Brainscape's Knowledge GenomeTM

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


See full index

Repro > 18. Neoplasms Of The Reproductive Tract > Flashcards

18. Neoplasms Of The Reproductive Tract Flashcards

1
Q

What type of cancer are vulval cancers usually?

A

Squamous cell carcinoma.

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

How are vulval squamous neoplastic lesions related to HPV infection? When do non HPV related vulval cancers usually occur?

A

Approx 30% related to HPV - usually HPV 16, peak age in 60s.
Approx 70% unrelated to HPV - peak age in 80s, often occur in longstanding inflammatory and hyper plastic conditions of the vulva eg lichen sclerosis.

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

What is vulvar intraepithelial neoplasia (VIN)?

A

Atypical squamous cells within the epidermis (no invasion), which is an in situ precursor of vulval squamous cell carcinoma.

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

How does vulval squamous cell carcinoma spread?

A

Spreads initially to the inguinal, pelvic, iliac and para-aortic lymph nodes. Also tho the lungs and liver.

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

How does HPV cause cervical intraepithelial neoplasia (CIN) and cervical carcinoma?

A

Almost all cases related to one of 15 high risk HPVs, mainly HPV 16 and HPV 18. Infect immature metaplasia squamous cells in the transformation zone of the cervix. Produce viral proteins E6 and E7, which interfere with the activity of tumour suppressor proteins to cause inability to repair damaged DNA and increased proliferation of cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why doesn’t everyone who contracts a genetically HPV infection get cervical cancer?

A

Most genital HPV infections are transient and eliminated by the immune response in months.

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

Give 6 risk factors for HPV related vulvar squamous neoplasia, CIN and cervical carcinoma?

A 
Sexual intercourse.
Early first marriage.
Early first pregnancy.
Multiple births.
Many partners.
Promiscuous partner.
Long term use of oral contraceptive pill.
Partner with carcinoma of the penis.
Low socio-economic class.
Smoking.
Immunosuppression.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does cervical screening involve?

A

Cells from the transformation zone are scraped off, stained with Papanicolaou stain and examined microscopically.
Starts age 25, and offered every 3 years till 50. 50-65 offered every 5 years.
If abnormal refer for colposcopy and biopsy.

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

What does vaccination for HPV involve?

A

Gardasil vaccination against high risk HPVs given to girls aged 12-13 years. Protects for up to 10 years as when at highest risk of contracting HPV, so reduced risk of cervical, vulval and vaginal cancers, genital warts, oral cancers and anal cancers.

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

What is cervical intraepithelial neoplasia (CIN)?

A

Dysplasia of squamous cells within the cervical epithelium, induced by infection with high risk HPVs.

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

What are the 3 stages of CIN?

A

CIN I - most regress spontaneously, only a small percentage progresses to:
CIN II - a proportion of which progress to:
CIN III - carcinoma in situ. 10% progresses to invasive carcinoma in 2-10 years.
Approx 7 years from CIN I to CIN III.

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

What is the treatment for CIN?

A

CIN I - follow-up or cryotherapy.

CIN II & CIN III - superficial excision of transformation zone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Of the 10% of CIN III that progresses to invasive cervical carcinoma, which types of carcinoma does this cause?

A

80% - squamous cell carcinomas.

15% - adenocarcinoma.

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

How does invasive cervical carcinoma usually spread?

A

Locally to the para-cervical soft tissues, bladder, ureters, rectum, vagina.
Lymph nodes - para-cervical, pelvic, para-aortic.
Distal.

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

How does cervical carcinoma present?

A

Screening abnormality.

Post coital, intermenstrual or postmenopausal vaginal bleeding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is cervical carcinoma treated?

A

Microinvasive carcinomas are treated with cervical cone excision.
Invasive carcinomas are treated with hysterectomy, lymph node dissection and if advanced radiation and chemotherapy.

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

How is endometrial hyperplasia associated with endometrial carcinoma?

A

Endometrium lines the internal cavity of the uterus and consists of glands within a cellular stroma. Endometrial hyperplasia leads to an increased gland to stroma ratio.

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

Endometrial hyperplasia of the uterus is associated with prolonged oestrogenic stimulation. Give 2 causes of this?

A

Annovulation.
Endogenous sources (eg adipose tissue).
Exogenous oestrogen.

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

How is endometrial hyperplasia of the uterus treated if complex and atypical?

A

Hysterectomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does endometrial adenocarcinoma usually present?

A

Irregular or postmenopausal vaginal bleeding.

21
Q

What is the prognosis for endometrial adenocarcinoma?

A

Overall, 75% 10 year survival.

22
Q

What are the 2 types of endometrial adenocarcinoma? Describe each and how they spread.

A

Endometrioid - more common, mimics proliferative glands, typically arises in setting of endometrial hyperplasia. Associated with unopposed oestrogen and obesity. Spreads by myometrial invasion and direct extension to adjacent structures to local lymph nodes and distant sites.
Serous carcinoma - poorly differentiated, aggressive, worse prognosis. Exfoliates, travels through Fallopian tubes, implants on peritoneal surfaces.

23
Q

What is the commonest tumour of the myometrium of the uterus?

A

Leiomyoma = fibroid (BENIGN).

24
Q

What does a uterine leiomyoma look like?

A

Well circumscribed, round, firm and whitish in colour, bundles of smooth muscle that resembles normal myometrium.

25
Q

How does a uterine leiopmyoma usually present?

A

May be asymptomatic, or can cause heavy/painful periods, urinary frequency (bladder compression), infertility.

26
Q

What is a malignant tumour of the myometrium of the uterus?

A

Uterine leiomyosarcoma. Is uncommon, highly malignancy and metastasises to the lungs.

27
Q

How do ovarian tumours present?

A

Most are non-functional, so produce symptoms when they become large, invade adjacent structures or metastasise. Mass effects are seen as abdominal pain, abdominal distension, urinary, gastrointestinal symptoms and ascites.
Some cause hormonal problems such as menstrual disturbances and inappropriate sex hormones.

28
Q

What can be used in diagnosis and to monitor recurrence and progression of malignant ovarian tumours?

A

Serum CA-125.

29
Q

What genetic mutation are some malignant ovarian tumours associated with?

A

BRCA mutations.

30
Q

How can BRCA mutation carriers that predisposes them to malignant ovarian tumours be treated prophylactically?

A

With a prophylactic saplingo-oophrectomy.

31
Q

Ovarian tumours are classified depending on the tissue from which they have arisen. What are the 4 tissue types?

A 
Mullerian epithelium (including endometriosis).
Germ cells (pluripotent).
Sex cord-stromal cells (from the endocrine apparatus of the ovary, so can be functional).
Metastases.
32
Q

What are the 3 main histological types of ovarian epithelial tumours? What can they all be further classified as?

A

Histological types - serous, mucinous, endometrioid.

Can all be further classified as - benign, borderline, malignant.

33
Q

Give 3 risk factors for ovarian epithelial tumours.

A 
Nulliparity or low parity.
Heritable mutations eg BRCA1 or BRCA2.
Smoking.
Endometriosis.
(Oral contraceptive pill is protective).
34
Q

How do serious ovarian tumours (epithelial) spread?

A

Often spread to peritoneal surfaces and omentum, therefore are commonly associated with ascites.

35
Q

What are mucinous ovarian tumours?

A

An ovarian epithelial tumour. Are often large, cystic masses filled with sticky thick fluid. Are usually benign or borderline.

36
Q

What is pseudomyxoma peritonei?

A

Cancer that usually begins in the appendix, but frequently involves the ovaries. Is a mutinous ovarian tumour, with extensive mutinous ascites. Epithelial implants on peritoneal surfaces. Can cause intestinal obstruction.

37
Q

What do endometriosis ovarian tumours contain and when can they arise?

A

Tubular glands resembling endometrial glands.

Can arise in endometriosis.

38
Q

What are most types of germ cell ovarian tumours?

A

Teratomas, which are usually benign.

39
Q

What are the 3 groups of ovarian teratomas?

A

Mature (benign).
Immature (malignant).
Monodermal (highly specialised).

40
Q

What are the pathological features of ovarian mature teratomas?

A

Usually contain hair, sebaceous material, skin like structures, teeth. Also tissue from other germ layers present eg cartilage, bone, thyroid, neural tissue.

41
Q

What is the most common monodermal ovarian teratoma? What is this?

A

Struma ovarii - a benign tumour, composed entirely of mature thyroid tissue. May be functional and cause hyperthyroidism.

42
Q

What are ovarian sex cord-stromal tumours derived from?

A

Ovarian stroma (which is derived from the sex cords of the embryonic gonad).

43
Q

What does the sex cord produce in the testes and ovaries? (Tumours resembling all of these 4 cell types can be found in the ovary).

A

Testes - Sertoli and Leydig cells.

Ovaries - granuloma and theca cells.

44
Q

What are the two types of ovarian sex cord-stromal tumours? Are they masculinising or feminising?

A

Granulosa/therca cell tumours - feminising.

Leydig cell tumours - masculinising.

45
Q

What are the clinical features of granuloma cell tumours (ovarian sex cord-stromal tumours)?

A

Most occur in post-menopausal women.
May produce large amounts of oestrogen - so in pre-pubertal girls may produce precocious puberty and in adult women may be associated with endometrial hyperplasia, endometrial carcinoma and breast disease.

46
Q

What are the clinical features of Sertoli-Leydig cell tumours (ovarian sex cord-stromal tumours)?

A

Peak incidence in teens or twenties.
Often functional, in children may block normal female sexual development. In women can cause de feminisation and masculinisation eg breast atrophy, amenorrhoea, sterility, hair loss, hirsutism with male hair distribution, criterial hypertrophy, voice changes.

47
Q

What cancers most commonly metastasise to the ovaries?

A

Mullerian tumours from the uterus, Fallopian tubes, contralateral ovary, pelvic peritoneum.
Also GI tumours and breast.

48
Q

What is a krukenberg tumour?

A

Metastatic GI tumour within the ovaries. Is often bilateral and usually from the stomach.

49
Q

What are the 3 classification of tumours in the testes?

A

Germ cell tumours - seminomas and non-seminomatous germ cell tumours (many are mixed type of yolk sac tumours, embryological carcinomas, choriocarcinomas and teratomas).
Sex cord-stromal tumours - Sertoli cell tumours and Leydig cell tumours.
Lymphomas.

Repro (18 decks)

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