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Woman's Health > 3.2 Genital tract cancers > Flashcards

3.2 Genital tract cancers Flashcards

1
Q

What are the top 10 cancers in women?

A

1) breast
2) colorectum
3) lung
4) endometrial
5) ovarian
6) skin
7) lymphoid
8) stomach
9) thyroid
10) cervical

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2
Q

what genetic condition predispose to type 1 endometrial cancer?

A

HNPCC/Lynch syndrome

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3
Q

is oestregen related to type 1 endometrial cancer?

A

Oestrogen-related (background of endometrial hyperplasia from unopposed oestrogen-mediated proliferative phase of the endometrial cycle)

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4
Q

what is seen in the histology for type 1 endometrial cancer?

A

Endometrioid adenocarcinoma

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5
Q

when is type 1 endometrial cancer diagnosed?

A

Average age: 63 years (lower grade; occurs in younger age group)

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6
Q

what stage is when type 1 endometrial cancer diagnosed?

A

Early stage (70%)

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7
Q

what is the survival for type 1 endometrial cancer?

A

5-year: 83%

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8
Q

what genetic condition predispose to type 2 endometrial cancer?

A

p53 mutations (abnormal accumulation of p53 protein)

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9
Q

is oestregen related to type 21 endometrial cancer?

A

Non-oestrogen-related (background of atrophic oestrogen-deficient endometrium) → serous carcinomas develop from endometrial intraepithelial carcinomas (EIC)

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10
Q

what is seen in the histology for type 2 endometrial cancer?

A

Non-endometrioid, serous/clear cells

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11
Q

when is type 2 endometrial cancer diagnosed?

A

Average age: 67 years (older age group)

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12
Q

what stage is when type 2 endometrial cancer diagnosed?

A

Advanced stage (50%)

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13
Q

what is the survival for type 2 endometrial cancer?

A

5-year: 53% (serous), 62% (clear

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14
Q

What are the risk factors for type 1 oestrogen relataed endometrial cancer?

A
  • Anovulation and polycystic ovarian syndrome (PCOS)
  • Nulliparity (never given birth to children before)
  • Early menarche (first occurrence of menstruation)
  • Hormone replacement therapy (HRT) without progestin
  • Tamoxifen (for breast cancer) predisposes to cystic hyperplasia of endometrium
  • Obesity/diabetes mellitus: increased risk of hyperoestrogenaemia (due to insulin resistance and reduced SHBG levels)
  • Breast and ovarian cancer
  • Genetic factors: hereditary non-polyposis colon cancer (HNPCC/Lynch syndrome) → high risk of colon and endometrial cancers
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15
Q

How is endometrial hyperplasia which occurs in Type I EC classified under WHO 1994 classification?

A

Based on complexity of glandular architecture and presence of atypia (higher risk of progression to malignancy)

  • simple hyperplasia: mildly crowded glands, widely spaced with stroma in between
  • complex hyperplasia: >50% gland to stromal ration, the gland to stroma ratio is higher in complex compared to simple hyperplasia
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16
Q

How is endometrial hyperplasia which occurs in Type I EC classified under WHO 2014 classification?

A

Based on presence/absence of cytological crypts

  • Hyperplasia without atypia: risk of progression to EC < 5% over 20 years
  • Atypical hyperplasia: high risk of progression to malignancy
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17
Q

What are the features of EC during the early tumour growth?

Characterised by the following features:
• ____________ (growing outwards beyond the surface of the epithelium) and spreading pattern
• __________ (breaks down easily → vaginal bleeding)
• ___________ invasion and growth towards _____________

A

Exophytic;

Pliability;

Myometrial;

cervix

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18
Q

where does endometrial cancer locally extend normally?

A

Invasion of adjacent structures (most common progression): myometrium, serosa, cervix, vagina, parametrium, ovary, tubes

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19
Q

What is the clinical presentation of endometrial cancer?

A

• Abnormal uterine bleeding (most common sign; ~80%): pre/peri-menopausal heavy prolonged bleeding, post-menopausal bleeding, vaginal discharge
o Post-menopausal bleeding must be investigated with priority due to the possibility of EC

• Pelvic pressure (causing urinary/bowel symptoms)
• Manifestations of metastatic disease
• Incidental finding on US pelvis (in PCOS) → increased endometrial thickness
• Abnormal Pap smear (atypical glandular cells/AGUS on endometrial origin → 1.5% risk of EH and 3% risk of EC)
o 50% of patients in stage II – IV EC have abnormal Pap smear findings

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20
Q

what is the ddx of endometrial cancer when presented with post menopausal bleeding?

A

endometrial/vaginal atrophy, endometrial hyperplasia, polyps, cervical and vaginal pathologies

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21
Q

what are hpv strains which are cancer causing?

A
  • HPV 16, 18, 31, 33, 45, 52, 58

- Types 16 & 18 are responsible for >75% of cervical cancers and >50% of vaginal and vulvar cancers

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22
Q

what are the risk factors for cervical cancer?

A

The risk of developing cervical cancer is increased by obesity, sexual history, multiparity, lower socioeconomic status and some co-factor interactions

Sexual history

  • Early age of sexual activity: RR 2.5 if age < 18 years
  • Multiple sexual partners: RR 2.8 if ≥ 5 partners
  • Partner with multiple sexual partners or known HPV infection or intercourse with high-risk men

Co factors

  • Cigarette smoking: both active and passive (2 – 3-fold increased incidence of HSIL and invasive cancer)
  • Infection by other microbes: Chlamydia, gonorrhoea, HSV, Trichomonas
  • Sex hormonal influences: long-term OCP use (2-fold for >5-year use)
  • Immunosuppression (exogenous/endogenous)
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23
Q

where does cervical cancer expand locally to normally?

A

Extension to endocervix or vaginal fornixes → progressive infiltration of parametrium, uterine corpus, bladder, rectum

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24
Q

where does endometrial cancer drain to by lymphatics?

A

To pelvic and para-aortic nodes, vagina, inguinal nodes (rare)

25
Q

where does endometrial cancer spread to haematogenously?

A

Rarely occurs; to the lungs (mostly), liver, bone, brain (rare)

26
Q

where does cervical cancer drain to by lymphatics?

A

Pelvic LNs → common iliac and para-aortic LN chains

27
Q

where does cervical cancer spread to haematogenously?

A

Distant implants in lungs, bones, liver parenchyma, others

28
Q

How does advanced stage of cervical cancer normally present with?

A

Cervical cancer is often asymptomatic until the advanced stages of disease: • Abnormal vaginal bleeding (PCB, IMB, PMB, irregular bleeding patterns)
• Malodorous foul-smelling vaginal discharge (in absence of STIs)
• Pressure symptoms (of the bowel and bladder)
• Vaginal passage of urine and faeces
• Advanced stages (with parametrial invasion): pelvic pain/lower backache, haematuria/rectal bleeding (if bladder/rectal invasion), leg swelling & ankle oedema (due to lymphatic involvement in pelvis)

29
Q

what is the most common type of ovarian cancer?

A

Epithelial ovarian cancers (EOC)

• Serous (46%), mucinous (36%), endometrioid (8%), clear cell (3%), transitional (2%), undifferentiated (2%), mixed (3%)

30
Q

when is the peak incidence of ovarian cancer?

A

Peak incidence of 56 – 60 years (only <2% before the age of 20)

31
Q

what are the risk factors for ovarian cancer?

A
  • 1st degree relative suffering from breast/ovarian cancer
  • Obesity: Positive association between BMI and risk of ovarian cancer
  • Low parity/infertility: Prolonged exposure to ovulation
  • Fertility drugs: Controversial risk factor. Slight increase → reverts to normal after stopping for a few years
  • Genetic factors: 10 – 14% of patients have BRCA1 or BRCA2 (breast cancer susceptibility gene) mutations → often develop cancer before 50:
    • Autosomal dominant TSG which help to ensure DNA stability and prevent uncontrolled cell growth
32
Q

which chromosome is the BRCA1 gene on?

A

chromosome 17 → 28 – 44% lifetime risk of ovarian cancer (mostly develop after 40)

33
Q

which chromosome is the BRCA2 gene on?

A

chromosome 13 → 27% lifetime risk of ovarian cancer (more likely in the postmenopausal age group; with hereditary tumours occurring about 10 years earlier)

34
Q

what kind of cancers does lymch II syndrome predispose to?

A

LYNCH II syndrome (HNPCC): ovarian, endometrial, colon

35
Q

What are the protective factors against ovarian cancers?

A

The protective factors against ovarian cancer include interruption ovulation (pregnancy, breastfeeding, oral contraceptive use), tubal ligation, salpingectomy (at time of hysterectomy for benign diseases), multiple pregnancies, pregnancy before 35, and OCP (50% reduction with > 5 years of use).

36
Q

how does incessant ovultion leads to ovarain cancer?

A

Ovulation (follicular rupture) → physical trauma → breach in the ovarian surface epithelium (OSE):
• Repeated damage and repair → dedifferentiation → poorly differentiated tumour

37
Q

Pathogenesis of ovarian cancer

OSE- CIC model: Ovarian surface develops numerous invaginations into the _________________ with age → frequently pinch off and become entrapped in the stroma → forms _________________(CICs – circular OSE-lined structures):
• Epithelial cells lining CIC are exposed to new hormone-rich milieu (gonadotrophins, oestrogens, androgens) inside the ovary → induces ________________→ more complex epithelium (resembling Mullerian-derived organs) → tumours
• Alternatively: __________________ → remnants of the Mullerian-derived epithelia adhere to the ovarian surface → incorporated into CICs

STIC: ______________ serves as a site of origin (fimbrial end of Fallopian tube gives rise to precursor lesions) → STIC (serous tubal intraepithelial carcinomas) → ovarian cancer

A

cortical stroma;

cortical inclusion cysts ;

proliferation and differentiation/metaplasia;

endometriosis/endosalpingiosis;

Fallopian tube epithelium

38
Q

where does ovarian cancer expand locally to normally?

A

Capsular invasion and peritoneal seeding (most common pattern → frequent involvement of omenta and diaphragm)

39
Q

where does ovarian cancer drain to by lymphatics?

A

Para-aortic nodal tissue (through ovarian arteries arising from the aorta) and pelvic nodes (most common for cancers of the uterus and cervix)

40
Q

where does ovarian cancer spread to haematogenously?

A

To the liver parenchyma, lungs, and bones

41
Q

what is the clinical presentation of ovarian cancer?

A
  • GI symptoms: abdominal bloating/distension, dyspepsia (indigestion, acid reflex), nausea, early satiety, altered bowel habits, abdominal discomfort/pain
  • Urinary frequency and urgency
  • Vaginal bleeding
  • Shortness of breath, tiredness, weight loss
  • Incidental ultrasound finding of complex adnexal tissues
  • Often misdiagnosed as stress, depression, IBD, or gastritis → correct diagnosis requires a high index of suspicion
42
Q

What are the risk factors for fallopian cancers?

A

Age (usually diagnosed at 60 – 66 years), family history, gene mutations (BRCA gene mutations esp. BRCA1, genes causing HNPCC)

43
Q

Primary Fallopian tube cancers account for 1 in 100 gynaecological cancers (metastatic cancers are more common than primary cancers):
• Rare cancer which only accounts for 0.3% of malignancies
• >95% are _________________ (very few sarcomas)
• Exact cause and risk factors are poorly understood (very rare)

A

papillary serous adenocarcinomas

44
Q

what is the clinical presentation of fallopian tube cancer?

A

Adnexal mass, vague abdominal/pelvic discomfort/bloating/pain, vaginal bleeding, postmenopausal bleeding (PMB):
• Less than 1/3 of patients present with the triad of hydrops tubae profluens (pelvic pain, copious watery discharge, adnexal mass)

45
Q

Primary cancers of the vagina are rare (3% of gynaecological cancers) → classified as cervical cancer if there is a simultaneous cervical cancer/lesion:
• Secondary vaginal malignancies/metastases are direct extensions from the __________________ or from lymphatic/haematogenous spread from the ____________________

A

endometrium, cervix, vulva;

ovary, breast, rectum, and kidneys

46
Q

85% of vaginal cancers are _____________________ (followed by adenocarcinomas, sarcomas, melanomas) → may be ulcerative or exophytic:
• Usually involves the _________________ of the vagina (may be multimeric)
• Different stages of histological differentiation in vaginal cancer + possible microinvasive carcinoma + invasive cancer → continuum of transformation
• Vaginal intraepithelial neoplasia (VAIN): intraepithelial cancerous abnormality for the vagina → high grade VAIN is associated with CIN and VIN in 50 – 90% of cases

A

squamous cell carcinomas;

posterior wall of upper third

47
Q

What are the risk factors for vaginal cancer?

A
  • 75% of vaginal cancers are associated with high risk HPV (16, 18):
    • Pathogenesis of squamous cell vaginal cancers → field effect (entire genital tract is at risk of squamous cell CA once malignancy occurs anywhere along the tract)
  • Other anogenital cancers increase risk of vaginal/vulvar cancers
- Family history 
Autoimmune disorders (e.g. SLE), immunosuppression (increases risk of HPV persistence and HPV-related cancers)
  • Prior pelvic radiation therapy, women who have previously undergone hysterectomy for CIN 3/cervical cancer
  • Diethylstilboestrol (DES): medication used to prevent miscarriage
    • Linked to risk of clear cell adenocarcinomas of vagina in daughters of women who were treated with the drug
  • Smoking
48
Q

where does vaginal cancer expand locally to normally?

A

Anteriorly to bladder, urethra; posteriorly to rectum, laterally to paracolpium, parametrium, and lateral pelvic wall

49
Q

where does vaginal cancer drain to by lymphatics?

A

Middle to upper vagina: superiorly with lymphatics of cervix → obturator LNs → internal/external iliac chains → para-aortic LNs

Distal third of vagina: inguinal LNs → pelvic LNs

Posterior wall: rectal lymphatics → inferior gluteal, sacral, rectal LNs

50
Q

where does vaginal cancer spread to haematogenously?

A

Late spread to the lungs, liver, bone, skin

51
Q

what is the clinical presentation of vaginal cancer?

A

Vaginal cancer is often asymptomatic in the early stages, and picked up incidentally (abnormal vaginal cytology, vaginal mass on pelvic exam, vaginal ulcer/exophytic tumour):
• Painless bleeding and discharge (due to ulcerative lesions), PCB/PMB, irregular unscheduled bleeding
• Watery blood-tinged malodorous vaginal discharge
• Advanced cases: weight loss, lower limb oedema, pain due to extension to pelvic wall and neurovascular structures
• Tumour impinging upon rectum/bladder: dysuria, haematuria, constipation, melena

52
Q

Vulval cancer accounts for 5% of genital tract cancers with _________________ being the most common histological type (>80%):
• _______________ are the second most common type of vulval cancer (2 – 10%)
• Other types: verrucous carcinoma (variant of SCC), basal cell carcinoma (2 – 8%), extramammary Paget disease, Bartholin gland carcinoma, sarcoma

A

squamous cell carcinoma;

Melanomas

53
Q

___________________ is the premalignant lesion of vulval cancer:
• Vulval squamous cell carcinoma can occur in areas of epithelial neoplasia → develops into a small nodule which may break down and ulcerate → small/warty/cauliflower-like growths may arise (may be confused with _______________)

A

Vulva intraepithelial neoplasia (VIN);

condyloma acuminata

54
Q

What is the presentation of a patient with HPV independent vulva intraepithelial neoplasia?

A

Commonly occurs in older women → associated with differentiated VIN on the background of atrophic changes in lichen sclerosus or in hypertrophic epithelium

55
Q

What is the presentation of a patient with HPV dependent vulva intraepithelial neoplasia?

A

Commonly occurs in younger women (<50 years) who are smokers → associated with uVIN (predisposes to vulval cancer) → warty type and basaloid type of SCC

56
Q

where does vulva cancer expand locally to normally?

A

To the vagina, urethra, bladder, and rectum (malignant lesions can appear anywhere on the vulva → ¾ arise primarily on the labi

57
Q

where does vulva cancer drain to by lymphatics?

A

Occurs early (vulva being rich in lymphatics):
• Directly related to death of stromal invasion, size of primary lesion
• Spreads in an organised fashion: superficial inguinal LNs → deeper nodal chains (inguino-femoral, pelvic)
• Lateral tumours: only ipsilateral groin nodes involved
• Midline tumours (clitoris, urethra, vagina, perineal body, anus): lymph nodes become involved bilaterally

58
Q

where does vulva cancer spread to haematogenously?

A

Usually late manifestation → to the lungs, liver, and bone

59
Q

what is the clinical presentation of vulva cancer?

A

In about half of the patients diagnosed with vulval cancer, the following signs are present:
• Prolonged pruritus vulvae, vulval ulcer, palpable nodule/mass, exophytic growth (warty/cauliflower-like), lesion from background of lichen sclerosus
• May have complaints of dyspareunia and dysuria
• Advanced cases: enlarged groin LNs, oedema in the lower extremities

Woman's Health (29 decks)

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