Neuroendocrine Flashcards

1
Q

4 neurohormones of the hypothalamus, not including GnRH

A

TRH
CRH
GHRH
Dopamine(!)

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2
Q

Where in the hypothalamus can you find the GnRH cell bodies?

A

The arcuate nucleus

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3
Q

Where do GnRH cells originate from?

A

The olfactory area (hence why the x linked Kallman syndrome is a due to failure of GnRH migration

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4
Q

When do primordial germ cells reach the genital ridge?

A

6 weeks

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5
Q

Describe a primordial FOLLICLE (no germ cell)

A

Single layer of squamous like granulosa cells

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6
Q

Describe a secondary follicle

A

Multiple layers of granulosa cells, with beginning of theca cell development

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7
Q

What is characteristic on an antral follicle?

A

Accumulation of follicular fluid

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8
Q

Where do male germ cells undergo spermatogenesis?

A

Seminiferous tubules

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9
Q

Define spermatogenesis?

A

The process by which an immature diploid spermatogonium becomes an haploid spermatozoa

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10
Q

Where do sertoli cells live?

A

They are secretory cells that line the seminiferous tubules

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11
Q

What are the first signs of gonadotropin independent primordial follicle maturation?

A

-Granulosa cells become cuboidal
-Increase in oocyte size
-Gap junction development between oocyte and

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12
Q

What happens to antral follicles that aren’t “rescued” by FSH

A

The undergo specifically, apoptosis, or programmed cell death

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13
Q

How does actually FSH promote follicle growth?

A

FSH stimulates the aromatase activity in granulosa cells creating the estrogenic environment required for continued cell growth (an androgenic environment fosters cellular atresia)

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14
Q

Besides size, how is the dominant follicle different then the other follicles?

A

More FSH receptors and more advanced microvasculature compared to the other follicles, allowing it to continue to grow

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15
Q

When in the luteal phase do progesterone levels peak?

A

midluteal phase

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16
Q

when are gonadotropins at their nadir?

A

Late luteal phase

17
Q

What part of the HPO axis does stress, weight loss, and eating disorders effect?

A

The hypothalamus, inhibiting GNRH neuronal activity, leading to dysfunctional gonadotropin secretion and anovulation (even though gonadotropin levels might be normal when checked.)

18
Q

What is the most common way that PCOS affects gonadotropin levels?

A

There is an INCREASE in serum LH due to increases in LH pulse frequency and amplitude, and normal to LOW concentrations of serum FSH. This causes disordered follicular development and ovarian hyperandogenism

19
Q

How does chronically elevated estrogen causes anovulation?

A

It inhibits FSH secretion necessary for follicular development, and then the poor follicular development doesn’t generate the estradiol levels necessary for the LH surge. (This is also why you dont get your period when your pregnant)

20
Q

Do you measure free or total T for PCOS?

A

Both. Total is the actual value, free is calculated

21
Q

Prometrium is what kind of progestin and what is the dose for women with POI?

A

Micronized progesterone. 200mg daily for 12 days a month

22
Q

What are the proteins produced by the liver that increase with estrogen?

A

thyroxine-binding globulin (TBG), corticosteroid-binding globulin (CBG), sex hormone-binding globulin (SHBG), triglycerides, high-density lipoprotein (HDL) cholesterol, and clotting factors

23
Q

Estrace is what type of estrogen?

A

micronized estradiol

24
Q

1mg of oral estradiol (estrace) is equivalent to what dose of oral conjugated estrogens (premarin)?

A

0.625mg conjugated estrogens

and 0.05mg transdermal estrogen

25
Q

What is considered a low dose ESTRADIOL patch (for HRT)?

A

0.014mg estradiol

26
Q

What does the National Academy of Clinical Biochemistry consider the upper limit of normal for TSH?

A

2.5mIU/L, because 95% of people without evidence of thyroid disease have a TSH <2.5. However if they lowered the upper limit from 4.5 to 2.5 then an additional 28 million people would be diagnosed with HypoT

27
Q

What is the ASRM’s 2015 statement on SCH (with TSH >2.5) and miscarriage?

A

There is FAIR evidence that SCH, defined
as a TSH level >4 mIU/L during pregnancy, is associated with
miscarriage, but insufficient evidence that TSH levels between
2.5 and 4 mIU/L are associated with miscarriage

28
Q

What composes a gonad

A

Germ cells AND somatic cells

29
Q

Where to primordial germ cells migraine from?

A

Hindgut/yolk sac where they originate to gonadal ridge, *Between 4-6 weeks

30
Q

What is the gene on SRY region of chromosome Y that determines a gonads becomes a testes?

A

TDF (testes determining factor)

31
Q

When do primordial germ cells differentiate into sertoli cells?

A

7 weeks. Sertoli cells +spermatogonia = testicular cords. Important because TCs produce AMH for mullerian regression, and ABP (androgen binding protein) to maintain high local adrogen environment for spermatogenesis

*Leydig cells differentiate at 8 weeks!

32
Q

The hormone produces by Leydig cells *starting at 8 weeks

A

Testosterone. Maintained by LH and maternal/placental HCG. Maternal HCG is why patients with Kallman syndrome still produce testosterone in utero and so have phenotypic appearance at birth

33
Q

What are the wolffian duct structures specifically

A

Epididymis, vas deferns, seminal vesicles * dependent on testosterone*
and
male external genitalia, urethra and prostate dependent on DHT

34
Q

Two genes necessary for ovarian developement

A

WNT-4, RSPO1- they suppress SOX9

35
Q

If the germ cells are undergoing mitosis for rapid aggregation of oogonia between 6-8 weeks, when do the oogonia undergo MEIOTIC division to become a primary oocyte arrested in prophase 1?

A

During the 11-12th week. Male spermatogonia do NOT undergo meiosis in utero

36
Q

In the neonate, how many oocytes have been lost since they reached there max at 20 weeks GA

A

80%! Now only 500,000-2 million by birth

37
Q
A