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REPRO > Lecture 21: Tumours of the reproductive tracts > Flashcards

Lecture 21: Tumours of the reproductive tracts Flashcards

1
Q

Are vulval cancers common?

A

No, 3% of all female cancers

-arise in older patients (80-84)

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2
Q

What is the most common cancer seen in the vulva?

A

The vulva is skin, so they are skin cancers

  • squamous cell carcinoma (commonest)
  • basal cell carcinoma
  • malignant melanoma
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3
Q

What do vulval cancers appear as?

A

-lumps/bumps
-ulcerations
-pigmentation changes
-changes in sensation
-pain
(may be a delay to presentation as in intimate region, so usually advanced)

Histologically: no distinct layers in the skin, cells are atypical
-squamous cell carcinomas produce keratin so will see swirls of spherical keratin formation

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4
Q

What is VIN?

A

Vulvar intraepithelial neoplasia (in situ- contained within the basal layer)

  • precancerous skin condition
  • may progress to squamous cell carcinoma
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5
Q

Does HPV cause VIN and vulval squamous cell carcinoma?

A

-in 30% of cases, HPV16 does cause it
-im majority of cases, HPV does not relate to VIN and VSCC
(they are related to long standing chronic inflammatory conditions)

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6
Q

How do malignant cells spread?

A
  • direct extension
  • lymphatic vessels
  • blood vessels
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7
Q

Where do vulval cancers commonly spread to?

A

Lungs and liver

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8
Q

What are the parts of the cervix?

A

Ectocervix: incommunication with the vagina (acidic environment so it stratified squamous epithelia)
Endocervix: not in contact with the vagina, epithelial lining is simple columnar
At mestruation, oestrogen causes: evertion (pushes outwards), so simple columnar epithelium is now exposed to the acidic vagina: get inflammation
-simple columnar cells undergo metaplasia to become stratified squamous= TRANSFORMATION ZONE
-metaplasia good in short term but increases risk of dyplasia

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9
Q

What does HPV cause?

A

HPV is sexually transmitted
Low risk HPV (6 and 11): warts
High risk HPV (16 and 18): lead to cancer, preferentially infects the transformation zone, produce viral proteins e.g. E6/7, inactive tumour suppressor genes (6: p53, 7: retinoblastoma gene)

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10
Q

What is CIN?

A

Cervical intraepithelial neoplasia

  • dysplasia confined to the cervical epithelia (in situ), no breaking through the basement membrane
  • if they do break through the membrane=invasion: invasive squamous cell carcinoma
  • HPV causes CIN
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11
Q

What are the classifications of CIN?

A

1 (bottom 1/3), 2 (2/3rds), 3 (full thickness)

-determined by the thickness of the cervical epithelium that is dyplastic

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12
Q

What are the risk factors for CIN and cerivcal squamous cell carcinoma?

A
  • HPV (multiple sexual partners, early intercourse increase risk of HPV exposure)
  • early first pregnancy
  • multiple births
  • low socio-economic status
  • smoking
  • immunosuppression
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13
Q

How do you treat CIN?

A
  • CIN1 often regresses spontaneously
  • CIN2 and 3 denote risk of developing into squamous cell carcinoma
  • urgent colcoscopy (look at cervix)
  • can remove transformation zone
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14
Q

When des the cervical cancer screening programme start?

A

24 1/2, every 3/5 years

  • brush used on transformation zone
  • cells sent to cytology (tested for HPV, if positive the cells undergo microscopy, if negative they go back to routine follow up)

-vaccination available now and targets the most common high risk subtypes of HPV, given at age of 12-14

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15
Q

What other types of cancers can HPV cause?

A

Oral and anal cancers (why men also have the vaccine)

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16
Q

What other type of cancer can be seen in the cervix?

A

Glands in the stroma of the cervix, can become neoplastic-rare
-gives rise to adenocarcinoma

17
Q

How does invasive cervical cancer present?

A
  • bleeding, post-coital bleeding, intermenstrual bleeding, post-menopausal bleeding
  • palpable abdominal mass
18
Q

How is cervical cancer staged?

A

TNM staging

gynaecological cancers are also staged by FIGO

19
Q

What is the treatment for invasive cervical cancer?

A
  • hysterectomy (removal of cervix and uterus)
  • if lymphnodes are involved, they are removed
  • option for chemotherapy/radiotherapy
20
Q

What is the endometrium comprised of?

A

Glands: lined by simple columnar cells lining an empty space
Stroma: supporting cells

21
Q

What is endometrial hyperplasia?

A

Increased gland to stroma ratio

  • USS done to look at thickness of endometrium
  • if thicker a biopsy is taken
  • presents with bleeding
  • caused by excessive oestrogen (obesity, as fat cells convert androgens to oestrogens, early menarche and late menopause, tumours secreting oestrogen, hormones replacement therapy, tamoxifen stimulates oestrogen receptors in the endometrium, irregular menstrual cycles)
  • can progress into a type of invasive endometrial cancer
22
Q

What is the most common malignancy to arise from the endometrium?

A

Most common: Endometrioid adenocarcinoma-typically arises from endometrial hyperplasia (malignant cells resemble endometrial glands, but glands are complex, they grow into each other, cells look atypical)
-spreads by direct invasion, lymphatic and blood vessels also invaded

Less common: serous adenocarcinoma, more aggressive, cells don’t resemble normalendometrial glands, poorly differentiated

  • exfoliates, cells break off main tumour and escape through the fallopian tubes into the peritoneal cavity: transcoelomic spread)
  • see spherical collections of calcium: psammoma bodies
23
Q

How do you manage endometrial cancer?

A
  • surgical: hysterectomy
  • bilateral salpingoophorectomy (removal of both fallopian tubes and ovaries)
  • lymphnode involvement?
  • chemotherapy/radiotherapy
24
Q

What is a leiomyoma?

A

Benign tumour of the myometrium (fibroids)

  • common
  • see streaming on histology
  • symptoms of fibroids depend on size
  • large: pelvic pain, heavy periods, compress on other organs e.g. urinary frequency/GI symptoms
25
Q

What is a leiomyosarcoma?

A

Malignant tumour of the myometrium
-cells are abnormal: pleomorphism, irregular nuclei
(leiomyoma does not progress to leiomyosarcoma)
-can occassionally metastasise to the lung

26
Q

Why is there a delayed diagnosis in ovarian cancer?

A

Ovarian cancer presents in a vague non-specific way

-abdo pain, bloating, GI/urinary symptoms

27
Q

What protein is released by ovarian cancer?

A

CA125 (cancer antigen)

28
Q

Do mutations to BRCA1/2 lead to ovarian cancers?

A
  • BRCA1/2 are usually tumour suppressory genes

- mutations to BRCA1/2 are associated with high grade serous cancers

29
Q

What is the anatomy of the ovary?

A

-epithelial lining
-follicles (have germ cells in them)
-stroma
Those are the 3 sources of primary ovarian tumours

30
Q

What do epithelial ovarian tumours present as?

A

Cystic mass
-serous/mucinous/endometreoid adenocarcinoma
(can be benign/malignant)

31
Q

What are the types of teratoma?

A

Mature- fully differentiated cell types from all 3 germ cell layers, benign
Immature- no recognisable structures, malignant
Monodermal- composed of one cell type
(more scary it looks, with teeth, bone etc- less harmful as it contains fully differentiated cell types)

32
Q

What are sex cord stromal tumours?

A
  • Testes: stroma give rise to sertoli cells, leydig cells
  • mass (enlarged testicle) +/- pain
  • use of tumour markers and scan to detect

Ovaries: stroma give rise to theca and granulosa cells (these cells aid development of the follicle)
-produce oestrogen (if tumour before puberty, this will accelerate the development of the secondary sexual charcteristics, after puberty the excess oestrogen can cause breast cancer/endometrial hyperplasia)

Leydig and sertoli cells can be found in the ovaries so can get cancer of these
-in female not been through puberty, testosterone will prevent secondary sexual characteristics, if after puberty it results in ammenorrhoea, infertility, hirsutism

33
Q

What are some tumour markers in germ cell testicular tumours?

A
  • beta-hCG: choriocarcinoma (present in testes and ovaries)

- AFP (alpha fetoprotein): present in yolk sac tumours, also produced in liver cancer

34
Q

What are the different types of testicular cancer?

A 
Germ cell
-seminomatous (seminoma) or non-seminomatous 
Non-germ cell
-sex-cord stromal tumours
-lymphoma metastases
35
Q

What is the most common testicular cancer?

A

Seminoma

36
Q

What is the most common invasive cancer of the female genital tract?

A

Endometrial adenocarcinoma

37
Q

What is the most significant risk factor for the development of germ cell tumours?

A

Cryptorchidism

-undescended testes

REPRO (18 decks)

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