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kris Endocrinology > Section 7- Reproductive endocrinology > Flashcards

Section 7- Reproductive endocrinology Flashcards

1
Q

Sequential process of sexual differentiation

A
  1. Establishment of genetic sex
  2. Translation of genetic sex into gonadal sex
  3. Translation of gonadal sex into phenotypic sex
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2
Q

Which duct is typical for males and which is for females?

which organs does each of those ducts give rise to?

A

Females: mullerian duct-> Female tract (oviduct, uterus, upper vagina)

Males: Wolffian duct-> Male tract (Epididymis, vas deferens, seminal vesicle)

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3
Q

What is urogenital sinus?

A

common primordium for external genitalia

Will develop in either Clitoris and vulva in females, or penis and scrotum in males

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4
Q

What happens if we remove testes from embryos? What happens to female embryos that had their gonads removed?

What does that mean?

A

embryos developed a female reproductive tract and female genitalia.

But, gonadectomised female embryos also developed into female features

it means that The TESTES are essential for male sexual differentiation, but the ovaries are NOT necessary for female differentiation

-> embryos develop in females by default and a switch is requried for an embryo to start developign in a male

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5
Q

Which of the developmnet pathways (male or female) are dependent on hormones? Why

A

Male development pwathway is hormonal dependent as hormones act as a switch to swith from default female pathway into male pathway

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6
Q

Pre-requisites for normal sex differentiation

A

Normal intact chromosome complement
Fully functioning sex determination genes

Intact steroidogenic pathway and receptors

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7
Q

Is female fomration abolutelty default?

A

No, it stil requires some signalling but less than in males

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8
Q

Allozome vs isozome

A 
allozome= sex chromosomes
isozome= all chromosomes
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9
Q

What are the functions of sexes that result form sexual differentiation

A

Males: provision of sprem, provision of different set of chromosomes

Females: Provision of eggs, Fertilization, Pregnancy, Lactation

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10
Q

Classification of sexual differences: Chromosomal, gonadal, inernal ducts, external genitalia, Phenotypic, behavioural

A
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11
Q

What are all the possible male and female phenotypes?

A
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12
Q

Presence of _ = MALE

A

Presence of Y = MALE

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13
Q

How does sexual reproduction produce new combinations of genes? Why is it beneficial?

A

recombination occurs between homologous chromosomes-> genetic variation-> benefit for survival

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14
Q

Which regions of sex chromosomes can participate in recombination

A

only a small portions on either ends of X and Y that can participate in recombination-> these are called pseudoautosomal regions

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15
Q

What is MSY region

A

MSY does not participate in recombination at all; it is the whole of Y chromosome, but the PAR region (Pseudoautosomal region that participates in recombination)

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16
Q

Does the whole X chromosome participate in recombination?

A

The whole X chromosome participates in recombintion only if 2 Xs are present

if X and Y are present, only the PAR regions of X participate in recombination

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17
Q

What is SRY? Where is it found?

A

Sex determining region of Y

Present in MSY (Male specific region of Y)

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18
Q

Proof of the role of the SRY gene

A

male Y chromosome was cut up in chunks
DNA pieces were injected into pronuclei in hope for integration into a sex chromosome

Some embryos contained ovaries, some contained testis

They were interested in those, that contained tesits as they had male phenotype, but had female chromosomal pattern XX

some fetuses had XX but yet had testes due to SRY gene DNA- Thus SRY is required for testis development and male phenotype

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19
Q

What is the effect of SRY on Bipotential Genital ridge

A

Converts Bipotential Genital ridge into testis

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20
Q

Why is the location of SRY in MSY a bit problematic

A

SRY is oacted close to the region that participates in recombination

1) Can lead to XX male
2) Y chromosome can have abnormal SRY-> Deleted/mutant SRY gene-> XY female

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21
Q

What is the role of HMG proteins

A

bend the DNA after they bind to it

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22
Q

SRY has DNA __ capability

A

SRY has DNA binding capability

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23
Q

in which region of DNA are SRY genes found?

A

In DNA binding domain

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24
Q

SRY protein binds to DNA to __ because it is a __

A

SRY protein binds to DNA to induce trancription of other genes because it is a transcription factor

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25
Q

What is the consequence of SRY absence in sex determination?

Se

A

SRY absence: Ovary is formed-> female

SRY presence: SOX9-> testis-> male

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26
Q

At what day is SRY expressed in bipotential gonad?

A

day 10-12

27
Q

SOX9 expression is __ throughout embryonic development in the gonad

A

SOX9 expression is continuous throughout embryonic development in the gonad

28
Q

SOX9 and SRY relationship

A

SOX9 is the target gene of SRY

As pregnancy progesssess:

SOCS9 takes over the role of SRY

SOCS9 inhibits the expression of SRY

29
Q

How does SOX prevent the embryo from becoming a female

A

other factors + SOX9 lead to amh expression
- anti mullerian hormone (or MIS Mullerian inhibiting substance)-> responsible for destruction of mullerian duct (which transforms into female reproductive organs)
Wolffian duct takes over-> male is formed

Female phenotype requires other hormones and proteins (WNT4 and RSPO1) along with TF FOXL2 determines ovary formation and thus female phenotype - these have to be present to form fa female (thus it is not formed by default)

30
Q

What is the site of GnRH production?

A

hypothalamus is the site of GnRH production as there ar GnRH neurones

31
Q

WHat are the 2 centers of the hypothalamus that release GnRH?

A

It is synthesized in two different centres of the hypothalamus, the tonic (male) and the ovulatory or surge centre (female).

32
Q

Estradiol entrance to the brain: male vs female fetus

What is the consequent effect

A

In male fetus, testosterone freely enters brain and converted to estradiol by aromatase

  • as testosterone is not bound to a protein that is produced only during fetal period
  • this protein is called alpha-fetal protein; produced by fetal liver

In female, estradiol cannot cross the blood-brain barrier (binds to alpha-Fetoprotein)

  • this is why estradiol doesn’t end up in the brain and de-feminize the surge center
    absence of estrogen causes the surge center to mature and become functional post-puberty
  • Female retains surge center + tonic center to control LH/FSH after puberty

this estrogen presence in the brain is responsible for de-feminization, lack of maturation of another center called surge center

33
Q

what is the imortance of the surge center in females?

A

surge center is important for females in the post puberty period where there’s a surge release of GnRH, leading to a surge release of gonadotropins that are responsible for ovulation and reproductive cycle

34
Q

The hypothalamo-pituitary-gonadal axis

A

hypothalamus produces GnRH
which stimulates the production of FSH and LH from the pituitary
They act upon gonads to produce gonadal hormones that can have negative impact on hypothalamus and pituitary

35
Q

The function of the gonads

A
  1. Gametogenesis
  2. Hormonogenesis (mostly steroids)
    1. Electrolyte homeostasis
    2. Fuel and protein metabolism
    3. Adiposity and muscle mass
36
Q

Effect of plasma testosterone levels at various ages in human males

A

testosterone levels at fetal stage are responsible for Sexual differentiation (maturation of testis and their descent, formation of reproductive organs, formation of tonic center and inhibition of surge center)

testosterone levels at neonatals stage are a tiny bit hihger than at fetal, but the function is unknown; some infants show pimple development because of this increase

Pre-puberty: Gonads quiescent in both sexes

Surge in pubertal perdiod and remains high durign adulthood (same increases are seen in estradiol in females )

37
Q

What are the chnages that occur in puberty

A

Includes all physiological, morphological & behavioral changes

v Gonads/brain/phenotype change from adolescent to adult

v In females, first menstrual cycle – menarche

v In males, first ejaculation - semenarche

38
Q

GnRH, FSH and Lh levels: Prepubertal period vs Puberty

A

Prepubertal period

  • minimal GnRH release; low amplitude and low frequency
  • FSH and LH low
  • minimal to no folliculargenesis or spermatogenesis

Puberty

  • increase in the pulse frequency and amplitude of GnRH release
  • once the puberty occurs, the tonic center produces more frequent GnRH pulses; in case of adult females only, the surge center becomes active and results in massive release of GnRH
  • increase in FSH and LH pulses
  • folliculargenesis and spermatogenesis occur
39
Q

What are the changes in that occur in hypothalamic senstitivity to estradiol and negative feedback that allow puberty to occur

A
40
Q

Gonadotrophin Releasing hormone- structure

A

vSmall peptide of 10 a.a. cleaved from a larger precursor

vSynthesized by about 1000-3000 neurons in the hypothalamus

41
Q

Where do axons of neruones that release Gonadotrophin Releasing hormone terminate? What is their consequent role?

Where else is GnRh made and what is the role?

A

vMost axons terminate in the hypophyseal portal capillaries and release GnRH → Stimulation of gonadotrophs in the anterior pituitary

vSome axons terminate in other brain areas and may affect sexual behavior

GnRH is also synthesized in the placenta, gonads, breast, lymphocytes and the pituitary, but function unknown

42
Q

Structure of Gonadotropins LH and FSH

A

Glycoprotein

43
Q

What are the subunits of Gonadotropins LH and FSH

A

Common α-subunit and different β-subunit that provides specificity (there’s LH-beta and FSH-beta gene).

the alpha-gene is not only common for gonadotropins, but also for TSH

44
Q

What are the consequences of changes in glycosylation of Gonadotropins LH and FSH that may occur in circulation

A

different isoforms with slightly different biological properties

45
Q

What is the receptor and pathways used by LH and FSH

A

G-linked: Activation of adenylate cyclase and also phospholipase C (PKA and PKC pathways)

46
Q

What is the release pattern of LH and FSH

A

Pulsatile release (in response to GnRH)

47
Q

Which cells have LH receptors? What is the pathways tiggered by LH binding in these cells?

A

Thecal cells in females; Leydig cells in males

1) Adenylel cyclase-> cAMP-> PKA
2) Phospholipase C-> DAG-> PKC
2) Phospholipase C-> IP3-> Ca2+

48
Q

Which cells have FSH receptors? Which pathways are triggered in these cells by FSH binding?

A

Granulosa cells; sertoli cells

Adenylel cyclase-> cAMP-> PKA

49
Q

What is the overall effect of gonadotropins on gonads

A

Oogenesis, spermatogenesis, steroidogenesis

Target cells and actions differ in male and female

  • Testis: Only LH is steroidogenic (acts on Leydig cells)-> produce testosterone
  • Ovaries: Both LH and FSH are steroidogenic act on two cell types (theca and granulosa cells)
50
Q

What are the actions of LH and FSH in non-gonadal tissues?

A

v Increase of intracellular cholesterol.

v Transport of cholesterol to the inner mitochondrial membrane by StAR

v Conversion to pregnenolone; effect and mechanism similar to ACTH action in adrenal cortex

51
Q

What is the role of sertoli cells?

A

sertoli cells main role is to support spermatogenesis, but they can also produce some estrogen when stimulated by FSH; thus sertoli cells also have some steroidogenic role

52
Q

What are the 2 stages of follicules

A
  • primordial
  • primary
  • secondary
53
Q

What are the types of somatic cells in follicles

A

1) Theca cells are the endocrine cells associated with ovarian follicles that play an essential role in fertility by producing the androgen substrate required for ovarian estrogen biosynthesis.
2) A granulosa cell or follicular cell is a somatic cell of the sex cord that is closely associated with the developing female gamete

54
Q

What is a follicular antrum?

A

The follicular antrum is the portion of an ovarian follicle filled with follicular

55
Q

What is the role of corpus luteum?

A

it is the main producer of progesterone which is essential for the establishment of pregnancy and maintenance

56
Q

Positive and netative feedback of estrogen

A

low estrogen can have a negative effect at the level of pituitary and tonic center as a negative feedback loop. It will inhinbit LH and FSH release
but higher levels of estrogen can act upon the surge centre as a positive feedback which results in GnRH surge release-> pre-ovulatory FHS and LH surge-> ovulation

57
Q

Do we have just 1 follicule growing at one particular time?

A

group of follicles grow together at a certain period of time, but there is one follicle that will continue to grow; other follicles will undergo attrition (death)
this one follicle becomes large- dominate follicle

58
Q

When would dominant follicule ovulate?

A

dominant follicle doesn’t ovulate unless there’s and LH surge; will die if it doesn’t occur

59
Q

Hormonal profile changes during estrous cycle

A

LH peak in the beginning- responsible for ovulation of the dominant follicle from the previous cycle
One at the end- initiation of the next cycle
LH has one peak per cycle, and then remains at a lower concentration for the rest of the cycle

Progesterone concentrations starts to increase after the begging of the cycle
This is because there’s a corpus luteum that is formed in the beginning of the cycle after ovulation
Remains functional for some time; then undergoes luteolysis and progesterone levels decrease
When progesterone levels are high: luteal phase
Low levels of progesterone: follicular phase as there’s only the follicle that is present (releases estrogen); responsible for LH surge

Estrogen there are periodic increases and decreases
Estrogen surge preseeds LH surge; this is the postive feedback that results in LH release

FSH surge along with LH surge
Smaller periodic increases in FHS
Peak estrogen levels is associated with low levels of FSH; low estrogen levels are associated with peak FSH levels- reverse relationship between FHS and estrogen- negative feedback regulation

60
Q

how does the level of estrogen change as follicule growth?

A

as follicle growth, estradiol levels increase as dominant follicle is the main source of estrogen in females

61
Q

What happens when a dominant follicule dies>

A

As dominant follicle dies, estrogen levels go down -> no negative feedback-> increase in FSH-> next wave

62
Q

Surge in which hormone leads to ovulaion

A

FSH

63
Q

What are the hormonal levels durign the Follicular phase

A

low progesterone levels, increased levels of estrogen-> stimulation of pre-ovulation gonadotropin surge-> ovulation

kris Endocrinology (17 decks)

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