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RER2.10_Female Repro_ZACHOW > Part 7: > Flashcards

Part 7: Flashcards

1
Q

Non-hormonal signs of menopause (3):

A
  1. variable cycle length.
  2. skipped cycles.
  3. amenorrhea.
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2
Q

Menopause is characterized by how many months of amenorrhea?

A

12.

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3
Q

Menopause hormonal signs (2):

A
  1. decreased estrogen.
  2. increased FSH:LH ratio.
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4
Q

Menopause prior to age 40 is abnormal and classified as:

A

primary ovarian insufficiency.

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5
Q

The decrease in E2 and inhibin B production in menopause is due to:

A
  • severely limited number of growing follicles, which produce E2.
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6
Q

The increase in FSH production in menopause is due to (2):

A
  1. loss of E2 negative feedback.
  2. decreased inhibition by Inhibin B.

Both E2 and Inhibin B are produced by growing GCs.

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7
Q

Source and function of anti-Mullerian hormone (AMH) in reproductive-aged females:

A
  • Source: granulosa cells within small growing follicles.
  • Function: suppresses follicular recruitment via reducing young follicle FSH-sensitivity.
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8
Q

What occurs to anti-Mullerian hormone (AMH) levels during the years leading up to menopause?

A
  • decreases due to less granulosa cells within small growing follicles.
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9
Q

What leads to an increase in recruitment and accelerated atresia/exhaustion of the follicular reserve (primordial cells) during the years leading up to menopause (2)?

A
  • decreasing levels of anti-Mullerian hormone (AMH).
  • increasing levels of FSH due to decreased E2 and inhibin B levels.
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10
Q

Draw levels of E2 and FSH during the menopausal transition:

A
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11
Q

With increasing maternal age, what birth risks increase (3)?

A
  1. decreased chance of live birth; due to less viability of oocytes.
  2. increased risk of maternal mortality.
  3. increased risk of embryo aneuploidy.
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12
Q

Risk factors that have to be evaluated prior to hormonal therapy (4)?

A
  1. cardiovascular disease
  2. thromboembolism
  3. breast cancer
  4. prior stroke or TIA
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13
Q

E2-associated benefits in perimenopausal women include (3):

A
  1. decreased cardiovascular risk.
  2. bone density.
  3. vasomotor control.
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14
Q

Hormonal therapy for a woman with a uterus:

A

E2 + P4.

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15
Q

Hormonal therapy for a woman without a uterus:

A

E2 only.

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16
Q

Why is E2 + P4 hormonal therapy given to women with uteruses?

A
  • E2 triggers proliferation and angiogenesis of endometrial tissue; cancer risk.
  • High P4 levels downregulates P4-R and ERα expression in endometrium.
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17
Q

Endometriosis is caused by:

A
  • abnormal extra-uterine deposits of E2-responsive endometrial tissue.
18
Q

By which mechanism do endometrial fragments become deposited within the extrauterine environment?

A

retrograde menstruation.

19
Q

Extrauterine endometrial lesions most commonly form in which regions of the female anatomy (3)?

A
  1. pelvic peritoneum.
  2. ovaries.
  3. rectovaginal septum.
20
Q

Symptoms of endometriosis include (3):

A
  1. dysmenorrhea (painful periods).
  2. dyspareunia (painful sex).
  3. infertility.
21
Q

What genetic changes occur in the cells of extrauterine endometrial lesions (5)?

A
  1. ability to evade immune destruction.
  2. growth factors for neoangiogenesis.
  3. nerve recruitment.
  4. increased CYP19 (aromatase; increases E2 supply).
  5. decreased progesterone receptors.
22
Q

How do cells of extrauterine endometrial lesions elevate local E2 levels?

A
  1. express high levels of CYP19 (aromatase); E2 production favored.
  2. express prostaglandins that promote increased CYP19 expression.
23
Q

What drugs can be utilized to decrease E2 levels in the setting of endometriosis, and why (4)?

A
  1. GnRH agonists; alter GnRH pulsality.
  2. Progestins; decrease LH>FSH secretion.
  3. Aromatase inhibitors; decreases E2 production.
  4. Androgens.
24
Q

Key diagnostic features of PCOS (2):

A
  1. anovulation (amenorrhea or oligomenorrhea).
  2. elevated androgens.
25
Q

Androgen-linked physcial symptoms of PCOS:

A
  • hirsuitism
  • acne
26
Q

Congenital adrenal hyperplasia (CAH) is a disruption in adrenal cortical steroidogenesis due to:

A

21-hydroxylase enzyme mutation.

27
Q

Function of the enzyme 21-hydroxylase:

A
  • required for cortisol and aldosterone production in the adrenal cortex.
28
Q

How can hyperandrogenemia result from a 21-hydroxylase enzyme mutation (CAH)?

A
  • androgen precursor (DHEAS and androstenedione) steroidogenesis favored since only functioning cortical steroidogenic pathway.
  • Theca cells convert to testosterone; hyperandrogenemia results.
29
Q

How do increased circulating androgens (testosterone) lead to infertility?

A
  1. testosterone converted to E2 via hypothalamic CYP19.
  2. E2 binds to hypothalamic ERα receptors.
  3. FSH > LH secretion mainly blocked.
30
Q

How can HyperPRLemia and Cushing’s Syndrome cause infertility?

A
  • Prolactin and cortisol both inhibit LH/FSH secretion.
31
Q

Body type of most women presenting with PCOS:

A

android obesity.

32
Q

The insulin model of PCOS:

A
  1. increased abdominal fat leads to insulin resistance.
  2. hyperglycemia occurs in response to insulin resistance.
  3. hyperinsulinemia occurs due to hyperglycemia.
  4. LH + insulin has a synergistic effect on Theca cell androgen production.
  5. Hyperandrogenemia decreases LH/FSH secretion.
  6. anovulation results due to decreased FSH levels.
33
Q

What molecule has a synergistic effect of LH-stimulated androgen production in Theca cells?

A
  • insulin.
34
Q

LH model of PCOS:

A
  1. Altered GnRH pulse generator firing frequency.
  2. Excess LH secretion.
  3. Hyperactivation of Theca cells; androgen production increased.
  4. Hyperandrogenemia results.
  5. Hyperandrogenemia decreases LH/FSH secretion.
  6. Anovulation results due to decreased FSH levels.
35
Q

Effect of anovulation on LH levels:

A
  1. No ovulation.
  2. Very low progesterone production.
  3. Large decrease in progesterone-mediated negative feedback on LH secretion.
  4. Increased LH.
36
Q

Adrenal model of PCOS:

A
  1. excess adrenal cortical androgen precursors (DHEAS and androstenedione).
  2. steroid sulfatase in the ovaries converts DHEAS to DHEA.
  3. Theca cells use DHEA and androstenedione to produce testosterone.
  4. hyperandrogenemia results.
  5. hyperandrogenemia decreases LH/FSH secretion.
  6. anovulation results due to decreased FSH levels.
37
Q

Anabolic androgen steroids decrease levels of (4):

A
  • sex-hormone binding protein (SHBG).
  • LH/FSH (negative feedback).
  • Testosterone.
  • Estrogen.
38
Q

Low sex-hormone binding protein (SHBG) =

what testosterone levels?

A

high testosterone.

39
Q

High sex-hormone binding protein (SHBG) =

what testosterone levels?

A

low testosterone.

40
Q

What enzyme levels are extremely elevated in CAH?

A

17α-hydroxyprogesterone.

RER2.10_Female Repro_ZACHOW (7 decks)

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