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Reproductive System > Tumours Of The Reproductive Tract > Flashcards

Tumours Of The Reproductive Tract Flashcards

1
Q

Vulval cancers are relatively uncommon.

What type are most of them?
Who’s affected mostly?

A

Squamous cell carcinomas (produce keratin)

Older women

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2
Q

What causes Vulval Cancer in Older women?

A

Undone cause, but suspected to be due to chronic irritation and long-standing dermatoses

(Lichen Sclerosus and Squamous Hyperplasia)

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3
Q

What causes Vulval Cancer in Pre-menopausal women?

A

Main factor appears to be HPV, with invasion developing from precursor- VIN

(Vulval Intraepithelial Neoplasia, doesn’t invade through BM)

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4
Q

Vulval cancer spreads locally.

Where does it metastasise to primarily?
What does definitive surgery include?

A

Inguinal lymph nodes

Includes removing primary tumour and lymph nodes

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5
Q

In what percentage of cases does HPV cause VIN and Vulval Cancer?

A

30%

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6
Q

What classification is used to classify Cervical Cancer?

A

FIGO system

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7
Q

Compare the epithelia of the Endocervix and Ectocervix

A

Endo;
- Glandular (Simple columnar) epithelium

Ecto;
- Stratified squamous (as in contact with acidic vagina)

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8
Q

What are 2 significant things about the Transformation Zone of the Endocervix?

A
  • This is the part removed for histology in a Loop Excision

- This is where metaplasia occurs between the 2 types of cervical epithelium (can lead to dysplasia and neoplasia)

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9
Q

What percentage of Cervical carcinomas are Adenocarcinomas and Squamous Cell Carcinomas?

A

Adenocarcinoma- 15%

Squamous cell- 80%

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10
Q

Describe the common aetiology of Cervical Adenocarcinomas and Squamous Cell carcinomas?

A
  • Infection by HPV, which produces E6 and E7

- These proteins inactivate TS genes p53(E6) and pRB(E7)-> Unregulated cell proliferation-> Neoplasia

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11
Q

What is CIN (Cervical Intraepithelial Neoplasia)?

What can CIN lead to?
What is a common cause of CIN?

A
  • Confined Neoplasia of cervical epithelia, without invasion of BM (In Situ)
  • Can lead to Squamous Cervical Cell carcinoma
  • Commonly due to HPV Infection (99%)
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12
Q

There are 3 classes of CIN.

Explain them

A

CIN 3: Full thickness of cervical epithelia is displaying abnormal cellular features

CIN 2: Bottom 2/3 “”

CIN 1: Bottom 1/3 ”” (Resolves spontaneously, smear 1 year later)

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13
Q

Since 2008, girls aged 12-13 have been offered HPV vaccine.

How long this vaccine protect against?

A

Up to 10 years

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14
Q

Suggest some risk factors for CIN-> Cervical cancer

A
  • Multiple partners or one with confirmed HPV
  • Early age of 1st intercourse
  • Smoking
  • Early 1st pregnancy
  • Low socioeconomic status
  • Immunosuppression

Anything that could increase HPV exposure

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15
Q

Cervical screening is done to detect a pre-invasive lesion and excise the involved area completely

(Colposcopy to look for, Diathermy to remove)

What does cervical screening look for?

A

Cells with abnormally enlarged nuclei and abnormal chromatin (dyskaryotic cells)

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16
Q

Where can cervical cancer spread to?

What structures can be affected locally?
How does this present?

A
  • Initially to the Iliac lymph nodes, then to Aortic nodes, before systemic spread
  • Ureters, Bladder, Rectum
  • Pain and fistula formation
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17
Q

What can HPV cause in men?

A

Oral and Anal cancers

Hence vaccinated, but also to achieve herd immunity

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18
Q

How can Invasive Cervical cancer present?

A

Bleeding;

  • Inter menstrual
  • Post menopausal
  • Post coital
  • Possible palpable abdominal mass
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19
Q

Define Endometrial Hyperplasia
What is it caused by?

How is it investigated?

What can it lead to?

A
  • Increased Gland to Stroma ratio of endometrium
  • Excessive Oestrogen (Obesity)
  • USS to look at thickness
  • Biopsy if thickness> 7mm
  • Can progress to Invasive Endometrial Endrometroid Carcinoma
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20
Q

How can Obesity causes excessive endogenous oestrogen

List 5 other causes of excessive oestrogen

A

Adipocytes can convert androgens to oestrogen

  • Oestrogen secreting tumour
  • Early Menarche or Late Menopause (More oestrogen made over lifetime)
  • Oestrogen administration (Pill, HRT)
  • Tamoxifen (Used to treat breast cancer)
  • Irregular menstrual cycles (PCOS)
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21
Q

Endometrial Adenocarcinoma occurs in Peri-menopausal and Older women.

What are 2 types of Endometrial Adenocarcinoma?
How do they differ in incidence and outcome?

A
  • Endometroid (More common)

- Serous (More aggressive, with worse prognosis)

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22
Q

When can advanced endometrial carcinoma spread to?

Compare the method of spread of Serous and Endometroid carcinoma

(Direct invasion, Via blood, via lymph, Transcoelomic)

A

Cervix, Bladder, Rectum

  • Endometroid: Lymphatics and Direct Invasion
  • Serous: Transcoelomic
23
Q

What sign of Serous Carcinoma may you see on histology?

A

Psammoma Bodies: Spherical collections of Ca

Dark purple in colour

24
Q

How can Endometrial cancer be treated

A
  • Surgery (Removal of Cervix, Uterus, Fallopian tubes, possibly lymph nodes)
  • Possibly Radio and Chemo
25
Q

What are Fibroids/ Leiomyomas?

What are some symptoms?

A

Benign tumours of uterine smooth muscle, whose growth is Oestrogen dependent and usually regress after menopause

  • Menorrhagia
  • Infertility
  • Pelvic pain
  • If big enough/ numerous enough, compressive symptoms (Urinary frequency, GI symptoms)
26
Q

What is a Leomyosarcoma? (Unknown aetiology, no development from Fibroids)

How do they present?

A

A malignant tumour of uterine smooth muscle

Similarly to Fibroids/ Leiomyomas

27
Q

Describe the Spread of Leiomyosarcomas

A
  • Infiltrate locally

- Metastasise by blood to the lungs then systemically

28
Q

What does ‘Endometroid’ mean?

Can these cancers occur only in the Endometrium

A

Looks like Endometrial tissue

No, can occur outside of endometrium

29
Q

What are 3 classes of Primary ovarian tumour?

Which class is the majority?

A
  • Epithelial tumours; majority of primary Ovarian tumours
  • Germ cell tumours (from follicles)
  • Sex-cord Stromal tumours
30
Q

Epithelial Ovarian tumours often present as a cystic mass, containing fluid

Describe the classification of Epithelial Ovarian tumours

A

Can be classed into;

  • Serous
  • Mucinous
  • Endometrioid

Each of these can further be classed into;

  • Benign
  • Borderline
  • Malignant
31
Q

Malignant epithelial tumours usually don’t preset until late stage so prognosis is poor.

Where can they spread and what 3 things can they lead to?

A

Within abdomen

Can lead to;

  • Ascites
  • Intestinal obstruction
  • Death
32
Q

What is the link between BRCA1 and 2 genes and Epithelial Ovarian cancer?

A

These genes are markers for Familial Ovarian Epithelial Carcinoma, however this represents < 1% of cases

33
Q

Germ cell tumours are usually benign in women.

What is the most common type?

A

Dermoid Cyst/ Mature Cystic Teratoma

For these tumours, mature means benign as more differentiation has occurred

34
Q

Germ cell tumours can contain tissues from which Germ cell layers?

A

From any of the three germ cell layers

35
Q

In a Germ cell tumour, what does presence of immature tissue indicate?

(E.g primitive neuroepithelium)

A
  • Malignancy
  • Risk of intrabdominal spread
  • Potential to cause death
36
Q

List 4 malignant germ cell tumours

Suggest 2 useful tumour marker for this group of tumours

A
  • Dysgerminoma (testis)
  • Yolk sac tumour
  • Choriocarcinoma
  • Embryonal carcinomas
  • hCG
  • AFP
37
Q

What are Sex-cord Stromal Tumours derived from?

What are 2 types?

A

From ovarian stroma, which is derived from the sex cord of the embryonic glands

  • Granulosa cell tumours
  • Sertoli-Leydig cell tumours
38
Q

Describe Granulosa Cell tumours

A
  • Resemble cells lining the ovarian follicle

Commonly produce oestrogen so can cause;

  • Endometrial hyperplasia and adenocarcinoma (if after puberty)
  • Precocious puberty
39
Q

Describe Sertoli-Leydig cell tumours

A
  • Rare sex-cord stromal tumours

May produce Androgens causing;

  • Defeminisation
  • Masculinisation
  • Amenorrhoea
  • Infertility
40
Q

List 4 tumours that can metastasise to Ovaries

A
  • From Mullerian epithelium (Uterus, Tubes, other ovary etc)
  • GI
  • Breast
  • Kruckenberg tumours (usually from stomach)
41
Q

What are 2 classes of Testicular tumours?

A
  • Germ cell tumours (Not the same as in women)
  • Non Germ cell tumours

(Also can be affected by Lymphomas via metastases)

42
Q

Sex-cord Stromal tumours are a type of Non-Germ Cell Testicular tumour.

What are the commonest types seen in the testes?

A

Sertoli or Leydig cell tumours

These are uncommon and benign

43
Q

In post-puberty males, 95% of testicular tumours are germ cell tumours.

Describe the aetiology of Germ cell tumours in men

A
  • Possible genetic predisposition
  • Cancer in 1 testis is associated with increased risk in the other
  • Increased risk of testicular cancer in Cryptorchidism (increased risk in BOTH testes)
44
Q

What is Cryptorchidism?

This can increase risk of testicular cancer.

What can be done about this condition to decrease risk of cancer?

A

Failure of testicular descent into scrotum (Can be bilateral)

Orchiopexy (Surgical placement of testis into scrotum) before puberty decreases risk of cancer

45
Q

How does Testicular cancer present usually?

What is Intratubular Germ Cell Neoplasia?

What are the 2 types of Germ Cell Testicular tumours?

A
  • Painless testicular mass
  • A pre-invasive precursor of germ cell tumours
  • Seminomas
  • NSGCTs (Non Seminomatous Germ Cell Tumours)
46
Q

50% of Germ Cell Testicular tumours are Seminomas.
The peak age for development is 40-50 years

Describe their spread

A
  • Confined to testis for long time periods
  • Metastasise by Lymphatics to Iliac and Para-aortic nodes
  • Further spread is rare
47
Q

Describe the spread of NSGCTs, in contrast to Germ Cell tumours

A
  • Metastasise early via Lymphatics and Blood

- May present with metastases with a non-palpable primary testicular tumour

48
Q

Many NSGCTs are Mixeed, containing at least 2 Pure NSGCT components.

List 4 Pure NSGCTs

A
  • Yolk sac tumours
  • Embryonal carcinomas
  • Choriocarcinomas
  • Teratomas
49
Q

Describe the Incidence, Prognosis and Tumour Marker production of Yolk Sac tumours in men.

A
  • In young children
  • Very good prognosis
  • Almost all produce AFP which can be detected in blood
50
Q

In men, describe the Incidence and Tumour Marker production of;

  • Choriocarcinomas
  • Embryonal Carcinomas
  • Mixed NSGCTs
A
  • Occur in young adults
  • All Choriocarcinomas produce hCG
  • Most Mixed NSGCTs produce BOTH hCG and AFP
51
Q

Describe the Incidence, Severity and Tumour Marker production of Teratomas

A
  • Occur in men of all ages
  • Benign if arise BEFORE puberty
  • Malignant if arise AFTER puberty
  • Produce hCG
52
Q

10% of Seminomas (a type of Germ Cell Testicular tumour) produce hCG.

What is response for this?

A

Presence of Syncytiotrophoblastic cells that produce hCG

53
Q

How are Germ Cell Testicular tumours treated?

Whichever type it is, treatment is often successful resulting in a cure

A
  • Radical Orchiectomy

If Seminoma;
- Radiotherapy (these are very radiosensitive, best prognosis of al the Germ Cell tumours)

If NSGCT;
- Aggressive Chemotherapy

Reproductive System (21 decks)

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