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Endo/Repro II Test 1 > Uterus and Endometrium > Flashcards

Uterus and Endometrium Flashcards

1
Q

What is the myometrium and endometrium?

A
  • Myometrium = tightly woven bundles of smooth muscle cells that form the wall of the uterus
  • Endometrium = glands embedded in stroma that line the internal cavity of the uterus.
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2
Q

What are the myometrium and endometrium hormonally responsive to?

A
  • Myometrium = Oxytocin during parturition (childbirth)
  • Endometrium = Sex-steroid hormones
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3
Q

A drop in _____ causes the functionalis layer to degenerate or shed due to a breakdown/bleeding into stroma.

A

Progesterone, when the CL involutes at day 15 if ovulation does not occur.

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4
Q

Proliferative phase is driven by ________ =>

A

Estrogen => proliferation of glands and stroma from the basalis to form a new functionalis

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5
Q

Features of the Proliferative phase

-Glands, stroma, mitotic figures, mucus secetion/vaculoizeation-

A
  • Glands = straight, tubular structures with regular, tall pseudostratified columnar cells
  • Stroma = actively prolifearting spindle cells with SCANT cytoplasm
  • Numerous mitotic figures
  • No mucus secretion/vacuoliztion
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6
Q

Proliferative phase ends at ______

A

ovulation

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7
Q

What hormone begins the secretory phase?

A

Progesterone downregulates of estrogen receptors in the glands and stroma => supresses proliferation

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8
Q

How does the location and histology of the secretory vacuoles change over the course of the secretory phase (post-ovulation) during the menstrual cycle?

A
    • Marked by the appearance of secretory vacuoles
  • Day 16-17: Early secretory phase with secretory Subnuclear vacuoles –> supranuclear vacuoles (3rd week of cycle)
  • Day 18-24: Glands dilate when secretion is maximal –> tortuous and serrated or “saw-toothed” by week 4
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9
Q

What stromal changes are seen in the late secretory phase of the menstrual cycle, which is IMP FOR DATING THE ENDOMETRIUM.

A
  1. Day 21-22: Prominent spiral arterioles appear + ↑ ground substance and edema btw stromal cells
  2. Day 23-4: Stromal hypertrophy –> ↑ cytoplasmic eosinophilia (predecidual change) + increase stromal mitoses
  3. Day 24-28- Predecidual changes spread throughout functionalis + sparse infiltrate of neutrophils and lymphocytes
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10
Q
  • Which hormone is responsible for driving the proliferation of glands and stroma during the proliferative phase of the menstrual cycle?
  • Between which days of the menstrual cycle will you see dilation of gland which appear tortuous and serrated or “saw-toothed?”
A
  • Estrogen
  • Day 18-24
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11
Q

“Dating” the endometrium by its histologic appearance may be used to assess hormonal status, document ovulation, and determine causes of endometrial bleeding and infertility

A
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12
Q

what may contribute to the development of ectopic endometrial tissue and endometrial cancer?

A

endometrial stem cells

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13
Q

What is the most common cause of AUB (abnormal uterine bleeding)?

A

DUB due to anovulation (failure to ovulate) due to subtle hormone imbalances => no progesterone => unopposed estrogen stimulates the endometrium.

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14
Q

Anovulation leading to dysfunctional uterine bleeding is most common during what 2 periods of a woman’s life?

A

Menarche and peri-menopausal period

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15
Q

Endocrine causes of hormonal imbanlance that can lead to anovulation?

A
  1. Thryoid,
  2. Adrenal
  3. Pituitary
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16
Q

Ovarian causes of hormonal imbanlance that can lead to anovulation?

A
  1. PCOS (Stein-Leventhal syndrome)
  2. Granuloma cell tumors
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17
Q

Metabolic causes of hormonal imbanlance that can lead to anovulation?

A
  1. Obesity
  2. Malnutrition
  3. Chronic systemic disease
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18
Q

What is the most common cause of abnormal uterine bleeding in the pre-puberty age group?

A

Precocious puberrt (hypothalamic, pituitary, or ovarin origin)

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19
Q

When their is failure of ovulation what hormonal imbalance occurs?

A

Excessive endometrial stimulation by estrogen that is unopposed by progesterone

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20
Q

What is the most common appearance of the endometrium during anovulation?

A
  1. Lacks progesterone-dependent features (glandular secretory changes and stroma pre-deciduation)
  2. Contains pseudostratified glands and scattered mitotic figures
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21
Q

What is inadequate luteal phase?

When do we see when we biopsy?

A
  • Infertility + increased bleeding or amenorrhea due to inadequare progesterone during post-ovulatory period.
  • Biopsy: slow, developing “secretory endometrium”, lagging behind for expected dates.
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22
Q

Why are the endometrium and myometrium relatively resistant to infection?

A

Endocervix forms a barrier to ascending infection

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23
Q

Acute endometritis is uncommon and caused by what?

A
  • Bacterial infections that arise after delivery or miscarriage due to retained products of conception.
  • Bacteria: Group A hemolytic strep (GAHS), staphylococci, and others
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24
Q

In acute endometritis, there is _________ of the stroma.

A

Nonspecific inflammation

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25
Q

Treatment of acute endometritis.

A

Curettage of fragments + AB (B-lactams for staph and strep)

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26
Q

What finding does the diagnosis of chronic endometritis depend on?

A

Plasma cells in the stroma of the endometrium

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27
Q

What is the MCC of chronic endometritis?

A

Ascending infection (especially chlamydia)

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28
Q

Chronic Endometritis is associated with:

A
  1. PID (mostly chylamidia)
  2. Retained gestational tissue
  3. IUD
  4. TB = rare in western countries
  5. Chylamydia
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29
Q

Chronic endometritis presentaion

A
  1. ABNL bleeding
  2. Pain
  3. Discharge
  4. Infertility
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30
Q

Pelvic TB MC infects what?

A
  1. BOTH fallopian tubes + endometrium (50%) of the time
  2. RARELY infects: [cervix, vagina, uterus]
  3. If ovaries, only surface.
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31
Q

Morphology of Pelvic TB (2)

  • Detected on what stain?
A
  1. Multinucleated giant cells
  2. Histiocytes

Seen on [Kinyoun or Ziel-Neelsen fast-acid stain]

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32
Q

What is endometriosis?

When is it most common?

A
  • Ectopic endometrial tissues seen outside of the uterus (stroma and maybe glands).
  • 30-40YO (active reproducing childbearing years)
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33
Q

Symptoms of endometriosis

A
  1. Infertility (30-40%)
  2. Severe dysmenorrhea (cramps)
  3. Colicky pelvic pain
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34
Q

List the 8 most common sites of endometriosis in descending order of frequency.

A
  1. Ovaries

2. Uterine lig.

3. Rectovaginal septum

4. Cul de sac

5. Pelvic peritoneum

  1. Large and small bowel and appendix
  2. Mucosa of cervix, vagain, and fallopian tubes
  3. Laparotomy scars
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35
Q

How does ectopic tissue form in endometriosis?

A
  1. Regurgitation theory: retrograde flow of menstrual endometrium through the fallopian tubes => implants at ectopic sites (occurs in 90% of W)
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36
Q

What is the benign metastases theory in relation to the pathogenesis of endometriosis?

A

Endometrial tissue spreads via blood and lymph to distant sites

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37
Q

What is the metaplastic theory in relation to the pathogenesis of endometriosis?

A

Endometrium arises from coelomic mesothelium or mesonephric remnant that undergo endometrial differentiation giving rise to ectopic tissue

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38
Q

What is the extrauterine stem/progenitor cell theory in relation to the pathogenesis of endometriosis?

A

Bone marrow derived stem/progenitor cells differentiate into endometrial tissue

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39
Q

How is ectopic endometrial tissue (which still undergoes menstruation) different from regular endometrial tissue?

A
  1. Ectopic endometrial stroma has high levels of the aromatase (not present in normal endometrium) => make its own estrogen => survival and persist.
  2. Secretes pro-inflammatory factors.
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40
Q

Epigenetic alterations seen in endometriosis lead to what kind of response to estrogen and progesterone?

A
  • ↑ responsivness to estrogen
  • ↓ responsivness to progesterone
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41
Q

Women with endometriosis have a 3x greater risk for development of what 2 cancers?

A

Ovarian and clear cell types

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42
Q

Endometriotic lesions bleed periodically in response to extrinsic (ovarian) and intrinsic hormones, producing what?

A

Red-blue => yellow-brown nodules on or just beneath the mucosal and/or serosal surfaces at site involved

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43
Q

When the lesions of endometriosis are extensive, organizing hemorrhage causes what?

A

Fibrous adhesions btw structures (tubes, ovaries and other structures) and obliterates the pouch of Douglas

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44
Q

What can form when ectopic endometrial tissue forms on ovaries?

A

Chocolate cysts/ endometrioma= large cysts filled with brown fluid as a result of previous hemorrhage

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45
Q

What is the significance of atypical endometriosis?

A

Precursor to cancer (endometrosis-related ovarian and cell cell carcinoma)

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46
Q

Based on histology what must be present for the diagnosis of endometriosis to be readily made?

A

When both endometrial GLANDS and STROMA are present, with or without hemosiderin.

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47
Q

Why might a patient with endometriosis present with pain during defecation or dysuria?

A

Involvement of the

  • Rectal wall = pain on defecation
  • Bladder serosa = dysuria
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48
Q

Treatment of endometriosis?

A

Aromatase inhibitors or surgery

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49
Q

What is adenomyosis?

A

Endometrial tissue WITHIN the uterine wall (myometrium) that can co-exist with endometriosis.

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50
Q

What is seen on microscopic examination of adenomyosis?

A

Irregular nests of endometrial stroma, w/ or w/o glands, arranged within myometrium, separated from basalis by at least 2-3mm

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51
Q

What is the appearance of endometrial polyps?

MC when?

A
  • Exophytic masses (single or multiple) and usually sessile in the endometrial cavity.
  • Occasionally large and pedunculated
  • Reproductive age, peri and postmenopausal F.
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52
Q

Endometrial polyps may become hyperplastic in association with what; what is their response to hormones?

A
  • In assoc. w/ generalized endometrial hyperplasia
  • Responsive to estrogen but show little or no response to progesterone
53
Q

Endometrial polyps have been observed in association with what drug?

A

Tamoxifen, used in breast cancer therapy due to its anti-estrogenic activity on the breast; has weak pro-estrogenic effects on endometrium

54
Q

Endometrial hyperplasia is defined as an increase in the proliferation of what?

A

↑ proliferation of glands relative to the stroma = ↑ gland:stroma ratio due to prolonged estrogenic stimulation of the endometrium,

55
Q

Endometrial hyperplasia is an important cause of ____________ and is also important due to what?

A
  • Abnormal bleeding
  • Frequent precursor to the most common type of endometrial carcinoma
56
Q

What associated clinicopathologic and epidemiologic conditions cause increased estrogen, which can lead to endometrial hyperplasia?

A
  1. Anovulation
  2. Obesity = peripheral conversion of androgens –> estrogens
  3. Menopause
  4. Prolonged administration of estrogenic substances (estrogen replacement therapy)
  • Polycystic ovarian syndrome
  • Granulosa cell tumor of the ovary
  • Excessive ovarian corticalfunction (cortical stromal hyperplasia)
57
Q

What mutation is a common in both endometrial hyperplasia and endometrial carcinomas; which pathway does this regulate?

A
  • PTEN, a tumor supressor that regulates PI3K/AKT pathway
  • Loss of PTEN => overactivation of PI3K/AKT pathway
58
Q

Which AD disorder is due to germline mutations of PTEN and is associated with high incidence of endometrial carcinoma and breast cancers?

A

Cowden syndrome (multiple harmatoma syndrome)

59
Q

What is the relation of the PI3K/AKT pathway to estrogen?

A

PI3K/AKT signaling enhances the ability of the estrogen receptor to stimulate gene expression in target

60
Q

Is the loss of PTEN seen in endometrial hyperplasia predictive of progression to carcinoma?

A

NO

61
Q

What are the 2 major categories of endometrial hyperplasia (precursor lesions) recommended by the WHO?

A
  1. Non-atypical hyperplasia
  2. Atypical hyperplasia (aka endometrial intraepithelial neoplasia)
62
Q

Cardinal morphological feature of non-atypical hyperplasia of the endometrium

A

- ↑ in gland-to-stroma ratio due to persistant estrogen stimulation

  • Glands MAY be back-to-back, but usually there is intervening stroma
63
Q

What is the likelihood of non-atypical hyperplasia of the endometrium progressing to adenocarcinoma; what may be seen morphologically when estrogen is withdrawn?

A
  • Rarely progress to cancer (1-3%)
  • When estrogen with withdrawn after menopause => undergoes cystic atrophy
64
Q

What are the morphological and cellular features (chromatin and nucleoli) which encompass atypical hyperplasia (EIN) of the endometrium? (4)

A
  1. Complex pattern of proliferating gland with nuclear atypia
    1. Back-to-back glands that branch
    2. Loss of orientation of nuclei to BM
    3. Chromatin is open (vesicular) chromatin
    4. Conspicuous nucleoli
65
Q

Morphology of atypical hyperplasia of the endometrium IS VERY SIMILAR to well-differentiated endometrioid adenocarcinoma; how can the distinction be made?

A

May not be possible without hysterectomy, where 1/2 patients are found to have cancer.

66
Q

In patients who want to be fertile, how do we treat endometrial intraepithelial neoplasia (EIN)?

A
  • Progesterone therapy and close follow up.
  • If it does NOT regress => hysterectomy
67
Q

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

  • Peak age
  • Earliest sign
A

Endometrial adenocarinoma

  • 55-65 YO
  • Vaginal bleeding in older women
68
Q

Of the 2 classifications of endometrial carcinoma, which is the most common type accounting for 80% of cases?

A

Type I (endometriod) Adenocarcinoma

69
Q

5 disorders associated with development of Type 1 (endometriod) Endometrial Carcinoma?

A
  1. Obesity
  2. DB (abnormal GTT in 60%)
  3. HTN
  4. Infertility
  5. Unopposed estrogen stimuulation
70
Q

Type 1 Endometroid Carcinoma

  • Age
  • Morphology
  • Precursor
  • Mutated genges
  • Behavior
A
  • Age = 55-65YO
  • Morphology = endometriod (most are well-differentiated and mimic endometrial glands)
  • Precursor= atypical hyperplasia
  • Mutated genes = MSI
  • Behavior= low grade, indolent, spreads via lymphatics
71
Q

Type 2 Serous Carcinoma

  1. Age
  2. Morphology
  3. Precursor
  4. Mutated genes
  5. Behavior
A
  1. Age: 65-75 YO; more common in AA
  2. Morphology: Poorly-differentiated; [Serous, clear cell or mixed mullerian tumor]
  3. Precursor: serous endometrial intraepithelial carcinoma
  4. Mutated genes
  5. Behavior: aggressive and spreads intraperitoneal and lymphatcs
72
Q

What is the hallmark mutation associated with type I endometrial carcinoma?

A

Multiple mutations => ↑ signaling via PI3K/AKT pathway => increase sensitivity to estrogen.

73
Q

What mutation is commonly found in: [type I endometrial carcinoma, ovarian endometroid AND clear cell carcinomas that arise in endometriosis]?

A

LOF of ARID1A

74
Q

Why are endometrial carcinomas common in women from families w/ HNPCC (aka Lynch Syndrome)?

A

Epigenetic silencing (hypermethylation) of DNA mismatch repair genes

75
Q

What mutation has a important role in the INVASION of type 1 endometrial carcinomas?

A

activation of PIK3CA oncogene

76
Q

In sporadic endometrioid carcinomas, loss of expression of DNA mismatch repair genes is commonly caused by what? (like in Lynch Syndrome)

A

Epigenetic silencing (via promoter hypermethylation)

77
Q

What does Endometroid carcinoma (Type 1) typically look like?

A
  • Localized polypoid tumor or one that diffusely infiltrates the endometrial lining
78
Q

How does Endometriod carcinoma spread?

A
  1. Myometrial invasion => direct extension into adjacent structures =>
    1. If broad ligament=> palpable
  2. Regional LN => lymphatics to lungs, liver bone.
79
Q

How is Endometroid Adenocarcinoma graded histologically ?

A
  1. Grade 1 = well-differentiated, well-formed lgands
  2. Grade 2 = Moderately differentiated, well formed glands + solid sheets of cells causing < 50% solid growth
  3. Grade 3 = Poorly differentiated with 50% solid growth
80
Q

Well- differentiated endometrial carcinomas may be differentiated from hyperplasia by what?

A

Cancer has lack of intervening stroma btw glands (top right)

81
Q

Stage I-IV for [Type I and II Endometrial Adenocarcinoma] & [malignant mixed mullerian tumor]

A
  • Stage I: confined to corpus uteri
  • Stage II: involves corpus AND cervix
  • Stage III: extends outside the uterus, but NOT outside true pelvis
  • Stage IV: extends outside the true pelvis or involves mucosa of bladder or rectum
82
Q

A 52 year old Caucasian female presents with abnormal vaginal bleeding. Menarche age 12, last normal menstrual period age 49. Pap smear history normal. PE: BMI 32, BP 140/92, Pulse 85, normal external genitalia, uterus slightly enlarged on bimanual exam. Hgb 10 g/dl. Transvaginal ultrasound reveals endometrial thickness of 14mm (normal 8-11), and endometrial biopsy performed. Most likely diagnosis in this setting?

A

Type 1 Endometriod Adeno

- white, between 55-65, obese-

83
Q

Type II (serous) endometrial carcinoma is most in who?

A

African-Americans

84
Q

Type II endometrial carcinoma typically arises in the setting of _________

A

Endometrial atrophy => Serous endometrial intraepithelial carcinoma (precursor lesion)

85
Q

What are the 3 morphological subtypes of type II endometrial carcinoma and which is most common?

A
  1. Serous = most common
  2. Clear cell
  3. Mixed müllerian tumor
86
Q

Type II endometrial carcinomas are by definition what grade of tumor?

At presentation, already spread where?

A
  • Poorly differentiated (Grade 3) with poor prognosis bc travel through fallopian tube => implants on peritoneal
  • Uterus
87
Q

Mutations in what gene are seen in at least 90% of type II (serous) endometrial carcinomas; what does this mutation cause?

A

- TP53 missense mutations

  • Mutations results in accumulation of the altered protein in the nucleus
88
Q

What is the precursor of type II (serous) endometrial carcinoma and what can be this lesion be stained for immunohistochemically?

A
  • Serous endometrial INTRAepithelial carcinoma (pic top left)
  • Can stain for TP53 (pics on right)
89
Q

What is the behavior of type II (serous) endometrial carcinomas and how does it spread?

A
  • Aggressive, when found already attacks uterus
  • Intraperitoneal –> travel through fallopian tubes and implants on peritoneal surfaces and lymphatic spread
90
Q

What is necessary for establishing the diagnosis of endometrial carcinoma?

A

Histological examination of tissue obtained by biopsy or curettage

91
Q

What is the 5-year prognosis for stage I (grade 1 or 2) endometrial carcinomas following surgery +/- irradiation?

A

90% = excellent

92
Q

What makes serous endometrial intraepithelial carcinoma a pre-malignant lesion if the cells are the same as serous carcinoma?

A

Confined to epithelial surface and HAS NOT invaded stroma.

93
Q

What is the morphology of Type II serous endometrial carcinoma?

A
  1. Papillary like growth-pattern
  2. Malignant cells with cytologic atypia: high nuclear:cytoplasmic ratios, atypical mitotic figures, hyperchromasia, prominent nucleoli.
94
Q

Some type II (serous) endometrial carcinomas will have a predominantly glandular growth pattern; how can they be distinguished from type I (endometrioid) carcinoma?

A

Marked cytologic atypia

95
Q

If a women has endometrial cancer and presents with post-menopausal bleeding, we can often assure her that what?

A

Can be cured bc often leads to early detection

96
Q

What are malignant mixed müllerian tumors (aka carcinosarcomas)?

A

Endometrial adenocarcinomas w/ a malignant mesenchyma component (has malignant glandular + mesechynak cells)

97
Q

The epithelial and stromal components of malignant mixed müllerian tumors are derived from what?

A

The same founding cell

98
Q

Which genes are involved in malignant mixed müllerian tumors?

A

Same genes mutated in endometrial carcinomas, such as PTEN, TP53, and PIK3CA

99
Q

What is the gross morphology and size of malignant mixed müllerian tumors?

Histo?

A

Often bulky and polypoid, and may protrude through the cervical os

  • Glandular (adenocarcinoma) + sarcomatous (malignant mesenchymal) elements
100
Q

The sarcomatous component of malignant mixed müllerian tumors may mimic what tissues?

Outcome?

A

Heterogenous elements = Striated muscle, cartilage, adipose tissue, and bone = worse outcome

101
Q

Metastases from m_alignant mixed müllerian tumors_ usually contain which component of the tumor?

A

Epithelial components

102
Q

What is the common presentation and in whom for malignant mixed müllerian tumors?

A

Postmenopausal female w/ bleeding

103
Q

The outcome/prognosis of malignant mixed müllerian tumors is dependent on what?

Which has the WORST prognosis?

A
  • Depth of invasion AND stage ****
  • Also the differentiation of the mesenchymal component
  • Heterologous mesenchymal components = worse prognosis
104
Q

Genetically, what do malignant mixed mullerian tumors (MMMTs) resemble genetically?

survival?

A

Endometrial carcinoma; POOR outcome (25-30% 5year survival if high stage)

105
Q

Diagnosis of adenosarcomas of the endometrium is dependent on the finding of a tumor composed of what?

A

Malignant-appearing stroma, which coexists w/ benign but abnormally shaped endometrial glands

106
Q

What type of malignancy are adenosarcomas?

A

Low grade

107
Q

How do adenosarcomas of the endometrium most typically present and what is the principle diagnostic dilemma w/ these tumors?

A

- Large, broad, polypoid growths that can prolapse thru the cervical os

  • Dilemma = distinguishing these tumors from large benign polyps
108
Q

Why is it important to make the distinction between adenosarcomas and large benign polyps of the endometrium?

A

Adenosarcoma is estrogen-sensitive and responds to oophorectomy

109
Q

Endometrial stromal neoplasms are divided into what 2 categories?

A

1) Benign stromal nodules = well-circumscribed
2) Endometrial stormal sarcomas (high- or low-grade)

110
Q

Endometrial stromal sarcomas are associated with translocations that create fusion genes.

Which chromosomal translocation has been linked to low-grade endometrial stromal sarcomas?

A

JAZF1-SUZ12 fusion gene

111
Q

Which benign neoplasm of the myometrium is perhaps the most common tumor in women?

A

Uterine leiomyomas (fibroids) = Smooth m. neoplasm

112
Q

How do leiomyomas most often present and there is an increased incidence in which ethnic group?

A

Most often presents as multiple, well-circumscribed grey-white benign tumors

  • ↑ incidence in African Americans
113
Q

Rearrangements of what chromosomes and involving what genes implicated in other benign neoplasms are seen in about 40% of leiomyomas?

A

Cr. 12q14 and 6p –> HMGIC and HMGIY

114
Q

Mutation of _______ => allows uncontrollable cell division has been implicated in 70% of leiomyomas (fibroid)?

A

MED12, a mediator that controls cell division

115
Q

Leiomyomas that occur beneath endometrium => _____

A

Submucosal

116
Q

What are the characteristic microscopic features which distinguish leiomyomas? (3)

A
    • Bundles of whorled smooth m. cells, which are uniform in size and shape
    • Oval nucleus + long bipolar cytoplasmic processes
    • RARE mitotic figures
117
Q

How can we distinguish leiomyomas from leimyosarcomas?

A

Leiomyomas have SCARCE mitotic figures.

118
Q

What is the typical clinical presentation of leiomyomas?

A
  • Often asymptomatic
  • Common sx’s: [abnormal bleeding] + [urinary frequency (bc compressed bladder)] + [_sudden pain]_from infarction of a large or pedunculated tumor and [impaired fertility]
119
Q

What are the complications which may arise due to leiomyomas in a pregnant woman?

A
  1. ↑ frequency of
    1. Spontaneous abortion
    2. Fetal malpresentation
    3. Uterine inertia (failure to contract w/ sufficient force)
    4. Post-partum hemorrhage
120
Q

What is the likelihood of a leiomyoma undergoing malignant transformation to a leiomyosarcoma?

A

Extremely rare

121
Q

How does the karyotype of leiomyosarcomas differ from that of leiomyomas?

A
  • Leiomyosarcoma = complex, highly variable karyotypes that frequently include deletions; subset contains MED12 mutations
  • Leiomyomas = normal karyotypes
122
Q

What are leiomysosarcomas?

MC occur when?

A
  • Uncommon, malignant neoplasms that arise from myometrium or endometrial stromal precursor cells (RARELY from leiomyomoas).
    • STUMP = smooth muscle tumor of uncertain malignant potential
  • 40-60YO (before and after menopause)
123
Q

What mutations are virtually unique to uterine smooth muscle tumors?

A

MED12

124
Q

What are the 2 distinct patterns by which leiomyosarcomas grow within the uterus?

A

1) Bulky, fleshy masses that invade uterine wall
2) Polypoid masses that project into uterine lumen

125
Q

Distinction of leiomyosarcoma from leiomyoma is based on what cellular features?

A

Nuclear atypia + mitotic index + zonal necrosis

126
Q

What is the behavior and prognosis of leiomyosarcomas like?

A
  • OFTEN recur after surgey
  • > 50% metastasize hematogenously —> lungs, bone, and brain; may also disseminate throughout abdominal cavity
  • Overall 5-year survival = 40%, but anaplastic lesions = 10-15%
127
Q

Based on the anatomy why do leiomyosarcomas often metastasize to the lung?

A

Tumor invades uterine vein and goes straight to lungs

128
Q

Leiomyosarcomas are malignant if:

A
  1. 10 mitosis/hpf
  2. 5 mitosis/hpf + nuclear atypia or large cells.

Endo/Repro II Test 1 (23 decks)

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