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Endo/Repro > Uterus - Hyperplasia, Malignant tumors of Endometrium, Stroma, and Myometrium & Fallopian Tubes > Flashcards

Uterus - Hyperplasia, Malignant tumors of Endometrium, Stroma, and Myometrium & Fallopian Tubes Flashcards

1
Q

What is endometrial hyperplasia defined as?

A
  • An increase in the number of glands relative to the stroma, appreciated as crowded glands, often with abnormal shapes
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2
Q

What causes endometrial hyperplasia?

A
  • The balance between estrogen and progesterone is disturbed, resulting in absolute or relative increases in the amount of estrogen, with consequent hyperplasia of the endometrial glands
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3
Q

What does endometrial hyperplasia cause?

A
  • Abnormal uterine bleeding
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4
Q

What conditions cause increased estrogen?

A
  • Anovulation
  • Obesity
  • Menopause
  • Prolonged administration of estrogenic substances
  • Polycystic ovarian syndrome
  • Excessive ovarian cortical funciton
  • Functioning ovarian tumors
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5
Q

What is a common genetic alteration seen in endometrial hyperplasia and endometrial cancer?

A
  • Inactivation of PTEN tumor suppressor gene
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6
Q

What is Cowden syndrome?

A
  • Multiple hamartoma syndrome

- Germline PTEN mutation and high incidence of endometrial and breast cancer

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7
Q

What does a loss of PTEN lead to?

A
  • Overactivation of the PI3K/AKT pathway
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8
Q

What does the PI3K/AKT pathway do?

A
  • Up-regulates the activity of glucose transporters and multiple glycolytic enzymes, thus increasing glycolysis
  • Promotes shunting of mitochondrial intermediates to pathways leading to lipid biosynthesis
  • Stimulates factors that are required for protein synthesis
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9
Q

What are the two major types of endometrial hyperplasia?

A
  1. Typical hyperplasia

2. Atypical hyperplasia

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10
Q

What is the cardinal feature of typical hyperplasia?

A
  • Increase in gland to stromal ratio
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11
Q

What are some features of typical hyperplasia?

A
  • Variation in size and shape of glands (dilated)
  • Can be back to back glands but usually intervening stroma remains
  • Rarely progresses to cancer
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12
Q

What is seen in atypical hyperplasia?

A
  • Complex pattern of proliferating glands displaying nuclear atypia
  • Glands are back to back and branching
  • Loss of orientation of nuclei to basement membrane
  • Nuclear chromatin open
  • Conspicuous nuclei
  • Overlap with well differentiated cancer
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13
Q

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

A
  • Endometrial cancer
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14
Q

What is the peak age for type 1 endometrial cancer?

A
  • 55-60
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15
Q

What are some clinical features of endometrial cancer?

A
  • No screening test available
  • May be asymptomatic for a period, usually produces irregular or postmenopausal bleeding which helps lead to early detection and cures
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16
Q

How is a diagnosis made in endometrial cancer?

A
  • Histologic examination of tissue obtained by biopsy or curettage
  • Analyzed for evidence of DNS mismatch repair defects because 3%-5% of women with endometrial cancer have Lynch syndrome and are at high risk for colon cancer
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17
Q

What is the peak age for type 2 endometrial cancer?

A
  • 65-75
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18
Q

What is the clinical setting for type 1 endometrial cancer?

A
  • Unopposed estrogen
  • Obesity
  • Hypertension
  • Diabetes (abnormal GTT in 60%)
  • Infertility
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19
Q

What is the clinical setting for type 2 endometrial cancer?

A
  • Atrophy

- Thin physique

20
Q

What is the morphology of type 1 endometrial cancer?

A
  • Endometrioid
21
Q

What is the morphology of type 2 endometrial cancer?

A
  • Serous
  • Clear cell
  • Mixed Müllerian tumor
22
Q

What is the precursor lesion in type 1 endometrial cancer?

A
  • Hyperplasia
23
Q

What is the precursor lesion in type 2 endometrial cancer?

A
  • Serous endometrial intraepithelial carcinoma
24
Q

What mutated genes are seen in type 1 endometrial cancer?

A
  • PTEN

- MSI

25
Q

What mutated genes are seen in type 2 endometrial cancer?

A
  • TP53
26
Q

What is the behavior of type 1 endometrial cancer?

A
  • Indolent

- Spreads via lympatics

27
Q

What is the behavior of type 2 endometrial cancer?

A
  • Aggressive

- Intraperitoneal and lymphatic spread

28
Q

What are the different stages of endometrial cancer?

A
  • Stage 1: confined to corpus uteri itself
  • Stage 2: Involves the corpus and the cervix
  • Stage 3: Extends outside the uterus but not outside the true pelvis
  • Stage 4: Extends outside the true pelvis or involves the mucosa of the bladder or rectum
29
Q

What are malignant mixed müllerian tumors?

A
  • Endometrial adenocarcinomas with a malignant mesenchymal component
  • Mutations similar to endometrial carcinomas in the epithelial component (TP53, PTEN, PIK3CA)
  • Sarcomatous mesenchymal component
30
Q

What is the presentation of malignant mixed müllerian tumors?

A
  • Postmenopausal bleeding
  • Outcomes depend on depth of invasion and stage
  • Heterologous elements (cartilage, muscle, adipose tissue, bone) = worse outcome
31
Q

What genes are involved in leiomyoma?

A
  • HMGIC and HMGIY

- MED12 in 70% (encodes a component of Mediator which allows cells to divide in an uncontrolled way)

32
Q

What are the gross features of a leiomyoma?

A
  • Sharply circumscribed
  • Single of multiple
  • Small or large
  • Firm grey-white mass
  • Subswersal, myometrial, submucosal
  • Rarely uterine ligaments, LUS, or cervix
33
Q

What are some microscopic features of leiomyoma?

A
  • Bundles of smooth muscle cells
  • Uniform in size and shape, oval nucleus, long bipolar processes
  • Rare mitoses
  • Can degenerate
34
Q

What are some clinical signs of a leiomyoma?

A
  • Even when large, could be asymptomatic
  • Abnormal bleeding
  • Urinary frequency
  • Sudden pain from infarction of a large or pedunculated tumor
  • Impaired fertility
35
Q

What do leiomyomas cause in pregnant women?

A
  • Increase the frequency of spontaneous abortion/premature delivery, fetal malpresentation, uterine inertia, and postpartum hemorrhage
36
Q

Do leiomyomas transform to leiomyosarcomas?

A
  • Rarely
37
Q

What are some features of leiomyosarcomas?

A
  • Uncommon
  • Peak age 40-60
  • Arise from myometrium or a stromal precursor cell
  • Complex karyotypes that include deletions (also the MED12)
  • Recurrence common
  • More than half metastasize
38
Q

What are some microscopic features of a leiomyosarcoma?

A
  • Nuclear atypia
  • Increased mitotic index (10 or greater is diagnostic) = malignant
  • Zonal necrosis
39
Q

What is the outcome for leiomyosarcoma?

A
  • 5 year survival is 40%

- High grade tumors only 10%-15%

40
Q

Why is lung the most common site of mets for leiomyosarcoma?

A
  • Uterine vein goes up to the IVC which goes to the lung
41
Q

What are the major disorders that affect the fallopian tubes?

A
  • Infections associated inflammatory conditions
  • Ectopic pregnancy
  • Endometriosis
42
Q

What are the most common bacteria that cause infection in the fallopian tubes?

A
  • N. gonorrhea in 60%

- Chlamydia in the rest

43
Q

What is tuberculous salpingitis?

A
  • Rare in this country
  • Cause of infertility where endemic
  • Have necrotizing granulomas
44
Q

What is the most common primary lesion of the fallopian tube?

A
  • Translucent cysts that are filled with a clear serous fluid calle paratubal cysts
  • If found near the fimbriated end of the tube, they are call hydatids of Morgagni
45
Q

What is a benign tumor of the fallopian tubes?

A
  • Adenomatoid tumors (mesothelioma)
46
Q

What is a malignant tumor of the fallopian tubes?

A
  • Primary adenocarcinoma of the fallopian tubes (rarest gynecological malignancy)

Endo/Repro (31 decks)

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