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Maternal Adaptations During Pregnancy > Hormonal Coordination of Maternal Adaptations to Pregnancy > Flashcards

Hormonal Coordination of Maternal Adaptations to Pregnancy Flashcards

1
Q

what is the hormone detected by home pregnancy kits, which can even be detected in low amounts

A

hCG

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2
Q

what type of hormone is hCG

A

glycoprotein

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3
Q

when does hCG synthesis begin and by what cells

A
  • hCG synthesised by trophoblast cells in blastocysts, starting before implantation
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4
Q

at what point in hCG synthesis can home pregnancy kits detect it

A
  • hCG synthesis by trophoblasts in blastocyst before implantation
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5
Q

as embryos begin to implant and early into pregnancy, what happens to hCG concentrations & why

A
  • hCG concentrations rise quickly
  • as hCG mostly synthesised by syncytiotrophoblast cells (specialised trophoblast cell soon after implantation)
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6
Q

when do hCG concentrations peak
they decline gradually after this

A

around week 8-9 of pregnancy

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7
Q

what is hCG critical for in body to recognise & why

A
  • pregnancy recognition
  • without, corpus luteum will regress -> lose progesterone production
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8
Q

how does hCG maintain and promote progesterone synthesis that is essential to pregnancy

A

by binding to LHR on corpus luteum
(sim to LH hence why hCG can also trigger ovulation)

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9
Q

what happens to corpus luteum without pregnancy

A

-no hCG -> regression of CL and loss of progesterone
- marking end of cycle where implantation has not occurred
- menstruation occurs (shedding of endometrium)

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10
Q

what type of hormone is progesterone (P4)

A
  • steroid hormone
  • synthesied from LDL cholesterol
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11
Q

what synthesises progesterone initially and later on

A
  • initially / early pregnancy from luteal cells in corpus luteum (~wk 6/7/8 have drop in production from CL)
  • later placental production becomes dominant
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12
Q

key functions of progesterone

A
  • promote implantation (decidualisation - preparing endometrium)
  • maintains pregnancy
  • drives maternal respiratory adaptations - increasing sensitivity of respiratory centre to O2
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13
Q

how does progesterone maintain pregnancy (2)

A
  • myometrial quiescence: suppress (myometrium) contractions
  • [maternal] immune tolerance: to developing embryo
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14
Q

how does progesterone promote implantation

A
  • initiating changes in decidua (modified endometrium) making it receptive to implantation
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15
Q

what hormone is essential for pregnancy

A

progesterone

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16
Q

if woman not have corpus luteum during pregnancy eg/ IVF (since embryo implanted straight into uterus) what happens regarding progesterone for pregnancy

A
  • supplemental progesterone used
  • essential to establish and maintain pregnancy
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17
Q

in addition to progesterone, human placenta makes multiple other what

A

steroid hormones

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18
Q

what are some of the steroid hormones the human placenta makes

A
  • oestrogens (including oestradiol)
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19
Q

can human placenta make oestrogens by itself, if not, what is used?

A
  • no
  • some of the substrates for production of oestrogens by placenta are actually coming from the foetal adrenal (eg/ 19-C androgen precursors made in foetal adrenal)
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20
Q

key functions of oestrogens in pregnancy

A
  • vasodilators
  • regulate placental progesterone production
  • stimulate maternal RAS -> incr blood volume
  • promote mammary development
  • promote foetal adrenal steroid synthesis
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21
Q

how does oestrogen function of vasodilator result in

A
  • utero-placental blood system exposed to very high levels oestrogen coming from placenta
  • oestrogens important for driving increase in blood flow thru uteroplacental bed
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22
Q

how does oestrogen regulate placental progesterone production

A
  • oestrogens increase expression of LDL receptor on placenta
  • important for placenta to be able to take up LDL cholesterol
  • which is the precursor for progesterone production
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23
Q

how does oestrogen promote foetal adrenal steroid synthesis

A
  • oestrogens stimulate LDL cholesterol production from foetal liver
  • which is a substrate for many steroids produced by foetal adrenal (eg/ corticosteroids)
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24
Q

why do corticosteroids need to increase in late pregnancy (produced by foetal adrenals)

A

important driver of foetal organ maturation

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25
Q

what synthesises growth hormone initially and later on

A
  • initially anterior pituitary (drops to low later on alongisde placenta production)
  • later on high placental production dominates
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26
Q
  • key function of GH in pregnancy
  • importance of this
A
  • induces insulin resistance: shifts maternal metabolism to using lipids rather than glucose
  • to preserve glucose for foetal supply
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27
Q

is the GH produced from placenta the same as anterior pituitary, what are the consequences?

A
  • not same
  • still binds to GH receptor (ie/ no consequence said)
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28
Q

in what way is GH released from anterior pituitary gland & when does this stop

A
  • pulsatile
  • most pulses lost by mid-pregnancy
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29
Q
  • after pulses of GH lost around midpregnancy, what happens to GH levels, especially into late pregnancy
  • what does this reflect
A
  • very high GH concentration
  • reflects production of GH from placenta
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30
Q

why does GH from pituitary gland fall during late human pregnancy

A
  • GH coming from placenta -> negative feedback at hypothalamus & anterior pituitary -> suppress production GH from pituitary
31
Q

can you definitely conclude what is happening in a human body with GH from mouse studies

A

no

32
Q

which maternal adaptations during human pregnancy is GH important for

A

metabolic adaptations (feeding and digestive maternal adaptations)

33
Q

what is a potential metabolic adaptation (incr food intake) that GH has on pregnancy as a key function of GH

A
  • in mice
  • GH acts on nerves in stomach -> downregulate nerve signals that signal stretch of stomach -> decreasing satiety signals => may allow increased food intake
34
Q

where is placental lactogen (hPL) produced from

A

placenta (syncytiotrophoblast - specialised trophoblast cells of blastocyst)

35
Q

key functions of placental lactogen

A
  • promotes insulin secretion - by promoting beta cell expansion (through increased proliferation and reduced apoptosis), enhancing insulin release from beta cells (by increasing sensitivity of glucose sensors in beta cells)
  • mammary gland development and function
  • promote foetal growth by promoting IGF production
36
Q

what is the increase of placental lactogen like throughout pregnancy

A

steadily increases

37
Q

if a pregnancy is complicated with placental insufficiency, what would we expect placental lactogen levels to look like

A

low

38
Q

how do placental lactogens act

A
  • mostly binds to prolactin-receptor (PRL-R)
39
Q

describe what it means to increase glucose sensors, in situation of increasing insulin secretions

A
  • to increase insulin secretion in response to glucose
40
Q

which 3 hormones are part of prolactin-growth hormone family (PRL-GH family)

A
  • growth hormone (GH)
  • placental lactogen (hPL)
  • prolactin
41
Q

where is prolactin made from

A
  • pituitary
  • but increased in pregnancy in response to oestrogens and progesterones
  • decidua?
42
Q

list 8 hormones that increase during pregnancy & (+1) help coordinate maternal adaptations to pregnancy

A
  • human chorionic gonadotrophin (hCG)
  • progesterone
  • other steroid hormones: oestrogens
  • growth hormone
  • placental lactogen
  • prolactin
  • relaxin
  • ## leptin
  • insulin (not increase during pregnancy)
43
Q

which 2 hormones mentioned does not come from placenta

A

prolactin
insulin

44
Q

key functions of prolactin

A
  • promotes insulin secretion - by promoting beta cell expansion (through increased proliferation and reduced apoptosis), enhances insulin release from beta cells (by increasing sensitivity of glucose sensors in beta cells)
  • mammary gland development and function
  • anti-inflammatory
45
Q

which 2 hormones in prolactin-growth hormone family have similar key functions & why

A
  • placental lactogen (hPL)
  • ## prolactin
  • because both are primarily binding to prolactin receptor
46
Q

what has prolactin been seen to promote

A
  • mammary gland ductal branching
  • formation of alveoli
  • promotion of milk protein production
47
Q

what is the link between insulin and placenta

A
  • placental signals have significant effects on insulin secretion and insulin sensitivity
48
Q

which hormones mentioned induce insulin resistance
which hormones mentioned increase insulin secretion

A
  • insulin resistance: growth hormone
  • insulin secretion: placental lactogen (hPL), prolactin
49
Q

when are increases in insulin secretion and decreases in insulin sensitivity / increased insulin resistance particularly seen in pregnancy based on hormone production time

A
  • late pregnancy
50
Q

at what other intermittent times during pregnancy does insulin secretion increase higher than what would be expected in non-pregnancy
MoA for this increase

A
  • in response to glucose
  • due to increase responsiveness of beta cells to glucose (hPL, prolactin)
51
Q

decrease in insulin sensitivity could also be considered as what

A

increased insulin resistance
ie/ body’s cells become less responsive to effects of insulin, leading to impaired glucose uptake and regulation

52
Q

from what hormone and why is insulin resistance seen in pregnancy

A
  • GH
  • as a maternal metabolic adaptation
  • to preserve glucose for foetal supply
53
Q

what kind of protein is relaxin

A

protein hormone

54
Q

what is chorion

A

outermost membrane surrounding embryo; contributes to placenta formation

55
Q

what is relaxin coming from

A

corpus luteum

56
Q

what pregnancy would result in no relaxin production

A
  • anovulation pregnancies since no corpus luteum
57
Q

when does relaxin release occur (which trimester), when does it fall, when does it stabilise

A
  • relaxin production occurs in first trimester of pregnancy
  • falls in second trimester and remains stabilised in third trimester
58
Q

key functions of relaxin

A
  • systemic vasodilator
  • renal vasodilator
  • cervical softening and ripening (MMM -> ECM remodeling)
59
Q

due to the vasodilator key functions of relaxin, what effects do these have on the body (maternal adaptations)

A
  • increased cardiac output & cardiovascular performance in pregnancy due to systemic vasodilaton
  • increased renal function and increased renal blood flow due to renal vasodilation
60
Q

MoA for relaxin result in cervical softening and ripening

A
  • relaxins induce production of enzymes such as matrix metalloproteinases (MMM)
  • (MMM can digest and remodel ECM)
    => extracellular matrix remodeling
  • ECM remodeling important in timing of labour
61
Q

in regards to relaxin causing cervical softening and ripening, if relaxin levels are elevated in early pregnancy -> would this be more likely to cause a preterm delivery, full-term delivery, late-term delivery

A

pre-term delivery

62
Q

what type of hormone is leptin

A

protein hormone

63
Q

what does leptin come from if not pregnant

A
  • adipose tissue
64
Q

generally, what does increase in leptin do to food intake appetite

A
  • increase leptin -> reduced food intake appetite
65
Q

where does leptin come from in pregnancy

A
  • both adipose and placenta (syncytiotrophoblast cells)
  • increased in response in BOTH to hCG and oestrogen (released in pregnancy)
66
Q

when do levels of leptin peak in pregnancy

A
  • second trimester / mid-pregnancy 24-28 weeks
67
Q

explain what 2 pathways syncytiotrophoblasts in placenta are increasing leptin

A
  • produce leptin
  • express leptin receptor
68
Q

what would explain the actions leptin has on the placenta (which produces leptin)

A

syncytiotrophoblasts in placenta expressing leptin receptor

69
Q

functions of leptin

A
  • in vitro: enhances placental nutrient transport, placental angiogenesis
  • central leptin resistance in pregnancy: leptin does not reduce food intake in pregnancy
70
Q

what is placental angiogenesis

A
  • formation of blood vessels within placenta
  • pivotal process
  • establishes fetomaternal circulation
71
Q

what about the formation of the placenta allows the link between mother and foetus in placental angiogenesis if its blood vessels within only placenta

A

-angiogenesis: formation of new blood vessels; involves branching of new microvessels from pre-existing larger blood vessels

  • placenta is made up of maternal tissue and foetal tissue
  • maternal blood enters placenta through maternal arteries in uterine wall
    (placenta is attached to uterine wall)
  • maternal arteries come in close contact to foetal blood vessels within placenta)
  • foetal blood vessels in developing placenta initially not fully formed
  • placental angiogenesis occurs which further develops foetal blood vessels closer to maternal blood supply for greater capacity of exchange through close proximity.
72
Q

what do these key functions of hormones contribute to in pregnancy

A

maternal adaptations in pregnancy

73
Q

in regards to leptin, what state is pregnancy in

A

state of leptin resistance

74
Q

studies show that increased leptin levels in first trimester of humans had increased or decreased weight gain

A

increased weight gain
ie/ leptin resistance

Maternal Adaptations During Pregnancy (4 decks)

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