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gynaecological cancers DONE Flashcards

1
Q

what is endometrial hyperplasia

A

thickening of the inner lining of the womb (uterus)

excess of the hormone oestrogen not balanced by progestrone hormone

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2
Q

what are the two types of endometrial hyperplasia

A

hyperplasia without atypia. In this type, the lining of the womb is thicker, as more cells have been produced. The cells are all normal, however, and are very unlikely to ever change to cancer. Over time, the overgrowth of cells may stop on its own, or may need treatment to do so.

Atypical hyperplasia. In this type, the cells are not normal (they are said to be atypical). This type of hyperplasia is more likely to become cancerous over time if not treated.

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3
Q

Sx of endometrial hyperplasia

A 
red flags
above 55
vaginal bleeding which is different to your usual pattern. 
PMB
 vaginal discharge

inbetween their periods

heavier or irregular

HRT you may get bleeding

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4
Q

causes of endometrial hyperplasia

A 
overweight
diabetic
HRT
no children
PCOS
tumour of the ovary
tamoxifen
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5
Q

tests for endometrial hyperplasia

A

US scan - exclude other causes such as polyps or cysts

after menopause lining is thin usually

endometrial biopsy

hysteroscopy

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6
Q

Mx for endometrial hyperplasia without atypia

A

nothing and repeat biopsy

IUS is the best treatment releases progestorn which thins the lining of the women.

stays in at least for 6 months but for upo 5 years

repeat sampling in 3-4 months

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7
Q

when may hysterectomy endometrial hyperplasia without atypia be required

A

The hormone treatments are not working after 6-12 months.

The condition comes back after treatment.

You go on to develop atypical hyperplasia.

You prefer to have an operation than to take regular medication or have an IUS

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8
Q

Mx for atypical endometrial hyperplasia

A

total hysterectomy with bilateral salpingo-oophorectomy

menopause - removal of ovaries and fallopian tubes may be suggested

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9
Q

most common gynaecological cancer

A

endometrial

Rare before the age of 35
Peak age group 64 – 74
Declines after 80
Commoner in western world

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10
Q

high risk factors for endometrial cancer

A 
Obesity
Early menarche-late menopause
Nulliparity
PCOS
Unopposed oestrogen
Tamoxifen
Previous breast or ovarian cancer
BRCA 1/2
Endometrial polyps
Diabetes
Parkinson’s

all result in excess oestrogen

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11
Q

risk factors that reduce endometrial cancer

A 
Continuous combined HRT
Combined oral contraceptive pill
Smoking
Physical activity
Coffee
Tea
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12
Q

presentation of endometrial cancer

A

Pre-menopausal (1% risk)
Prolonged, frequent vaginal bleeding
Intermenstrual bleeding

Postmenopausal
Postmenopausal Bleeding (PMB) (10% risk)
Less commonly blood stained, watery or purulent vaginal discharge
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13
Q

pathology of endometrial hyperplasia

A

Pre-malignant condition
Classification simple, complex, atypical
With atypical, malignancy co-exists in 25-50% of cases, and 20% will develop Ca within 10 years.
Treatment with progestagens/ surgery

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14
Q

classification of endometrial adenocarcinoma

A

TYPE 1 (80%): Endometrial Adenocarcinoma

TYPE 2 (20%):

Papillary Serous
Clear cell Carcinosarcoma

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15
Q

endometrial FIGO staging

A

1A - confined to cervix - <7mm wide
1B - confined to cervix - >7mm

2 - Cervical spread NOT TO PELVIC WALL

3 - Uterine serosa
Ovaries / Tubes Vagina
Pelvic / Para-aortic Lymph Nodes to pelvic wall

4 - Bladder / bowel involvement
Distant metastases

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16
Q

diagnostic tests for endometrial cancer

A

Endometrial sampling by Pipelle or (less commonly) D&C - dilataion and caradarch

Hysteroscopy: gold standard to assess uterine cavity
Transvaginal Ultrasound: useful for investigation of PMB, use >5mm cut off for endometrial thickness

1) women >= 55 years who present with postmenopausal bleeding should be referred using the suspected cancer pathway
2) first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
3) hysteroscopy with endometrial biopsy

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17
Q

other Ix for endometrial cancer

A
  • Metastases rare at presentation in Type 1 cancers
  • Intraperitoneal, lung, bone, brain
  • FBC, U&E, LFT
  • CT chest/abdo/pelvis
  • MRI Pelvis
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18
Q

preferref Mx for endometrial cancer and factors influencing it

A

Surgical treatment is the preferred treatment option where possible.

Factors influencing primary treatment are stage, age & fitness for surgery, patient preference

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19
Q

surgical Mx for endometrial cancer

A

Hysterectomy PLUS bilateral salpingo-oophorectomy, peritoneal washings
Laparoscopic / Open

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20
Q

non-surgical alternatives for endometrial cancer

A

Progestagens

Primary Radiotherapy

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21
Q

adjuvant radiotherapy if high risk of recurrence of endometrial cancer

A

External beam

Brachytherapy

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22
Q

advanced disease/inoperatble disease/ unfit for surgery for endometrial cancer

A

Chemotherapy
Radiotherapy
Hormones
Palliative Care

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23
Q

what will happen at one stop postmenopausal bleeding

A

History & Examination
FBC
Transvaginal ultrasound
Hysteroscopy and endometrial biopsy

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24
Q

epidemiology of ovarian cancer

A
  • Second commonest gynae cancer in the UK
  • Incidence is rising
  • Lifetime risk 1:50
  • Peak age 70-74 years, occurs predominantly in 5th, 6th and 7th decade
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25
Q

pathology of ovarian cancer

A 
cystadenocarcinoma - commonest histological subtype
surface epithelium 
- most common serous
- mucinous
 endmetriod
- clear cell
brenner tumpurs

germ cells

  • dysgerminoma
  • teratoma
  • yolk sac
  • choriocarcinoma

stroma

  • granulosa
  • theca
  • sertoli-leydig

krukenberg tumour from stomach or breast cancer

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26
Q

which types of ovarian cells can be benign/malignant

A

serous

mucinous

teratoma

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27
Q

high risk factors for ovarian cancer

A
  1. Genetic
    - FH of ovarian cancer
    - BRCA 1/2
    HNPCC
  2. Environmental
    - asbestos exposure
    - talcum powder use
  3. physical
    - Obesity
  4. Hormonal
    - Nulliparity
    - Early Menarche
    - Late Menopause
    - Unopposed Oestrogen HRT
  5. Medical Hx
    - Endometriosis / cysts
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28
Q

risk factors that reduce ovarian cancer

A 
Combined oral contraceptive pill
Pregnancy
Breastfeeding
Hysterectomy
Oophorectomy
Sterilisation
? Statins
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29
Q

ovarian cancer presentation

A

not specific

  • abdominal swelling
  • pain
  • anorexia
  • N/V
  • weight loss
  • vaginal bleeding
  • bowel Sx

adenocarcinoma cells and a complex pelvic mass

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30
Q

Ovarian cancer diagnosis and work up

A

CA125 - baseline

Pelvic examination
Ultrasound
FBC, U&E, LFT

(CXR) - staging

CT to assess peritoneal, omental and retroperitoneal disease
Cytology of ascitic tap

Surgical exploration
Histopathology

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31
Q

ovarian cancer staging

A

1 - Limited to ovary / ovaries

2 - Spread to pelvic organs

3 - Spread to rest of peritoneal cavity
Omentum
Positive Lymph nodes

4 - Distant metastatsis
Liver parenchyma
Lung

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32
Q

epithelial ovarian cancer Tx

A

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

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33
Q

non-epithelial ovarian tumours Tx

A

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

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34
Q

Tx if recurrent ovarian tumours

A

palliative chemotherapy

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35
Q

factors that increase risk of cervical cancer

A
  • HPV
  • Young age at first intercourse
  • Multiple sex partners
  • Exposure (no barrier contraception)
  • Smoking
  • Long term use of COCP
  • Immunosuppression/HIV

Non compliance with cervical screening

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36
Q

factors that may reduce cervical cancer

A

HPV vaccine

Cervical screening compliance

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37
Q

which HPV types increase risk of cervical cancer

A

16, 18

38
Q

what is HPV

A

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

Most women will be infected at some time

HPV infection is common in late teens and early twenties

Infection lasts on average 8 months

39
Q

history of HPV

A

Asymptomatic

Can be cleared or persist or cause CIN

40
Q

CIN history

A

Asymptomatic

Can regress, persist or progress to cancer

41
Q

what is CIN

A

Pre-malignant condition

Occurs at the TZ

Asymptomatic

42
Q

diagnosis of cervical cancer

A

histological

43
Q

cervical presentation

A

PCB
PMB
IMB
Blood stained vaginal discharge

In very advanced disease:
Fistulae, renal failure, nerve root pain, lower limb oedema

44
Q

staging of cervical cancer

A

1
Confined to cervix A Microinvasive (depth<5 mm/width<7mm)
B Clinical lesion

2
Beyond cervix but not pelvic side wall or lower 1/3 of vagina

A Upper 1/3 Vagina

B Parametrium

3
Pelvic spread, reaches side wall or lower 1/3 of vagina

A Lower 1/3 of vagina, hydronephrosis

B Extends to pelvic side wall, hydronephrosis

4
Distant spread
A Invades adjacent organs (bladder/bowel)

B Distant sites

45
Q

Mx for cervical cancer

A

Microinvasive carcinoma: can be more conservative. If fertility is an issue, then cone biopsy can be used. Once family is complete, hysterectomy is appropriate.

Clinical Lesions (1b - 2a): Wertheim’s radical hysterectomy or chemoradiotherapy (survival same)

  1. Clinical lesions beyond stage 2a: Chemoradiotherapy
  2. Postoperative radiotherapy: with lymph node involvement
  3. Recurrent disease: Radiotherapy, chemotherapy, exenteration, palliative care
46
Q

surgical complications of cervical cancer Mx

A

Surgery:

Infection
VTE
Haemorrhage
Vesicovaginal fistula
Bladder dysfunction
Lymphocyst formation
Short vagina
47
Q

radiotheraphy complications of cervical cancer

A 
Vaginal dryness
Vaginal stenosis
Radiation cystitis
Radiation proctitis
Loss of ovarian function
48
Q

Principles of cervical screening

A

The condition should be an important health problem.
There should be a treatment for the condition.
Facilities for diagnosis and treatment should be available.
There should be a latent stage of the disease.
There should be a test or examination for the condition.
The test should be acceptable to the population.
The natural history of the disease should be adequately understood.
There should be an agreed policy on whom to treat.
The total cost of finding a case should be economically balanced in relation to medical expenditure as a whole.

49
Q

cervical smear frequency

A

First invitation age 25

3 yearly from 25 to 50

5 yearly from 50 – 65

After 65 selected patients only

50
Q

cervical cytology

A

Cells collected from cervix (transformation zone) and exfoliated morphology examined
Liquid based cytology- UK

51
Q

classification of cytology

A 
Normal
Inadequate
Borderline
Mild Dyskaryosis
Moderate Dyskaryosis
Severe Dyskaryosis
Possible Invasion
52
Q

what is colposcopy

A
  • Low-power binocular microscopy of cervix

To look for features suggestive of CIN or invasion

  • — abnormal vascular pattern (mosaicism, punctation)
  • — abnormal staining of the tissue (aceto-white, brown iodine)
53
Q

Mx for CIN

A

See-and-treat concept

Excisional: LLETZ (large loop excision of the transformation zone), cold knife cone

Destructive: cryocautery, diathermy, laser vaporisation (less common in UK)

Following colposcopy, follow up depends on results, but may be 6 monthly, yearly for 10 years, or routine recall

54
Q

what vaccination is given preveneting cervical cancer

A

Gardasil: 6,11,16,18
Cervarix:16 & 18

3 injections over 6 months

Ideally prior to SI

5 years protection
Still need smears (HPV 31, 45 & others)

55
Q

how does vulval cancer look

A

ulcerated lesion or raised in labia or clitoris

56
Q

what is VIN vulval intraepithelial neoplasia

presentation

Mx

A

Pre malignant condition

  • Can resolve spontaneously
  • Can progress to vulval cancer

Can be asymptomatic
Can present with itching/burning/pain

Treatment
Conservative: Antihistamine
Medical: Imiquimod
Surgical: Excision

57
Q

risk factors for VIN

A 
Herpes Simplex Virus Type 2
Smoking
Immunosuppression
Chronic vulvar irritation
Conditions such as Lichen Sclerosus
58
Q

vulval cancer cell type

A

SCC caused by HPV

59
Q

Meig’s syndrome three features

A

a benign ovarian tumour
ascites
pleural effusion

60
Q

what is serous cystadenoma

A

benign

Most common benign ovarian tumour, often bilateral
Cyst lined by ciliated cells (similar to Fallopian tube)

61
Q

what is serous cystadenocarcinoma

A

malignant

Often bilateral
Psammoma bodies seen (collection of calcium)

62
Q

what is mucinous cystadenoma

A

benign

Cyst lined by mucous-secreting epithelium (similar to endocervix)

63
Q

what is mucinous cystadenocarcinoma

A

malignant

May be associated with pseudomyxoma peritonei (although mucinous tumour of appendix is the more common cause)

64
Q

what is brenner tumour

A

Contain Walthard cell rests (benign cluster of epithelial cells), similar to transitional cell epithelium. Typically have ‘coffee bean’ nuclei.

benign

65
Q

what is teratoma

Ix

A 
Mature teratoma (dermoid cyst) - most common: benign
Immature teratoma: malignant

Ix - AFP, LDH, hCG

Account for 90% of germ cell tumours
Contain a combination of ectodermal (e.g. hair), mesodermal (e.g. bone) and endodermal tissue

66
Q

what is dysgerminoma

A

malignant

Most common malignant germ cell tumour
Histological appearance similar to that of testicular seminoma
Associated with Turner’s syndrome
Typically secrete hCG and LDH

67
Q

what is yolk sac tumour

A

malignant
secrete AFP

Schiller-Duval bodies on histology are pathognomonic

68
Q

what is choriocarcinoma

A

malignant

estational trophoblastic disease
Typically have increased hCG levels
Often characterised by early haematogenous spread to the lungs

69
Q

what is granulosa cell tumour

A

malignant

Produces oestrogen leading to precocious puberty if in children or endometrial hyperplasia in adults.
Contains Call-Exner bodies (small eosinophilic fluid-filled spaces between granulosa cells)

70
Q

what is sertoli-leydig tumour

A

benign

Produces androgens → masculinizing effects
Associated with Peutz-Jegher syndrome

71
Q

what is fibroma

A

benign

Associated with Meigs’ syndrome (ascites, pleural effusion)
Solid tumour consisting of bundles of spindle-shaped fibroblasts
Typically occur around the menopause, classically causing a pulling sensation in the pelvis

72
Q

what is krukenberg tumour

A

malignant

Metastases from a gastrointestinal tumour resulting in a mucin-secreting signet-ring cell adenocarcinoma

73
Q

if a woman is pregnant but she is due for cervical smear what should u do

A

3 months post-partum

74
Q

for ovarian cancer if it spread lymphatically where will it go first and its haematological where will it go first

A

lymphatically - para-aortic lymph nodes

haematological - liver

75
Q

epidemiology of ovarian cancer

A

leading cause of death from gynaecological cancer

most common in the postmenopausal group

76
Q

what investigations are done to assess ascites

A
  • ascitic tap for cytology
77
Q

exudative causes of ascites

A

malignant infiltration peritoneum
pancreatitis
abdominal TB

78
Q

transudative causes of ascites

A

cardiac failure
hypoalbuminaemia
hepatic cirrhosis
renal failure

79
Q

cervical screening interpretation
HRPV +VE
HRPV -VE

A

-ve -> routine recall

+ve -> cytology

cytology abnormal -> colposcopy

cytology normal -> repeat test
if the repeat test is now hrHPV -ve → return to normal recall
if the repeat test is still hrHPV +ve and cytology still normal → further repeat test 12 months later:
If hrHPV -ve at 24 months → return to normal recall
if hrHPV +ve at 24 months → colposcopy

sample inadequate

  • repeat within 3 months
  • > if two consecutive inadequate samples then → colposcopy
80
Q

why may be a cervical sample be inadequate

A

Was taken but the cervix was not fully visualized.
Was taken in an inappropriate manner (for example, using an unapproved device).
Contains insufficient cells.
Contains an obscuring element (for example lubricant, inflammation, or blood).
Is incorrectly labelled.

81
Q

role of a colposcopy

chemicals used

A

look for abnormal changes
pre cancerous CIN
cancer

acetic acid - abnormal areas turn white (ACETOWHITE)

iodine solution - normal tissue outside of cervis stains brown

82
Q

epidemiology of endometrial cancer

A 
Commonest gynaecological cancer in UK
Incidence is rising
Rare before the age of 35
Peak age group 64 – 74 
Declines after 80
Commoner in western world
83
Q

epidemiology of cervical cancer

A

Worldwide - in some areas commonest cancer in women
UK 3rd commonest gynae cancer
80% of cervical cancer occurs in developing world
5% lifetime risk in some regions

Incidence declined by 40% with cervical screening
Bimodal age distribution (30s and 80s)
More common in low socio-economic groups
2/3 are squamous & ca 15% are adenocarcinoma

84
Q

symptoms of lichen slerosis

A 
 Itch
 Soreness
 Dyspareunia if introital narrowing
 Urinary symptoms
 Other symptoms, e.g. constipation, can occur if there is peri-anal
involvement
 Can be asymptomatic, but this is rare
85
Q

signs of lichen sclrosus

A

 Pale, white atrophic areas affecting the vulva
 Purpura (ecchymosis) is common
 Fissuring
 Erosions, but blistering is very rare
 Hyperkeratosis can occur
 Changes may be localised or in a ‘figure of eight’ distribution including
the perianal area
 Loss of architecture may be manifest as loss of the labia minora and/or
midline fusion. The clitoral hood may be sealed over the clitoris so that
it is buried

86
Q

complications of lichen sclerosus

A

 Development of squamous cell carcinoma
 Development of clitoral pseudo cyst
 Sexual dysfunction
 Dysaesthesia

87
Q

Mx of lichen sclerosus

A

ultra potent steroids

88
Q

DDx of PMB

A 
incomplete cessation of menses
cervical cancer
ovarian cancer
cervical poly
endometrial polyp
atrophic vaginitis
89
Q

Risks of hysterectomy w bilateral salpingo-oopherectomy

A

damage to urethra, ureters, bowel
thromboembolism
stress incontinence
risk of herniation through scat site

90
Q

other gynae conditions requiring hysterectomy

A 
severe endometriosis 
fibroids
other gynae cancers
menorrhagia
PID w chronic pain

repro (28 decks)

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