L36- Ovarian Pathology I Flashcards

1
Q

list the types of ovarian lesions

A

Cysts: cystic follicle, follicular cyst, luteal cyst, chocolate cyst, PCOD

Tumors:

  • metastasis (colon, GI, breast), 5%
  • primary ovarian tumors: surface epithelium (90%), germ cell (3-5%), sex cord stromal (2-3%)
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2
Q

list the types of ovarian cysts

A

Non-Neoplastic:
-follicular, corpus luteum, chocolate, PCOD

Neoplastic:

  • serous cystadenoma / carcinoma
  • mucinous cystadenoma / carcinoma
  • dermoid cyst
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3
Q

Follicular Cysts:

  • stem from (1)
  • (2) size
  • (3) clinical features
  • (4) Dx
A

1- unruptured follicle OR ruptured follicle that is immediately sealed off

2- 2cm, up to 4-5 cm

3- silent, pain, endometrial hyperplasia

4- US

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4
Q

Chocolate Cysts:

  • stem from (1)
  • chocolate color results from (2), which also induces (3) processes
  • (4) appearance
A

1- endometriosis (endometrial tissue in ovary)

2- repeated cyclical hemorrhage

3- fibrosis, adhesions, pain

4- normal endometrial glands + stroma + RBC + hemosiderin

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5
Q

Chocolate Cysts:

  • mainly needs to be distinguished from (1)
  • may grow / extend with (2)
  • associated with (3) as a symptom or complication
A

1- corpus luteum cysts
2- pelvic ligaments
3- infertility

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6
Q

PCOD, aka (1):

  • (2) most commonly affected women
  • (3) main Sxs
A

1- Stein Leventhal Syndrome

2- young, post-menarche, those with persistent anovulation

3- oligomenorrhea, secondary amenorrhea, hirsutism, obesity (40%), infertility

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7
Q

PCOD: describe hormonal changes and why

A
  • inc androgen => 50% hirsutism, rarely virulization (poorly regulated enzymes)
  • inc LH // dec FSH
  • insulin resistance
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8
Q

PCOD causes increase in circulating androgens:

  • (1) is the main fate of androgens
  • (2) and (3) are the hormonal effects of (1)
  • (4) is the connection to repeat this cycle
A

1- androgens –> (adipose) –> estrogens

2- inhibits FSH release
3- stimulates GnRH release –> inc LH release (but not FSH)

4- LH stimulates theca cell androgen production

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9
Q

PCOD, describe the direct or symptomatic effects of:

  • (1) excess estrogen
  • (2) excess androgen
A

1- endometrial hyperplasia, stimulates adipose cells in body –> obesity

2- hirsutism, virilization + processed thru adipose / liver –> excess estrogens

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10
Q

PCOD ovarian changes

A
  • 2x larger
  • subcortical cysts, 0.5-1.5 cm
  • large, thick capsule, multiple unruptured follicles as cysts lined by granulosa cells and hypertrophied theca interna cells
  • thick hypertrophied stroma
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11
Q

PCOD Dx

A
  • hormonal assay

- transvaginal US

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12
Q

PCOD Tx

A

-depends on age and Sxs

Hormonal: break cycle; clomiphene induces ovulation if fertility is desired

Previously: wedge resection of ovary to help ovulation to reduce mass

Sxs:

  • hirsutism - spironolacone
  • DM - metformin
  • obesity - weight loss
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13
Q

list the many clinical features of ovarian disease

A

-clinically silent for long time –> lots of space to grow

Mass Effects (mostly): pressure, swelling, ascites –> abdominal pain / enlargement, pelvic discomfort, frequent micturation, GI issues

Hormonal Effects (rare): endometrium (menstrual irregularities), breast enlargment, hirsutism

  • infertility (no ovulation)
  • Advanced CA: cachexia, weight loss, weakness
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14
Q

list the ovarian tumor investigations

A
  • abdominal palpation
  • US, CT scan
  • FNAC via pouch of douglas
  • ascitic fluid tap
  • mass biopsy (uncommon)
  • CA125 levels in serum
  • hormone estimation
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15
Q

CA125 is described as (1) and is mainly used for (2). (3) is a main caveat to its use. (4) is its main value clinically.

A

1- high MW glycoprotein

2- tumor marker –> endometrial CA

3- inc in a variety of non-specific conditions that irritate peritoneum + tumors limited to ovary are 50% negative

4- possible use as screening in asymptomatic post-menopausal women, BUT mainly for monitoring response to therapy / disease progression

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16
Q

(1) is the most common gynecological malignancy. (2) and (3) generally reduce risk of (1). (4) is the main issue with diagnosing (1).

A
1- ovarian cancer
2- pregnancy
3- OCTs
(+ FHx is important)
4- late detection --> majority are clinically silent
17
Q

Ovarian Tumors:

  • mostly (benign/malignant)
  • (normally/rarely) functional
  • (3) describe malignant spread
A

1- 80% benign, mostly 20-45 y/o //// malignant more in 40-65 y/o

2- rarely functional

3-

i) peritoneum (ascites, omental caking)
ii) LNs- illiac, para-aortic
iii) blood- lungs, liver, GIT

18
Q

describe the classifications of ovarian tumors

A

(based on origin)
-Surface epithelium: serous, mucinous (intestinal, endocervical), endometroid, clear cell, Brenner, mixed, undifferentiated

  • Germ Cell: teratoma, dysgerminoma, endodermal sinus tumor, chorioarcinoma
  • Sex Cord stromal: fibroma/fibrothecoma, granulosa tumor, sertoli leydig tumor

Metastasis

19
Q

describe (simplistic) classification of Surface Epithelial tumors (ovarian)

A

Serous- columnar cells w/ cilia (towards fallopian tube)

Mucinous- tall mucin secreting cells (towards endocervix)

Endometroid- non-ciliated columnar cells (towards endometrium)

Brenner tumor- transitional cells (toward transitional epithelium)

20
Q

Ovarian Epithelial Tumor:

  • benign = (1)
  • borderline / intermediate has (high/low) malignant potential
  • malignant = (3)
A

1- cystadenomas

2- low

3- cystadenocarcinomas (usually aggressive)

21
Q

describe gross appearances of surface epithelial ovarian tumors

A

Cystic, no solid areas / papillary excrescences – generally benign

Solid- homogenous, benign

Solid- variegated (nodular, fleshy, papillae), generally malignant

22
Q

Serous Tumors:

  • (1) prevalence
  • mostly (benign/malignant)
  • mostly (uni/bi)-lateral
A

1- 30% of all ovarian tumors

2- benign (60%) more in younger people, 20-50 y/o // malignant (25%) mostly >50 y/o

3- unilateral if benign, bilateral if malgnant

23
Q

list the risk factors of Serous Ovarian Tumors

A
  • Nulliparity (no pregnancies)
  • FHx
  • BRCA1/2
  • KRAS, BRAF mutations (low-grade)
  • p53 mutation (high-grade)
24
Q

describe general structure of Benign Serous Cystadenoma (ovarian)

A
  • cysts filled with serous fluid
  • 10-15 cm
  • smooth and glistening lining, single layer of tall ciliated columnar cells

Variant- cystadenofibrma had fibrous tissue under epithelium (benign)

25
Q

Borderline / Malignant Serous Ovarian Tumors:

  • (1) changes are more numerous structurally
  • (2) nodules are most worrisome / dangerous
  • (3) borderline specific (+ 10yr survival rate)
  • (4) malignant specific (+ 10yr survival rate)
A

1- papillae, polyploid changes
2- solid nodules

3- (75%) multi-layering, moderate mitosis, nuclear atypia (NO stromal invasion)
4- multi-layering, nuclear atypia, Stromal invasion

26
Q

Mucinous Ovarian Tumors:

  • (1) prevalence
  • mostly (benign/malignant)
  • mostly (uni/bi)-lateral
  • (4) are main risk factors (hint- 1 genetic, 1 environmental)
A

1- 30% of all ovarian tumors

2- benign (80%)

3- unilateral, 95%

4- KRAS, smoking??

27
Q

malignancy of mucinous tumors (ovarian) are based on….

  • mucus composition
  • general size
A
  • # locules (cavities) in cysts- more present => more likely to be malignant
  • solid composition

Extra:

  • sticky gelantinous material, rich in glycoproteins
  • very large mass, one of the largest in ovary
28
Q

Mucinous Ovarian Tumors:

  • (1) cell description
  • importantly lacking (2)
  • (better/worse) prognosis in comparison to serous carcinoma
A

1- tall columnar cells w/ apical mucinous vacuole, no cilia

2- no papillae, psammoma bodies

3- better

29
Q

Pseudomyxoma Peritonei:

  • (1) definition
  • (2) most cases location
  • (3) most end-results
A

1- extensive mucinous ascites = ‘jellybelly’ / mucoid material in peritoneal cavity implanted over abdominal and ovarian surfaces

2- extraovarian (appendiceal usually) w/ secondary ovarian and peritoneal spread

3- fatal