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brs (phase 1b) > (dev&age) pregnancy, parturition and late fetal development > Flashcards

(dev&age) pregnancy, parturition and late fetal development Flashcards

1
Q

what is parturition?

A

childbirth

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2
Q

what is embryo-fetal growth like in the first trimester?

A

very limited and slow

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3
Q

what is early embryo nutrition in the first trimester described as?

A

histiotrophic embryo nutrition

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4
Q

what is late embryo nutrition in the second trimester onwards described as?

A

haemotrophic embryo nutrition

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5
Q

what is histiotrophic nutrition?

A

provision of nutrients for the embryo via the uterine gland secretion and the breakdown of surrounding endometrial tissue

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6
Q

what two things is histiotrophic embryo nutrition reliant on?

A

uterine gland secretions (of uterine milk)

breakdown of surrounding endometrial tissue

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7
Q

what do the uterine glands secrete and why is this important?

A

uterine milk

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8
Q

what is uterine milk?

A

nutritive secretion from the uterine glands that nourishes the embryo

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9
Q

how do syncitiotrophoblast cell contribute to histiotrophic nutrition?

A

invade and degrade the maternal endometrial cells

the products of the endometrial tissue breakdown AND the nutrients from the maternal capillaries = give nutrients to the embryo

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10
Q

how does the rate of foetal growth change from the first trimester onwards?

A

increases rapidly in the second and third trimester

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11
Q

how does embryo nutrition change from the first to the second trimester?

A

switches from histiotrophic to haemotrophic nutrition

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12
Q

why does the type of embryo nutrition change from the first to the second trimester?

A

the rate of foetal growth increases significantly and histiotrophic nutrition is not enough to keep up with this increased growth rate

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13
Q

what is haemotrophic nutrition?

A

the provision of nutrients for the embryo via the exchange of nutrients across the maternal and fetal circulations

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14
Q

when does haemotrophic nutrition begin?

A

at the start of the second trimester

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15
Q

what type of placenta is present in humans?

A

haemochorial-type placenta

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16
Q

why is the haemochorial-type placenta important for?

A

essential for enabling haemotrophic nutrition from the start of the second trimester

enables the maternal blood to be directly in contact w the fetal membranes

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17
Q

what is a haemochorial-type placenta?

A

a placenta type wherein the blood supply (maternal) is directly in contact with the fetal membranes

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18
Q

what causes the switch of nutrition from histiotrophic to haemotrophic and what does this cause?

A

the activation of the hameochorial-type placenta at around week 12 of gestation (i.e. start of the second trimester)

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19
Q

what is the chorion?

A

the outermost layer of the embryo

develops from the outer fold of yolk sac

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20
Q

differentiate between histiotrophic and haemotrophic development

A

histiotrophic nutrition comes from the uterine gland secretions and the breakdown of the surrounding endometrial cells

whereas haemotrophic nutrition is the provision of nutrients from the maternal blood to the fetal membranes via direct contact

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21
Q

what type of growth occurs in the early implantation stage?

A

histiotrophic growth

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22
Q

what are the main sources of nutrients for the embryo in the early implantation stage?

A

uterine secretions from the glands (of uterine milk)

nutrients from the maternal capillaries + the breakdown of endometrial tissues

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23
Q

what is the amnion?

A

the inner fetal membrane (derived from the epiblast) that forms a fluid-filled cavity (amniotic sac) enclosing the embryo

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24
Q

what is the amnion derived from?

A

epiblast cells

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25
Q

what does the amnion give rise to?

A

forms a fluid-filled cavity called the amniotic sac that encloses the embryo

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26
Q

what is the amniotic sac?

A

fluid-filled cavity that encloses the embryo

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27
Q

what are the two fetal membranes?

A

chorion (outer)

amnion (inner)

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28
Q

how are the fetal membranes arranged?

A

chorion on the outside and amnion on the inside, containing amniotic fluid

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29
Q

how does the amnion form the amniotic sac?

A

forms due to the amnion cells secreting fluid which accumulates, causing an expansion of the amniotic cavity

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30
Q

which cells give rise to the yolk sac?

A

hypoblast cells

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31
Q

what is the function of the connecting stalk?

A

grows from the embryo to connect the developing embryo unit to the chorion

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32
Q

what is the connecting stalk?

A

precursor to the umbilical cord

extraembryonic tissue that connects the embryo unit to the chorion

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33
Q

what are the trophoblastic lacunae?

A

large spaces filled with maternal blood formed from the breakdown of maternal capillaries and uterine glands

= become intervillous spaces

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34
Q

how do trophoblastic lacunae form?

A

when syncytiotrophoblast cells invade and degrade the maternal capillaries and the endometrial tissue (i.e. uterine glands) etc break down = large spaces are left

fuse together to create continuous canals along which maternal blood flows

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35
Q

what do trophoblastic lacunae become?

A

intervillous spaces (i.e. maternal blood spaces)

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36
Q

what are intervillous spaces?

A

maternal blood spaces

i.e. large spaced filled w maternal blood that are formed from uterine gland and maternal capillary breakdown

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37
Q

name the two main fetal membranes

A

amnion, chorion

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38
Q

what are fetal membranes?

A

extraembryonic tissue that forms a tough, but flexible sac that encapsulates the fetus and forms the basis of the maternal-fetal interface

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39
Q

what kind of tissue are fetal membranes?

A

extraembryonic tissue

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40
Q

what is the function of the fetal membranes?

A

for a tough but flexible sac that encapsulates the fetus and forms the basis of the maternal-fetal intereface

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41
Q

how does the amnion come into contact with the chorion?

A

accumulation of amniotic fluid in the amniotic cavity (due to secretion from the amnion cells) pushes the amnion out to the chorion

they eventually fuse together (at week 14-16) to form amniotic sac

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42
Q

how do the amnion and chorion interact?

A

usually fuse together between week 14 and week 16 of gestation (closing the chorioamniotic separation)

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43
Q

what is the space between the amnion and the chorion called?

A

anechoic space

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44
Q

when do the amnion and chorion fuse?

A

approx week 14-16 o gestation

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45
Q

why is the fusion of the amnion and chorion important?

A

leads to the formation of the amniotic sac

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46
Q

what is the amnion?

A

inner fetal membrane

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47
Q

what is the chorion?

A

outer fetal membrane

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48
Q

name all the fetal membranes

A

chorion
amnion
allantois

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49
Q

what is the allantois?

A

outgrowths of the yolk sac

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50
Q

which cells does the amnion come from?

A

epiblast cells (but does not contribute to the fetal tissue)

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51
Q

what does the amnion give rise to?

A

forms a closed, avascular amniotic sac

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52
Q

what do the amnion cells secrete?

A

at week 5, they being to secrete amniotic fluid

leads to the formation of the amniotic sac that encapsulates and protects the fetus

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53
Q

when do the amnion cells begin to secrete amniotic fluid?

A

approx week 5 of gestation

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54
Q

why is the amniotic sac important?

A

essential for encapsulating and protecting the fetus

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55
Q

what gives rise to the chorion?

A

formed from yolk sac derivatives and the trophoblast

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56
Q

differentiate between the amnion and chorion in terms of vascularity

A

the amnion is avascular whereas the chorion is highly vascularised

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57
Q

what is the vascularity of the chorion like?

A

chorion is highly vascularised

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58
Q

what does the chorion give rise to?

A

gives rise to chorionic villi (outgrowths of cytotrophoblast) from the chorion that form the basis of the fetal side of the placenta

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59
Q

what are the chorionic villi?

A

outgrowths of cytotrophoblast from the chorion

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60
Q

what is the purpose of the chorionic villi?

A

(form from the cytotrophoblast from the chorion)

form the basis of the fetal side of the placenta

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61
Q

what forms the basis of the fetal side of the placenta?

A

the chorionic villi (form from the cytotrophoblast)

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62
Q

where does the allantois grow?

A

grows along the connecting stalk from the embryo to the chorion

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63
Q

which structure is the allantois linked to?

A

connecting stalk (grows along it)

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64
Q

how does the allantois develop with time?

A

becomes coated with mesoderm and become vascularised to form the umbilical cord

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65
Q

why is the vascularisation of the allantois important?

A

leads to the formation of the umbilical cord

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66
Q

which structure does the allantois give rise to?

A

umbilical cord

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67
Q

describe how the amniotic sac is formed

A

the amnion cells being to secrete amniotic fluid into the amniotic cavity that accumulates over time and causes an expansion of the amnionic membrane so it is forced into contact with the chorionic membrane with which it fuses to form the amniotic sac

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68
Q

describe the structure of the amniotic sac

A

two layers: inner amnion (contains amniotic fluid and fetus) and outer chorion (contains amnion and part of the placenta)

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69
Q

what are the two functions of the allantois?

A

contributes to the embryonic bladder

becomes vascularised to form the umbilical cord

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70
Q

what is the umbilical cord?

A

a narrow tube that connects the baby to the placenta for the provision of nutrients and removal of waste products

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71
Q

why is the umbilical cord important?

A

enables the provision of nutrients for the developing fetus and the removal of toxic waste substances

(i.e. circulatory link to the fetal side of the placenta)

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72
Q

what does the amnion encapsulate?

A

the amniotic fluid and the developing fetus

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73
Q

what does the chorion encapsulate?

A

the amnion and part of the placenta

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74
Q

how do the primary chorionic villi form?

A

cytotrophoblast proliferates and form finger-like projection that extend past the syncitiotrophoblast into the maternal endometrium

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75
Q

into which layer do the chorionic villi protrude?

A

extend past the syncitiotrophoblast into the maternal endometrium

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76
Q

what are the main function of the cytotrophoblast?

A

main = act as a dividing cell population that proliferates to constantly replenish and contribute to the syncitiotrophoblast cell population

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77
Q

where do the chorionic villi develop?

A

outside of the chorion (past the syncitiotrophoblast into the maternal endometrium)

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78
Q

what do the chorionic villi contribute to?

A

the maternal-fetal interface

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79
Q

how are the chorionic villi adapted to their function?

A

they are highly branched and so provide a larger surface area for the exchange of gases and nutrients

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80
Q

what are chorionic villi?

A

finger-like projection stemming from the cytotrophoblast, that then undergo branching to contribute to the fetal side of the placenta

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81
Q

name the three phases of chorionic villi development

A

primary, secondary and tertiary chorionic villi development

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82
Q

describe the three phases of chorionic villi development

A

primary = outgrowth of the cytotrophoblast and branching of these extensions to form primary villi

secondary = growth of the fetal mesoderm into the primary villi

tertiary = growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature

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83
Q

what occurs in primary chorionic villi development?

A

outgrowth of the cytotrophoblast and branching of these extensions to form primary villi

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84
Q

what occurs in secondary chorionic villi development?

A

growth of the fetal mesoderm into the primary villi

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85
Q

what occurs in tertiary chorionic villi development?

A

growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature

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86
Q

what is chorionic villi development?

A

the process by which fetal primary chorionic villi form and become invaded by mesoderm and blood vessels to ensure maximal contact between maternal and fetal blood for efficient exchange

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87
Q

why is chorionic villi development important?

A

the invasion of the primary villi by the mesoderm and blood vessels is essential to provide
1) close contact
2) a large SA
= between maternal and fetal blood for efficient exchange of gases and nutrients

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88
Q

which blood vessels grow into the villus mesoderm in tertiary chorionic villi development?

A

uterine and umbilical arteries

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89
Q

what structure grows into the primary villi in secondary chorionic villi development?

A

fetal mesoderm

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90
Q

describe the microstructure of the terminal villus

A

villus is arranged in a convoluted knot of vessels

vessels are dilated

whole structure is covered in trophoblast

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91
Q

how does the structure of the terminal villus ensure it is adapted to its function?

A

convoluted knot and the dilated vessels

= ensure the flow of blood is slowed

= so maximal efficiency in the exchange of nutrients and gases between maternal and foetal blood

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92
Q

what is the terminal villus coated in?

A

trophoblast

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93
Q

what two structural features of the terminal villus maximise efficient exchange between the maternal and foetal blood?

A

convoluted knot structure

vessel dilation

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94
Q

why is it important that the terminal villus has a convoluted knot?

A

ensures the flow of blood is slowed to allow maximal efficiency of gas and nutrient exchange between the maternal and foetal blood

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95
Q

why is it important that vessel dilation occurs at the terminal villus?

A

ensures the flow of blood is slowed to allow maximal efficiency of gas and nutrient exchange between the maternal and foetal blood

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96
Q

describe the structure of the terminal villus during early pregnancy

A

150-200µm in diameter

10µm trophoblast thickness between capillaries and maternal blood

(i.e. maternal blood spaces surround the capillaries)

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97
Q

describe the structure of the terminal villus during late pregnancy

A

40µm in diameter

1-2µm trophoblast thickness between capillaries and maternal blood

(i.e. maternal blood spaces surround the capillaries)

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98
Q

how does the terminal villus change structurally as pregnancy progresses?

A

there is a decrease in the diameter of terminal villi

thinning of the trophoblast layer coating the terminal villi

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99
Q

explain why the structural changes in the terminal villi are important as pregnancy progresses

A

trophoblast thinning and diameter decrease

= essential as the blood vessels become close to the maternal blood supply so the diffusion distance for gases and nutrients is significantly reduced

= can keep up with the increased rate of fetal development and increased demand

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100
Q

how does trophoblast thickness change at the terminal villus as pregnancy progresses?

A

trophoblast layer thins from 10µm to approx 1-2µm

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101
Q

how does vessel diameter change at the terminal villus as pregnancy progresses?

A

vessel diameter falls from 150-200µm to approx 40µm

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102
Q

what is the impact of trophoblast layer thinning AND diameter decrease in terminal villi as pregnancy progresses?

A

the blood vessels will become closer to the maternal blood supply = reduced diffusion distance

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103
Q

describe the maternal blood supply to the endometrium

A

the ovarian and uterine arteries anastomose to give rise to the arcuate artery

arcuate artery branches to give rise to the radial arteries

radial arteries branch to give rise to the basal arteries

basal arteries spiralise to form the spiral arteries

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104
Q

list the arteries and their branches supplying the endometrium

A

ovarian + uterine artery

(myometrium)
arcuate artery
radial artery
basal artery

(endometrium)
spiral artery

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105
Q

which two arteries anastomose to give rise to the arcuate artery?

A

ovarian and uterine arteries

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106
Q

what does the arcuate artery give rise to?

A

radial artery

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107
Q

what do the radial arteries give rise to?

A

basal artery

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108
Q

what do the basal arteries form?

A

spiralise to form spiral artery

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109
Q

what are the three uterine layers?

A

perimetrium
myometrium
endometrium

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110
Q

which arteries supply the myometrium?

A

arcuate, radial, and basal arteries

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111
Q

which arteries supply the endometrium?

A

spiral arteries

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112
Q

how does the endometrial blood supply develop through the menstrual cycle?

A

menstrual cycle progresses and endometrial thickening occurs

terminal basal arteries will grow and spiralise to form the spiral arteries form and grow out further during endometrial development

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113
Q

how does successful implantation affect the endometrial blood supply?

A

if implantation is successful, the spiral arteries remain intact and stabilise

= provide maternal blood supply to the foetus

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114
Q

how does failed implantation affect the endometrial blood supply?

A

if implantation is unsuccessful

= regression of the spiral arteries

= endometrium is lost due to lack of blood supply (i.e. the monthly menstrual period)

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115
Q

what causes the regression of the spiral arteries?

A

unsuccessful implantation of an embryo

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116
Q

when do the basal arteries form the spiral arteries?

A

during endometrial development

terminal basal arteries spiralise to form spiral arteries

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117
Q

what does failed implantation result in and how?

A

a menstrual period

regression of the spiral arteries causes loss of the thickened endometrial lining

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118
Q

why are the spiral arteries important?

A

responsible for the endometrial blood supply

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119
Q

describe how the tertiary chorionic villi are arranged in relation to the endometrium

A

tertiary chorionic villi are arranged above the endometrium

with their trophoblast layer in close contact with the endometrium

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120
Q

what is EVT?

A

a form of differentiated trophoblast cells of the placenta

extra-villus trophoblast (EVT) are cells that are found on the surface of the tertiary chorionic villi that will invade down into the maternal spiral arteries

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121
Q

what action is carried out by EVT?

A

invade down into the maternal spiral arteries to form endovascular EVT

(stimulate by IGF-II and IGFBP-I)

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122
Q

once the EVT invade the maternal spiral arteries, what forms?

A

endovascular EVT

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123
Q

what is endovascular EVT?

A

a form of differentiated trophoblast cells of the placenta

responsible for the remodelling of spiral arteries to control oxygenation and blood perfusion in the developing placenta

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124
Q

what is the function of endovascular EVT?

A

break down the maternal endothelium and underlying smooth muscle AND form new endothelial layer with EVT coating the inside

  • to enable the de-spiralisation of the spiral arteries (for control of the oxygenation and blood perfusion of the placenta) -
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125
Q

how does endovascular EVT cause spiral artery remodelling?

A

the breakdown of the maternal endothelium and the underlying smooth muscle causes the spiral arteries to open up into straight channels

= change from being highly convoluted, high-pressure vessels TO low pressure, high capacity conduits for blood flow

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126
Q

how are the spiral arteries converted by endovascular EVT?

A

spiral arteries will de-spiralise and become open, straight channels (due to maternal endothelium and smooth muscle breakdown)

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127
Q

why is the conversion of spiral arteries by endovascular EVT important?

A

change from being highly convoluted, high-pressure vessels TO low pressure, high capacity conduits for increased blood flow

= to meet the increased demand for placental and foetal growth and haemotrophic nutrition in the second and third trimester

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128
Q

describe the change in spiral artery structure due to endovascular EVT

A

change from being highly convoluted, high-pressure vessels TO low pressure, high capacity conduits for blood flow

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129
Q

explain the change in spiral artery structure due to endovascular EVT

A

(from being highly convoluted, high-pressure vessels TO low pressure, high capacity conduits)

to increase blood flow to the developing placenta and fetus to keep up with increased growth rate and haemotrophic nutrition

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130
Q

why is it important that the spiral arteries are remodelled?

A

so when there is an increase in demand for blood by the developing placenta and fetus, the blood flow can be increased accordingly to meet the requirements for heterotrophic nutrition and increased growth

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131
Q

what do endovascular EVTs regulate?

A

regulate oxygenation and blood perfusion during early placental development

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132
Q

how do the endovascular EVTs regulate oxygenation of the placenta during histiotrophic nutrition?

A

plug maternal spiral arteries to maintain hypoxia and blood perfusion

= protects fetus and placenta from oxidative stress during development in the histiotrophic nutrition stage

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133
Q

how do the endovascular EVTs regulate oxygenation of the placenta in during haemotrophic nutrition?

A

the EVT plugs dissolve and blood perfusion and oxygenation of the placenta is restored allowing further development of the fetus and placenta

134
Q

how does the type of fetal nutrition influence endovascular EVT action on the spiral arteries?

A

in histiotrophic nutrition = EVT plug the spiral arteries and prevent blood perfusion and oxygenation as nutrition is derived from the uterine glands and tissues

in haemotrophic nutrition = EVT plugs dissolve and the blood perfusion and oxygenation is restored as nutrition is derived from the maternal blood

135
Q

how does EVT become endovascular EVT?

A

when the EVT cells coating the tertiary chorionic villi invade down into the spiral arteries, endovascular EVT is formed

136
Q

where is endovascular EVT found?

A

coating the inside of the new, wider spiral arteries

137
Q

which nutrients are exchanged across the placenta?

A 
oxygen
glucose
water
electrolytes
calcium
amino acids
138
Q

how is oxygen exchanged across the placenta?

A

simple diffusion due to a steep diffusional gradient between the high maternal oxygen tension and the low fetal oxygen tension

139
Q

how is glucose exchanged across the placenta?

A

facilitated diffusion by transporters on the maternal side and the fetal trophoblast cells

140
Q

how is water exchanged across the placenta?

A

mainly by diffusion but there are some local hydrostatic gradients

(placenta is the main site of water exchange but some does occur at the amnion-chorion)

141
Q

how are electrolytes exchanged across the placenta?

A

both diffusion and active (energy-dependent) co-transport

142
Q

how is calcium exchanged across the placenta?

A

active transport via the magnesium-calcium ATPase pump

143
Q

how are amino acids exchanged across the placenta?

A

reduce maternal urea excretion AND active transport of amino acids to fetus

144
Q

how does pregnancy affect cardiac output in the mother?

A

maternal cardiac output increases by 30% during the first trimester

(i.e. increased stroke volume and heart rate)

145
Q

how does pregnancy affect peripheral resistance in the mother?

A

maternal peripheral resistance decreases by up to 30%

146
Q

how does pregnancy affect blood volume in the mother?

A

maternal blood volume increase by up to 40% near term

147
Q

how does pregnancy affect pulmonary ventilation in the mother?

A

maternal pulmonary ventilation increases by up to 40%

148
Q

what changes does the mother go through to meet the increased metabolic demand during pregnancy?

A

maternal cardiac output increases by up to 30%

(combined with a 30% decrease in peripheral resistance and a 40% increase in blood volume)

maternal pulmonary ventilation increases by up to 40%

149
Q

how much glucose and oxygen does the placenta consume?

A

consumes 40-60% of the glucose and oxygen it is supplied

150
Q

how does the composition of fetal blood compare to that of maternal blood?

A

fetal blood has a lower oxygen tension than maternal blood

but fetal and maternal oxygen saturation and content is similar

151
Q

compare adult haemoglobin to fetal/embryonic haemoglobin

A

embryonic/fetal haemoglobin has a greater affinity for oxygen than adult haemoglobin so bind to oxygen more strongly

152
Q

why is the altered structure of embryonic/fetal haemoglobin advantageous?

A

(HbF in fetal haemoglobin has a greater affinity for oxygen than HbA in adult haemoglobin so binds more strongly to oxygen)

= enables the transfer of oxygen from mother to fetus prenatally to meet the demands of the developing fetus

153
Q

in which trimester do organ systems form?

A

first trimester

154
Q

in which trimester do organ systems mature and develop?

A

second and third trimester

155
Q

what is the initial circulatory system for the fetus in the first few weeks?

A

tube of mesoderm that pumps blood at day 22

156
Q

by when does the fetus have a relatively complete circulatory system?

A

by the second trimester

157
Q

where does gas exchange take place in the fetus?

A

placenta acts as the main site for gas exchange for the fetus (not lungs)

158
Q

how do the ventricles act in the fetus as opposed to in a human?

A

ventricles pump in parallel rather than in series

159
Q

how is the fetal circulatory system adapted for fetal development?

A

vascular shunts bypass hepatic and pulmonary circulation = permits the heart to drive oxygenated blood from the placenta to the developing tissues that require it the most (i.e. brain)

160
Q

what is the function of the vascular shunts in the fetus?

A

bypass the hepatic and pulmonary circulation (to enable the direction of oxygenated blood to where demand is greatest)

161
Q

how do the lung structures develop in the fetus?

A

lung bud develops around the forgut

then branches in the first trimester = to give other lung structures

162
Q

when do the primitive air sacs form in the fetus?

A

approx week 20

163
Q

when does lung vascularisation take place in the fetus?

A

approx week 28

164
Q

when does surfactant production take place in the fetus?

A

approx week 20 (upregulated towards term)

165
Q

how does surfactant production change towards term?

A

upregulated towards term

166
Q

how does the foetus prepare for the breathing reflex?

A

spends 1-4 hours a day making rapid respiratory moments during REM sleep

167
Q

what gives rise to the gastrointestinal system?

A

gut tube from the endoderm and yolk sac

168
Q

when does the pancreas form during pregnancy?

A

pancreas fully functional at the start of the second trimester

(insulin secretion begins mid-second trimester)

169
Q

when does the pancreas begin secretin insulin during pregnancy?

A

insulin secretion begins in the middle of the second trimester

170
Q

how does glycogen deposition change towards term?

A

liver glycogen is progressively deposited and accelerated towards term

171
Q

when does the fetal liver form during a pregnancy?

A

begins to form at approx day 23

172
Q

what does the fetus do to the amniotic fluid?

A

fetus will inhale and swallow the amniotic fluid

173
Q

what does the swallowing of the amniotic fluid by the fetus result in?

A

the ingested debris and bile acids will form the meconium (first stool)

174
Q

what is the meconium?

A

the first stool of the newborn

175
Q

what does the meconium consist of?

A

ingested amniotic fluid, debris (lanugo, intestinal cells and pancreatic enzymes) and bile salts and pigments

176
Q

when do fetal movements begin?

A

in the late first trimester

177
Q

when are fetal movements detectable by the mother?

A

approx by week 14

178
Q

when does the fetus develop stress responses?

A

approx week 18

179
Q

when does the fetus develop thalamus-cortex connections?

A

approx week 24

180
Q

does the fetus show conscious wakefulness?

A

no - fetus is mostly in slow-wave or REM sleep most of the time

181
Q

what are developmental changes in the fetus said to be orchestrated by?

A

simultaneous increase in fetal corticosteroids (towards the end of a pregnancy)

182
Q

what is organ maturation coordinated by?

A

fetal corticosteroids

183
Q

what is labour?

A

the process by which the fetus is safely expelled from the uterus at the correct time

184
Q

what are three purposes of labour?

A

safe expulsion of the uterus at the correct time

expulsion of the placenta and the fetal membranes

resolution and healing of the uterus to permit future reproductive events

185
Q

how does labour prepare the body for future pregnancies?

A

after the fetus, fetal membranes and placenta have been safelt expelled, the uterus undergo resolution and healing = preparing the uterus for future pregnancies

186
Q

what is expelled during labour?

A

fetus, fetal membranes, placenta

187
Q

what kind of reaction is labour?

A

pro-inflammatory reaction

188
Q

what two occurrences make labour a pro-inflammatory reaction?

A

immune cell infiltration

cytokine and prostaglandin secretion

189
Q

how many phases are there to labour?

A

four

190
Q

name the four phases of labour

A

quiescence (phase 1)
activation (phase 2)
stimulation (phase 3)
involution (phase 4)

191
Q

what is phase 1 of labour?

A

quiescence = prelude to parturition

192
Q

what is phase 2 of labour?

A

activation = preparation for labour

193
Q

what is phase 3 of labour?

A

stimulation = processes of labour

194
Q

what is phase 4 of labour?

A

involution = parturient recovery

195
Q

what happens during phase 1 of labour?

A

contractile unresponsiveness, cervical softening

uterus is quiet but some changes in cervix

196
Q

what happens during phase 2 of labour?

A

uterine preparedness for labour, cervical ripening

cervical development for dilation

197
Q

what happens during phase 3 of labour?

A

uterine contraction, cervical dilation, fetal and placenta expulsion (three stages of labour)

198
Q

what happens during phase 4 of labour?

A

uterine involution, cervical repair, breast feeding

restores uterus to original size, repairs cervix and onset of lactation

199
Q

what happens after phase 1 of labour?

A

initiation of parturition

200
Q

what happens after phase 2 of labour?

A

onset of labour

201
Q

what happens after phase 3 of labour?

A

delivery of conceptus

202
Q

what happens after phase 4 of labour?

A

restoration of fertility

203
Q

why does the uterus undergo resolution and healing after labour?

A

during pregnancy, the uterus undergoes a lot of expansion, tissue remodelling and distention = so to return uterus to original size and shape for future pregnancies

204
Q

during labour, into where do immune cells infiltrate?

A

the cells of the female reproductive tract

205
Q

what inflammatory molecules are secreted during labour?

A

prostagalndins and cytokines

206
Q

why are cytokines and prostaglandins secreted during labour?

A

to orchestrate the timing and sequence of the events of labour

207
Q

how many stages of labour are there?

A

three

208
Q

name the stages of labour

A

first stage (split into latent phase and active phase)

second stage

third stage

209
Q

differentiate between the phases and the stages of labour

A

there are four phases of labour (quiescence, activation, stimulation, involution)

there are three stages of labour (occur in the stimulation phase of labour)

210
Q

what happens during the first stage of labour?

A

uterine contractions and cervical dilation

  • slow dilation in the latent phase up to 2-3cm
  • followed by rapid dilation to 10cm in the active phase
211
Q

what happens during the second stage of labour?

A

delivery of the fetus

  • commences at 10cm maximal cervical dilation
  • maximal myometrial contractions
212
Q

what happens during the third stage of labour?

A

delivery of the placenta

  • expulsion of the placenta and fetal membranes
  • post-pastum repai
213
Q

what are the two segments of the first stage of labour?

A

latent phase (slow cervical dilation to 2-3cm)

active phase (rapid cervical dilation to 10cm)

214
Q

how is cervical dilation spilt into segments?

A

slow cervical dilation to 2-3cm = latent phase

rapid cervical dilation to 10cm = active phase

215
Q

what stimulates expulsion of the fetus?

A

maximal cervical dilation at 10cm

216
Q

how does the rate of cervical dilation change?

A

initially slow up to 2-3cm and then rapid up to 10cm

217
Q

what happens at maximal cervical dilation?

A

stimulates expulsion of the fetus

218
Q

what is maximal cervical dilation?

A

at 10cm

219
Q

how long is labour usually in the first delivery?

A

approx 8-18 hours

220
Q

how long is labour usually last in the first delivery?

A

approx 8-18 hours

221
Q

how long is labour usually last in subsequent deliveries after the first?

A

approx 5-12 hours

222
Q

what is the key role of the cervix during pregnancy?

A

retains the fetus in the uterus during pregnancy

223
Q

describe the structure of the cervix

A

bundles of collagen fibres that are embedded in a proteoglycan matrix

= high connective tissue content that provides rigidity and enables stretch resistance

224
Q

why is it important that the cervix has a high connective tissue content?

A

provides cervical rigidity and ensures it is stretch-resistant

= to keep cervix closed

225
Q

what are the structural changes that take place during cervical softening?

A

measurable changes in compliance but retains cervical competence

226
Q

what are the four parts to cervical remodelling?

A

cervical softening
cervical ripening
cervical dilation
post-partum repair

227
Q

when does cervical softening begin?

A

begins in the first trimester

228
Q

what happens during cervical softening?

A

measurable changes in compliance but cervical competence is retained

229
Q

what is cervical competence?

A

the ability of the cervix to stay closed and keep the fetus inside

230
Q

when does cervical ripening begin?

A

weeks and days before birth

231
Q

what happens during cervical ripening?

A

monocyte infiltration

IL-6 and IL-8 secretion

hyaluronic acid deposition

232
Q

when does cervical dilation begin?

A

the ninth month of pregnancy, closer to the due date

233
Q

what happens during cervical dilation?

A

increased hyaluronidase expression to break down deposited hyaluronic acid

matrix metalloproteinases decrease collagen content

234
Q

why is hyaluronic acid deposited during cervical ripening?

A

to increase tissue water content = increases cervical ripening

235
Q

why is hyaluronidase increasingly expressed during cervical dilation?

A

to increase the breakdown of the deposited hyaluronic acid

= contributes to increased cervical elasticity

236
Q

what is the function of matrix metalloproteinases in cervical dilation?

A

decrease collage content to contribute to the increased cervical elasticity

237
Q

what are MMPs?

A

matrix metalloproteinases

238
Q

what happens during post-partum repair in cervix remodelling?

A

recovery of tissue integrity and competency

239
Q

why does cervical ripening take place?

A

to allow extensive immune cell infiltration, IL6 and IL8 secretion and hyaluronic acid deposition into the uterus

240
Q

why does cervical dilation take place?

A

to breakdown collagen and hyaluronic acid to increase cervical elasticity

241
Q

why does cervical post-partum repair take place?

A

to prepare the cervix for future reproductive events

242
Q

why is cervical remodelling important?

A

needs to soften cervix to allow dilation and let the fetus pass through, out of the uterus

243
Q

what stimulates parturition?

A

the fetus determines the timing of partirition through changes in the fetal HPA axis

244
Q

which hormone increases in maternal blood towards the end of pregnancy?

A

the CRH levels rise exponentially towards the end of pregnancy

245
Q

why does CRH bioavailability increase towards the end of pregnancy?

A

there is a decline in CRH binding protein levels so CRH bioavailability increases towards the end of pregnancy

246
Q

how do CRH and CRP-BP levels change towards the end of pregnancy?

A

while CRH-BP levels decrease, the CRH levels increase exponentially

247
Q

what are the functions of fetal CRH in labour?

A

promotes fetal ACTH production and fetal cortisol release

increased fetal cortisol stimulates placental CRH production

increased fetal cortisol stimulates fetal adrenal DHEAS production = increased oestrogen production

248
Q

describe the positive feedback loop triggered by fetal CRH

A

fetal CRH stimulates fetal adrenal cortisol production

fetal cortisol acts on the placent to stimulate placental CRH production

placental CRH positively feeds back to the fetal hypothalamus and stimulates fetal CRH production

249
Q

how does fetal CRH affect the placenta?

A

stimulates fetal adrenal cortisol production

fetal cortisol acts on the placenta to stimulate placental CRH production

250
Q

how does fetal CRH affect the fetal adrenal cortex?

A

stimulates the fetal adrenal cortex to produce cortisol

251
Q

what is DHEAS?

A

dihydroepiandrosterone sulphate

252
Q

what is the function of DHEAS?

A

acts as a substrate for oestrogen production in the placenta

253
Q

how do progesterone levels vary throughout pregnancy?

A

increase steadily to very high levels and drop rapidly as term approaches

254
Q

how do oestrogen levels vary throughout pregnancy?

A

increase steadily to moderately high levels and drop rapidly as term approaches

255
Q

how do hCG levels vary throughout pregnancy?

A

increase rapidly to week 7 and fall rapidly and remain low by week 10

256
Q

how does the serum oestrogen : progesterone ratio change as a pregnancy progresses?

A

serum O:P ration may shift in favour of oestrogen (possibility)

257
Q

how does progesterone receptor expression change as term approaches?

A

as term approaches, there is a switch from PR-A isoforms (activating) to PR-B and PR-C isoforms (repressive) expressed in the uterus

258
Q

what is functional progesterone withdrawal?

A

as term approaches, there is a switch from PR-A isoforms (activating) to PR-B and PR-C isoforms (repressive) expressed in the uterus

259
Q

what are the activating isoforms of the progesterone receptor?

A

PR-A

260
Q

what are the repressive isoforms of the progesterone receptor?

A

PR-B and PR-C

261
Q

describe the shift in progesterone receptor isoforms

A

expression shifts from PR-A (activating) isoforms to PR-B and PR-C (repressive) isoforms in the uterus

262
Q

how does oestogen receptor expression vary with pregnancy?

A

as term approaches, there is a rise on oestrogen receptor alpha expression

263
Q

what is the impact of functional progesterone withdrawal on the uterus?

A

blinds the uterus to progesterone action and makes it increasingly sensitised to oestrogen action

264
Q

why is it important that the uterus is blinded to progesterone action during labour?

A

high progesterone levels through pregnancy maintain uterine relaxation

so when progesterone withdrawal occurs = uterine relaxation cannot be maintained so uterine contraction can take place during labour

265
Q

how does the progesterone receptor shift stimulate uterine contractions?

A

progesterone receptors shift from being activating to repressive so progesterone can no longer carry out its function of maintaining uterine relaxation

thereby allowing uterine contractions during labour (when there is a shift in receptor isoforms)

266
Q

how does the uterus respond to changes in progesterone and oestrogen receptor expression?

A

uterus becomes blinded to progesterone action and more sensitised to oestrogen action

267
Q

what is the function of progesterone during pregnancy?

A

maintains uterine relaxation

268
Q

what type of hormone is oxytocin?

A

nonapeptide (9 AAs) hormone

269
Q

what is a nonapeptide hormone?

A

a peptide hormone with nine amino acids

270
Q

where is oxytocin synthesised?

A

mainly in the maternal pituitary gland and utero-placental tissues

271
Q

when does uterine oxytocin production rapidly increase?

A

uterine oxytocin production rapidly increases at the onset of labour
(due to rise in oestrogen levels)

272
Q

what drives the increase in uterine oxytocin secretion?

A

rise in oestrogen levels

273
Q

what stimulates the release of oxytocin in the uterus?

A

promoted by vaginal stretch receptors (i.e. Ferguson reflex)

274
Q

what is the Ferguson reflex?

A

as fetus starts to bear down on cervix and vagina, vaginal stretch receptors signal to hypothalamus

then hypothalamus signals onto the poster pituitary gland

oxytocin then released into the bloodstream

act on uterine myometrium to stimulate uterine contraction

275
Q

what does oxytocin signal through?

A

G-protein coupled oxytocin receptors in the uterus

276
Q

what type of receptors are oxytocin receptors?

A

G-protein couple dreceptors

277
Q

what controls oxytocin receptor expression pre-labour?

A

increased progesterone levels pre-labour will inhibit oxytocin receptor expression

(so uterine relaxation can be maintained)

278
Q

how does oxytocin receptor expression pre-labour affect the uterus?

A

pre-labour, less OXTR expression (due to elevated progesterone) so the uterus remains relaxed (i.e not contracting)

279
Q

describe the change in uterine oxytocin receptor expression that takes place as term approaches

A

uterine OXTR expression increases greatly

280
Q

explain the change in uterine oxytocin receptor expression that takes place as term approaches

A

during labour, progesterone levels fall + oestrogen levels rise = so uterine OXTR expression increases greatly

281
Q

what are the functions of oxytocin in the uterus?

A

increases connectivity of the myocytes in the myometrium (syncitium formation)

destabilises membrane potentials so there is a lower threshold for muscle contraction

enhances liberation of intracellular Ca2+ ion stores for muscle contraction

(also stimulates prostaglandin release via uterine OXTR signalling pathways)

282
Q

how and why does oxytocin affect the myometrium?

A

increases connectivity of the myocytes in the myometrium (syncitium formation)

  • oxytocin promotes the formation of gap junctions between myocytes so the myometrium is more connected (i.e. can act as a syncitium)
283
Q

how does oxytocin affect muscle contraction?

A

destabilises membrane potential to lower the threshold for muscle contraction

enhances the liberation of intracellular Ca2+ ion stores for muscle contraction

= increasing myometrial contractions

284
Q

which hormone dominates most of a pregnancy?

A

progesterone

285
Q

how does high progesterone affect oxytocin receptor expression pre-labour?

A

elevated progesterone levels will inhibit myometrial OXTR expression pre-labour to maintain uterine relaxation

286
Q

how does high oestrogen affect oxytocin receptor expression pre-labour?

A

rapidly increased oestrogen levels will stimulate OXTR expression in the myometrium (during labour) when uterine relaxation is no longer necessary and uterine contraction must occur

287
Q

what are the primary prostaglandins synthesised during labour?

A

PGE2, PGF2alpha, PGI2

288
Q

what stimulates prostaglandin action in the uterus?

A

rising oestrogen levels drive prostaglandin action in the uterus

289
Q

how do rising oestrogen levels stimulate prostaglandin action in the uterus?

A
  • activate phospholipase A2 enzyme, generating more arachidonic acid for prostaglandin synthesis
  • stimulates OXTR expression which promotes prostaglandin release through oxytocin signalling
290
Q

what is the function of PGE2?

A

cervical remodelling (especially cervical softening and ripening)

291
Q

how does PGE2 carry out its function?

A

promotes leukocyte infiltration, IL8 secretion and collagen bundle remodelling

292
Q

what is the function of PGF2alpha?

A

stimulates myometrial contractions

293
Q

how does PGF2alpha carry out its function?

A

promotes the connectivity of myocytes (together with oxytocin)

destabilises membrane potentials to lower the threshold for muscle contraction

294
Q

what is the function of PGI2 and how is this carried out?

A

uterine relaxation

promotes myometrial smooth muscle relaxation and relaxation of the lower uterine segment (*between contractions)

295
Q

what do prostaglandins work in conjunction with?

A

oxytocin

296
Q

why is the function of PGI2 essential?

A

stimulate myometrial relaxation between contraction to allow blood to flow back to the uterus and placenta = to maintain blood flow to the fetus

297
Q

why is the function of PGI2 essential?

A

stimulate myometrial relaxation between contractions to allow blood to flow back to the uterus and placenta = to maintain blood flow to the fetus

298
Q

how does DHEAS affect oestrogen levels?

A

as DHEAS acts as a substrate for oestrogen production, increased DHEAS stimulates increased placental oestrogen levels

299
Q

what do rising oestrogen levels cause?

A

increased oxytocin release from the PPG and the utero-placental tissues

upregulation of uterine OXTR

300
Q

what does placental oestrogen stimulate?

A

upregulation of uterine OXTR

301
Q

which hormone upregulates oxytocin receptor expression in the uterus?

A

oestrogen

302
Q

which hormone inhibits oxytocin receptor expression in the uterus?

A

progesterone

303
Q

how does oxytocin act in the uterus?

A

stimulates myometrial connectivity

stimulates more vigorous muscle contraction (destabilising membrane potentials + enhanced intracellular calcium release)

! stimulates prostaglandin release via the uterine OXTR !

304
Q

what does increased oxytocin result in the production of?

A

increased prostaglandin relelase (via uterine OXTR signaling pathways)

305
Q

to what do vigorous myometrial contraction feedback positively?

A

more vigorous muscle contractions in the uterus

= 1) increased prostaglandin production
= 2) increased oxytocin secretion

306
Q

how is the uterus sensitised to the pituitary production of maternal oxytocin?

A

upregulation of uterine OXTR expression (towards term) = stimulates muscle contraction

(vaginal stretch receptors also stimulate oxytocin release via Ferguson reflec)

307
Q

what stimulates syncitium formation in the uterus?

A

oxytocin release (following rising oestrogen levels) stimulates increased myometrial myocyte connectivity

308
Q

where do myometrial contraction start and how do they progress?

A

start from the myometrial syncitium in the fundus and spread down the upper segment

(remain in the upper uterine segment)

309
Q

what is the effect of only the upper myometrial segment contraction?

A

the myometrial syncitium of the fundus causes the contractions to be transmitted down the upper segment

= pulls up the cervix and lower segment to create one large birth canal for the foetus to transit out of

310
Q

describe the type of myometrial contraction during labour

A

brachystatic (i.e. the muscle fibres do not relax completely and retain some muscle shortening)

311
Q

define brachystatic

A

the muscle fibres do not relax completely and retain some muscle shortening (i.e. do not return to full length on relaxation)

312
Q

what is the effect of the brachystatic myometrial contraction of the shape of the uterus?

A

as muscle fibres do not relax completely and retain some muscle shortening = the cervix progressively opens until complete dilation is achieved

313
Q

which part of the uterus actively takes part in myometrial contractions?

A

upper segment

syncitium of myometrial muscle cells w extensive gap junctions in between

314
Q

which part of the uterus passively takes part in myometrial contractions?

A

lower segment

315
Q

explain the process of fetal expulsion

A

head engages w the pelvic space at 34-38 weeks

pressure on hind of fetus and head causes chin to press against chest (Flexion)

fetus rotates so fetal belly faces maternal spine

head expelled and then shoulders delivers sequentially followed by torso

(then much quicker expulsion of rest of the body)

316
Q

when does the fetal head engage with the pelvic space?

A

at approx 34-38 weeks

317
Q

how does pressure change within the uterus to cause fetal expulsion?

A

pressure on hind of fetus due to myometrial contraction AND pressure of fetal head on the cervix

= causes flexion of fetal head forward towards chest and rotation (prepped for expulsion)

318
Q

what must occur before the fetus is expelled from the uterus?

A

must rotate so the fetal belly faces the maternal spine

319
Q

how is the fetus expelled from the uterus?

A

head expelled first

shoulders delivered sequentially

torso and then rest of the body (much quicker)

320
Q

what happens to the uterus after the fetus has been expelled?

A

uterus shrinks rapidly after fetal delivery (causing the area of contact between the placenta and the endometrium to shrink)

but uterus remains contracted (to prevent inter-uterine bleeding)

321
Q

what does uterine shrinkage in turn cause?

A
  • causing the area of contact between the placenta and the endometrium to shrink
  • causing the folding of fetal membranes so they peel off the endometrium
322
Q

why is the umbilical cord clamped after birth?

A

to stop fetal blood flow to the placenta

323
Q

what is the impact of clamping the umbilical cord after birth?

A

= villi collapse

= haematoma forms between decidua and placenta

= subsequent contractions expel the placental and fetal membranes

324
Q

what stimulates the contractions that cause expulsion of the placenta and fetal membranes?

A

clamping of the umbilical cord = villi collapse and then haematoma formation between the decidua and placenta = leads to contractions

325
Q

what happens when the placental villi collapse when their blood supply is cut off?

A

heamatoma forms between the decidua and placenta

326
Q

what are the layers of the uterus immediately post expulsion of the fetus?

A

amnion
chorion
decidua vera
myometrium

327
Q

why does the uterus remain contracted after delivery?

A

to prevent inter-uterine bleeding

to facilitate thrombosis and healing of the blood vessels

328
Q

how is the risk of inter-uterine bleeding post-delivery prevented?

A

the uterus remains contracted even after delivery

329
Q

why do uterine involution and cervical repair occur?

A

to restore the non-pregnant state

330
Q

why do uterine involution and cervical repair occur?

A

to restore the non-pregnant state

shielding uterus from commensal bacteria that live in the female reprodcutive ttract

restore endometrial cyclicity in response to hormones

brs (phase 1b) (71 decks)

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