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Metabolic Endocrinology > Reproductive endocrinology > Flashcards

Reproductive endocrinology Flashcards

1
Q

what are the 2 sequential steps involved in sexual differentiation

A
  • establishment of genetic sex (XX or XY)
  • translation of genetic sex into gonadal sex (ovaries or testis)
  • translation of gonadal sex into phenotypic sex (secondary characteristics + reproductive organs)
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2
Q

About the X chromosome

A
  • 160 megabases
  • 5% of haploid genome
  • encodes 850 proteins of which several regulate gametogenesis and hypothalamus-pituitary functions BUT most result non-reproductive functions
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3
Q

About the Y chromosome

A
  • 60 megabaess long (2% of genome)

- encodes 57 proteins of which most genes regulate reproductive functions

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4
Q

most genes found on the X chromosome regulate reproductive functions. true or false

A

false, most genes regulate non-reproductive functions

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5
Q

what is Klinefelter syndrome

A

47 chromosomes with XXY

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6
Q

what is Turner’s syndrome

A

45 chromosomes with XO

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7
Q

which genotype of sex chromosomes is nonviable

A

45 chromosomes OY

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8
Q

what causes sex chromosome aneuploidy

A

nondisjunction of sister chromatids during meiosis

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9
Q

what causes sex chromosome mosaicism

A

nondisjunction of sister chromatids in zygote

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10
Q

if there is a Y chromosome with the ____ gene, there will always be a ____ phenotype

A

Y chromosome with functional SRY -> male

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11
Q

what does the non-viability of OY confirm?

A

Confirms that X chromosome is important for development of female reproductive tract but also for non-reproductive functions such as development of embryo

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12
Q

the Wolffian duct develops in _____

A

male reproductive tract

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13
Q

the Mullerian duct develops in ______

A

female reproductive tract

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14
Q

the ______ will differentiate into external genitalia depending on ______

A

urogenital sinus

depending reproductive tract

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15
Q

_____ are essential for male sexual differentiation, but the _____ are not necessary for female differentiation

A

testes are necessary for male sexual differentiation

ovaries are not necessary for female differentiation

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16
Q

germ cells are not _____ in origin

A

gonadal

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17
Q

pathway to go from primordial germ cells to testis or ovaries

A
  1. primordial germ cells differentiate in allantoic ectoderm
  2. they migrate into endoderm
  3. migration along endoderm and hindgut to the genital ridges
  4. genital ridges develop in ovaries or testis depending on the sex chromosomes brought by primordial germ cells
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18
Q

how do the primordial germ cells migrate

A

HORMONAL guiding with secretion of local factors

  • they put be polar during migration
  • migration involves cell protrusion and adhesion in the leading edge and retraction of the lagging edge
  • guiding cells biochemically direct the migration
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19
Q

what is the typical male development events during gestation

A
  1. germ cell migration until genital ridges -> differentiation into testis (week 5-6)
  2. Sertoli cells -> Mullerian duct regression
  3. Leydig cell -> Wolffian duct stabilization
  4. Male external genital differentiation
  5. external genital growth (week 20)
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20
Q

____ cells are involved in regression of the Mullerian duct and _____ cells stabilize the Wolffian duct

A

Sertoli cells -> regression of M duct

Leydig cells -> stabilization of W duct

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21
Q

what are the 3 pre-requisites for normal sex differentiation

A
  1. normal intact chromosome complement
  2. fully functioning sex determination genes
  3. intact steroidogenic pathway and receptors
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22
Q

genital ridges are considered to be _____ as they can differentiation either into testis or ovaries

A

bipotential

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23
Q

_____ are the regions on the X and Y chromosome s that can undergo recombination

A

Pseudoautosomal region PAR

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24
Q

the _____ region of the Y chromosome contains the ______ gene that allows for development of the testis

A

Male specific region of Y (MSY) contains the Sex determining region of Y (SRY)

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25
Q

how can fertilization by sperm produces an XX male?

A

The SRY gene is located very closely to the PAR1 region that undergoes recombination. Therefore, if there is recombination beyond PAR1, the SRY gene will be transferred to X chromosome leading to a sperm with X + SRY => fertilization by sperm produce an XX male

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26
Q

how can XY genotype result in an female phenotype

A

the Y chromosome may have a deletes/muted SRY gene therefore the primordial gonad will develop into an ovary -> XY female

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27
Q

what is the role of the HMG box found on the SRY gene

A

HMG box is the DNA binding domain which can regulate transcription of target genes

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28
Q

what are the consequences of mutations in the DNA binding domain of SRY gene

A

non-functional SRY -> female phenotype development although XY chromosomes

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29
Q

gonadial differentiation is based on the presence or absence of _____

A

SRY

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30
Q

development of testes depend on _____ and _____ factors

A

transcription and paracrine factors

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31
Q

which transcription factor gene is expressed by SRY

A

SOX9

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32
Q

SOX9 drives the expression of _____ and ____ which are paracrine factors

A

FGF9, Amh, PGD2

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33
Q

If there is no SRY, there is no SOX9 thus the biopotential gonad develops into ovary due to _____, _____, and ____

A

WNT4, RSPO1, FOXL2

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34
Q

if there is an ovary, the ____ duct continues to grow and _____ duct undergoes regression

A

mullerian duct

wolffian duct

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35
Q

if there is testis, the _____ duct undergoes regression

A

mullerian duct

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36
Q

How does the presence of testes results in male reproductive tract development?

A

if there are testes, Sertoli cells produce anti-mullerian hormones which bind to TGF-beta receptor 2 causing heterodimerization with TGF-beta receptor 1
-> phosphorylation of TGF-bR1 drives phosphorylate of transcription factors Smad: heterodimerization of Smad2 and 3 followed by trimerization with Smad4
Trimer complex translocates from cytoplasm to nucleus and binds to promoter region of genes expressing pro-apoptotic genes causing regression of mullerian duct

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37
Q

which genes cause regression of mullerian duct

A

pro-apoptotic genes

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38
Q

which nuclear receptor signals regression of wolffian duct, resulting in female reproductive tract and phenotype

A

NR2F2

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39
Q

what is the mechanism of action of NR2F2

A

NR2F2 inhibits FGF paracrine factor allowing for Wolffian duct regression

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40
Q

which are the survival factors for Wolffian duct

A

FGF

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41
Q

what are the various errors that can occur during sex differentiation

A
  1. defects in testosterone synthesis or actions

2. congenital adrenal hyperplasia

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42
Q

what are the consequences of defects in testosterone synthesis or actions

A

androgen insensitivity syndrome -> there is testicular feminization

  • phenotypic female with XY genotype
  • no ovaries
  • gonads develop into testes but cryptorchidism (undescended testicle)
  • infertile (spermatogenesis is disrupted)
  • blind ending vagina
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43
Q

in androgen insensitivity disorders, where can the error come from?

A

there is either disruption/problem with any of the enzymes involved in steroidogenesis converting cholesterol into androgen (steroidogenesisi stops at previous step) OR all the enzymes are functional and androgen metabolites are produced in sufficient amounts BUT problem is at the receptor level

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44
Q

what is congenital adrenal hyperplasia CAH

A

masculinization of external genitalia at birth due to hyperplasia of adrenal glands before birth -> excessive androgen production -> masculinization of genitalia

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45
Q

which enzyme is mission in CAH that causes reduced synthesis of aldosterone and cortisol but excessive androgen production

A

CYP21A2

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46
Q

what is the normal development of females external genitalia

A
  • primordial gonad develops into ovary as there is not Y chromosome with SRY gene
  • no testosterone -> no development of wolffian duct or male reproductive tract and no DHT (dihydrotestosterone)
  • no anti-mullerian hormone AMH therefore mullein duct is maintained -> uterus
    => female external genitalia
47
Q

what happens in CAH females in terms of phenotype development

A
  • primordial gonad develops into ovary as there is not Y chromosome with SRY gene
  • no anti-mullerian hormone AMH therefore mullein duct is maintained -> uterus
  • HOWEVER there is more androgen synthesis from bona reticular due to lack of CYP21A2 therefore DHT (dihydrotestosterone) concentration Is high -> masculinization of external genitalia
48
Q

what is responsible for masculinization of external genitalia in CAH female

A

high dihydrotestosterone DHT concentration due to increased androgen synthesis

49
Q

when does sexual differentiation in brain (marked differences between the sexes - structural and behavioural) occur in primates

A

3-6 months prenatal

50
Q

there is ______ in terms of brain structure

A

sexual dimorphism

51
Q

how is sexual differentiation of the hypothalamus in male carried out

A
  • the fetal testis secretes testosterone which freely enters the brain and is converted to estradiol/estrogen
  • estrogen defeminizes the surge centre in males (does not develop)
  • male has tonic cents to control LH/FSH post-puberty
52
Q

unlike males, females have both _____ and _____ that are active

A

females have both tonic and surge centers

53
Q

what is the difference between male and females in regards to sexual differentiation of the hypothalamus

A
  • males have fetal testes that secrete testosterone which can cross the blood Brian barrier and be converted into estradiol which eventually inactivates the surge centre (defeminization) and keeps only tonic centre active to control LH/FSH post-puberty
  • in females, estradiol produced by fetal ovary cannot cross the blood brain barrier as it binds to alpha-FetalProtein (a-FP) thus, the female restainssurge centre + tonic centre to control LH/FSH after puberty
54
Q

the lack of estrogen inside the CNS allows for development of ______

A

surge center

55
Q

what are the functions of alpha-fetal protein

A

a-FP is produced very early in embryonic development, it is also produced by fetal liver and functions as albumin, binding to fat soluble molecules
it can also bind to estrogen in females which allows for the development of the surge centre since estrogen won’t be able to cross the BBB

56
Q

describe the hypothalamo-pituiary-gonadal axis

A
  • environmental factors + physiological factors act on brain/hypothalamus -> secrete GnRH -> acts on pituitary -> LH and FSH are secreted and acts on gonads -> gametogenesis, gonadal growth, steroidogenesis (testosterone or estrogen)
    Steroidogenesis has a negative feedback on hypothalamus and pituitary
57
Q

what are the functions of the gonads (testis and ovaries)

A

gonads -> gametogenesis and steroidogenesis

Steroidogenesis -> electrolyte homeostasis, fuel and protein metabolism, adiposity ad muscle mass

58
Q

describe the plasma testosterone levels at various ages in human males

A
  • increase during fetal development
  • increase during Neo-natal period
  • gonads quiescent pre-pubertal period (super low levels)
  • exponential increase in levels during puberty
  • slow decrease during adulthood and onwards
59
Q

what are the signs of female puberty? male puberty

A
  • females: first cycle - menarche in women
  • males: first ejaculation - semenarche/spermache
    => both events do not signify fertility (fertility reaches its maximum later than puberty)
60
Q

GnRH is released in a ____ fashion. It controls _____

A

pulsatile fashion

controls puberty/sexual development

61
Q

tonic enters are extremely sensitive to ________

A

steroid negative feedback

62
Q

what happens before puberty and after puberty in regards to changes in hypothalamic secretion of GnRH

A

Before puberty: in female and male, GnRH neurons in both the tonic centre and the surge centre of the hypothalamus release low amplitude and low frequency pulses of GnRH
After puberty: in female, the tonic centre controls basal levels of GnRH but they are higher than in prepubertal female because the pulse frequency increases. The surge centre control the preovulatory surge of GnRH. the male does not develop the surge centre

63
Q

what controls the preovulatory increases of GnRH

A

the surge centre -> controls preovulatory surge in GnRH

64
Q

what causes the increase in GnRH pulses (amplitude and frequency)

A

decreased sensitivity of TONIC centre to negative feedback from gonadal steroids

65
Q

which neurons regulate pulsatile secretion of GnRH

A

Kisspeptin KISS1 neurons

66
Q

where are Kisspeptin neurons located

A

located in anteroventral periventricular and arcuate nuclei of the hypothalamus
=> AVPV and ARC nuclei

67
Q

the KISS1 enrols in ARC are initiated by _____ and regulate ______

A

inhibited by steroid feedback and regulate tonic centre => negative feedback

68
Q

the KISS1 neurons in AVPC are activated by _____ and regulate _____

A

activated by estradiol and regulate tonic centre

69
Q

GnRH neurons don’t express _____ thus their regulation is done by other neurons _____

A

GnRH neurons don’t express steroid hormone receptors (androgen receptors) thus are regulated by KISS1 neurons

70
Q

GnRH stimulate gonadtraophs in ______

A

anterior pituitary

71
Q

GnRH is only synthesized in the hypothalamus. true or false

A

false, it is also synthesized din the placenta, gonads, breast, lymphocytes and pituitary but the function is unknown

72
Q

FSH and LH have a common ____ sub and different ____ subunit

A

common alpha subunit

different beta subunit

73
Q

the alpha chain of FSH and LH is also common to ____

A

TSH

74
Q

LH stimulates GPCR receptors and activate which pathways?

A

cAMP/PKAabd PLC-> IP3 and DAG

75
Q

FSH stimulates GPCR receptors and activate which pathway

A

Granulosa cells and sertoli (male) cells -> cAM/PKA

76
Q

what are the actions of LH and FSH

A

similar to ACTH on adrenal cortex cells

  • increase of intracellular cholesterol
  • trnasport of cholesterol to the inner mitochondrial membrane by StAR (rate limiting step)
  • conversion to pregnennolone by side chain cleavage (CYP11A1)
77
Q

what are the target cells of LH and FSH in tetsis

A

LH acts on Leydig cells (testosterone) and FSH on Seertoli cells (estradiol)

78
Q

what are the target cells of LH and FSH in ovaries

A

LH acts on theca interna (testosterone), granulosa cells (estradiol) and luteal cells (progesterone) and FSH acts on granulosa cells (estradiol)

79
Q

what are the three difference cell types of importance in spermatogenesis

A
  • spermatogonia
  • sertoli cells
  • leydig cells
80
Q

which are the most important androgens secreted by testes

A

DHEA and testosterone

81
Q

adrenal and testes contribution to DHEA and testosterone secretion is equivalents. true or false

A

false, testes have a greater contribution to androgen secretion -> adrenal secretion contribution is less than 5%

82
Q

98% of testosterone and DHEA secretion is in bound form. what do they bind to

A

albumin and sex-hormone binding globulin SHBG

83
Q

testosterone can be converted into ____ (its active form) or _____

A

DHT or estradiol

84
Q

what is the action of androgens

A

powerful anabolic hormones

  • production of steroid hormones -> secondary sex characteristics at puberty
  • spermatogenesis, skeletal muscle growth, larynx development, hard growth, behavioral changes, changes in excretion of sebaceous gland (acne)
85
Q

the oocyte is surrounded by single cell layer of granulosa to form ______

A

primordial follicles

86
Q

there is a _____ in number of primordial follicles before brith and a _____ of primordial follicles after birth

A

an increase in number until 5th month of gestation

after that -> continuous loss

87
Q

which follicles en up ovulating

A

mature follicles

88
Q

the remnant of ovulated follicle forms ______

A

corpus luteum

89
Q

what is the relationship between theca/LH and granulosa/FSH cells

A

the cells of the theca interna contain receptors for LH. Theca cells produce testosterone from cholesterol that diffuses into the granulosa cells that contain FSH receptors. Binding of FSH to the granulosa cell receptors causes the synthesis of enzymes that are responsible for the conversion of testosterone to estradiol

90
Q

which enzyme is responsible for the conversion of cholesterol into testosterone in theca cells

A

CYP17A1

91
Q

which enzyme is responsible for the conversion of testosterone to estradiol E2 in granulosal cell

A

CYP19A1

92
Q

ovarian follicles have 2 somatic cells which are

A

granulosa cells and theca cells

93
Q

what are the 2 conditions for estradiol to have a positive feedback on surge centre

A
  1. high estradiol

2. low progesterone

94
Q

inhibit produced by granulosa cells of ovary specifically inhibits ____- secretion

A

FSH

95
Q

what is he difference between tonic vs surge centre

A
  • tonic center relates small episodes of GnRH in a pulsatile fashion similar to a dripping faucet -> episodic release is continuous throughout reproductive cycle
  • surge centre is sensitive to positive feedback and releases high amplitude, high frequency pulses of GnRH (gushing, wide-opened faucet) in a relatively short period after estrogen reaches a threshold level
96
Q

ovulation occurring at the middle of menstrual cycle is preceded by a dramatic increase in LH. why?

A

the dramatic release is due to preovulatory LH surge from surge centre positively regulated by high estradiol and low progesterone

97
Q

what are the changes occurring during the menstrual cycle

A
  • in the early part of the menstrual cycle, there is an increase in FSH (follicle stimulating hormone) which stimulates follicle growth and maturation
  • the maturing follicle will release estradiol
  • high estradiol concentration in combination with low progesterone will have a positive feedback on the surge centre and stimulate GnRH release
  • GnRH release will cause a dramatic increase in LH right before ovulation happening mid-cycle => pre-ovulatory LH surge
    > all of this describes the FOLLICULAR PHASE
  • once ovulation occurred, the remnants of the follicle will develop into corpus luteum
  • the corpus luteum produces a lot of progesterone -> surge in progesterone concentration + increase in estradiol
  • decrease in progesterone and estradiol + increase in FSH -> luteolysis
    > LUTEAL PHASE
98
Q

what are the 2 phases involved in the menstrual cycle

A
  • follicular phase

- luteal phase

99
Q

women have ____ cycles where are bovine have _____ cycles

A 
menstrual cycle (mess at the beginning and end of cycle, ovulation in the middle)
estrous cycle (ovulation occurs at the beginning and end of cycle)
100
Q

what is the hormonal profile during estrous cycle

A
  • Luteal phase: increase in FSH which stimulates follicular wave development increase in progesterone and estradiol for follicular development -> no LH surge -> no ovulation + FSH peak with low estradiol -> negative feedback on pituitary (GnRH)
  • Follicular phase: low progesterone, high estradiol -> positive feedback on surge centre -> pre-ovulatory LH surge -> ovulation
    after ovulation, corpus luteum development > progesterone increases -> goes back to luteal phase
101
Q

the dominant follicle is the one to secrete ____. if at this time there is high progesterone due to _____, there will be no _____.

A

dominant/mature follicle secretes estradiol. if at this time there is high progesterone due to corpus luteum, there will be no LH surge and in turn no ovulation

102
Q

reduction fo estradiol allows for _____ to increase causing a second follicular wave

A

FSH concentration

103
Q

pre puberty there are waves of _______ but due to insufficient ______ there is no _____ and atresia occurs

A

follicular growth but due to insufficient FSH/LH there is no maturation and atresia occurs

104
Q

how does the resumption of the first meiosis occur

A

the pre-ovulatory LH surge causes the breakdown of the gap junctions between the granulosa cells and oocytes therefore the molecules inhibitory of meiosis will no longer be provided by granulosa cell -> resumption of meiosis

105
Q

how does the preovulatory LH surge allow for fertilization

A

preovulatory LH surge breaks-down the gab unction between granulosa cell and oocyte -> removal of meiotic inhibition -> first polar body (small daughter cell) -> haploid oocyte, 2nd polar body (big daughter cell ) -> can undergo fertilization

106
Q

fertilization can only occur if _____ occurs

A

ovulation (haploid oocyte has to get out of follicle)

107
Q

what are the ovarian events caused by the preovulatory LH surge leading to ovulation

A
  • increase in blood flow to ovary and dominant follicle -> increase in follicular pressure
  • increase in PGF2alpha -> increase in contraction of ovarian smooth muscle and release of lysosomal enzyme -> increase in follicular pressure and follicle wall weakens, respectively
  • shift from estradiol to progesterone by dominant follicle -> follicle wall weakens
    => increase in follicular pressure + follicle wall weakens => ovulation
108
Q

what are the 3 factors allowing for ovulation

A
  • follicular rupture
  • luteinization
  • resumption of meiosis
109
Q

LH stimulates the corpus luteum to secrete ____

A

progesterone

110
Q

the formation of corpus sputum is also known as ____

A

luteinization

111
Q

what are the effects of the progesterone secreted by CL

A
  • P4 has negative feedback on GnRH neurons of hypothalamus -> GnRH, LH/FSH suppressed -> little sterogen produced
  • P4 exerts positive influence of endometrium of uterus -> embryo development
  • P4 has negative effect on contractility of myometrium
  • involved in development of mammary gland if fertilization occurs
112
Q

if there is no fertilization, what happens to CL

A

luteolysis

113
Q

what is the proposed mechanism of luteolysis in primates

A

increased concentration of oxytocin within ovary that contain CL which increases protaglandin F2 alpha -> luteolysis -> reduction of progesterone and estradiol -> menses

Metabolic Endocrinology (10 decks)

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