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General Gynecology > Androgen disorders > Flashcards

Androgen disorders Flashcards

1
Q

What are the three types of androgens produced by the Ovaries?

A

DHEA, Androstenedione, Testosterone

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2
Q

What is the main androgen produced by the adrenal glands?

A

DHEAS

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3
Q

The ovary produces what androgen in the highest amount?

A

Androstenedione

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4
Q

What percent of circulating testosterone is bound to SHBG?

A

80%

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5
Q

PCOS affects what percent of women in the US?

A

5-10%

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6
Q

What is the cardinal feature of PCOS?

A

Hyperandrogenism

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7
Q

What are the 2 outcomes of hyperandrogenism in PCOS?

A

interference with follicular development, Decreases SHBG

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8
Q

T/F: Insulin resistance is common in PCOS and leads to hyperinsulinemia

A

True

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9
Q

What is the most current definition of PCOS?

A

Hyperandrogenism AND oilgo ovulation or polycystic ovaries

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10
Q

What percent of women with PCOS have hirsutism?

A

65 - 75%

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11
Q

Hair follicular growth are stimulated by what hormone?

A

DHT

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12
Q

Testosterone is converted to DHT by what enzyme?

A

5 alpha reductase

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13
Q

What is the term for rapid hair loss following delivery?

A

Telogen effluvium

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14
Q

Why do women loose their hair following delivery?

A

All hair is in the resting teolgen phase during pregnancy

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15
Q

If a patient has signs of virulization what conditions should you be worried about?

A

Adrenal hyperplasia, androgen producing tumors

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16
Q

What percentage of testosterone is bound?

A

99%

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17
Q

What percent of testosterone is bound by SHBG and what percent is bound by albumin?

A

80% bound by SHBG, 19% bound by albumin

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18
Q

What percentage of women with PCOS have irregular menstrual cycles?

A

60 - 85%

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19
Q

How do you verify ovulation?

A

Serum progesterone on day 20 -24 of menstrual cycle

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20
Q

What level of serum progesterone signifies ovulation?

A

Progesterone > 3 ng/ml

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21
Q

What is the definition of polycystic ovaries?

A

12 or more follicles measuring 2-9mm and/or ovarian volume > 10 ml

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22
Q

What percentage of women with PCOS have polycystic ovaries?

A

> 80%

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23
Q

What percentage of women WITHOUT PCOS have polycystic ovaries?

A

20 - 30%

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24
Q

What is a cause of hirsutism in pregnancy?

A

Pregnancy luteoma

25
Q

If a patient has a luteoma, what is the possible outcome in the neonate?

A

female infants will be virilized

26
Q

In a patient with PCOS the LH/FSH ratio is often ____as ___ is elevated and ____ is normal

A

elevated as LH is often elevated and FSH is normal

27
Q

What percentage of women with PCOS are insulin resistant?

A

50 - 70%

28
Q

What labs should be ordered when evaluating a patient with PCOS?

A

Total testosterone, free testosterone, SHBG, DHEAS, progesterone, TSH, Prolactin, 17-OHP

29
Q

What is the first choice for ovulation induction in a patient with PCOS?

A

Letrozole

30
Q

What is the mechanism of letrozole?

A

Aromatase inhibitor

31
Q

How do OCPs improve Hirsutism?

A

Increase SHBG (estrogen), Inhibit 5 alpha reductase (progesterone) supress LH and ovarian steroidogenesis

32
Q

What does the estrogen do in OCPs to improve hirsutism?

A

Increases SHBG

33
Q

What does the progesterone do in OCPs to improve Hirsutism?

A

inhibit 5 alpha reductase

34
Q

How does spiranolactone treat hirsutism?

A

Inhibits androgen synthesis, inhibits 5 alpha reductase, competes for androgen receptor

35
Q

What is the mechanism spiranolactone?

A

aldosterone antagonist

36
Q

What are the side effects of spiranolactone?

A

AUB, hyperkalemia

37
Q

What is the mechanism of flutamide?

A

nonsteroidal antiandrogen

38
Q

What is the mechanism o Finasteride?

A

5 alpha reductase inhibitor

39
Q

How does eflornithine cream slow hair growth?

A

blocks ornithine decarboxylase

40
Q

True or False: Weight loss alone can lead to resumption of ovulation in patients with PCOS?

A

True

41
Q

What type of genetic inheritance is congenital adrenal hyperplasia?

A

Autosomal Recessive

42
Q

In CAH, Decreased production of ______, leads to increased ______ and high levels of adrenal androgens

A

Cortisol, ACTH

43
Q

What is the most common enzyme deficiency of CAH?

A

21 hydroxylase deficiency

44
Q

What steroid is increased in patients with 21 hydroxlase deficiency?

A

17 OHP

45
Q

21 Hydroxylase deficiency accounts for what percentage of CAH cases?

A

95%

46
Q

What are the classical findings in the neonate of 21 hydroxylase deficiency?

A

sexual ambiguity, virilization, salt wasting

47
Q

What are the classical findings of 11B Hydroxylase deficiency?

A

Virilization, Hypertension, volume overload.

48
Q

How do you diagnose CAH?

A

Oder 17 OHP

49
Q

In 11 B hydroxylase deficiency what androgen will be elevated?

A

11 deoxycortisol

50
Q

How do you differentiate between 21 hydroxylase and 11 B hydroxylase deficiency?

A

Order 11 deoxycortisol

51
Q

What is the mainstay of treatment of CAH?

A

Give cortisol and aldosterone

52
Q

What medications and dosing do you use to treat CAH?

A

Hydrocortisone 10 mg/day, fluorohydrocortisone 100 mg/day

53
Q

How do you diagnose CAH prenatally?

A

CVS to detect mutations

54
Q

T/F: 17 OHP and androstendione are detectable in amniotic fluid

A

True

55
Q

When should you initiate treatment with dexamethasone during pregnancy for fetuses at high risk?

A

4-5 weeks gestation

56
Q

What is the difference between classical and non classical CAH?

A

Presentation of nonclassical CAH is at puberty or later.

57
Q

What is the treatment for nonclassical CAH?

A

Dexamethasone 0.25 mg nightly

58
Q

What labs are included in the initial evaluation of a patient with hirsutism?

A

Total testosterone, SHBG, DHEAS, 17 OHP

General Gynecology (11 decks)

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