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Endocrinology and Reproduction > Female Reproductive Endocrinology V > Flashcards

Female Reproductive Endocrinology V Flashcards

1
Q

Recall that peripheral fat expresses CYP19; thus this tissue can utilize the abundance of androstenedione and testosterone for the production of

A

Estrone (E1) and E2 respectively

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2
Q

Mildly, but chronically elevated E2 (generally in the mid-follicular phase range) with an increased E1: E2 ratio is common in

A

PCOS

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3
Q

These estrogens with elevated testosterone exert negative feedback on

A

FSH secretion

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4
Q

Many endocrine tissues can purportedly feed into PCOS, and these include the

A

Ovary, adrenal. and HPA

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5
Q

There are several genetic links coupled to PCOS inducing disruptions in

A
  1. ) Insulin sensitivty
  2. ) Androgen production
  3. ) Gonadotropin secretion
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6
Q

Regarding gonadotropin secretion and PCOS, an abnormally elevated GnRH pulse frequency is not uncommon, and this leads to an increase in

A

LH secretion while impairing FSH secretion

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7
Q

Recall that LH stimulates theca cell androgen production; and interestingly, insulin has a synergistic effect of

A

LH-stimulated androgen synthesis in theca cells

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8
Q

Androgen production (notably testosterone) is driven above that which occurs in normal ovaries with

A

Excess LH and slightly elevated Insulin

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9
Q

Of note is that abdominal obesity exacerbates many symptoms that can manifest during

A

PCOS

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10
Q

Glucose intolerance, insulin resistance, hyperandrogenemia, and others are examples of

A

Symptoms that we can see in PCOS

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11
Q

It should be mentioned that insulin resistance is essentially universal in the case of PCOS women with a body-mass index of

A

Greater than 30

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12
Q

How can we find BMI?

A

BMI = Weight (kg) / Height (m^2)

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13
Q

There is overlap in many of the symptoms of PCOS with those describing the

A

Metabolic syndrome

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14
Q

To summarize, the more “typical” PCOS phenotype is one of

A

Overweight w/ abdominal obesity, anovulation, and hyperandrogenism

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15
Q

First and foremost in the management of PCOS in overweight women is weight loss since this can reverse

A

Insulin resistance and hyperandrogenism

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16
Q

Has been correlated with restored ovulatory function and reduction in androgens in some PCOS women

A

Weight loss of 2-7%

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17
Q

Because of its effectiveness, lifestyle modifications should be considered as a first course of action in

A

Overweight PCOS women

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18
Q

Can help to normalize menstrual cyclicity and reduce any incidence of endometrial hyperplasia due to unopposed E2 seen in PCOS

A

The use of OCPs

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19
Q

A GnRH agonist which can assist in restoring normal gonadotropin secretion

A

Clomiphene

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20
Q

An insulin-sensitizing drug qhich by normalizing insulin responsiveness can assist in restoring ovulation

A

Metformin

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21
Q

Can aid in reversing hirsutism

-not commonly used

A

Antiandrogens (flutamide)

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22
Q

FSH (rFSH) can be used, but this technique is not routine since it can induce

A

Ovarian hyperstimulation syndrome

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23
Q

Following an rFSH regimine, we can also see an increased risk of

A

Multiple-fetus pregnancies

24
Q

Can be used in the event of elevated DHEAS in PCOS women

A

Exogenous glucocorticoids

25
Q

The neuroendocrine system is made up of the

A

Hypothalamus and pituitary

26
Q

Often occurs at the cellular/molecular level as a result of acute and/or chronic over-stimulation by a hormone

A

Desensitization

27
Q

Desensitization often works as a cellular failsafe system that prevents sustained

A

Hyperstimulation

28
Q

When the hormone affects the cell population from which it is released

A

Autocrine function

29
Q

When the hormone affects a neighboring population of different cells; without requiring the circulatory system as a vehicle

A

Paracrine function

30
Q

Use of the circulatory system to affect a target tissue

A

Endocrine function

31
Q

The genes for many protein hormones encode for the transcription and translation of immature (inactive) precursor hormone molecules known as

A

Pre-hormones or prohormones

32
Q

Often required in order for the mature hormone to be identified for secretion by the Golgi apparatus

A

Post-translational modifications

33
Q

Peripheral fat tissue, the brain/neural, heart, liver, and many other tissues possess some

A

Steroidogenic function

34
Q

Rely upon the physiology of positive feedback or feed forward

A

Stimulation tests

35
Q

One example of a stimulation test uses the physiology controlling the secretion of gonadotropin-releasing hormone (GnRH) and its stimulation of the

A

Gonadotropins

36
Q

During puberty, the hypothalamic hormone GnRH stimulates the secretion LH and FSH from the

A

Anterior pituitary

37
Q

Prior to puberty, has little effect on gonadotropin secretion

A

GnRH

38
Q

This endogenous mechanism is useful in the diagnosis of precocious puberty, and is the basis of the

A

GnRH stimulation test

39
Q

A child with signs and symptoms of precocious puberty can be given a dose of GnRH, and later, blood is drawn in order to measure

A

LH

40
Q

An elevation in LH above the reference standard for the child’s age and gender would indicate that

A

His/her pituitary has been prematurely activated

41
Q

This leads to the diagnosis of

A

Central (neuroendocrine) precocious puberty

42
Q

What are 5 other stimulation tests?

A
  1. ) ACTH
  2. ) CRH
  3. ) GH
  4. ) TRH
  5. ) OGTT
43
Q

Rely upon the physiology of negative feedback or some direct suppression of an endocrine system

A

Suppression tests

44
Q

ACTH is down regulated by

A

Cortisol

45
Q

TSH in down-regulated by

A

Thyroid hormones

46
Q

Gonadotropins are down-regulated by

A

Gonadal steroid hormones estradiol-17B, testosterone, and progesterone

47
Q

Growth hormone is down-regulated by

A

Hyperglycemia

48
Q

Aldosterone is down-regulated by an

A

Oral salt load

49
Q

One classic example where physiology was instrumental in evaluating endocrine function was in the use the

A

Dexamethasone (Dex) suppression test

50
Q

The dex suppression test was based upon the physiology of cortisol-dependent negative feedback on

A

ACTH secretion

51
Q

An extremely potent pharmacological derivative of Cortisol

A

Dex

52
Q

This test was thus used to diagnose

A

Hypercortisolism (Cushing’s disease and Cushing’s syndrome)

53
Q

Hypercortisolism driven by excess ACTH of pituitary origin; e.g., a pituitary adenoma

A

Cushing’s Disease

54
Q

In patients with Cushing’s disease, feedback inhibition \ upon ACTH by cortisol is reset to a much higher threshold. In this case, a high enough dose of dex suppresses

A

ACTH and cortisol

55
Q

Certain tumors can also secrete ACTH, and some of these neoplasms are not subject to negative feedback by

A

Dex

56
Q

Thus, if a patient has Cushing’s syndrome due to ectopic production of ACTH, the high dose dex suppression test may have little if any effect on

A

ACTH or cortisol levels

57
Q

In today’s world there are more direct methods to evaluate the presence and etiology of cortisol excess. Most commonly we measure

A

Salivary or urine free cortisol

Endocrinology and Reproduction (15 decks)

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