • peritoneal washings (explores abdominal cavity)
  • appendectomy for mucinous tumours
  • treatment is similar to ideal treatment during low grade ovarian cancer, minus assessment of retroperitoneal nodes.
144
Q

Sentinel node mapping is most established with which gynae malignancy? Benefit?

A

Vulval cancer

Sentinel lymphadenectomy is assoc with a lower rate of lymphoedema compared to complete groin lymphadenectomy.

145
Q

5y.o with vulvar scratching, well demarcated white area around introitus, with the overlying skin appearing thin with extensive fissuring. Likely diagnosis?

A

White, thin skin with fissuring + severe pruritus = think lichen sclerosus

146
Q

What are the histological features of lichen sclerosus?

A

Atrophic epidermis
Overlying hyperkeratosis
Effaced dermoepidermal junction
Superficial dermal hyalinisation
Lymphocytic infiltration

147
Q

What is the appearance of vulval psoriasis?

A

Well defined, beefy red/pink, uniform/smooth and symmetrical lesions on the SKIN of the vulva.
- Vaginal mucosa not involved.

Not scaly like on the other areas of the body.
—check nails and scalp

148
Q

What is the histological findings for vulval psoriasis?

A

Papillomatosis
Parakeratosis
Neutrophil exocytosis
Spongiform pustules

149
Q

What is the treatment for vulval psoriasis?

A

Emollients
Soap substitutes
Topical steroids
Calcipotriene

150
Q

What is the effectiveness of HPV vaccines in presenting cervical abnormalities assoc with HPV types 16 & 18?

A

> 99% in women previously not infected with those serotypes

151
Q

Factors that reduce ovarian ca?

A

They reduce ovulation:
Pregnancy
Breastfeeding
Multiparity
OCPs

Gynae (9 decks)

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