Path of Polycystic Ovarian Synd. Flashcards

0
Q

3 NIH criteria for PCOS?

A

Hyperandrogenemia.
Chronic amenorrhea or oligomenorrhea.
Not caused by other defined disorder.

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1
Q

What’s the most common endocrine disorder affecting women of child-bearing age?

A

Polycystic Ovarian Syndrome (PCOS)

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2
Q

What is the criterion that the Rotterdam criteria have in addition to those of the NIH?

A

Polycystic ovaries on ultrasound.

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3
Q

Which criterion is most important?

A

The hyperandrogenemia criterion (can be symptomatic or measured free T). Many adolescents will have irregular periods with polycystic ovaries but not progress to PCOS.

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4
Q

2 features of oligo-ovulation / anovulation in PCOS?

A

Less than 6-9 menses / yr.

Low mid-luteal progesterone levels.

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5
Q

What 2 endocrine disorders that could cause oligo-ovulation / anovulation must be ruled out when making PCOS Dx?

A

Hypothyroidism

Hyperprolactinemia

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6
Q

3 clinical features of hyperandrogenemia?

A

Hirsutism
Acne
Male-pattern baldness

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7
Q

Which androgens are measured when working up PCOS?

A

Testosterone

DHEA

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8
Q

What’s the definition of “polycystic” ovaries?

A

12 or more follicles seen on ultrasound that are above a certain size. Presence in single ovary is sufficient.

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9
Q

Simplistic model for what’s going on in PCOS?

A

Non-dominant follicles are more responsive to FSH.

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10
Q

Does PCOS have any racial differences?

A

Seems to be more severe in African Americans.

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11
Q

Is obesity part of the PCOS diagnosis? What’s obesity got to do with with PCOS?

A

Nope. But obesity/metabolic symptom and PCOS are correlated……

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12
Q

How is GnRH release different in PCOS?

A

Higher frequency -> favors LH release more.

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13
Q

How is feedback different in PCOS?

A

Hypothalamus is less sensitive to sex hormone feedback.

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14
Q

What’s a hypothesis as to the etiology of PCOS?

A

Increased exposure to androgens may decrease sensitivity feedback in the HPO axis.

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15
Q

How is the response to FSH different in granulosa cells in PCOS?

A

Granulosa cells make more estrogen in response to FSH.

16
Q

How do numbers of germ cells compare in PCOS vs. normal?

A

More germ cells in the ovaries of women with PCOS.

17
Q

What’s insulin got to do with PCOS?

A

Theca cells are more sensitive to insulin -> androgen production.
Insulin resistance is tissue selective (i.e. not in the ovaries) and is highly prevalent in PCOS population.

18
Q

What’s a sign of insulin resistance often seen in PCOS?

A

Acanthosis nigricans - black, velvety skin.

19
Q

What causes the insulin resistance in PCOS?

A

Post-receptor mechanisms, so far as we know.
(decreased activity of a serine kinase -> decreased phosphorylation of a serine in the cytoplasmic domain of the insulin receptor…)

20
Q

Genetics of PCOS?

A

Polygenetic: lots of candidate genes with a small effect.

21
Q

Treatment for infertility caused by PCOS? How well does it work?

A

Clomiphene followed by FSH if necessary.
Seems to work pretty well - study shown had about 70% pregnancy at 2 years. (but it’s hard to say how infertile women were to begin with)

22
Q

What’s risk to patient with PCOS who does get pregnant?

A

Higher risk for eclampsia, gestational diabetes, pre-term birth, and perinatal mortality.

23
Q

4-5 treatments for PCOS?

A

OCPs / cyclic progesterone
Anti-androgens (topical or systemic)
Weight loss
Insulin-sensitizing (agent)