7. Ovary Flashcards

1
Q

Disorders of the ovary

A
  1. Non-neoplastic ovarian cysts
    - Follicular cysts
    - Corpus luteal cysts
    - Theca lutein cysts
    - Endometriotic cysts
    - Multiple follicular cysts (polycystic ovary syndrome)
  2. Ovarian neoplasms
    a. Epithelial ovarian tumours
    i. Benign
    - Ovarian serous cystadenoma
    - Ovarian mucinous cystadenoma
    - Brenner tumour
    ii. Malignant
    - Serous cystadenocarcinoma
    - Mucinous cystadenocarcinoma
    - Endometrioid carcinoma
    - Clear cell tumours

b. Ovarian germ cell tumours
i. Benign
- Mature cystic teratoma
- Mature teratoma
ii. Malignant
- Immature teratoma
- Yolk sac tumour of the ovary
- Dysgerminoma
- Nongestational choriocarcinoma

c. Sex cord-stromal tumours of the ovary
i. Benign
- Ovarian fibroma
- Theca cell tumour
- Sertoli-leydig cell tumour
ii. Malignant
- Granulosa cell tumour

d. Krukenberg tumour

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2
Q

Follicular cysts

A
  1. Most common ovarian mass in young women
  2. Develops when a Graafian follicle does not rupture and release the egg (ovulation) but continues to grow
  3. Eventually develops into a large cyst (∼ 7 cm) lined with granulosa cells
  4. Associated with hyperestrogenism and endometrial hyperplasia
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3
Q

Corpus luteum cyst

A

Enlargement and buildup of fluid in the corpus luteum after failed regression following the release of an ovum

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4
Q

Theca lutein cysts

A
  1. Often multiple cysts that typically develop bilaterally
  2. Result from exaggerated stimulation of the theca interna cells of the ovarian follicles due to excessive amounts of circulating gonadotropins such as β-hCG
  3. Strongly associated with gestational trophoblastic disease and multiple gestations
  4. Usually resolve once β-hCG levels have normalized
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5
Q

Epidemiology of polycystic ovary syndrome

A

6–12% of women in their reproductive years in the US

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6
Q

Pathophysiology of polycystic ovary syndrome

A
  1. Strong association with obesity → ↑ in peripheral estrogen synthesis from adipose tissue and ↓ in peripheral sensitivity to insulin
  2. Reduced insulin sensitivity (peripheral insulin resistance) and the consequent hyperinsulinemia result in:
    - Epidermal hyperplasia and hyperpigmentation (acanthosis nigricans)
    - ↑ Androgen production in ovarian theca interna cells → imbalance between androgen precursors and the resulting estrogen produced in granulosa cells
    i. ↑ LH secretion disrupts the LH/FSH balance → impaired follicle maturation with cyst formation due to lack of follicle rupture and anovulation/oligoovulation → infertility
    ii. ↑ Androgen precursor release and ↑ estrogen production in adipose tissue
    - Inhibition of sex hormone-binding globulin (SHBG) in the liver → ↑ free androgens and estrogens
    i. ↑ Unopposed estrogen (lack of progesterone) during anovulatory cycles → endometrial hyperplasia → ↑ risk of endometrial carcinoma
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7
Q

Clinical features of polycystic ovary syndrome

A
  1. Menstrual irregularities
    - Primary or secondary amenorrhea
    - Oligomenorrhea
    - Menorrhagia
    - Infertility or difficulties conceiving
  2. Insulin resistance and associated conditions
    - Metabolic syndrome (especially obesity)
  3. Skin conditions
    - Hirsutism
    - Acne vulgaris
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8
Q

Complications of polycystic ovary syndrome

A
  1. Cardiovascular disease
  2. Type 2 diabetes mellitus
  3. Increased cancer risk (before menopause)
  4. Endometrial cancer
  5. Increased miscarriage rate
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9
Q

Epidemiology of cystadenoma

A

Most (serous) and second most common (mucinous) benign ovarian tumor

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10
Q

Pathology of Ovarian serous cystadenoma

A
  1. Cysts with watery fluid
  2. May contain small papillary projections
  3. Psammoma bodies
  4. Cyst is lined by serous epithelial cells (similar to the epithelium of fallopian tubes)
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11
Q

Pathology of Ovarian mucinous cystadenoma

A
  1. Smooth or bosselated appearance
  2. Cyst is loculated; loculi contain gelatinous material
  3. Cyst is lined by columnar epithelium that secretes thick mucus (similar to the epithelium of cervix)
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12
Q

Epidemiology of Brenner tumour

A
  1. Rare

2. Peak age: 40–60 years

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13
Q

Pathology of Brenner tumour

A
  1. Encapsulated, pale yellow solid tumor
  2. Similar to transitional cells of the bladder (urothelium)
  3. Circular patches of cells with coffee bean nuclei
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14
Q

Epidemiology of serous cystadenocarcinoma

A

Most common malignant ovarian tumor

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15
Q

Pathology of serous cystadenocarcinoma

A
  1. Cysts with watery fluid
  2. Tumor cells with papillary structures and small cytoplasm
  3. Psammoma bodies are a typical feature.
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16
Q

Epidemiology of mucinous cystadenocarcinoma

A
  1. Rare

2. Can also be metastatic from GI malignancies (e.g., of the appendix)

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17
Q

Pathology of mucinous cystadenocarcinoma

A
  1. Cysts filled with mucoid material, cellular debris, and/or blood
  2. Cystic or colloid type, depending on intracellular or extracellular mucin deposition
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18
Q

Epidemiology of endometrioid carcinoma

A
  1. 10% of epithelial tumors

2. Concomitant endometrial carcinoma in 10–15% of cases

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19
Q

Pathology of endometrioid carcinoma

A
  1. Possible appearances are:
    - Smooth surface with cystic spaces filled with blood-stained fluid
    - Completely solid with necrosis/hemorrhage
  2. Characteristic confluent glandular/expansile pattern
    - Tightly packed, back-to-back glands lined with tumor cells
    - Absent intervening stroma
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20
Q

Epidemiology of clear cell tumour

A
  1. 5–10% of epithelial tumors

2. Most commonly occur in perimenopausal women

21
Q

Pathology of clear cell tumour

A
  1. Endometriosis-associated tumors are filled with chocolate-colored fluid
  2. Variable appearance: tubulocystic, papillary, and solid
22
Q

Tumour marker for epithelial ovarian tumours

A

CA-125

23
Q

Epidemiology of mature cystic teratoma

A
  1. Most common of all germ cell tumors (90% of all cases)

2. Most common ovarian tumor in women < 30 years

24
Q

Pathology of mature cystic teratoma

A

Contains somatic tissue (e.g., hair, teeth, sebaceous glands) from any of the three embryonic germ layers:

  • Endoderm
  • Mesoderm
  • Ectoderm
25
Q

Epidemiology of mature teratoma

A

∼ 5% of all ovarian teratomas

26
Q

Pathology of mature teratoma

A

Endodermal differentiation into thyroid tissue

27
Q

Epidemiology of immature teratoma

A
  1. Rare

2. Peak age: women < 20 years of age

28
Q

Pathology of immature teratoma

A

Composed of immature neuroectodermal tissue

29
Q

Epidemiology of Yolk sac tumor of the ovary

A

Occurs mainly in children and adolescents

30
Q

Pathology of Yolk sac tumour of the ovary

A
  1. Macroscopic appearance: yellow, friable mass (due to hemorrhage)
  2. Schiller-Duval bodies (resemble glomeruli on microscopy)
31
Q

Tumour marker for immature teratoma

A
  1. LDH
  2. AFP
  3. CA-125
32
Q

Tumour marker for yolk sac tumour of the ovary

A
  1. LDH

2. AFP

33
Q

Epidemiology of ovarian fibroma

A

Peak age: postmenopause

34
Q

Pathology of ovarian fibroma

A
  1. Smooth, lobulated
  2. Cut surface: chalky, firm, yellow-to-white color
  3. Clusters of spindle-shaped cells (fibroblasts)
35
Q

Epidemiology of theca cell tumour

A

Peak age: postmenopause

36
Q

Pathology of theca cell tumour

A
  1. Solid yellow-orange tumor

2. Ovarian stromal cells filled with lipids on microscopy

37
Q

Epidemiology of sertoli-leydig cell tumour

A
  1. Rare

2. Peak age: 30–40 years

38
Q

Pathology of sertoli-leydig cell tumour

A
  1. Small, yellow-brown tumor

2. Seminiferous-like tubules lined by Sertoli cells and Reinke crystals

39
Q

Epidemiology of granulosa cell tumour

A
  1. Most common type of sex cord-stromal malignancy (∼ 90%)

2. Peak age: 50–55 years

40
Q

Pathology of granulosa cell tumour

A
  1. Tan/yellow color
    Encapsulated; smooth lobulated surface, possibly with areas of necrosis/hemorrhage
  2. Call-Exner bodies: granulosa cells arranged in clusters surrounding a central cavity with eosinophilic secretions, resembling primordial follicles
41
Q

Tumour marker for granulosa cell tumour

A

Inhibin

42
Q

Krukenberg tumour

A

Secondary ovarian tumor that most commonly arises from metastatic spread of gastric carcinoma

  • Often bilateral
  • Characteristic mucin-secreting signet ring cells on histology
43
Q

Clinical feature of ovarian fibroma

A

May be associated with Meigs syndrome: ascites and pleural effusion in association with a benign ovarian tumor

44
Q

Clinical feature of sertoli-leydig cell tumour

A

Symptoms of excessive androgens and/or estrogen production

  1. ↑ Testosterone
    - Virilization, hirsutism, acne, temporal balding
    - Amenorrhea, clitoral enlargement, ↓ fertility
  2. ↑ Estrogen
    - Menstrual bleeding abnormalities
    - Endometrial polyps and hyperplasia
45
Q

Clinical feature of granulosa cell tumour

A
  1. Symptoms caused by estrogen and/or progesterone secretion
    - Adult subtype: menstrual irregularities (e.g., postmenopausal bleeding, endometrial hyperplasia with metrorrhagia)
    - Juvenile subtype: precocious puberty
  2. Breast tenderness
  3. Associated with increased risk of endometrial cancer
46
Q

Spread of malignant ovarian neoplasms

A
  1. Local infiltration into broad ligament
    - Urethral obstruction
    - Bladder involvement
  2. Peritoneal spread
    - Ascites with malignant cells in fluid
    - Peritoneal nodules
  3. Lymphatic spread
  4. Hematogenous spread
    - Lung nodules
47
Q

Epidemiology of dysgerminoma

A

Most common malignant ovarian germ cell tumor in adolescents and young women

48
Q

Pathology of dysgerminoma

A

Equivalent to seminoma (e.g., presence of fried egg cells)

49
Q

Tumour markers of dysgerminoma

A
  1. LDH

2. hCG (rare: ∼ 5%)