Chapter 19: Uterus, Fallopian Tubus and Ovaries Flashcards

1
Q

What is meant by adenomyosis?

A

The presence of endometrial tissue in the myemetrium. (Here, nests of endometrial stroma, glands or both are found deep in the myometrium interposed between muscle bundles.)

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

What results from adenomyosis?

A

It induces reactive hypertrophy of the myometrium, resulting in an enlarged globular utereus, often with a thickened uterine wall.

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

What is endometriosis?

A

The presence of endometrial glands and stroma in a location outside the uterus.

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

What pelvic structures can be involved in endometriosis (don’t learn by heart)

A

Ovaries, pouch of Douglas, uterine ligaments, tubes and rectovaginal septum. Less frequently, distant areas of the peritoneal cavity of periumbilical tissues are involved. Uncommonly, distant sites such as lymph nodes, lungs and even heart, skeletal muscle, or bone are affected.

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

Four hypotheses have been put forth to explain the origin of dispersed endometriotic lesions (endometriosis). Describe the four theories (regurgitation, beign metastases, metaplastic and extrauterine stem cell theory).

A

-Regurgitation theory proposes that menstrual backflow through the fallopian tubes leads to implantation. -Benign metastases theory proposes that endometrial tissue from the uterus can spread to distant sites via blood vessels and lymphatics. -Metaplastic theory says that endometrial differentiation of coelomic epithelium is the source. -Extrauterine stem cell theory proposes that circulating stem cells from the bone marrow differentiatie into endometrial tissue.

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

Is endometriotic tissue in endometriosis only misplaced or is something else also wrong?

A

It is also abnormal, it exhibits increased levels of inflammatory mediators (PGE2) (results from recruitment and activation of macrophages by factors made by endometrial stromal cells.)

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

What factors lead to enhancement of survival and persistence of endometriotic tissue within a foreign location?

A

Inflammation by inflammatory mediators such as PGE2. But most importantly, stromal cells that produce aromatase. Aromatase stimulates estrogen production, which are important for survival and peristence of endometriotic tissue within a foreign location.

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

Describe morphological characterisations of endometriosis.

A

-It consists of functioning endometrium, which undergoes cyclic bleeding. -They appear grossly as red-brown nodules because of blood build up. -They range in size from microscopic to 1 to 2 cm in diameter.

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

What is a chocolate cyst?

A

When the ovaries are involved, the lesions may form large, blood-filled cysts that turn brown as the blood ages.

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

What is a result of endometriosis and its cyclic bleeding?

A

Fibrosis, leading to adhesions among pelvic structures, sealing of the tubal fimbriated ends, and distortion of the fallopian tubes and ovaries.

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

Just read

A

Abnormal uterine bleeding: -Menorrhagia = profuse or prolonged bleeding at the time of the period. -Metrorrhagia = irregular bleeding between periods -Postmenopausal bleeding

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

What are the most common proliferative lesions of the uterine corpus?

A

Endometrial hyperplasia, endometrial carcinoma, endometrial polyps and smooth muscle tumors.

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

What can induce hyperplasia of the endometrium?

A

An excess of estrogen relative to progestin (if sufficiently prolonged or marked).

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

What is a common cause of estrogen excess?

A

Obesity, adipose tissue converts steriod precursors into estrogens. (Other causes are failure of ovulation, administration of estrogenic steroids without counterbalancing progestin and estrogenproducing ovarian lesions).

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

Why is endometrial hyperplasia placed into two categories (hyperplasia with and without atypia)?

A

The importance of this classification is that the presence of cytologic atypia correlates with the development or concurrent finding of endometrial carcinoma. So hyperplasia with atypia has a much higher risk.

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

In this picture you can see endometrial hyperplasia. Is this hyperplasia with or without atypia?

A

This is hyperplasia without atypia, you can see nests of closely packed glands (so you can still see some organized structures).

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

In this picture you can see endometrial hyperplasia. Is this hyperplasia with or without atypia?

A

This is hyperplasia with atypia, there’s glandular crowding (no organization) and cellular atypia.

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

Fill in: Endometrioid cancers arise in association with … (1) excess in the setting of endometrial … (2) in perimenopausal women, whereas serous cancers arise in the setting of endometrial … (3) in older postmenopausal women.

A
  1. estrogen 2. hyperplasia 3. atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Just read

A

The endometrioid type accounts for 80% of cases of endometrial carcinomas. These tumors are designated as endometrioid because of their histologic similarity to normal endometrial glands. Risk factors for this type of carcinoma include (1) obesity, (2) diabetes, (3) hypertension, (4) infertility, and (5) exposure to unopposed estrogen. Many of these risk factors result in increased estrogenic stimulation of the endometrium and are associated with endometrial hyperplasia.

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

What genes are mutated in early events in the stepwise development of endometrioid carcinoma?

A

Mismatch repair genes and the tumor suppressor gene PTEN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What genes are mutated in the serous type of endometrial carcinoma?

A

TP53 tumor suppressor gene, but mutations in DNA mismatch repair genes and PTEN are rare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is meant by exophytic?

A

Solid organ lesions arising from the outer surface of the organ of origin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What kind of endometrial carcinoma can be seen in this picture?

A

Endometrioid type, grade I, infiltrating myometrium and growing in glandular pattern (infiltrative).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What kind of endometrial carcinoma can be seen in this picture and what specific features?

A

Endometrioid type, grade 3, has a predominantly solid growth pattern (exophytic). And has severe atypia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What kind of endometrial carcinoma can be seen in this picture and what specific features?

A

Serous carcinoma of the endometrium, with papilla formation and marked cytologic atypia. There’s also nuclear pleomorphism, loss of polarity and an atrophic background.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Although endometrial polyps may occur at any age, they are most common…

A

Around the menopause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are riskfactors of endometrial polyps?

A

Obesity, late menopause and the use of tamoxifen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are leiomyomas and why are leiomyomas sometimes called fibroids?

A

Benign tumors that arise from the smooth muscle cells in the myometrium. They’re called fibroids because of their firmess.

29
Q

What are macroscopic and microscopic morphological characterisations of leiomyomas? (don’t learn this by heart)

A

Macroscopical leiomyomas are typically sharply circumscribed, firm gray-white masses with a characteristic whorled cut surface. They may occur singly, but more often occur as multiple tumors that are scattered within the uterus, ranging from small nodules to large tumors. Microscopically a leiomyoma appears as normal bundles of smooth muscle cells.

30
Q

Leiomyosarcomas differ from leiomyomas in some ways. What are these?

A

Leimyosarcomas arise from mesenchymal cells of the myometrium, they are almost always solitary and most often occur in postmenopausal women.

31
Q

What are three (histological) diagnostic features of leiomyosarcomas?

A

Tumor necrosis, cytologic atypia and mitotic acitivty.

32
Q

What can result from primary adenocarcinoma of the fallopian tube?

A

High-grade serous carcinomas, the fallopian tube may be the site of origin for many of the high-grade serous carcinoma long thought to arise in the ovary.

33
Q

From what anatomic structure do most of ovarian tumors arise from?

A

From the fallopian tube or epithelial cysts in the cortex of the ovary

34
Q

How can an epithelial cyst evolve into an ovarian tumor?

A

The epithelium lining the cysts may be derived from displaced ovarian surface epithelium or the lining of fallopian tube. These can become metaplastic or undergo neoplastic transformation to give rise to a number of different epithelial tumors.

35
Q

What is a cystademo?

A

Benign lesions that are cystic

36
Q

What is a cystadenofibroma?

A

Benign lesions that are cystic and are accompenied by a stromal component.

37
Q

What is a cysadenocarcinoma?

A

A cystic malignant tumor

38
Q

What is carcinoma?

A

Solid tumor

39
Q

What are borderline tumors?

A

Ovarian epithelial tumors that fall into an intermediate category (partly cystic, partly solid). They are usually benign, but can progress to carcinoma.

40
Q

What are risk factors of ovarian carcinoma?

A

Nulliparity (women who has never given birth), obesitas (due to estrogens), positive family history and germline mutations,(BRCA1 and 2 mutations), pregnancy/multiparity.

41
Q

How common and malignant are serous tumors?

A

They are the most common of the ovarian epithelial tumors and also make up the greatest fraction of malignant ovarian tumors (60% benign, 15% borderline, 25% malignant)

42
Q

What two types of serous carcinomas are there?

A

Low-grade and high-grade.

43
Q

How do low-grade serous carcinomas develop? What mutations accompany this development?

A

They arise in a stepwise manner to becoma invasive carcinoma. Mutations are in genes encoding signalling proteins, such as KRAS.

44
Q

How do high-grade serous carcinomas develop? What mutations accompany this development?

A

These type of tumors develop rapidly, they arise in the fimbriated end of the fallopian tubes. TP53 mutations are very common (also NF1 and RB, BRCA1 and 2).

45
Q

What is meant by the fact that about 25% of benign serous tumors are bilateral?

A

Cancer that occurs in both of a pair of organs, such as the ovaries.

46
Q

What is the difference between benign tumors and malignant serosal tumors?

A

In benign tumors, the serosal covering is smooth. The surface of adenocarcinomas has nodular irregularities. Also papillary projections are more common in malignant tumors.

47
Q

What are morphological/histological characterisations of benign serous tumors?

A

They contain a single layer of columnar epithelial cells (often ciliated) that line the cyst. In tips of pappilae, there are psammoma bodies (calcified concretions).

48
Q

What are morphological/histological characterisations of malignant serous tumors?

A

Here, cells are atypical, the pappilae are complex and multilayered and by definition nests or sheets of malignant cells invade the ovarian stroma.

49
Q

How do mucinous tumors differ from serous tumors?

A

The epithelium of mucinous tumors consists of mucin-secreting cells and these tumors arre less likeley to be malignant (only 10%)

50
Q

What is a krukenberg tumor?

A

A tumor that primary originates from metastasis of a mucinous adenocarcinoma from a gastrointestinal tract.

51
Q

Describe features of an endometrioid tumor.

A

Tumor is solid or cystic, sometimes develop in association with endometriosis. Within the lining of cystic spaces they from tubular glands.

52
Q

Which genes are frequently mutated in endometrioid tumors?

A

PTEN tumor suprressor gene, signaling gene PI3K-AKT.

53
Q

What is a teratoma?

A

They are germ cell tumors, they arise in the first 2 decades of life (the earlier, the more malignant).

54
Q

What is a characteristic of a benign (mature) cystic teratoma?

A

Tissue is dervied from all three germ cell layers: ecto-, endo-, mesoderm. (On cut section, they often are filled with sebaceous secretion and matted hair that, when removed, reveal a hair-bearing epidermal lining Sometimes there is a nodular projection from which teeth protrude. Occasionally, foci of bone and cartilage, nests of bronchial or gastrointestinal epithelium, or other tissues are present.)

55
Q

What are features of an immature malignant teratoma?

A

They are found early in life, typically bulky and appear solid on cut section and they often contain areas of necrosis.

56
Q

What does benign/usual hyperplasia of the endometrium look like?

A

It occurs after long term estrogen stimulation and looks almost normal as proliferative endometrium. Besides this it has a low risk to develop in endometrial cancer.

57
Q

What is seen when immunohistochemistry is performed on hyperplasia with atypia?

A

Inactivation of PTEN (it shows about 50% loss of PTEN.

58
Q

What adenocarcinoma is most common of all endometrial carcinomas (mucinous, squamous cell, clear cell, endometrioid, serous adenocarcinoma)?

A

Endometrioid adenocarcinoma

59
Q

What are risk factors for endometrial carcinoma (think of major and minor risk factors)? (don’t learn this by heart)

A

Major: obesitas, diabetes, hypertension, infertility, estrogen exposure. Minor: germline mutations, mutations in PTEN and DNA mismatch repair genes

60
Q

How is an endometrial carcinoma graded? Describe the three grades.

A

Based on the percentage of solid growth.

Grade 1 = well differentiated = 1-5% solid growth

Grade 2 = moderately differentiated = 6-50% solid growth

Grade 3 = poorly differentiated = >50% solid growth

61
Q

What is another name for hyperplasia with atypia?

A

Endometrial intraepithelial neoplasia (EIN)

62
Q

Name characterisations of endometrioid carcinoma (don’t learn this by heart)

A

Often grade 1, looks like normal endometrium, squamous or mucinous differentiation, low mitotic activity, atypical hyperplasia.

63
Q

What is seen when immunohistochemistry is performed on endometrioid type carcinoma?

A

P16 patchy (tumor suppressor), ER+ and p53 wild type (normal).

64
Q

What can arise from endometrial carcinoma grade 3?

A

Serous carcinoma or clear cell carcinoma

65
Q

What can be seen in clear cell carcinoma (grade 3 endometrial carcinoma)?

A

Clear cells with distinct borders (glycogen+), nuclear atypia, round/cystic spaced.

66
Q

What is hobnailing?

A

A hobnail cell is a cell with a characteristic appearance, including a bulbous nucleus and nuclear projections into the cytoplasm

67
Q

Serous tumors are often bilateral and contain psamomma bodies. They are classified under benign, borderline or malignant. Describe the histological features of these types of serous tumors.

A

Benign: unilocular cyst (single-chambered/one cavity), no atypia Borderline: more complex papillary structures, little atypia Malignant: high-grade atypia, high mitotic rate.

68
Q

What is the most common malignant uterine tumor?

a) Endometrial stromacel sarcoma
b) Leiomyosarcoma
c) Endometrial carcinoma
d) Serous carcinoma

A

(c) Endometrial carcinoma