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Endocrinology > reproduction > Flashcards

reproduction Flashcards

1
Q

what is a primordial follicle?

A

it is a primary oocyte surrounded by granulosa cells

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2
Q

what is the single most important hormone for reproduction?

A

GnRH

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3
Q

what is special about GnRH secretion?

A

released in a pulsatile manner to act on GnRH-1 receptors in the anterior pituitary. continuous release of GnRH - causes down regulation of those receptors

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4
Q

what causes the LH surge?

A

positive feedback from oestrogen

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5
Q

what is the most reliable indicator of ovulation?

A

a serum progesterone level of 30mmol/L at 21 days

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6
Q

what happens in the follicular phase of the menstruation cycle?

A

FSH stimulates the granulosa cell of the primordial follicle to develop into a secondary follicle which is able to produce oestrogen, oestrogen increases the number of FSH receptors on the granulosa cells. but also inhibits FSH, so that only follicles that express enough FSH-R survive and the rest atrophy. once cell is selected to around which theca cells develop under the influence of lH

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7
Q

what happens during the luteal phase?

A

progesterone is being secreted by the corpus luteum, and so is oestrogen - this inhibits FSH and LH release. inhibin is also released which acts specially to inhibit FSH release and thereby increasing the inhibitory effects of those two molecules

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8
Q

what are the hormone levels during the menopause?

A

because menopause marks a depletion in germ cells, there is a decline in oestrogen production by the ovaries, meaning there is no negative feedback on LH and FSH.
low oestrogen
high FSH and LH

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9
Q

what is the LH surge dependant on?

A

this is dependant on intrinsic properties of the anterior pituitary rather than the hypothalamus.

increasing levels of oestrogen, seem to sensitise the anterior pituitary to GnRH and increases the number of GnRH receptors it expresses, and this causes the surge

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10
Q

how can we prove that the lH surge is not dependant on the hypothalamus?

A

hypogondal women, or women with Kallman’s syndrome can be given analogues of GnRH and they can achieve the LH surge

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11
Q

how are oestrogens synthesised?

A

androgens are made in the theca cells under the influence of LH (which activates lyase 17,20) - androgens then diffuse into the granulosa cell where they’re converted to oestrogen’s under the influence of FSH- which activates P150-aromtase

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12
Q

how are oestrogens synthesised?

A

androgens are made in the theca cells under the influence of LH (which activates lyase 17,20) - androgens then diffuse into the granulosa cell where they’re converted to oestrogen’s under the influence of FSH- which activates P450-aromtase

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13
Q

why is masculinisation seen in women with PCOS?

A

those women have a high LH: FSH ratio and have no ovulation.

the LH makes androgens, but the lack of FSH means they cannot be converted to oestrogen

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14
Q

what are the effects of the LH surge?

A

the LH surge causes ovulation it also causes lutenisation and the formation of the corpus leuteum. progesterone is produced from the corpus letuem under the influence of LH acting on the LH-receptors. but progesterone inhibits lH so eventually there will be so little LH that it cannot sustain the corpus leutum, this degenerates and causes mutation. unless fertilisation has occurred, and the blastocyte secretes hCG and this maintained CL by acting on the LH-R

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15
Q

what does hCG do?

A

it acts on the corpus luetum (and mimics LH) so that it maintains it and keeps it secreting progesterone

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16
Q

what is the most important function of the SRY gene?

A

testis formation (it allows the differentiation of the gonads and the reproductive tract)

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17
Q

what is gonadal function in males?

A

spermatogenesis begins at puberty and continues until death. meaning PGC invade the embryonic gonad and enter mitotic arrest as spermatogonia until puberty

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18
Q

what is gondal function in females?

A

oogenesis is discontinuous and begins in foetal life

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19
Q

what phase is the egg at during ovulation?

A

metaphase II

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20
Q

what phase is the egg frozen at during growth?

A

prophase I

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21
Q

what is egg growth dependant on?

A

absolutely dependant on granulosa cells, without those cells the egg would atrophy. there is bidirectional and homeostatic communication between both

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22
Q

what is the relevance of connexion mutations?

A

connexion are a family of gap junctions, involved in the communication between granulosa cells and the oocyte, if they’re mutated and the communication is disturbed, this causes atrophy of the egg

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23
Q

what is menopause an example of?

A

it is an example of primary gonadotropic failure

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24
Q

what is capacitation?

A

it is the final stage of sperm maturation. it can only occur in the female reproductive tract. and it is required for the sperm to be able to undergo the acrosome reaction (this reaction is required for the sperm to be able to penetrate the zona pellucida)

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25
Q

what are the effects of sertoli cells in males?

A

sertoli cells, under the influence of testosterone allows spermatogenesis to occur under the influence of FSH they also form oestrogens

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26
Q

what are the effects of the Laydig cells in males?

A

those produce testosterone which diffuses into the sertoli cells. this production of testosterone is under the influence of LH

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27
Q

what are the effects of the Laydig cells in males?

A

those produce testosterone which diffuses into the sertoli cells. this production of testosterone is under the influence of LH

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28
Q

how is polyspermy prevented?

A

this is prevented by the modification of ZP2 and ZP3 by calcium currents that are due to sperm and egg fusion

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29
Q

what is the acrosomal reaction

A

this occurs when the acrosome binds to the ZP3 receptor and ZP2 on the zona pellucida. this induces it to release its enzymes so that it can penetrate and degrade the ZP

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30
Q

What are necessary and sufficient for egg activation?

A

calcium currents

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31
Q

where do the calcium currents required for egg activation come from?

A

they seem to be an intrinsic property of the sperm rather than the egg. because sperm lack PLC zeta 1 fail to initiate the first step of embryonic development

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32
Q

what is pregnancy hormonally characterised by?

A

characterised by high oestrogen and high progesterone, with low FSH and Low LH

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33
Q

On average what is the size of the egg when it is ready to rupture?

A

about 10mm?

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34
Q

what is the best indication of ovulation?

A

a progesterone level of greater than 30nmol/L on day 21

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35
Q

what is the best indicator of pregnancy?

A

hCG levels in urine

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36
Q

what is hCG?

A

this is a powerful leutotrophic hormone

37
Q

what type of oestrogen is produced during pregnancy?

A

estratriol (rather than estradiol)

38
Q

describe the changes in hCG levels during pregnancy

A

hCG levels peak at about week 8 - and this is because it is released by the syncitotrophblast to maintain the progesterone secreting corpus luteum.

at about the 4th month, the levels of hCG have decreased and remain low.

the levels of hCG rapidly decline after the 10th week because the placenta takes over the role of progesterone secretion (the pregnancy is autonomous)

39
Q

explain what is meant by the term autonomous pregnancy?

A

this is when the placenta starts secreting progesterone, and this progesterone maintains the endometrium

40
Q

describe the levels of progesterone levels during:

  • multiple pregnancies
  • end of pregnancies
  • compared to the luteal phase
A
  • during multiple pregnancies very high (the peak in its concentration)
  • the progesterone levels shift towards the end of pregnancy
  • and it is up-to 10x higher than the luteal phase
41
Q

what is a good indicator of placental function? and what is the role of this hormone?

A

a good indicator of placental function is PL (sommatomatropin hormone)

  • this hormone inhibits glucose uptake by the mother, sparing the glucose for the developing foetus (link there to gestational diabetes?)
  • it also increases breath growth, by encouraging protein synthesis
42
Q

what is a good indicator of placental function? and what is the role of this hormone?

A

a good indicator of placental function is PL (sommatomatropin hormone)

  • this hormone inhibits glucose uptake by the mother, sparing the glucose for the developing foetus (link there to gestational diabetes?)
  • it also increases breath growth, by encouraging protein synthesis
43
Q

what is the role of progesterone in pregnancy?

A

progesterone inhibits myometrial contractility (probably by inhibiting prostaglandin formation)
it causes the glandular development of the breast (acts on the alveolar epithelial cells)

44
Q

what is mifepristone?

A

this is a progesterone antagonist. a progesterone antagonist will cause myometrial contractility, and this drug can be used to induce a medical abortion

45
Q

what is the role of oestrogen during pregnancy?

A

onset of partition
foetal development
stimulates urine blood flow
and development of breast for lactation

46
Q

where is progesterone synthesised during pregnancy?

A

synthesised in the placenta from a steroid

47
Q

where is oestrogen synthesised during pregnancy?

A

oestrogen cannot be formed from pregnanlone in the foetus or the placenta, it requires the co-operation of both

progestrone is converted to androgens by the placenta - using the enzyme 17,20 lyase

48
Q

where is oestrogen synthesised during pregnancy?

A

oestrogen cannot be formed from pregnanlone in the foetus or the placenta, it requires the co-operation of both

progestrone is converted to androgens by the foetus - using the enzyme 17,20 lyase. then androgens are converted into oestrogens via aromatase enzyme in the placenta

49
Q

why are estratriol levels a good indicator of placental function?

A
  • because the placenta does not possess all the enzymes required for oestriol synthesis
  • therefore, it is in part reliant on the foetus for the synthesis of oestrogen
50
Q

explain the consequence of sulphatase deficiency?

A

so steroids are conjugated in the foetal liver (this is because high concentration of steroids can virulise the sex of the baby)

in the placenta those sulphate conjugates (which make the steroids biologically inert) are removed by sulphatases. without sulphatases estratriol deficiency would occur

51
Q

where is CRH released from during pregnancy and what effects does it have during pregnancy?

A

CRH is released from the placenta. it causes ACTH release from foetal anterior pituitary and cortisol release from the adrenal.

this is particularly true for during the end of pregnancy because:

  • cortisol is a lung surfactant required for lung maturation
  • cortisol is responsible in the peak of oestrogen which promotes birth during the end of pregnancy
  • recall the import ants of 11B HSD-2 (inactivation of cortisol by the placenta)
52
Q

what are the two most important factors in parturition?

A

oxytocin:
- secreted from posterior pituitary due to cervical stimulation
- causes contraction of the myometrium (by increasing its excitability)
oestrogen:
- this increases the number of oxytocin receptors in the endometrium
- causes the number of gap junctions between smooth muscles in the endometrium
PDG-2Fa:
- increased by both factors
- causes cervical contractility and softening

53
Q

what is the most important hormone involved in the onset of partition (hint: change in dominance)

A

cortisol produced by the adrenal glands seem to increase the conversion of progesterone to oestrogen

54
Q

what is the most important hormone involved in the onset of partition (hint: change in dominance)

A

cortisol produced by the adrenal glands seem to increase the conversion of progesterone to oestrogen. and this shifts the hormonal dominance from hormones that inhibit myometrial contractility to hormones that increase myometrial contractility

55
Q

briefly explain what the fergusson reflex is?

A

this refers to the positive feedback manner in which oxytocin is released during pregnancy. it starts by the foetus stimulating the cervix, and ends by the expulsion of the foetus

56
Q

what is the role of relaxin

A

it is produced by the placenta during pregnancy

it relaxes the pubic symphsis
inhibits myometrial contraction
promotes cervical dilation at brith

57
Q

why despite the release of prolactin during birth, does lactation not occur?

A

this is because the high concentration of steroid hormones seem to inhibit the action of prolactin on alveolar epithelial cells

58
Q

what is the role of prolactin and oxytocin in lactation?

A

prolactin:
- this acts on the receptors of alveolar epithelial cells to cause milk secretion

oxytocin:
- this acts on myoepithelial cells to cause milk-let down

59
Q

why is there hyperplasia of the anterior pituitary during pregnancy?

A

because of the increase in prolactin secretion

60
Q

explain the effects of the sucking reflex

A

the only effective reflex in causing prolactin release

also causes oxytocin release (but oxytocin can be released in response to a baby crying or orgasmic intercourse)

this is a spinal reflex, and can be conditioned

61
Q

what is the significance of the mini-puberty?

A

this occurs only in boys:

  • seen by an increase in FSH and LH in the first few months of life
  • seems to be important for Sertoli cell replication
  • seems to prime and is important for spermatogenesis and testicular health in men
62
Q

what is the significance of the mini-puberty?

A

this occurs only in boys:

  • seen by an increase in FSH and LH in the first few months of life
  • seems to be important for Sertoli cell replication
  • seems to prime and is important for spermatogenesis and testicular health in men
63
Q

what is the single best trigger for the pulsatily of GnRH

A

leptin levels (beyond a critical concentration) - this would explain why puberty has been developing at a younger age (due to increase in obesity)

64
Q

what is the single best defining characteristic of puberty?

A

the onset of the release of GnRH in a pulastile fashion

65
Q

what is physiological amenorrhea

A

this refers to the fact that women who breast-feed full time have no periods and this is because the release of prolactin inhibits GnRH, LH and FSH

66
Q

what is the menopause hormonally dictated by?

A

high FSH and LH (although FSH rises higher and more than LH)

and low oestrogen levels

67
Q

how is ooccyte depletion characterised?

A

it is a logarithmic decline but beyond a certain age, there is a sharp decline

68
Q

describe the process of IVF

A

• Over-riding the natural hormonal cycle
o Exogenous analogues to prevent endogenous causes of ovulation
• Injections of GnRH agonists (high doses) to prevent spontaneous LH surges
o Those surges only occur when there is pulsatile GnRH secretion
• Injection of FSH analogues to prime follicles
• Injection of hCG (because it is an LH mimetic) to stimulate ovulation
• Transvaginal aspiration of follicle using ultrasound
• Collect 10 or more eggs just before ovulation
• Sperm collected and washed and prepared using swim-ups/percol gradients

69
Q

when is ICSI used?

A

when there is severe male infertility factor

70
Q

what is a haemochorial?

A

this is a placenta where foetal and maternal circulation are separated by foetal capillary endothelia and chorion

71
Q

what is the single best contributing factor to a successful pregnancy outcome

A

normal placental function and placental vascularisation

72
Q

what is a decidualised endoemtrium?

A

this is an endometrium prepared for implantation

73
Q

what is the most important component for placental development?

A

the extravillious portion of the cytotrophoblast.

if portion is well developed; the placenta is well embedded and can transition into normal circulation

if not developed well, only superficial implantation of the placenta occurs: leading to a shell like placenta which allows many of the complications associated with pregnancy (including intra-uterine growth restriction and pre-eclamspia)

74
Q

what is the syncitrophoblast?

A

this is the most active component of the placenta, concerned with hormonal production including hCG and PL

75
Q

what do the levels of hCG represent?

A

this reflect the invasive role of the placenta, and the rate of differentiation from cytotrophoblast into synctiotrophblast BUT NOT mass of placenta

76
Q

what is a syncitial sprout? what is its possible functions?

A

this is a villious offshoot from the synctiotrophoblast. it reaches pulmonary circulation and may play a role in immune tolerance

77
Q

describe the structure of a primary vilius

A

this has a cytotrophoblast core. and an outer synctiotrophoblast layer (With no villi)

78
Q

describe the structure of the secondary villus

A

has synctiotrophblast with microvilli, and the cytotrophoblast starts thinning out into a single layer, and there is invasion of extra-embryonic mesoderm into the core

79
Q

describe the structure of a tertiary villius

A

the core has now definitive foetal vessels, which are from extra-embryonic mesoderm.

80
Q

what are hofbaeur cells?

A

those are cells formed by macrophages, collagen fibres and mesenchymal cells involved in filtering out anti-foetal antibodies

81
Q

why is it necessary that the intravillious space is closed from maternal circulation unto 12 weeks

A

to prevent exposure of the early embryo to high oxygen tensions - foetus cannot deal with the oxygen load because has no enzymes e.g. SOD to deal with superoxide radicals

82
Q

briefly explain the placental structure

A

the decidua basalis on the maternal side and the chorion frondsum (villi from the embryonic pole) form the placenta

the uterine wall is obliterated by fusion of the decidua parietalis the chorion lavae (this is obliterated villi from the aembryonic pole, initially covered with decidua capsularis - which becomes displaced)

83
Q

what are the two steps of trophoblastic invasion?

A

1st 12 weeks: decidual invasion (superficial implantation)

week 14-16: myometrial invasion (Deep implantation)

84
Q

what is the effect of placentation on maternal blood flow?

A

involves modification of maternal blood flow to high capacitance low pressure system. this is done because the cytotrophoblast involves the change of the muscle and elastic tissue in the T.media of the spiral arteries into fibrinoid material which is loose and flaccid

this modification is done because the trophoblasts change their adhesion receptors, to resemble those of the endothelial cells they replace

85
Q

what is the best indication of placental insufficiency?

A

the retention of a characteristic notch form in spiral artery blood flow, this will lead into intrauterine restriction

86
Q

what causes placental insufficiency?

A

poor spiral artery transformation by the invasive trophoblasts

87
Q

what are syncitiotrophblasta?

A

those are post-mitotic fully differentiated cells, with no mitotic figures, they form a syncitium and produce hormones of the placenta

88
Q

what is the signalling molecule causing trophoblast invasion?

A

low oxygen tensions which prevail in the 1st trimester of pregnancy within the foetus (hence premature exposure to maternal blood is bad)

89
Q

what may be the cause of PET?

A

Low blood flow to placenta leads to placental insufficiency. the placenta produces ischaemic molecules which damage maternal endothelial cells.

it is through that PET is an outcome of the poor transformation function of the spiral artery by the cytotrophoblasts, mainly because they fail to change their phenotype (i.e. do not express cells that resemble the endothelial cells they replace) - this modulation in switch is thought to be due to low hypoxia

Endocrinology (6 decks)

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