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Repro > Tumours of Repro Tract 1 > Flashcards

Tumours of Repro Tract 1 Flashcards

1
Q

Possible presentations of cancer of repro tract

A

Ulcerating vulval lesion
Abnormal cervical cytology result
Post menopausal bleeding
6 month history of bloating
Unilateral testicular swelling

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2
Q

What is a tumour?

A

Any clinically detectable lump or swelling

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3
Q

Neoplasm definition

A

Abnormal growth of cells that persists after the initial stimulus is removed

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4
Q

What is malignant neoplasm?

A

Abnormal growth of cells that persists after initial stimulus is removed and invades surrounding tissue with potential to spread to different site

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5
Q

What is metastasis?

A

Malignant neoplasm that has spread to another site

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6
Q

What is dysplasia?

A

Pre-neoplastic alteration where cells show disordered organisation and abnormal appearances
Can be reversible

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7
Q

How common are vulval cancers?

A

Uncommon - 3% of all female cancers

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8
Q

Who do vulval cancers tend to affect?

A

Older people - 80-84 peak

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9
Q

What type of vulval cancers are there? Most common to least common

A

Squamous cell carcinoma
Basal cell carcinoma
Melanoma
Soft tissue tumours - rarer, fat, blood vessels, nerve

(all types of skin cancer as vulva is skin)

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10
Q

Clinical features of vulval cancer

A

Lumps/bumps
Ulceration
Skin changes - pigmentation, sensation, pain

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11
Q

Normal skin layers - 3

A

Epidermis
Dermis (collagen, blood vessels ect)
Subcutis (fat)

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12
Q

5 layers of epidermis

A

Stratum corneum
Stratum lucidum (only in hands and feet)
Stratum granulosum
Stratum spinosum
Stratum basale

(then basement membrane)

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13
Q

What happens histologically in squamous cell carcinoma?

A

Atypical squamous cells
Keratin formation - whorls of spherical keratin called keratin pearls

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14
Q

What happens when new squamous cells are produced in skin?

A

Produced in basale layer
As they rise up the layers the nucleus gets smaller
Eventually get to keratin layer or corneum layer

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15
Q

What is the in-situ precursor for vulval squamous cell carcinoma?

A

Vulval intraepithelial neoplasia (VIN)

  • abnormal cells with no breach of the basement membrane, may or may not develop into squamous cell carcinoma
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16
Q

What does in-situ mean?

A

No breach of the basement membrane

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17
Q

Typical features of neoplasia on histology

A

Increased nuclear size
Increased nuclei to cytoplasmic ratio
Pleomorphic cells - variation in size and shape of cells
Increased mitosis/mitotic figures
Abnormal mitotic figures - mercedes benz
Hyperchromasia - darker nuclei stain

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18
Q

Are Vulval intra-epithelial neoplasia and vulval squamous cell carcinoma related to HPV?

A

Yes and No

No - majority (70% of cases), usually associated with chronic inflammatory conditions instead, peak onset is older in 80s

Yes - minority (30%), peak onset younger in 60s, risk factors are same as cervical carcinoma

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19
Q

How does vulval cancer spread?

A

Direct - anus, vagina, badder
Lymph nodes - inguinal then iliac then para-aortic
Distant metastasis eg via blood - lung and liver

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20
Q

Inflammatory condition that can cause vulval cancer example (not HPV)

A

Lichen sclerosus - white patches of skin on genitals, anus or other parts of the body

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21
Q

Two parts of the cervix

A

Endocervix - internal os, not in contact with vagina
Ectocervix - external os, in contact with vagina acidic pH

22
Q

Different linings of endocervix vs ectocervix and why

A

Endocervix - columnar epithelium
Ectocervix - stratified squamous epithelium as it is exposed to harsh pH often

23
Q

What happens to the cervix during menstruation?

A

It everts - the endocervix simple columnar is then exposed to the acidic environment of the vagina so it gets inflamed and red, this is normal

24
Q

What is the region of simple columnar endocervix exposed the vagina during menstruation known as?

A

Ectropion

25
Q

What happens to the ectropian when it is exposed to acidic vaginal pH?

A

Metaplasia to squamous cell epithelium to cope

26
Q

What is the area of cervix undergoing metaplasia known as?

A

Transformation zone - increased risk of dysplasia

27
Q

What type of virus is HPV?

A

DNA virus, sexually transmitted

28
Q

Two types of HPV

A

Low risk - HPV 6 and 11 these cause warts

High risk - HPV 16 and 18 can cause cancer

29
Q

What region the cervix do HPV 16 and 18 infect?

A

Transformational zone - already at risk due to metaplasia

30
Q

What viral proteins does HPV produce and what do these do?

A

E6 - inhibits p53 tumour supressor gene
E7 - inhibits retinoblastoma gene (tumour supressor)

31
Q

What happens when E6 and 7 inhibit tumour supressor genes?

A

Uncontrolled cellular proliferation occurs

32
Q

What is cervical intraepithelial neoplasia (CIN)?

A

Precursor for squamous cell carcinoma of cervix - type of dysplasia confined to the cervical epithelium, no breach of BM

33
Q

What causes CIN?

A

99.9% HPV infections

34
Q

Division of CIN and meaning

A

CIN1 - dysplasia affects bottom 1/3rd of epithelia
CIN2 - affects bottom 2/3 of epithelia
CIN3 - affects all epithelia
CIN4 - breach of basememnt membrane, invasive squamous cell carcinoma

35
Q

Risk factors for cervical carcinoma, CIN and vulval intraepithalial neoplasia

A

Increased exposure to HPV- eg sexual partner with HPV, multiple partners or early age intercourse
Early first pregnancy
Multiple births
Smoking
Low socio-economic status
Immunosupression - eg HIV cannot clear HPV so exposed to virus for longer

36
Q

What often happens to CIN1?

A

Regress spontaneously
Can check via follow up 1 year following result

37
Q

Management of CIN2 and CIN3

A

Need treatment - colposcopy to examine cervix to decide if need LLETZ

Then large loop excision of transformation zone if needed (LLETZ)

38
Q

Cervical screening program age

A

Ages 25-49 is every 3 years
Ages 50-64 is every 5 years

Over 65 - only if recent abnormality

39
Q

What occurs in cervical smear?

A

Brush used to scrape cells from transformation zone and is tested for HPV

40
Q

What happens if cervical smear tests +ve for HPV?

A

Cells are looked at under microscope - cytology

41
Q

Prevention of HPV

A

Vaccine given to ages 12-13

42
Q

Vaccination for HPV info

A

Gardasil - recombinant vaccine against subtypes 6, 11, 16 and 18
Protects from cervical, vulval, oral and anal cancers

43
Q

Most common type of invasive cervical cancer

A

Squamous cell carcinoma
(CIN is precursor)

44
Q

Other type of cervical cancer

A

Adenocarcinoma - from endocervical glandular cells in stroma

45
Q

Presentation reasons for invasive cervical cancer

A

Bleeding - post coital, intermenstrual, post menopausal
Mass palpable in abdomen
Screening result

46
Q

What system is used to stage cervical cancer?

A

Figo

47
Q

Treatment of invasive cervical carcinoma

A

If advanced: Hysterectomy (removal of cervix and uterus)
Lymph node dissection
+/- chemoradiotherapy

48
Q

Normal endometrium structure

A

Simple columnar + glands + stroma

49
Q

What happens in endometrial hyperplasia?

A

Increased gland to stroma ratio
Thicked endometrium - due to increase in cell number
Can be precursor for endometrial cancer

50
Q

How is endometrial hyperplasia diagnosed?

A

Symptoms - intermentrual/postmenopausal bleeding + biopsy

51
Q

Cause of endometrial hyperplasia

A

Excessive oestrogen

52
Q

Causes of excessive oestrogen (which can cause endometrial hyperplasia and then cancer)

A

Endogenous:
Obesity - fat cells convert androgens to oestrogen
Early menarche/late menopause - more ovulations so more oestrogen exposure over life
Oestrogen secreting hormones

Exogenous:
Unapposed HRT oestrogen - need progesterone usually to appose
Tamoxifen - used to treat oestrogen receptor +ve breast cancer, inhibits receptor in breast but activates in endometrium

Irregular cycle - PCOS

Repro (22 decks)

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