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ESA 3 - Reproductive System > Cancers > Flashcards

Cancers Flashcards

1
Q

What are vulval cancers?

A

Uncommon

Over 80yrs old

Over 90% are squamous cell carcinoma

Also melanoma and Basal cell carcinoma

Present as: Lumps, ulcers, skin changes

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2
Q

What is VIN?

A

Vulval Intraepithelial Neoplasia

  • In situ precursor of vulval squamous cell carcinoma
    • -May or may not develop into SCC (squamous cell carcinoma)
  • Atypical squamous cells
  • Confined to epidermis
    • No invasions of basement membrane
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3
Q

Are VIN and vulval SCC related to HPV?

A

Depends on case

30% cases - YES

  • Usually HPV 16
  • 60s -onset
  • Risk factors same as cervical carcinoma
    • Expose to HPV
    • Ealry first pregnancy
    • Multiple births
    • Smoking

70% cases - NO

  • Usually associated with longstanding inflammatory conditions (e.g. Lichen sclerosus)
  • 80s -onset
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4
Q

How does vulval cancer spread?

A

Direct extension

  • Anus
  • Vagina
  • Bladder

Lymph nodes

  • Inguinal
  • Iliac
  • Para-aortic

Distant metastases

  • Lungs
  • Liver
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5
Q

What cells line the cervix and how does this change?

A

Transformation Zone:

Premenarchal: Endocervix (between internal and external os) is made from columnar epithelium and ectocervix is made from squamous epithelium.

Early reproductive age: Cervix everts under the influence of oestrogen (so the simple squamous becomes simple columnar). This means that the simple columnaris exposed to low vaginal pH. The low pH causes inflammation = ectropian.

Women in her 30s: Simple columnar epithelium undergoes metaplasia into stratified squamous to adapt to low pH. This metaplasia means there is an increases risk of dysplasia.

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6
Q

What is HPV?

A

DNA virus that can be sexually transmitted.

Many subtypes

  • HPV 6&11 = anogenital warts
  • HPV 16&18 = high risk subtypes
    • Infects trnasformation zone
    • Produces viral proteins E6 and E7
    • These inactivate tumour suppressor genes (P53 and Rb)
    • Results in uncontrolled cell growth and proliferation
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7
Q

What is CIN?

A

Cervical intraepithelial neoplasia

  • Dysplasia
  • Confined to cervical epithelium (in situ)
  • Caused by HPV infection (95%)
  • Divided into CIN 1,2,3
    • Increasing thickness of dysplasia
    • Increasing risk of progression to invasive squamous cell carcinoma.
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8
Q

What are the risk factors for CIN and carcinoma?

A
  • Increased risk of exposure to HPV
    • Sexual partner with HPV
    • Multiple partners
    • Early age of first intercourse
  • Early first pregnancy
  • Multiple births
  • Smoking
  • Low socio-economic class
  • Immunosuppression
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9
Q

How does the cervical cancer screeing program work?

A

Brush used to scrape cells from the transformation zone - send for cytological assessment.

Significant reduction in rates of cervical caner

  • Aged 25-49 = every 3 years
  • Aged 50-64 = eveyr 5 yeats
  • 65+ - Only if recent abnormality
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10
Q

Discuss the HPV vaccine

A

Gardasil

  • Vaccination against high risk HPV subtypes (6,11,16,18)
  • Given aged 12-13
  • Pretection from - cervical, vulval, oral and anal cancer
  • Not given to men (controvercial)
    • HPV> in penile, anal and oral cancers
    • Men are carriers for HPV
  • Screening has reduced rates of invasive cervical cancer
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11
Q

WHat is invasive cervical cancer and how do patients present?

A
  • Most commonly invasive squamous cell carcinoma (Precursor = CIN)
  • Also adenocarcinoma (arise from endocervical glandular mucosa)
  • Presentation:
    • Post-coital, inter-menstrual, post-monopausal bleeding
    • Mass - exophytic and infiltrative
    • Screening
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12
Q

How does cervical cancer spread?

A

..

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13
Q

How do you treat cervical cancer?

A

If advanced:

  • Hysterectomy
  • Lymph node dissection
  • Chemoradiotherapy
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14
Q

What is Endometrial hyperplasia and what causes it?

A

Thickened endometrium - >11cm

Can be a precursor to endometrial cancer

Inter-menstrual / post-menopausal bleeding.

Caused by excessive oestrogen:

  • Endogenous
    • Obeisity
    • Early Menarchy / late menopause
    • Oestrogen secreting tumours (granulosa cell tumours)
  • Exogenous
    • Unopposed oestrogen - HRT
    • Tamoxifen (partial agonist in endometrium)
  • Irregular cycles
    • PCOS
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15
Q

Hw does endometrial cancer present?

A
  • Intermenstrual bleeding
  • Postmenopausal bleeding
  • Mass
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16
Q

What are the types of endometrial cancer?

A
  • Endometrioid adenoarcinoma
    • Mostcommon
    • Resemble normal endometrial glands
    • Commonly arises from endometrial hyperplasia
  • Serous Carcinoma
    • Less common
    • More aggressive
    • Poorly differentiated cells
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17
Q

How do endometrioid cancers spread?

A

..

18
Q

How do serous carcinoma’s spread?

A
  • Exfoliates
  • Travels through Fallopian tubes
  • Deposits on peritoneal surface
  • Associated with collections of calcium (Psammoma bodies)
19
Q

How do you manage invasive endometrial cancer?

A
  • Hysterectomy
  • Bilateral salpingo-oophrectomy
  • +/- lymph node dissection
  • +/- chemoradiotherapy
20
Q

What tumours can o get in myometrium?

A

Leiomyoma

Leiomyosarcoma

21
Q

What is a leiomyoma?

A
  • Most common tumour of myometrium
  • Benign
  • Pale, homogenous, well circumscribed mass
22
Q

How does a leiomyoma present?

A
  • Asymptomatic
  • Pelvic pain
  • Heavy periods
  • Urinary frequency (bladder compression)
23
Q

What is a leiomyosarcoma?

A
  • Malignant tumour of smooth muscle
  • Cellsare bizarre and atypical
  • Doesn’t arise from a leiomyoma
  • Metastases to lung common
24
Q

How does an ovarian cancer present?

A

Early - vague, non-specific symptoms (leads to a delayed diagnosis)

Later - Abdominal pain, abdominal distention, urinary symptoms, GI symptoms, hormonal disturbances

25
Q

How can you hep diagnose ovarian cancer?

A

Ca-125 - a serum marker used in diagnosis and monitoring for recurrence

BRACA1/2 - High grade serous cancers, prophylactic salpingo-oophrectomy

26
Q

What are the normal places in ovaries cancer comes from?

A

Epithelial lining on outside

Follicles - germ cells

Stromal cells

Also metastasis to the ovary

27
Q

What are the subtypes of ovarian tumours?

A

Often presetn as cystic masses

Histological subtypes:

  • Serous
  • Mucinous
  • Endometrioid

Can all be:

  • Benign
  • Borderline (increased atypia, no stromal invasion)
  • Malignant
28
Q

What are ovarian serous tumours?

A

Highly atypical. pleomorphic cells.

Often show psammoma bodes (Ca collections)

Often spread to the peritoneal surface

29
Q

What are ovarian mucinous tumours?

A

Secrete mucin

Atypical epithelial cells

30
Q

What are ovarain endometrioid tumours?

A
  • Glands resembling endometrium
  • May arise in endometriosis
  • May have synchronous endometrial endometrioid adenocarcinoma
31
Q

What are the subtypes of a teratoma?

A

Teratoma is the most common germ cell tumour:

  • Mature (benign)
  • Immature (malignant)
  • Monodermal (highly specialised)
32
Q

What is a mature teratoma?

A

Dermoid cyst

Contain fully, mature, differentiate tissue from all germ cell layers

Can be bilateral

Often contains skin and hair structures

33
Q

What is an immature teratoma?

A
  • Contains immature, embryonic tissue
  • Malignant
34
Q

What is a monodermal teratoma?

A

A teratoma comprised entirely of one fully differentiated tissue type.

Most common = thyroid tissue (Struma Ovarii)

Benign

Can also cause hypo/hyperthyroidism

35
Q

What other germ cell tumours are there?

A
  • Dysgerminoma (equivalent of seminoma in testes)
  • Choriocarcinoma
  • Embryonal carcinoma
  • Yolk sac tumour
36
Q

What are sex cord stromal tumours?

A

From ovarian derived stroma

  • Stroma derived from sex cord of embryonic gonad
  • Sex cord produces:
    • Sertoli and Leydig cells in the testes
    • Granlosa and Theca cells in the ovaries
  • Tumours resembling all these cell types can arise in the ovary.
37
Q

What hormone do theca and granulosa cell tumours produce, therefore what does this predispose to?

A

Produce oestrogen

  • Pre puberty
    • Precocious puberty
  • Adult
    • Breast cancer
    • Endometrial hyperplasia
    • Endometrial carcinoma
38
Q

What hormone do sertoli-Leydig tumours produce, what can this lead to?

A

Prodice testosterone

  • Pre-puberty
    • Prevent normal, female pubertal changes
  • Adult
    • Sterility
    • Amenorrhoea
    • Hirsuitism
    • Male pattern baldness
    • Breast atrophy
39
Q

What cancers commonly metastasis to the ovary?

A
  • Breast Cancer
  • Gastro-intestinal cancers
    • Colon
    • Stomach
    • Biliary tract
    • Appendix
  • Krukenberg tumour
    • Metastatis GI tumour
    • Often gastric
    • Signet cells
  • Other gynae tumours
    • Endometrial
    • Other ovary
    • Fallopiaan tube
40
Q

What are the risk factors, presentation and investigations done for testicular cancer?

A

Risk factor: Cryptorchidism

Presentation: Mass +/- pain

Investigations: Scans (USS), Tumour markers

41
Q

What are the subtypes of testicular cancer?

A

Different histological subtypes are often mixed in the same tumour

42
Q

What are the testicular cancer tumour markers?

A

Germ cell tumours

B hCG -Choriocarcinoma

AFP -Yolk Sac tumours

Tumours may be benign / malignant depending on age of patient.

ESA 3 - Reproductive System (20 decks)

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