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Obstetrics + gynaecology > Gynaecological malignancy > Flashcards

Gynaecological malignancy Flashcards

1
Q

Pathophysiology of vulval cancer

A
  • Majority are SCC but can be adenocarcinoma
  • Warty type - a/w HPV
  • Keratinising type - a/w lichen sclerosus in elderly women

Usually spreads to the inguinal + femoral LNs, followed by the pelvic LN + haematogenous

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2
Q

How may vulval cancer present?

A
  • Pruritic raised lesion that may ulcerate + bleed
  • Occasionally affects mucus membrane causing a hyper pigmented ulcerated lesion
  • Most on labia majora
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3
Q

Management of vulval cancer

A
  • Stage IA: WLE + u/l groin node dissection

* >Stage 1: radical vulvectomy + b/l groin lymphadenectomy +/- radiotherapy, usually palliative

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4
Q

What are the types of vulval intraepithelial neoplasia and how do you manage it?

A

Loss of the epithelial architecture

  • Squamous VIN:
  • Usual VIN: affects 30-50yos, a/w smoking + HPV. Asymptomatic/itch/pain/dysuria/ulcer, white/pink/pigmented plaques/papules. 3-4% become invasive
  • Differentiated VIN: postmenopausal, a/w squamous hyperplasia/lichen sclerosus/lichen simplex chronicus, precursor to HPV-negative keratinising SCC

*Non-squamous VIN: Paget’s disease - papule lesions of various colours, rare

M: biopsy, search for neoplasia of the vagina or cervix, treat with imiquimod cream, laser or superficial excision

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5
Q

Vaginal intraepithelial neoplasia

A

Usually a/w cervical lesions, asymptomatic + superficial changes until develops into carcinoma

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6
Q

Vaginal adenosis

A

Columnar epithelium replaces squamous - usually this reverts but can become adenocarcinoma

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7
Q

Vaginal carcinoma

A
  • Usually SCC but can be adenocarcinoma, in UK usually mets from the cervix or endometrium
  • CF: irregular bleeding, offensive discharge, fistulae, exophytic lesion or indurated mass
  • Direct + LN spread
  • M: palliative radiotherapy unless stage I (surgery)
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8
Q

What is the aim of cervical screening and who is currently invited for it?

A

Aims to detect non-invasive precursor of cervical cancer (ie CIN) in asymptomatic population, to reduce morbidity mortality. There is a natural history of changes that may be over 10y from early changes to cancer

NHS programme for all women registered with a GP are invited every 3y (age 25-49) and 5y (age 50-64), and >65y if one of their last 3 tests were abnormal

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9
Q

What are the possible outcomes from cervical screening?

A

Cells taken from transformation zone and now all are tested for HPV- if HPV+ do cytology. Possible results:

  • Inadequate sample: not enough cells, cells not seen clearly or infection present. 3 inadeqaute-do colposcopy
  • Borderline nuclear change or mild dyskaryosis: if HPV positive colposcopy (as now all are tested for HPV), if negative back to routine recall
  • Moderate dyskaryosis CIN II - urgent colposcopy
  • Severe dyskaryosis CIN III - carcinoma in situ - urgent colposcopy
  • Suspected invasive cancer - urgent colposcopy
  • Glandular neoplasia - possible adenocarcinoma
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10
Q

Cervical intraepithelial neoplasia management

A
  • Low grade: cytological + colposcopy surveillance every 6m for a defined period
  • Higher grade: excise by scalpel/laser/LLETZ, destroy transformation zone by ablation/cryocautery/coagulation diathermy, cone biopsy if cannot see TZ
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11
Q

Pathophysiology of cervical cancer

A
  • 80% SCC and 20% AC, most occur in the transformation zone where columnar becomes squamous epithelium
  • RF: CIN, HPV infection (types 16+18 and 33), HIV, smoking, lower socio-economic status, immunosuppression, early age of 1st intercourse
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12
Q

How is cervical cancer staged?

A

I: IA microscopic, I cervix only
II: beyond cervix but not to the lower 1/3 vagina or pelvic wall
III: to pelvic wall/lower 1/3 of vagina or causes renal issues like hydronephrosis
IV: beyond pelvis to mucosa of bladder/rectum, IVB-distant spread

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13
Q

How may cervical cancer present if not on screening?

A
  • PCB, dyspareunia, IMB, irregular bleeding, PMB, foul discharge (thin + watery, may have blood)
  • Later: ureteric obstruction, renal failure, excruciating pain (bone + nerve), oedema of lower limbs, urinary/bowel sx
  • Colposcopy: white cells, small blood vessels below epithelium, don’t stain brown with Lugoli’s iodine, early cancer is raised/ulcerated/friable, more advanced often fixed/friable/warty
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14
Q

How is cervical cancer managed and what is the prognosis like?

A
  • Early stage (IA/I): LLETZ, local excision or hysterectomy if completed family
  • Later: surgery (usually radical hysterectomy + LN dissection, may keep ovaries), radiotherapy, platinum-based chemo

Stage I 5y survival 85% but stage IV 10%

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15
Q

What factors increase the risk of endometrial adenocarcinoma?

A
  • Hereditary syndromes e.g. HNPCC
  • High oestrogen levels: obesity, exogenous (e.g. HRT without progesterone), endogenous (e.g. granulosa cell tumours), Tamoxifen (acts as unopposed oestrogen - hyperplasia), nulliparity, late menopause, PCOS, DM
  • Endometrial hyperplasia itself
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16
Q

How may endometrial adenocarcinoma present?

A
  • PMB - endometrial cancer until proven otherwise
  • Irregular bleeding or HMB
  • Pyometria - uterus infection with purulent discharge
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17
Q

Endometrial cancer path

A
  • Type I - endometroid adenocarcinoma - the majority, a/w hyperoestrogenic states
  • Type II - other types eg clear cell, more aggressive

*Spread: myometrium, cervix, pelvic + para-aortic LN

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18
Q

How would you investigate suspected endometrial adenocarcinoma?

A
  • TV USS: <5mm endometrium v low risk, unreliable pre-menopause as thickness varies over the menstrual cycle
  • Endometrial aspirate (pipelle)
  • Hysteroscopy: pass through internal Os into uterus, visualise + take biopsies, can have with GA if cannot tolerate. Complications are small but include uterus perforation and pelvic infection
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19
Q

How is endometrial adenocarcinoma staged and managed?

A

Stage I-myometrium (good prognosis), stage II to cervix but not outside uterus, III local/regional spread, IV bladder/bowel/distant mets

  • TAH + BSO
  • Monitor CA-125
  • Adjuvant radiotherapy to reduce pelvic recurrence
  • Chemo
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20
Q

What are the non-epithelial uterine cancers? (3% of uterine cancers)

A
  • Stromal sarcomas - a/w adenomyosis and endometriosis, p/w discharge + bleeding
  • Mixed Mullerian tumours (carcinosarcomas) - from epithelium + stroma, have early spread
  • Leiomyosarcomas - may arise in a pre-existing fibroid, rapidly-growing ‘fibroid’ but often asymptomatic
21
Q

What are the features of ovarian lesions?

A
  • OFTEN ASYMPTOMATIC
  • Symptoms: abdo enlargement, ascites, pressure on bladder/rectum, torsion (pain, vomiting), ruptured cyst (pain, haemorrhage), disturbed menstrual cycle from hormones, bloating, reduced appetite
  • Signs: abdo distension, central dullness with resonant flanks, gross ascites, may be palpable on VE, usually non-tender, benign tumours are usually freely-mobile
22
Q

What are functional ovarian cysts?

A

They occur during menstrual life

  • Follicular cysts: commonest, walls of granulosa cells and contain clear fluid + sex steroids, they can cause endometrial hyperplasia and HMB, usually only last around 2 months
  • Lutein cysts: granulosa type (cysts of corpus luteum, can cause amenorrhoea or pain) and theca type (high hCG so seen in hydatidiform mole, rupture - haemorrhage)
  • Physiological cysts in early pregnancy are common and resolve from T2, reassure, are the corpus luteum
23
Q

Serous cystadenomas

A

Common type of benign cyst, often b/l, may become malignant (psammoma bodies seen-calcium collection). May be so large that they fill the peritoneal cavity and often replace the normal ovary

24
Q

Mucinous cystadenomas

A

Common type of benign cyst, often become very big, fluid contains mucin, secretory, less likely to become malignant than serous type

Mucinous ystadenocarcinoma: if ruptures may implant in the PC causing pseudomyxoma peritonii (tho mucin tumour of appendix more common cause)

25
Q

Granulosa cell tumours

A
  • Sex cord stromal tumour that secretes oestrogen
  • 1/4 malignant
  • Pre-puberty they cause precocious puberty
  • During repro life they cause hyperplasia + irregular prolonged bleeding
  • Post meno they cause PMB
  • Call-Exner bodies (eosinophilic fluid spaces between the cells)
26
Q

Theca cell tumours

A

Secrete oestrogen, often actually theca + granulosa cells. A sex cord stromal tumour

27
Q

Androblastomas / Sertoli-Leydig cell tumour

A

A sex cord stromal tumour of Sertoli-Leydig cells, rare, most in 20-30y, 1/4 malignant, secrete androgens so cause amenorrhoea, reduced breast tissue, hirsutism, enlarged clitoris
A/w Peutz-Jegher syndrome

28
Q

Germ cell ovarian tumours

A
  • Mature cystic teratoma (dermoid cyst): commonest solid ovarian tumour, benign, often no sx unless rupture causing a chemical peritonitis, rarely they have all embryonic elements (ectoderm eg hair, mesoderm eg bone, endodermal) or have a predominant tissue e.g. struma ovarii (causes hyperthyroidism)
  • Immature teratoma: malignant
  • V rare malignant types e.g. choriocarcinoma (of GTD, high hCG, spread to lungs), yolk sac tumour (secrete AFP, Schiller-Duval bodies on histology)
29
Q

Ovarian fibromas

A

Solid and rare, a/w ascites + pleural effusion (Meigs’ syndrome)

Typically occur around menopause, pulling sensation in pelvis

30
Q

What are the risk factors for ovarian cancer?

A

Genetics (a/w BRCA 1/2), nulliparity, unsuccessful infertility treatment, early menarche, late menopause

31
Q

What is the commonest type of ovarian cancer?

A

Epithelial types make up 85%, of which serous cystadenocarcinoma is most common

32
Q

Outline the different possible types of ovarian cancers

A
  • Epithelial (85%): serous cystadenocarcinoma, mucinous cystadenocarcinoma (a/w appendix tumours), endometriosis cystuadenocarcinoma (a/w endometrial AC), clear cell cystadenocarcinoma (a/w endometriosis), Brenner/transitional cell cystadenocarcinoma
  • Sex cord stromal (6%): granulosa cell, Sertoli-Leydig cell
  • Germ cell tumours: dysgerminomas, teratomas (may make hCG/AFP/thyroxine)
  • Metastases from breast, GIT (Krukenberg’s), genital tract, blood
33
Q

How is ovarian cancer staged?

A

I-ovaries only
II-pelvic extension
III-peritoneal outside pelvis or retroperitoneal or inguinal LNs
IV-distant mets

34
Q

What Ix would you do in suspected ovarian cancer?

A

USS, CXR (effusions), CT/MRI CAP (spread), CA-125 (tho is normal in 15%)

In GP - CA125 initially, if raised >35 then urgent US Abdo+pelvis

35
Q

How is ovarian cancer managed?

A
  • TAH + BSO + omentectomy + sample pelvic + para-aortic LN
  • Adjuvant chemotherapy
  • Germ cell tumours are often chemo-sensitive
36
Q

What is endometrial hyperplasia?

A

An abnormal proliferation of the endometrium in excess of what occurs during the menstrual cycle, a minority develop endometrial cancer.

RF: unopposed oestrogen, obesity, late meno/early menarche, >35y, smoker, nulliparity, Tamoxifen (pro-oestrogen effect on uterus [anti oestrogen on breast])

Types: simple, complex, simple atypical and complex atypical

Features: abnormal vaginal bleeding e.g. intermenstrual/heavy, periods of amenorrhoea

Management

  • simple endometrial hyperplasia without atypia: high dose progestogens with repeat sampling in 3-4 months. The levonorgestrel intra-uterine system may be used
  • atypia: hysterectomy (+ BSO if post-memo) is usually advised cos of malignant potential
37
Q

What are the 4 main types of ovarian tumours?

A
  • Surface derived tumours - the cyst type ones
  • Germ cell tumours e.g. teratoma and choriocarcinoma
  • Sex cord stromal tumours: often produce hormones
  • Metastatic (5%) e.g. Krukenberg
38
Q

What is a Krukenberg tumour?

A

A malignant ovarian tumour metastases from a GI tumour

Is a mucin-secreting signet-ring cell adenocarcinoma

39
Q

Brenner tumour

A

Benign ovarian surface tumour, usually >50y

Contain Walthard cell rests (benign cluster of epithelial cells) and typical ‘coffee bean’ nuclei

40
Q

What is a dysgerminoma?

A

*Most common malignant germ cell tumour of ovary
*Histology similar to testicular seminoma
*A/w Turner’s syndrome
Secrete hCG + LDH

41
Q

Why is there no screening programme for ovarian cancer?

A
  • CA-125 lacks sensitivity for early stage disease (only raised in 50% of stage I, and early stage is what screening aims to pick up!)
  • CA-125 lacks specificity
42
Q

How is ovarian cancer monitored?

A

CA-125 trend is an important prognostic factor

43
Q

What markers are used in ovarian cancer?

A

CA-125 (HE-4 is more reliable but not in much use yet) - for epithelial origin (majority)
AFP and BHCG for germ cell origin tumours

44
Q

What may cause an elevated CA-125?

A
  • Ovarian cancer
  • Endometrial or cervical cancer
  • Cirrhosis with ascites, cirrhosis chronic active hepatitis
  • Endometriosis
  • Benign ovarian tumours
  • Acute salpingitis
  • Uterine myoma
  • Acute pancreatitis
  • Renal failure
45
Q

A woman who is 6m pregnant is called for her cervical screening. When would you do it?

A

Usually delayed until 3m postpartum unless they’ve had previous abnormal smears

46
Q

A woman had a colposcopy after her screening revealed CIN II. When should her next test be?

A

6m after treatment for any woman treated for CIN I, II or III

47
Q

How is the prognosis of ovarian cancer scored?

A

Risk malignancy index prognosis based on US findings, CA125 levels and menopausal status

48
Q

How often should women with HIV undergo cervical screening?

A

Every year

They are at higher risk of CIN + cancer because of reduce immune response + reduced clearance of HPV

Obstetrics + gynaecology (13 decks)

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