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Endocrinology > Female Repro > Flashcards

Female Repro Flashcards

1
Q

What ovarian tumors produce estrogen? MOA?

A

Granulosa cell tumors (produce estrogen through conversion of androstenedione to estradiol)
and
thecomas (solid, fibromatous, usually benign tumors made of theca cells from the ovarian stroma)

Do an ovarian venous sampling to assess autonomous estradiol secretion

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2
Q

when does combined ovarian and adrenal venous sampling performed?

A

to evaluate women with hyperandrogenism when clinical suspicion for an androgen-producing tumor is high, pelvic US is normal, and adrenal imaging is either normal or identifies a nodule or mass.

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3
Q

In the evaluation of irregular menstrual periods and secondary amenorrhea, what test is useful to distinguish between estrogen-sufficient amenorrhea vs estrogen-deficient amenorrhea?

A

the progesterone withdrawal test
estrogen sufficient leads to + withdrawal bleed (PCOS)
estrogen deficient leads to NO withdrawal bleed (secondary amenorrhea/hypogonadotropic hypogonadism/FHA)

Keep in mind that PCOS can co-occur with hypogonadotropic hypogonadism like FHA

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4
Q

explain the progesterone withdrawal test

A

It mimics the luteal phase of an ovulatory cycle to assess whether there is enough endogenous estrogen present to develop an endometrial lining. This would result in a menstrual period within 10 days of completing the progesterone 10-day treatment.

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5
Q

Combined ovarian and adrenal venous sampling
1. indications?
2. when is a unilateral source indicated?

A

1.when clinical suspicion for an androgen producing tumor is high, pelvic US is normal, and adrenal imaging is normal/shows a nodule or mass with benign features

2.
unstimulated T ovarian:IVC > 3
T adrenal:IVC > 3 AND –> means significant T production from that ovary
OR
ratio > 1.4 from one side

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6
Q

What agent is FDA-approved for use in women and is considered the first-line treatment of androgenetic alopecia?

A

topical minoxidil

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7
Q

Baseline or stimulated concentrations of 17-hydroxyprogesterone above [ ] are diagnostic of?

A

1000 ng/dl
21-hydroxylase deficiency (classic/non-classic CAH)

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8
Q

What are the updated Rotterdam consensus criteria for diagnosis of PCOS?

A
  1. anovulatory cycles (interval < 21 or > 35 days) or less than 8 periods per year or day 21 luteal phase progesterone < 3 if regular menses
  2. biochemical or clinically significant evidence for androgen excess
  3. PCO morphology with an antral follicle count greater than/equal to 20 or ovarian volume greater than/equal to 10 cc

2 of 3 criteria must be met

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9
Q

is ethinyl estradiol detected by estradiol assays?

A

no

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10
Q

what FSH and estrogen levels are expected in a woman on combined oral contraceptive pills?

A

low/low (or suppressed)

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11
Q

3 forms of progestin

A

norethindrone, levonorgestrel, norgestimate

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12
Q

transgender man taking testosterone while chestfeeding. What happens to breast milk?

A

Increased testosterone concentrations in the milk

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13
Q
  1. causes of hypogonadotropic hypogonadism
  2. what kind of infertility?
  3. tx?
A
    • congenital GnRH deficiency with (called Kallmann syndrome) or without anosmia
      - functional hypothalamic amenorrhea

2.anovulatory infertility
3.with the exception of FHA (since pituitary may recover), patients with hypogonad/hypogonadism need ovulation induction with BOTH FSH and LH (not just FSH), hence human menopausal gonadotropin. LH stimulates theca-cell androgen production, which are then aromatized to estrogen in the granulosa cells to stimulate endometrial growth. FSH along will cause growth of follicles that do not make estrogen.

pts with hypogonad/hypogonadism have high conception rates

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14
Q

in women with PCOS, what treatment is available for ovulation induction?

A

antiestrogen clomiphen citrate (or letrozole) –> increase in FSH and LH

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15
Q

A patient with PCOS and obesity starts COCs. Compared with women without obesity, there is [ ] difference in: contraceptive failure, impaired glucose tolerance, unscheduled bleeding, and weight gain.

A

NO

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16
Q

In perimenopause, what type of estrogen is best for addressing depression?

A

low-dose OCP (ethinyl estradiol), continuous –> suppresses HPO axis and decrease heavy bleeding. Ethinyl estradiol is also used in PCOS.

a physiologic dose of estrogen (17beta estradiol) would not do this

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17
Q

what is the advantage of incorporating a GnRH agonist into the hormone regimen for M to F transgender care?

A

causes profound suppression of endogenous testosterone so that only physiologic doses of estrogen need to be administered.

Unlike GnRH analogs, use of antiandrogens such as spironolactone causes more modest suppression of testosterone, so higher estrogen dosages are needed to achieve the desired degree of T suppression

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18
Q

Mullerian agenesis (aka?)
1. clinical characteristics
2. phenotype?
3. karyotype

A

aka Mayer-Rokitansky-Kuster-Hauser syndrome
1. variable uterine development (may be absent or underdeveloped) and congenital absence of the vagina
2. normal female. Ovaries are functioning (hence breast development is normal), normal external genitalia, normal pubic hair growth
3. 46,XX

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19
Q

Complete Androgen Insensivity Syndrome:
1. clinical characteristics?
2. defect in?
3. karyotype

A
  1. no pubic or axillary hair, full breast development
  2. the androgen receptor –> complete androgen resistance
  3. 46,XY
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20
Q

Menopause and tx of hot flashes
1. definition of menopause
2. age group to treat
3. best treatment for vasomotor symptoms
-tx for HTN and obesity
-tx for sexually active
4. alternative tx besides HRT (if CI’s exist) for hot flashes

A
  1. last menstrual period after 1 year OR an FSH > 25 mIU/mL
  2. healthy, young postmenopausal women in their late 40s-50s, within 10 years of their last period, tx for up to 5 years
  3. HRT if there are no CIs - with estradiol rather than conjugated estrogens. Add micrognized progesterone if + uterus
    -use transdermal estrogen for HTN/obesity
    -COCs until 55 yo
  4. paroxetine low dose; other SSRI’s, SNRI’s, gabas, clonidine
21
Q

general guidelines for pursuing additional workup for evaluation of an androgen-producing tumor

A
  1. total testosterone > 147 ng/dl; total testosterone > 63.5 ng/dl for postmenopausal women
22
Q

when to perform ovarian/adrenal venous sampling

A

when (1) clinical suspicion for an androgen-producing tumor is high, (2) pelvic US is normal, and (3) adrenal imaging is either normal or has a nodule w/benign features

23
Q

What’s the purpose of obtaining day 21 progesterone?

A

to document oligoovulatory and anovulatory cycles (in a woman with monthly menses)

A progesterone level >3 ng/mL is evidence of recent ovulation

24
Q

In a woman with PCOS, does a normal hemoglobin A1c exclude the possibility of impaired glucose tolerance?

A

No. Perform a 2-hr 75 g OGTT

25
Q

For PCOS, what treatment options are available to increase the frequency of ovulatory cycles?

A
  1. oral contraceptives
  2. if COCs are not tolerated or if contraindicated, alternate option is metformin
  3. metformin is also used to regulate menstrual cycle if COCs are contraindicated
26
Q

factors that are contraindicated in using COCs

A
  • cigarette smoking
  • HTN
  • migraines with aura
  • increased stroke risk: obesity, dyslipidemia, genetic variants predisposing to thrombosis
27
Q

Transmale patient with erythrocytosis on T injections. Next management?

A

switch to transdermal testosterone (causes less erythrocytosis than injections)
or
switching to longer-acting IM injections (testosterone undecanoate or SQ testosterone pellets)

28
Q

Treatments for patients with hirsutism and nonclassic CAH

A
  1. COCs are first line
  2. antiandrogen: spironolactone
29
Q

clomiphene citrate
1. MOA
2. site of action

A
  1. SERM (blocks estrogen receptor –> GnRH increases –> LH and FSH increase –> ovulation)
  2. hypothalamus
30
Q

letrozole (FDA off label use to induce ovulation)
1. MOA

A
  1. AI (decreases estradiol –> GnRH increases –> LH and FSH increase –> ovulation)
31
Q

In a perimenopausal women who does not desire pregnancy and is interested in hormonal treatment, what oral contraceptive should be used?

A

the lowest dose of ethinyl estradiol (20 mcg daily) - to decrease risk of VTE

32
Q

In a patient with primary ovarian insufficiency and positive 21-hydroxylase antibody, what is the next test to perform? Syndrome is called?

A

-get a morning cortisol and/or an ACTH stim test if am cortisol is < 18 ug/dl
-APS 2

33
Q

Mullerian agenesis:

  1. leads to? AKA?
  2. Affected persons have what type of phenotype at birth?
  3. karyotype?
  4. are breast development and growth of pubic hair normal?
A
  1. variable uterine development and congenital absence of the vagina. Termed the Mayer-Rokitansky-Kuster-Hauser syndrome. The uterus may be underdeveloped or absent.
  2. normal. Raised as girls, having functioning ovaries, normal external genitalia
  3. 46,XX
  4. yes

Mullerian structures: oviduct, uterus, cervix and upper vagina

34
Q

complete androgen insensitivity:

  1. clinical presentation?
  2. are Mullerian structures present or absent?
  3. this disorder is due to?
A
  1. primary amenorrhea, absence of axillary or pubic hair, serum testosterone within or above the normal range for boys and men, high LH, and normal FSH (due to inhibition by estrogen)
  2. absent (blind vaginal pouch and absent uterus and cervix)
  3. a defect in the androgen receptor that results in complete resistance to androgens
35
Q

Turner syndrome:

  1. clinical presentation?
  2. karyotype?
  3. appropriate screening?
A
  1. short stature, primary hypogonadism, a high rate of cardiovascular anomalies, a number of comorbidities
  2. 45,X
    • baseline echo/cardiac MRI - then f/u with cardiology as needed
      - annual TSH due to increased risk of hypothyroidism
      - annual fasting glucose and/or A1c due to increased prevalence of T2DM
      - serum vitamin 25OHD every 3-5 years
36
Q

Klinefelter syndrome:

  1. phenotype?
  2. karyotpe?
A
  1. male

2. 46,XXY

37
Q
  1. Postmenopausal hirsutism or virilization of recent onset with a serum T > 150 ng/dL or a serum DHEA-S > 700-800 ug/dL suggests?
  2. signs of virilization include?
  3. How does this differ from women with ovarian hyperthecosis?
A
  1. a neoplastic source of hyperandrogenism
  2. deepening of the voice, increased muscle mass and clitoromegaly
  3. for ovarian hyperthecosis, symptoms develop gradually
38
Q
  1. women with androgen-secreting adrenal tumors often present with?
A

Cushing syndrome + virilization.

Also often with DHEAS elevation (unlike ovarian tumors)

39
Q

androgen secreting ovarian tumors include?

A

Sertoli-Leydig-cell tumors, arrhenoblastomas, or hilus-cell tumors

40
Q

The first step in the evaluation of severe hyperandrogenism in postmenopausal women is?

A

transvaginal ultrasonography. If negative, then get adrenal CT (there are occasional cases of adrenal tumors that secrete only testosterone)

41
Q

Serum inhibin is a marker for?

A

some ovarian tumors, including granulosa-cell tumors and sex-cord stromal tumors

42
Q

serum 17-hydroxyprogesterone would be measured when there are concerns for?

A

nonclassic CAH due to 21-hydroxylase deficiency which is associated with HIRSUTISM, not virilization

43
Q

In a transgender man who has started testosterone therapy, what masculinizing features can occur within the first 6 months?

A 
oily skin (and sometimes acne);
after 6-12 months of therapy: deepening of the voice and increased muscle strength
44
Q
  1. what are the symptoms of premenstrual dyphoric disorder?
A
  1. premenstrual anger, irritability, and tearfulness that lasts for 1-2 weeks at a time. Accompanied by bloating, night sweats, and fatigue, with difficulty functioning at work.
    PMDD should resolve in the follicular phase.
45
Q

Case: 41 yo woman experiences severe hot flashes after total hysterectomy and bilateral salpingo-oophorectomy.
What is the treatment?

A

oral 17beta-estradiol, 2 mg daily or transdermal estrogen.
She is treated as one with primary ovarian insufficiency and therefore can prescribe higher dosages of estrogen than other women.

**Venlafaxine and gabapentin are options for some patients with breast cancer who cannot take estrogen

46
Q

A side-to-side gradient greater than [ ] in androgen concentrations correctly identifies most androgen-producing tumors

A

1.44

47
Q

Case: Patient with Prader-Willi syndrome p/w primary amenorrhea and stalled puberty. What is the most appropriate treatment?

A

Low dose estradiol (0.5 oral mg or 0.025 mg transdermal) and eventually progesterone to prevent endometrial hyperplasia from unopposed estradiol. This is PHYSIOLOGIC estradiol dose. Giving progesterone before breast development is complete can lead to less optimal breast development.

Do not use OCPs since doses are supraphysiologic and can lead to suppression of hypothalamus-pituitary-gonadal axis.

48
Q

a granulosa cell tumor of the ovary would present with?

A

HIGH estrogen levels

49
Q

Treatment of hirsutism in PCOS

A
  1. COCs (ethinyl estradiol + progesterone with low androgenic activity)

examples of progesterone with low androgenic activity: norgestimate, desogestrel, drospirenone, dienogest, ethynodiol, norethindrone, norethindrone acetate)

avoid: norgestrel and levonorgestrel (high androgenic activity and may contribute to hirsutism)

Endocrinology (8 decks)

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