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imed3003 > Pathology of the Ovary > Flashcards

Pathology of the Ovary Flashcards

1
Q

What are paratubal cysts?

A

They are cysts on ovaries derived from mullarian duct remnants and are very common with no clinical consequence.

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2
Q

What is an adenomatoid tumour?

A

Benign neoplasm derived from the mesothelium.

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3
Q

What kind of mutation or cancer affects the Fallopian tubes to cause premalignant STIC cancers?

A

Particularly prevalent in people with BRCA mutations and in women with high grade serous carcinoma of the ovary.

Frequently show p53 mutations

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4
Q

How are premalignant STIC or in situ serous carcinomas treated>

A

Spread rapidly through the peritoneum so removal of tubes prior to malignant spread is indicated to prevent ovarian cancer

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5
Q

What are BRCA mutations?

A

Breast cancer associated mutations

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6
Q

What does BRCA do?

A

Genes that make tumour suppressor proteins.

If there is a BRCA mutation then DNA is not repaired leading to mutations. People with inherited BRCA1 and BRCA2 are at risk of

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7
Q

What mutations result in breast and ovarian cancer?

A

Breast: Background lifetime risk = BRCA1/2

Ovarian: Background risk is 2% BRCA1 is 45% and BRCA2 is 80%

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8
Q

What kind of tumours are ovarian tumours classified as?

A

For exam: They are surface epithelial tumours.

However new research is showing that they arise from fimbrial end of fallopian tubes (so not from the ovary itself)

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9
Q

Where do ruptured cystic follicles come from?

A

They come from unruptured graafian or in follicles that ruptured but then stuck shut.

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10
Q

What is polycystic ovarian syndrome?

A

Lots of follicles are formed but no ovulation

High androgen production and insulin resistance.

Pathophysiology is poorly understood.

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11
Q

What are the associated disorders with polycystic ovarian syndrome?

A

Diabetes Mellitus 2

Obesity

Metabolic disorders

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12
Q

What are the macroscopic clinical symptoms of polycystic ovarian syndrome?

A

Macro: Globoid enlarged ovaries with multiple cysts ‘string of pearls USS’

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13
Q

What are the microscopic clinical symptoms of polycystic ovarian syndrome?

A

Thick ovarian capsule

Uniform cystic follicles

Partially regressing follicles

No corpus luteum or albicantia due to no cycling.

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14
Q

What percentage of cancers in women are ovarian cancer?

A

5% of cancers in women

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15
Q

What percentage of ovarian neoplasms are benign?

A

80%

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16
Q

What age group gets more benign ovarian neoplasms and what age group gets more malignant neoplasms?

A

Benign: 20 - 40 years

Malignant: 40 - 70 years

Malignant ones tend to present late and are more likely to be bilateral.

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17
Q

What are the following neoplasms called?

Benign and cystic

Benign, cystic and fibrous

Benign and mostly fibrous

Malignant

A

Cystadenoma

Cystadenofibroma

Adenofibroma

Adenocarcinoma or cystadenocarcinoma (late presenting, malignant and tend to be bilateral)

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18
Q

Why is ovarian cancer so deadly?

A

It is common (5th most common cancer in women)

Make up quarter of female genital tract cancer but cause half of deaths.

Vague clinical signs (bloating, fatigue, or no signs)

When advanced: Compressive sx ascites, mets.)

HIgh stage at presentation (late)

No screening tests available

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19
Q

What are the types of surface epithelial tumours of the ovary?

A

Serous: Benign / borderline / malignant forms. Malignant form is split into 2 categories (low and high grade serous carcinomas)

Mucinous: Benign / borderline / malignant forms

Endometrioid: Benign / borderline / malignant forms

Clear cell: Benign / borderline / malignant forms

Brenner: Benign / borderline / malignant forms

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20
Q

What are the types of mixed epithelial/stromal tumours of the ovaries?

A

Adenosarcomas

MMMT

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21
Q

What tumours can arise from the sex cord/stroma of the ovaries?

A

Granulosa/thecal tumours

Fibromas

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22
Q

What tumours arise from germ cells?

A

Teratomas

Dysgerminomas

Yolk sac tumours

Choriocarcinoma

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23
Q

Where do tumours of the ovary metastasize?

A

Colon

Appendix

Stomach

Breast

Pancreas

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24
Q

What mutation causes type 1 surface epithelial carcinomas?

A

KRAS/BRAF/ERBB2 mutations

Then loss of tp36 or CDKN2A/B

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25
Q

What are the classifications of surface epithelial tumours of the ovaries?

A

Type 1 - low grade that arise in setting of borderline tumours and/or endometriosis (eg low grade serous, endometrioid, mucinous)

Type 2 - STIC and high grade serous carcinoma

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26
Q

What mutations cause type 2 surface epithelial carcinomas?

A

p53 mutations

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27
Q

How are type 1 and type 2 lesions different?

A

Type 1: low grade with precursor lesion in a stepwise fashion, represented by cystadenomas and borderline tumours, most often presents early (low stage), often remains low grade by can progress to high grade. Mutation = K-ras/BRAF (65%) and TP53 (8%)

Type 2: High grade, arises de novo, and most often presents at high stage, is rapidly growing, aggressive, and caused by p53 mutation (in about 70% of cases), k-ras/BRAF are rare in these cancers.

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28
Q

Which cancers are type 1 and which are type 2?

A

Type 1 includes: Serous carcinoma, mucinous endometrioid, and clear cell carcinomas as well as transitional cell carcinoma. (Brenner and non-Brenner)

Type 2 includes: Serous carcinoma, and malignant mixed mullerian tumours.

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29
Q

What are the macroscopic and microscopic features of benign, borderline, and malignant tumours? What is the prognosis for these tumours?

A

Benign: Macroscopically a simple cyst, microscopically simple flat lining. Prognosis is excellent.

Borderline: Macroscopically a complex cyst, microscopically a branching complex architecture. Prognosis: may recur / progress.

Malignant: Macrscopically shows invasion, microscopically shows b/i plus solid and invasive areas. Prognosis is possibly lethal.

30
Q

What percentage of borderline serous tumours are bilateral?

A

25%

31
Q

What microscopic features do borderline serous ovarian lesions have?

A

They have papillary excrescences, non-invasive but recur, can implant into peritoneum, and have a small risk of malignant transformation.

32
Q

What microscopic features do benign serous ovarian lesions have?

A

Serous inclusion cysts / aka cortical inclusion cysts lined by tubal type ciliated cells. Benign serous cystadenoma same but bigger.

33
Q

What is the 5y survival rate of borderline serous ovarian lesions?

A

5y survival if confined to the ovary is 100%

If peritoneum is involved 60%

34
Q

What are the potential complications of low grade serous ovarian carcinomas?

A

Can widely spread to peritoneal surfaces but progress slowly and cause intestinal obstruction.

35
Q

What is 5y survival of high grade serous carcinomas?

A

<25%

36
Q

What are the important histological features of high grade serous ovarian carcinomas?

A

Markey nuclear atypia and ‘monster cells’

37
Q

What mutations are associated with high grade serous ovarian carcinoma?

A

P53 and BRCA

38
Q

How is histology different between benign and borderline mucinous ovarian lesions?

A

Benign: Tend to be multiloculated, huge, and seen in combo with benign teratoma. Have tall columnar cells with apical mucin. Mostly resembles intestinal epithelium, minority resemble endocervix.

Borderline: Older women, rarely bilateral, cystic and solid, more cytological and architectural atypia, non-invasive with intermediate prognosis.

39
Q

What causes “jelly belly”?

A

Was previously thought to be mucinous ovarian carcinoma but now is associated with appendix neoplasms.

40
Q

What mutations are associated with endometrioid ovarian lesions?

A

Alterations that increase PI3K/AKT pathway signalling (PTEN, PIK3CA, ARID1A and KRAS), MMR, and beta-catenin.

41
Q

What conditions are associated with endometrioid ovarian lesions?

A

May be synchronous with endometrial endometrioid adenocarcinoma.

May arise from endometriosis

42
Q

What is the 5y survival rate of endometrioid ovarian lesions if stage 1?

A

75%

43
Q

What percentage of endometrioid ovarian lesions are bilateral?

A

40%

44
Q

What ages are endometrioid ovarian lesions most common in?

A

50 - 60 yos

45
Q

What rare surface epithelial tumours affect the ovaries?

A

Brenner (transitional): majority are benign

Clear cell: Majority malignant, associated with endometriosis

MMMT (Malignant Mixed Mullarian Tumour): Always malignant poor prognosis, malignant epithelium + malignant stroma = MMMT. Dismal prognosis.

46
Q

What are the types of sex cord stromal tumours and what do they produce?

A

Granulosa and thecal cell -> Produce oestrogens

Sertoli-leydig -> androgens

Hilus (Pure leydig cell neoplasm) -> androgens.

47
Q

What are the types of sex cord stromal tumours that affect ovaries and what do they do?

A

Oestrogen producing tumours -> result in endometrial hyperplasia and carcinoma

Androgen producing tumours block puberty or cause amenorrhoea +/- hirsutism and clitoral enlargement.

48
Q

Who most commonly gets granulosa tumours?

A

Post menopausal women

49
Q

What mutations lead to granulosa tumours?

A

FOXL2 mutations

50
Q

What is a fibrothecoma? What is their prognosis?

A

When the thecoma > fibroma -> hormones

With ascites and R hydrothorax

Almost all are benign

51
Q

What is the prognosis like in granulosa tumours?

A

They are low grade but often recurs later in life

52
Q

What are the effects of sertoli-leydig tumours?

A

Masculinisation, 20 - 30yo, mostly benign

53
Q

What mutations lead to sertoli-leydig tumours?

A

DICER1

54
Q

What is the prognosis like in teratomas?

A

Most ovarian teratomas are benign. Most testicular teratomas are malignant with exception of those in prepubertal boys.

55
Q

What kind of tissue do teratomas form?

A

Can form all kinds of body tissues. (brain matter can be attacked by immune system which goes to brain and causes psychosis)

56
Q

What kind of tumours are immature teratomas?

A

Malignant, rare, seen in teens.

Tissue resembling foetal rather than mature tissue.

Usually immature neuroepithelium

Reasonable prognosis.

57
Q

What kind of tumours are monodermal teratomas?

A

Struma ovarii composed of ovarian tissue can be functional -> Hyperthyroidism. Rare can get follicular or papillary thyroid carcinoma

58
Q

What kind of behaviour do yolk sac tumours exhibit?

A

Differentiate along the extraembryonic yolk sac line and make AFP.

Schiller-Duval body. (looks like a glomerulus)

Rapidly growing mass, responds well to chemo

59
Q

What kind of behaviour do choriocarcinomas exhibit?

A

Can be placental or ovarian in origin. If ovarian they are very aggressive, metastasize early, are often fatal and make HCG.

60
Q

What tumours metastasize to the ovaries often?

A

Colon, appendix, stomach, breast, pancreas

61
Q

What is a krukenburg tumour?

A

Bilateral ovarian metastases - classically mucin producing signet ring gastric carcinoma (commonly from colon, appendix, and stomach.

62
Q

What is endometriosis?

A

Ectopic endometrial tissue outside of the uterus.

63
Q

What are the consequences of endometriosis?

A

Infertility

Pelvic pain

Dysmenorrhoea

64
Q

What are the microscopic and macroscopic features of endometriosis?

A

Macroscopic: Chocolate cyst, powder burns

Microscopic: Endometrial glands and stroma, haemorrhage.

65
Q

What causes endometriosis?

A

4 theories:

Regurgitation: retrograde flow through tubes (90% of women have retrograde menstruation but 10% have endometriosis)

Benign metastasis: Spread via blood vessels/lymphatics

Metaplasia: Endometriosis arises from mesonephric remnants or pelvic mesothelium

Extrauterine stem cells: Stem cells from bone marrow differentiate into endometrial tissue

66
Q

What conditions is endometriosis associated with?

A

Ovarian clear cell carcinoma

Ovarian endometrioid adenocarcinoma along with shared PTEN and ARID1A

67
Q

Where are ectopic pregnancies most common?

A

90% are tubal

68
Q

What are the chances of an ectopic pregnancy and what increases these chances?

A

Chances are 1/200 this is increased by:

PID

Adhesion

IUD

Endometriosis

69
Q

What are the symptoms of an ectopic pregnacny?

A

Pain

Shock +/- vaginal bleeding

Death

70
Q

How should women presenting with abdominal pain +/- PV bleeding be treated?

A

Pregnant until proven otherwise.

investigate with 2x cannula and take blood for group and hold

Pregnancy test

Then medical/surgical management.

imed3003 (48 decks)

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