Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA 4 > Repro: Gynaecological Tumours > Flashcards

Repro: Gynaecological Tumours Flashcards

1
Q

Why are cervical carcinomas more common in younger women?

A

Cervical carcinomas most common in the transitional zone, in younger women the transitional zone is larger so there is more to infect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Whats the most common cause of cervical carcinoma?

A

70% due to high risk HPV infection (type 16 and 18)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does HPV infection cause malignancy?

A

Produces viral proteins E6 and E7 which interfere with tumour suppressor proteins (eg p53 and RB)
Therefore there is inability to repair damaged DNA and increased proliferation of cells which predisposes to malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the risk factors for cervical intraepithelial neoplasia (CIN) and cervical carcinoma?

A

Most are related to HPV infection

  • sexual intercourse
  • early first marriage
  • multiple births
  • multiple partners
  • long term use of OCP
  • partner with carcinoma of the penis
  • low socioeconomic class
  • smoking
  • immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why is cervical screening so successful?

A
  • cervix is accessible to visual examination and sampling
  • there is slow progression from precursor to invasive cancer
  • pap test detect precursor lesions and low stage cancers allowing for early diagnosis and curative therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does screening need to be continued after the HPV vaccination has been introduced?

A

The vaccine doesn’t protect against all high risk types so screening needs to be continued

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is cervical intraepithelial neoplasia? (CIN)

A

Dysplasia of squamous cells induced by infection with high risk HPVs
CIN 1 - most likely to regress spontaneously
CIN 2 - a proportion will progress to 3
CIN 3 - carcinoma in situ, 10% will progress to invasive carcinoma in 2-10 years

CIN 1 -3 takes around 7 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is CIN treated?

A

CIN 1 - follow up or freeze

CIN 2 and 3 - excision, get all epithelia and some stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What age does invasive cervical carcinoma present?
How does it present?
What types are there?

A

Average age of presentation is 45 years, either picked up by screening abnormality, abnormal bleeding eg postcoital, intermenstrual or post-menopausal
80% are squamous cell carcinomas, 15% are adenocarcinomas (also caused by HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is cervical carcinoma treated?

A

Microinvasive carcinomas (mm)
Treated with cervical cone excision which has a 100% 5yr survival
Invasive carcinomas (cm)
Treated with hysterectomy, lymph node dissection, radiation, chemotherapy
Has a 60% 5 year survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is endometrial hyperplasia?

What is the risk?

A

Endometrial hyperplasia - increased gland to stroma ratio, associated with prolonged oestrogen exposure. Frequent precursor to endometrial carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some causes of prolonged oestrogen exposure?

A
  • annovulation (therefore OCP)
  • endogenous sources eg adipose tissue produces oestrogens so more common in obese
  • exogenous sources eg OCP, HRT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the clinical features of endometrial adenocarcinoma?

A

The most common invasive cancer of the female genital tract
Usually presents age 55-75 with irregular or post menopausal bleeding
Has a 75% 10 year survival, good prognosis because post menopausal bleeding a big red flag so women present early . Cure is often possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Whats the difference between polypoid and infiltrative endometrial adenocarcinoma?

A

Polyploid tends to grow to fill the uterus

Infiltrative begins to invade the myometrium, can grow all the way through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 2 types of endometrial adenocarcinoma?

A
  1. Endometrioid
    - most common
    - mimics the endometrium
    - usually arises from endometrial hyperplasia
    - spreads by myometrial invasion, direct extensions, local lymph nodes
  2. Serous carcinoma
    - poorly differentiated, aggressive, worse prognosis
    - exfoliates, cells from tumour fall off and travel through fallopian tubes and implants on peritoneal surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the most common tumour of the myometrium?

A

Leiomyomas (fibroids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Outline what fibroids are

A

A benign tumour of the myometrium
Often multiple, can be tiny or grow to fill the pelvis
Can be asymptomatic, cause menorrhagia, urine frequency (big and heavy so can compress bladder), infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the malignant tumour of the myometrium?

A

Uterine leiomyosarcoma
Uncommon but occurs 40-60
Highly malignant - metastasise to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical features of ovarian tumours?

A

80% are benign - occur ages 20-45
The malignant tumours occur aged 45-65

Many are bilateral
Many have spread beyond the ovary at time of presentation so have poor prognosis

20
Q

How do ovarian tumours present?

A
  • most are non functional (don’t produce hormones) so only produce symptoms when they become large, invade adjacent structures or metastasise: abdo pain, abdo distension, urinary and GI symptoms
  • some produce hormones: menstrual disturbances, inappropriate sex hormones (masculinisation, precocious puberty)
21
Q

What serum markers can be measured to detect and monitor ovarian tumours?

A

CA-125

22
Q

What are the 4 classifications of ovarian tumours

A

Dependent on the tissue from which they are arisen

  1. Mullerian epithelium
  2. Germ cells
  3. Sex cord-stromal cells
  4. Metastases
23
Q

What are the 3 main histological types of ovarian epithelial tumours?

A

Serous
Mucinous
Endometrioid
All can be classified as either benign, borderline or malignant

24
Q

What are the risk factors for ovarian epithelial tumours?

A
  • nulliparity or low parity
  • OCP is protective (presents ovulation, every ovulation there is a break in the epithelium which needs to heal causing turnover of cells)
  • inherited BRCA1/2 mutations
  • smoking
  • endometriosis (within the ovary increases risk of becoming malignant)
25
Q

Why are serous ovarian tumours associated with ascites?

A

They often spread to peritoneal surfaces

26
Q

Outline the condition of mucinous ovarian tumours

A

Large sticky masses - can be over 25kg

Usually benign or borderline

27
Q

Outline condition of endometrioid ovarian tumours?

A

They contain tubular glands resembling endometrial glands

They can arise in endometriosis

28
Q

What are the different types of germ cell ovarian tumours?

A
  • most are teratomas which are usually benign (whereas teratomas in testes are usually malignant)
  • other types are malignant eg non-gestational choriocarcinoma (produces HCG) which are agressive and often fatal (whereas gestational type are much easier to treat)
29
Q

What are the 3 types of ovarian teratomas?

A
  1. Mature and benign, most common in young women
  2. Immature and malignant, these are rare and contain immature fetal tissue
  3. Monodermal, high specialised and consist of 1 tissue type
30
Q

What are the clinical features of ovarian mature teratomas?

A

Most are cystic
Also known as dermoid cysts as they almost always skin like structures, as well as hair and teeth
Most common in women in their 20s
Other tissue types such as thyroid, neural, bone also present in some cases

31
Q

What is the most common type of monodermal ovarian tumours?

A

Struma ovarii - benign and composed entirely of mature thyroid tissue so can cause hyperthyroidisim. Indistinguishable from thyroid

32
Q

What are ovarian sex cord stromal tumours?

A

Derived from ovarian stroma which is derived from the sex cords of the embryonic gonad. The sex cord produces sertoli and leydig cells, and granulosa and theca cells) Tumours resembling all 4 types can be found in the ovary
The tumours can be feminising or masculinising

33
Q

What are the clinical features of granulosa cell tumours?

A

Most occur in post-menopausal women
Can produce large amounts of oestrogen so in pre-pubertal girls can cause precocious puberty
In adult women causes endometrial hyperplasia and breast disease

34
Q

What are the clinical features of ovarian sertoli-leydig cell tumours?

A

Often functional so in children block normal female sexual development
Can cause defeminisation - breast atrophy, hair loss, clitoral hypertrophy, amenorrhoea

Peak incidence in teens or twenties

35
Q

Where do metastasis from the ovaries arise?

A

Most commonly mullerian tumours - uterus, fallopain tubes, other ovary, pelvic peritoneum

Also GI tumours and breast
Krukenberg tumour - often bilateral metastasis from the stomach (via tran-colaemic spread)

36
Q

What are the clinical features of vulval tumours?

A

Uncommon
2/3rds occur in women over 60
Usually squamous cell carcinoma

37
Q

What can cause vulval squamous neoplastic lesions in older and younger women?

A 
Younger women (in 60s)
Usually infection with HPV 16
Older women (80s)
Usually in long standing inflammatory conditions such as lichen sclerosis. Inflammation and fibrosis of the vulva causes high cell turnover
38
Q

What is VIN?

A

Vulvar intraepithelial neoplasia
There is atypical squamous cells within the epidermic (no invasion). It is an in-situ precursor of vulval squamous cell carcinoma
Appears macroscopically as brown and white patches

39
Q

How is vulval squamous cell carcinoma treated?

A

All of vulva, and lymph nodes in groin removed, mutilating surgery.
Lesions less than 2cm have 90% 5yr survival after surgery

40
Q

How does vulval squamous cell carcinoma spread?

A

Initially spreads to inguinal, pelvic, iliac and para-aortic lymph nodes. These can fungate through the skin

Also spread to lungs and liver

41
Q

What is gestational trophoblastic disease?

What are the major types?

A 
Tumours and tumour-liek conditions which show proliferation of placental tissue 
Major types:
- hydatidiform mole 
- invasive mole 
- choriocarcinoma
42
Q

What is a hydatidiform mole?

A

Occurs in 1/1000 pregnancies. Can become malignant but this is rare.
There is cystic swelling of the chorionic vili and trophoblastic proliferation
Diagnosed in early pregnancy by USS, but can present with miscarriage

43
Q

What does a hydatidiform mole look like, how is it treated?

A

It is a friable mass on thin walled, translucent, grape like structures which are the oedematous vili

Treated with curretage - need to remove all tissue from uterus. HCG levels are monitored, if they dont fall the mole may be invasive

44
Q

What is gestational chorioncarcinoma?

A

A malignant neoplasm of trophoblastic cells from a previous normal or abnormal pregnancy

It is rapidly inasive, metastasises widely but has excellent repsonse to chemotherapy
(N.B non gestational choriocarcinomas arise from germ cells in the ovary and dont repsond well to chemotherapy)

45
Q

How does gestational choriocarcinoma present and how is it treated?

A

Usually presents with vaginal spotting
High HCG levels
Treated with uterine evacuation and chemotherapy - very high cure rate

ESA 4 (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions