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Foundations III > Ovarian Disorders > Flashcards

Ovarian Disorders Flashcards

1
Q

What are the 3 keys to Polycystic Ovarian Syndrome?

A 
1. Chronic anovulation (increased risk of endometrial cancer)
2 Hyperandrogenism (ex. hirsuitism, acne, male-pattern baldness)
3. Polycystic ovaries

-Insulin resistance/hyperinsulinemia (ex. acanthosis nigricans)

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2
Q

LH stimulates ____ cells to produce androgens

A

Theca

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3
Q

What finding on US is characteristic of PCOS?

A

“string of pearls”

>12 follicles, 2-9mm in diameter. No dominant follicle

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4
Q

Because there is insulin resistance with PCOS, what drug should be considered first line?

A

Metformin

-also helpful for anovulation

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5
Q

For the androgen excess of PCOS, what medications are indicated?

A

OCPs (central suppresion)

Spironolactone, Finasteride (peripheral androgen blockade)

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6
Q

In PCOS, which hormone dominates, LH or FSH?

A

LH&raquo_space;>FSH (so lack of stimulation to granulosa cells)

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7
Q

What effect does circulating insulin have on the ovary?

A

Increased insulin stimulates ovary to produce more androgens

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8
Q

What is the most common cause of infertility?

A

Polycystic ovarian Syndrome

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9
Q

How is the Rotterdam Criteria (2003) used to diagnose PCOS?

A

2 of 3 to dx

  1. Ovulatory dysfunction
  2. Clinical or biochemical signs of hyperandrogenism
  3. Polycystic ovaries
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10
Q

IF you suspect a patient has PCOS with hyperandrogenism, what is the first initial study to get?

A

Total testosterone*

Normal: 40-60ng/dL
Elevated: >60ng/dL, so get further labs

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11
Q

What do you need to rule out/exclude before trying to diagnose PCOS?

A
  1. Cushing’s Syndrome
  2. Hyperthyroidism
  3. Pituitary adenoma
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12
Q

If 12-OH progesterone is elevated (at 8AM), what should you suspect?

A

congenital adrenal hyperplasia

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13
Q

What is the initial treatment to recommend to someone with PCOS?

A

weight loss

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14
Q

What is 1st line treatment for hirsutism?

A

Combination of oral contraception with low androgenic activity

  • decrease LH–>decreased Testosterone
  • Increase testosterone binding capacity to lower free testosterone

Adjunct: spironolactone

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15
Q

What drug is used for endometrial protection in PCOS?

A

Provera 10mg QD

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16
Q

What do you need to educate the patient about regarding lifestyle modification?

A

it will be life long

17
Q

Pre-menarchal ovaries: palpable?

A

no

18
Q

Reproductive age ovaries: palpable?

A

~50% of the time

19
Q

When should ovaries become non-palbale in a post-menopausal women?

A

within 3 years of onset

20
Q

Benign US findings

A
  • Thin walls
  • Homogenous echogenicity (endometrioma)
  • <3cm premenopause, or <1cm postmenopause (simple cysts)
  • Hyperechoic nodule, distal acoustic shadowing (teratoma)
  • Network of linear or curvillinear pattern (hemorrhagic cyst)
21
Q

What are 3 ultrasound findings that would concern you for malignancy?

A
  1. thick septations
  2. Solid components
  3. Blood flow to solid component
22
Q

What are the 3 types of functional ovarian cysts?

A
  1. Follicular Cysts (MC**)
    - follicle isn’t resorbed, or non-dominants don’t go away
  2. Corpus Luteum Cysts
    - pt. will not have a period
  3. theca Lutein Cysts
    - elevated hCG
    - associated with abnormal pregnancies (hydatidiform mole, choriocarcinoma)
    - bilateral, clear straw-colored fluid
23
Q

Serous cystadenoma

A
  • MC epithelial cell neoplasm
  • non functional
  • 20% malignant
  • Aged 30-50 years
24
Q

Mucinous cystadenoma

A

-2nd most common epithelial cell neoplasm
-non functional
-LARGE!!
US: multilocular septations

25
Q

What is the most common of all benign ovarian lesions?

A

Benign cystic teratoma (dermoid cyst)

40-50% of benign neoplasms

26
Q

What do granulosa theca cell tumors produce?

A

estrogens

27
Q

What do Sertoli-Leydig cell tumors produce?

A

androgens

28
Q

Ovarian cancer: intro/general

A
  • 2nd MC gynecologic cancer

- MC cause of gynecologic cancer death in US

29
Q

Ovarian cancer: risk factors

A
  • Increased exposure to estrogens (nullparity, early menarche, late menopause, endometriosis, obesity)
  • Family history of breast, ovarian or colorectal cancer
  • BRCA1/BRCA2
  • Lynch Syndrome
  • White race
  • Turner’s Syndrome
30
Q

What is the best way to reduce risk for ovarian cancer?

A

Bilateral salpingectomy (remove fallopian tubes)

31
Q

What are the 4 major types of ovarian cancer?

A
  1. Epithelial** MC (high grade serous (MC)*, endometroid, clear cell, mucinous carcinomas)
  2. Germ cell (MC dysgerminoma)*
  3. Sex cord and stromal
  4. METs to ovary
32
Q

What is the tumor suppressor gene associated with ovarian cancer?

A

p53 tumor suppresor gene

“p53 signature” is located at the distal fallopian tube*

33
Q

Describe how a patient with ovarian cancer may present?

A
  1. Abdominal bloating or distention
  2. Abdominal/pelvic pain
  3. Decreased energy or lethargy
  4. Early satiety
  5. Urinary urgency
34
Q

Germ cell ovarian cancer: general

A
  • MC in women 20-30 yrs
  • Unilateral
  • Produce tumor markers**
35
Q

IF you are suspicious a patient may have ovarian cancer, what labs or imaging would help with diagnosis?

A
  • Elevated hCG, AFP, LDH*(suspect germ cell–> dysgerminoma)

- CA-125 elevation (suspect epithelial cancer)

36
Q

Which germ cell ovarian cancer is the only one that is bilateral?

A

Endodermal sinus tumor

Foundations III (34 decks)

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