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gynae oncology Flashcards

1
Q

what is endometrial hyperplasia?

A

abnormal proliferation of the endometrial layer of the uterus

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2
Q

what are the risk factors for endometrial hyperplasia?

A

unopposed oestrogen causes the endometrium to proliferate

  • obesity
  • PCOS
  • HRT (some forms)
  • tamoxifen
  • oestrogen secreting ovarian tumour
  • nulliparity

hereditary non-polyposis CRC
diabetes

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3
Q

how does endometrial hyperplasia present?

A

irregular bleeding
intermenstrual bleeding
post menopausal bleeding
menorrhagia

vaginal discharge

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4
Q

what are the two types of endometrial hyperplasia?

A

hyperplasia without atypica - less likely to become malignant
atypical hyperplasia - premalignant condition

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5
Q

what investigations should we do for endometrial hyperplasia?

A

Transvaginal USS - can see thickening of endometrium

endometrial biopsy

hysteroscopy and curettage - more accurate than above

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6
Q

how is endometrial hyperplasia managed?

A

reassure
address risk factors

progesterone treatment - Levonorgestrel IUS for 5 years or oral progesterone for 6 months

follow up:

  • endometrial biopsies 6 monthly until 2 negative
  • for those at high risk e.g. BMI >35 , annual biopsies there after

hysterectomy if not responding to treatment after 1 yr of progesterone, atypical hyperplasia or relapse after treatment

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7
Q

what are the different types of endometrial cancer

A

adenocarcinoma - type 1 - most common
types 2: papillary serous tumours, clear cell, carcinosarcomas
(rarely sarcomas)

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8
Q

what is the aetiology behind endometrial cancer?

A

Stimulation of the endometrium by oestrogen (in absence of progesterone = unopposed oestrogen)
this result in proliferation of endometrium = endometrial hyperplasia (pre-malignant condition) which can be simple, complex or atypical and can develop into cancer
progesterone is released from corpus luteum after ovulation and protects the endometrium from oestrogen effects and thus anything causing anovulation can result in increased risk.

endometrial cancers metastasise to para-aortic and pelvic nodes and then lung, bone, brain and intraperitoneum

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9
Q

which type of cancers of the endometrial cancers are most likely to have metastasised at presentation?

A

type 2

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10
Q

what are the risk factors for endometrial cancer?

A

upposed oestrogen:

  • tamoxifen,
  • PCOS - anovulation and high Oestrogens
  • HRT oestrogen only
  • obesity - peripheral conversion of androgens to oestrogen
  • early menarche/ late menopause - anovulation is more likely at extremes of age
  • granulosa cell tumours (ovarian tumours) - secrete oestrogen

other:

  • age (more common 65-75yrs)
  • immunosuppression e.g. HIV
  • lynch syndrome
  • diabetes / insulin resistance
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11
Q

what are the differentials for endometrial cancer?

A

cervical polyps/ cancer
endometrial hyperplasia
endometrial polyps

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12
Q

what are the clinical features of endometrial cancer?

A

abnormal bleeding - PMB, PCB, IMB
clear white vaginal discharge - less common
signs of mets: abdo pain/ distension, SoB, weight loss

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13
Q

what can you find on examination of someone with endometrial cancer?

A

abdo/pelvic mass

evidence of vaginal/vulval atrophy or cervical lesions

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14
Q

what investigations can be done for someone presenting with endometrial cancer ?

A

transvaginal USS - first line
pipelle/ curettage biopsy
hysteroscopy and biopsy - high risk patient = gold standard
MRI abdo/ pelvis
surgical exploration - also take samples of omentum (due to mets going here)

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15
Q

what suspicious findings are found on transvaginal USS of someone with endometrial cancer?

A 
endometrial thickening (>4mm) 
mixed echoes
calcifications 
mass 
free fluid
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16
Q

when is a biopsy of endometrium indicated ?

methods for this biopsy and comparison

A

if >4mm and post menopausal
pipelle doesn’t sample as deep as curettage (remember neither of them can sample myometrium for sarcomas)

these can confirm histology

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17
Q

what is the FIGO staging for endometrial cancer?

A

1: confined to uterus
2. uterus and cervix
3. uterus +/- cervix and beyond e.g. vagina, ovaries, serosa, pelvic/aortic nodes but all within pelvis
4. bladder/ bowel or distant sites

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18
Q

how is endometrial cancer managed (by stage) ?

A

stage 1: total abdominal hysterectomy + bilateral salpingo-oophorectomy. laparoscopic or open. peritoneal washings taken too

stage 2: radical hysterectomy, remove and assess lymph nodes. may be offered adjuvant radiotherapy

stage 3: maximal debulking surgery + chemoradiotherapy

stage 4: maximal debulking surgery. majority are palliative with low dose radiotherapy or high dose oral progesterones

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19
Q

what is cervical ectropion?

A

the endocervix of cervix becomes everted and is exposed to the vagina

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20
Q

what is the histology of the cervix? use this to explain pathophysiology of cervical ectropion.

A

ectocervix - stratified squamous epithelium. part that faces vagina
endocervix - within cervix - columnar epithelium

in cervical ectropion, the stratified squamous cells of ectocervix undergo metaplastic change and become simple columnar cells. this change is induced by high oestogen

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21
Q

what are the risk factors for cervical ectropion?

A 
adolescence
COCP
pregnancy 
menstruating age 
overall anything increasing O
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22
Q

what are the clinical features of cervical ectropion?

A

mostly asymptomatic
vaginal discharge - the glandular epithelium will secrete
bleeding - post coital - the glandular epithelium has fine blood vessles that can be easily broken (also intermenstrual bleeding)

on speculum exam - cervix appears red

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23
Q

what are the differentials for cervical ectropion?

A

cervical cancer/ CIN
cervicitis
pregnancy

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24
Q

what investigations can be carried out who may have cervical ectropion?

A

pregnancy test
twiple swabs - any suggestion of infection then endocervical and high vaginal swabs
cervical smear - rule out CIN

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25
Q

how is cervical ectropion managed?

A

normal variant does not need treatment unless symptomatic
first line - COCP
if symptoms persist can remove columnar epithelium typically by curettage or electrocautery

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26
Q

what is the aetiology of cervical cancer?

A

majority are squamous cell carcinomas, the rest are adenocarcinomas
develop from CIN over a course of 10-20yrs
most common site of metastasis = lung, liver, bone, bowel
majority caused by HPV

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27
Q

what is HPV? how is it linked to cervical cancer?

A

HPV = virus , many subtypes
most women have been infected and clear infection within 2 years.
however some women fail to clear the infection or get repeated infections
this increases risk of CIN developing

more over some are high risk strains (16 and 18) and carry oncogenes - p53 suppression

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28
Q

what are the risk factors for cervical cancer?

A

HPV- early age of first intercourse, multiple sexual partners
smoking
immunodeficiency
long term use of COCP (possibly because condoms not used)

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29
Q

how is cervical cancer prevented?

A 
screening - cervical smear
vaccines 
   - Gardasil - 6,11,16,18 
   - cervarix - 16,18
   - ideally before intercourse
   - 3 IM injections over 6 months 
   - still need smears
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30
Q

what are the clinical features of cervical cancer?

A

abnormal bleeding - PMB, PCB, IMB
vaginal discharge
dyspareunia
pelvic pain
may be asymptomatic and picked up from screening
2 peaks of incidence (24-35 and then >55)

advanced disease - weight loss, loin pain that radiates down thighs (radiculopathy), oedema, hydronephrosis, rectal bleeding, haematuria

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31
Q

what is found on examination of someone with cervical cancer?

A

cervix - irregular, febrile, bleeding, mass
bimanual - pelvic mass
abdominal - hepatomegaly, hydronephrosis, rectal mass/ bleeding

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32
Q

what investigations would you do for someone presenting with cervical cancer?

A

premenopausal - test for chlamydia (if positive treat and if symptoms don’t clear then colposcopy, if negative then colposcopy)

post menopausal - urgent colposcopy and biopsy
colposcopy - magnifies and uses stains (acetic acid to stain areas white that are abnormal)

basic bloods
CT CAP/ MRI pelvic / PET

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33
Q

describe the staging for cervical cancer?

A

0 - carcinoma in situ
1 - confined to cervix (A= only microscopic, B= gross)
2 - beyond cervix but not pelvic side walls or involves vagina but not lower 1/3. (A = no parametrial involvement, B= parametrial involvement)
3 - extends beyond pelvic side walls or lower 1/3 vagina, hydronephrosis
4 - extends to bladder/ rectum (A), distant (B)

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34
Q

how is cervical cancer managed?

A

consider stage and MDT approach (don’t forget psychological aspect)

surgical

  • stage 1a: radical trachelectomy if fertility is to be preserved otherwise hysterectomy
  • stage 1b/2a: radical hysterectomy
  • stage 4a: anterior/ posterior/ total pelvic extenteration

radiotherapy - stage 1b to 3 (offered in conjugation with chemo = gold standard)

chemo= cisplatin based - neoadjuvant or adjuvant

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35
Q

what is a radical trachelectomy?

A

remove cervix and upper vagina

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36
Q

how often are women treated for cervical cancer followed up?

A

reviewed every 4 months for 1st 2 years
then 6-12 months for 3 years
all follow ups include examination of vagina and cervix

37
Q

what are the complications of treatment for cervical cancer?

A

surgery - infection, VTE, haemorrhage, bladder dysfunction, short vagina, vesicovaginal fistula and lymphocyst formation

radiotherapy - vaginal dryness, vaginal stenosis, radiation cystitis, radiation proctitis, loss of ovarian function

38
Q

what is the pathophysiology behind CIN?

A

atypical changes to the transformation zone of the cervix whereby the columnar epithelium is replaced by squamous metaplasia. this is natural and occurs from vaginal acidity in young women. however if this is exposed to carcinogens (HPV) there is risk of CIN developing
CIN is premalignant

39
Q

what are the histological characteristics of CIN ?

A

nuclear polymorphism
increased mitotic activity
basal hyperplasia

40
Q

what are the different grades of CIN?

A

CIN I: low grade dyskaryosis, mild dysplasia. can spontaneously resolve. can extend 1/3 of squamous epithelium

CIN II: high grade dyskaryosis, moderate dysplasia. can resolve spontaneously or progress. extends 2/3 of squamous epithelium

CIN III: high grade dyskaryosis, severe dysplasia. high risk of developing into cervical cancer, even after removed. extends into final 3rd of squamous epithelium. develops into carcinoma within 10 years if untreated

41
Q

what is the difference between dyskaryosis and CIN?

A

dyskaryosis - cytological appearance

CIN = histological

42
Q

what is the UK cervical screening programme?

A

every 3 years for women 25-49 and then every 5 years from 50-64

cells are collected with a smear instrument (using speculum) and put into medium with Papanicolaou’s stain = pap smear)

this stains the cells so they can be examined under microscopy = liquid based cytology

43
Q

what can the results of a pap smear show?

A 
inadequate - not enough cells, incorrect label etc
normal - no abnormal cells found
abnormal cells found 
    = borderline changes
    = low grade dyskaryosis 
    = high grade dyskaryosis (moderate or severe)
    = invasive squamous cell carcinoma
    = glandular neoplasia
44
Q

how do we manage women depending on their smear results?

A

negative - continue on screening programme in 3 years
low grade dyskaryosis -
- HPV test - negative - continue on screening in 3 yrs
- positive - colposcopy
high grade - colposcopy

45
Q

in colposcopy stains are used to see abnormal cells. what stains can be used?

A

acetic acid = turns abnormal cells white

iodine - normal cells go brown

46
Q

how is high grade CIN treated?

A

LLETZ biopsy - large loop excision of transformation zone under general anaesthetic

47
Q

what are cervical polyps?

A

benign growths protruding from inner surface of cervix

48
Q

what is the pathophysiology of cervical polyps?

A

may be due to chronic inflammation, abnormal response to oestrogen or congestion of cervical vasculature
develop from endocervix (columnar epithelium)
more common in older women and multigravidum

49
Q

what are the clinical features of cervical polyps?

A

may be asymptomatic
abnormal bleeding - PMB, PCB, IMB, menorrhagia
vaginal discharge

on speculum can see polyp growth

50
Q

what investigations should be done for someone with cervical polyps?

A

swabs - rule out infection
smear - rule out CIN
histological examination - for definitive diagnosis

51
Q

how should cervical polyps be managed?

A

remove due to small risk of malignant transformation
polyp grasped with polypectomy forceps and twisted
larger ones may need diathermy loop excision
send for histological exam to rule out malignancy

52
Q

what are the complications of cervical polyp removal?

A

infection, haemorrhage, rarely uterine perforation

53
Q

how can ovarian cysts be classified?

A

simple - fluid filled sacs
complex - irregular, contain solid material, blood, septations or vascularity

neoplastic - have malignant potential
non-neoplastic

54
Q

what are the types of non-neoplastic ovarian cysts?

A

functional - follicular or corpus luteal cysts

pathological - PCOS or endometriomas

55
Q

what are the types of benign neoplastic ovarian cysts?

A

epithelial - serous , mucinous or breners
germ cell - cystic teratomas (contain teeth, hair)
other - fibroma, thecoma , adenoma

56
Q

how do fibromas (ovarian cysts) appear?

A

solid, small

meigs syndrome

57
Q

what is meigs syndrome?

A

triad of:

  • benign ovarian tumour
  • ascites
  • pleural effusion
58
Q

what are the risk factors for ovarian cysts?

A

non neoplastic ones have their own risk factors

benign epithelial have same risk factors as ovarian cancer

59
Q

how do ovarian cysts present?

A

asymptomatic
dull ache in lower abdo/ back
mass felt
swollen abdomen
dyspareunia
pressure effects - bladder (frequency), bowel (constipation), veins (varicose)
hormones secreted may lead to virilisation

rupture/ torsion - acute severe pain and fever and shock

60
Q

what investigations should be done for ovarian cysts?

A

need to rule out malignancy

  • pregnancy test
  • urinalysis
  • bloods - FBC, UEs, LFTs,
    • aFP, LDH and bHCG for <40s due to germ cell tumour
    • CA125
  • USS - transvaginal/ abdominal
  • pelvic examination for mass

other:

- diagnostic laparoscopy
- FNA
- CT CAP
61
Q

what is the risk of malignancy index?

A

A way to calculate the risk of an ovarian cyst being malignant
Ux M x Ca125

U = USS findings. look for acites, multilocular cysts, solid areas, metastasis, bilateral lesions. (1 =1 point, 2 or more = 3 points

M = post menopause = 3 points, pre menopause =1 point

Ca125

62
Q

what RMI value is low, moderate and high risk? and how should each be managed?

A 
0-25 = low risk  - follow up 1 year with USS and Ca125 if <5cm 
25-250 = moderate  - bilateral oophorectomy and if malignancy then follow up with oncology 
>250 = high risk  - refer for staging laparotomy
63
Q

what is the normal Ca125 value?

A

<35

64
Q

what are the complications of ovarian cysts?

A

torsion
haemorrhage (more likely in malignant ones)
rupture
infertility

65
Q

what is pseudomyxoma peritonei

A

rupture of mucinous ovarian cyst - can disseminate mucinous cells which produce mucins which can build up in viscera and cause death
needs debulking

66
Q

how are ovarian cysts managed?

A

expectant management:

- small simple cysts (<50mm) - generally do not require follow up 
- if 50-70mm = yearly USS

surgery:
- persistent cysts, >5-10cm, symptomatic, complex
- in young children/ women do cystectomy rather than oophorectomy

67
Q

how is ovarian torsion managed?

A

laparoscopically uncoil
may need oophorectomy
if vascular compromise - may need salpingoophorectomy

68
Q

what are the different types of ovarian cancer?

A

serous cystadenocarcinoma - most common
mucinous cystadenocarcinoma
germ cell - teratomas , dermoids
stromal - Sertoli, theca, granulosa cell tumours

69
Q

what are the risk factors for ovarian cancer?

A

ovulation appears to cause surface irritation to ovaries and thus anything increasing ovulation:
- early menarche, late menopause, nulliparous, women > 65

also unopposed oestrogen, obesity, lynch syndrome, BRCA positive and smoking

70
Q

what are serous cystadenocarcinomas and mucinous cystadenocarcinomas characterised by?

A

serous - psammona bodies

mucus - mucin vacuoles

71
Q

what are protective factors for ovarian cancers?

A

parity, breast feeding , COCP

72
Q

what cancers does lynch syndrome increase risk of?

A

endometrial, ovarian and bowel

73
Q

what can be offered to BRCA positive women?

A

prophylactic massectomy and bilateral salpingo-oophorectomy

74
Q

what are the clinical features of ovarian cancer?

A

asymptomatic
vague - dyspepsia, IBS like, urinary frequency, incontinence, tired, constipation

chronic pain due to pressure on bladder/ bowel. also dyspareunia
acute pain - rupture, torsion, haemorrhage. necrosis can give pain and fever

bleeding per vagina

later: weight loss, abdo distention, pleural effusion, DVT

75
Q

what investigations should be done for someone presenting with ovarian cancer?

A

same as for ovarian cysts

+ CT CAP, CXR, surgical exploration and histopathology

76
Q

describe the staging of ovarian cancers

A

1: limited to ovaries
2: spread to pelvic organs
3: spread to rest of peritoneal cavity , omentum and lymph nodes
4: distant mets, liver and lung

77
Q

what are the causes of a raised CA125?

A

endometriosis, uterine fibroids, pregnancy, menstruation, PID

inflammatory bowel - diverticulosis, liver cirrhosis

ovarian cancer

78
Q

what is krunkenburg tumour?

A

refers to ovarian cancers that have metastasized to gut / stomach

79
Q

how do we manage ovarian cancers?

A

surgery - staging laparotomy for those with high RMI to aim to debulk
adjuvant chemo - can use CA125 to assess progress
sometimes may need adjuvatnt chemo to shrink tumour before resection

chemo = carboplatin

chemo for palliative

follow up for 5 years by measuring Ca125

80
Q

is there a screening programme for ovarian cancer?

A

no , no pre-malignant stage

CA125 is too non-specific

81
Q

what are the risk factors for vulval cancer?

A 
HPV 
mostly in women >65
HSV
lichen sclerosus and lichen planus 
smoking
82
Q

what is the main type of vulval cancer?

A

squamous cell carcinoma

83
Q

what is VIN? how does it present

A

abnormal cells in vulva and at risk of becoming cancerous (pre-malignant)
there are 2 types - undifferentiated and differentiated

can resolve spontaneously

presents like vulval cancer - itching, pain etc

84
Q

what are the symptoms of vulval cancer?

A

itching, pain, tenderness, soreness
raised thickened patches of skin that can be white, red or dark
a lump/ wart like growth
bleeding/ open sore (pain when urinating)

85
Q

how is vulval cancer diagnosed?

A

examination and biopsy under local anaesthetic

other tests:

  • cervical smear test (due to common risk factor and more likely to get CIN from HPV than VIN)
  • cystoscopy - abnormal cells in bladder
  • lymph node biopsy

may require CT CAP or CXR for mets

86
Q

what staging is used for vulval cancer?

A

I - confined to vulva
2 - spread to near by structures - vagina, urethra, anus
3 - spread to nearby lymph nodes
4 - spread to other body parts

87
Q

what is the treatment for vulval cancers?

A

surgery to remove cancerous tissue from vulva and any lymph nodes that may be malignant
some also have radio/chemotherapy

radical wide local excision = cancer removed and margin of healthy tissue

radical partial vulvectomy = larger section of vulvula removed (one or both labia) and clitoris

radical vulvectomy = whole vulvula (inner and outer) + clitoris

psychological support

88
Q

how can lymph nodes be assessed in vulval cancer?

A

sentinel node biopsy

groin lymphadenectomy - all removed - risk of lymphoedema or infection

89
Q

how is VIN treated?

A

recommended that abnormal area is removed either chemically (imiquimod) or surgical excision

otherwise conservative treatment with antihistamines

gynaecology (7 decks)

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