Female Genital Tract 2 – Uterine & Pregnancy Pathology

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Question-and-Answer flashcards covering inflammatory, hyperplastic, dysfunctional, neoplastic, and pregnancy-related disorders of the uterus and placenta.

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46 Terms

1
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What infectious agents most commonly cause acute endometritis?

Neisseria gonorrhoeae and Chlamydia trachomatis

2
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Which histologic cell type is REQUIRED to diagnose chronic endometritis?

Plasma cells in the endometrial stroma

3
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List two classic clinical consequences of endometritis related to fallopian-tube damage.

Infertility and ectopic (tubal) pregnancy

4
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In what patient population is granulomatous (tuberculous) endometritis most often seen?

Immunocompromised patients in tuberculosis-endemic regions

5
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Define adenomyosis.

Growth of endometrial basal layer (glands & stroma) deep within the myometrium

6
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Why do adenomyotic foci not undergo cyclic bleeding?

Because they originate from the non-cycling stratum basalis of the endometrium

7
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What three main symptoms can adenomyosis produce?

Menorrhagia, dysmenorrhea, and pre-menstrual pelvic pain

8
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Define endometriosis.

Presence of normal endometrial glands and stroma outside the uterus

9
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Name two theories proposed to explain endometriosis.

Retrograde (reverse) menstruation theory and embryologic rest (metaplastic) theory

10
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Give four common anatomic sites of endometriosis.

Ovary (chocolate cysts), broad ligament, pelvic peritoneum, bowel (e.g., sigmoid, rectovaginal septum)

11
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What type of ovarian cyst is characteristic of endometriosis?

‘Chocolate cyst’ – a cyst filled with old hemorrhagic material

12
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Which hormone imbalance drives endometrial hyperplasia?

Excess estrogen relative to progesterone

13
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Identify the three histologic classes of endometrial hyperplasia.

Simple, complex, and atypical hyperplasia

14
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Which class of endometrial hyperplasia carries the highest cancer risk?

Atypical hyperplasia

15
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List four clinical or endocrine settings that cause unopposed estrogen exposure leading to hyperplasia.

Anovulation, prolonged estrogen therapy, polycystic ovary syndrome, estrogen-producing ovarian tumors (e.g., granulosa-theca cell tumors)

16
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Why is obesity a risk factor for endometrial hyperplasia?

Adipose tissue converts steroid precursors into estrogens, raising systemic estrogen levels

17
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Describe a typical endometrial polyp.

Sessile, hemispheric lesion composed of basalis-type endometrium with thick-walled vessels; may have cystically dilated glands

18
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What is the main clinical presentation of an endometrial polyp?

Abnormal uterine bleeding

19
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Define dysfunctional uterine bleeding (DUB).

Abnormal bleeding without an organic uterine lesion

20
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Name four major etiologic categories of DUB.

Failure of ovulation, inadequate luteal phase, contraceptive-induced changes, perimenopausal hormonal fluctuations

21
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What is the most common benign tumor of the female genital tract?

Leiomyoma (uterine fibroid)

22
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How do estrogens and oral contraceptives affect leiomyomas?

They stimulate growth; tumors often enlarge during reproductive years and regress after menopause

23
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List two common symptoms caused by leiomyomas.

Menorrhagia ± metrorrhagia and pelvic ‘dragging’ or mass effect

24
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Do leiomyomas commonly transform into sarcomas?

No, malignant transformation is rare

25
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How do leiomyosarcomas typically arise?

De novo from myometrial mesenchymal cells (not from pre-existing leiomyomas)

26
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Give three gross or microscopic features diagnostic of leiomyosarcoma.

Tumor necrosis, marked cytologic atypia, high mitotic activity

27
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What is the approximate 5-year survival rate for uterine leiomyosarcoma?

About 40%

28
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Differentiate endometrioid and serous endometrial carcinoma regarding pathogenesis.

Endometrioid: estrogen excess & hyperplasia with PTEN/DNA mismatch repair mutations; Serous: arises in atrophic endometrium with early TP53 mutations

29
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Which type of endometrial carcinoma is more aggressive with early metastasis?

Serous carcinoma

30
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State four classical risk factors for endometrioid endometrial carcinoma.

Obesity, diabetes mellitus, hypertension, and infertility (anovulatory cycles)

31
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What is the most important prognostic factor for both major types of endometrial carcinoma?

Tumor stage at diagnosis

32
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Define spontaneous abortion.

Loss of pregnancy before 20 weeks’ gestation

33
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What is an ectopic pregnancy?

Implantation of a fertilized ovum outside the uterine cavity, most commonly in the fallopian tube

34
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List the key placental anomalies discussed.

Accessory lobes, bipartite placenta, circumvallate placenta, placenta accreta

35
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Differentiate placental villitis from chorionamnionitis.

Villitis: inflammation of chorionic villi, usually hematogenous (TORCH); chorionamnionitis: inflammation of fetal membranes, usually ascending bacterial infection

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Which placental lesions are characterized by persistent elevation of hCG?

Hydatidiform mole and choriocarcinoma

37
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What are the two forms of hydatidiform mole and their karyotypes?

Complete mole – diploid (46,XX or 46,XY); Partial mole – triploid (69,XXY)

38
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Which type of mole contains fetal parts?

Partial hydatidiform mole

39
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State the approximate incidence of choriocarcinoma arising from complete hydatidiform moles.

About 2%

40
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Why do gestational choriocarcinomas respond better to chemotherapy than gonadal choriocarcinomas?

Placental tumors express paternal antigens, allowing maternal immune response to aid chemotherapy; gonadal tumors lack these antigens

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Give the three most common clinical settings in which gestational choriocarcinoma arises.

Complete mole (≈50%), after abortion (≈25%), during normal pregnancy (≈25%)

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What are classic presenting signs of choriocarcinoma?

Bloody or brownish vaginal discharge with markedly rising hCG levels

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Describe the typical metastatic pattern of choriocarcinoma.

Early hematogenous spread, especially to lungs and vagina; lymphatic spread is uncommon

44
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What perinatal complication is grouped under ‘toxemia of pregnancy’?

Pre-eclampsia/eclampsia

45
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Name two late-pregnancy conditions that contribute to intrauterine growth restriction (IUGR).

Placental insufficiency (e.g., vascular lesions, infections) and maternal toxemia (pre-eclampsia/eclampsia)

46
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Which placental anomaly involves chorionic villi attaching DIRECTLY to myometrium without decidua?

Placenta accreta