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Year 2 Development > Pregnancy, Parturition and Late Foetal Development > Flashcards

Pregnancy, Parturition and Late Foetal Development Flashcards

1
Q

What is early embryo nutrition?

A

Histiotrophic
Derivation of nutrients from the breakdown of surrounding tissues
Breakdown of maternal capillaries
Glands within the endometrium provide uterine milk

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2
Q

What is limited in the first trimester?

A

Growth

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3
Q

What happens between first and second trimester?

A

Rapid increase in rate of growtb

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4
Q

What happens in the second trimester?

A

Starts to derive nutrients from maternal blood

Achieved through haemochorial-type placenta where maternal blood directly contacts the foetal membranes

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5
Q

What is the second trimester nutrition called?

A

Haemotrophic

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6
Q

How is development supported via histitrophic nutrition in the early implantation stage?

A

Syncytiotrophoblast breaks down cells and uses their products to support embryo developement

Breakdown of maternal capillaries and uterine gland secretions exposes syncytiotrophoblast to maternal blood/milk from which it can derive nutrients

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7
Q

What is the amnion?

A

Derivative of epiblast

Does not go on to form part of foetus

First foetal membrane

Forms the amniotic cavity that goes on to become the amniotic sac (closed and avascular)

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8
Q

What is the second key foetal membrane?

A

Chorion

Outer membrane surround whole conceptus unit

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9
Q

What is the connecting stalk?

A

Part of extra embryonic tissues which grows from the embryo and connects the conceptus with the chorion

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10
Q

What is the trophoblastic lacunae?

A

Large spaces filled with maternal blood formed by breakdown of maternal capillaries and uterine glands
Become intervillous spaces aka maternal blood spaces

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11
Q

How is the trophoblastic lacunae formed?

A

Breakdown of maternal capillaries and glands

Lumens of the glands and capillaries start to fuse

Create a continuous space where maternal blood can flow

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12
Q

What are the fetal membranes?

A

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

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13
Q

What happens with the amniotic fluid at the 5th week?

A

Amnion begins to secrete amniotic fluid from 5th week – forms a fluid filled sac that encapsulates and protects the fetus

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14
Q

What are the main features of the chorion?

A

Formed from yolk sac derivatives and the trophoblast
Highly vascularized
Gives rise to chorionic villi

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15
Q

What are the chorionic villi?

A

Outgrowths of cytotrophoblast from the chorion that form the basis of the fetal side of the placenta

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16
Q

What is expansion of the amniotic sac caused by?

A

fluid accumulation forces the amnion into contact with the chorion, which fuse, forming the amniotic sac

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17
Q

What are the layers of the amniotic sac?

A

Amniotic sac: 2 layers;

amnion on the inside

chorion on the outside

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18
Q

What is the Allantois?

A

Outgrowth of the yolk sac

Grows along the connecting stalk from embryo to chorion

Becomes coated in mesoderm and vascularises to form the umbilical cord

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19
Q

What forms the umbilical cord?

A

Connecting stalk
Allantois
Additional mesoderm

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20
Q

What are cytotrophoblast cells?

A

Important in the development of the placenta

Cytotrophoblast forms
finger-like projections 
through 
syncitiotrophoblast layer
Into maternal
endometrium
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21
Q

What are the fingerlike projections called?

A

Primary chorionic villi

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22
Q

What are the chorionic villi?

A

Provide substantial surface area for exchange (gases and nutrients)

Finger-like extensions of the chorionic cytotrophoblast, which then undergo branching

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23
Q

What are the phases of chorionic villi development?

A

Primary
Secondary
Tertiary

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24
Q

What happens in the primary phase of chorionic villi?

A

outgrowth of the cytotrophoblast and branching of these extensions

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25
Q

What happens in the seconary phase of chorionic villi?

A

growth of the fetal mesoderm into the primary villi

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26
Q

What happens in the tertiary phase of chorionic villi?

A

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

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27
Q

What is the microstucture of terminal chorionic villi?

A

Blood vessel comes up through the villus
Coated in trophoblast
Surrounded by maternal blood

Convoluted knot of vessels and vessel dilation

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28
Q

What does the knot of vessel allow for?

A

Slows blood flow enabling exchange between maternal and fetal blood

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29
Q

How big are the villi in early pregnancy?

A

150-200µm diameter, approx. 10µm trophoblast thickness between capillaries and maternal blood.

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30
Q

How big are the villi in late pregnancy?

A

villi thin to 40µm, vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood.

Diffusion distance reduced

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31
Q

How is the endometrium supplied?

A

Uterine artery branches give rise to a network of arcuate arteries.

Radial arteries branch from arcuate arteries, and branch further to form basal arteries.

Basal arteries form spiral during menstrual cycle endometrial thickening.

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32
Q

What happens to the blood supply during menstrual cycle?

A

Basal arteries spiralise during menstrual cycle

Implantation does not occur: regression of spiral arteries

Implantation does occur: stabilise and provide the maternal blood supply

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33
Q

What happens in spiral artery re-modelling?

A

As the spiral arteries develop the trophoblast invade the maternal spiral arteries

Outgrowth of trophoblast down into maternal spiral arteries

Known as extra-villus trophoblast cells

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34
Q

What forms the endovascular EVT?

A

Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT.

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35
Q

What is the role of the endovascular EVT?

A

Replace the maternal endothelium of the blood vessels

As the e. EVT grow down they break down the maternal endothelium and maternal smooth muscle

Forms a new endothelial layer (foetal EVT)

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36
Q

What is the process of going from spiral to non-spiral arteries called?

A

Conversion

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37
Q

What is the affect of conversion?

A

Turns the spiral artery from a highly convoluted, high pressure vessels

Into a low pressure, high capacity conduit for maternal blood flow

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38
Q

What can problems with conversion cause?

A

Pre-eclampsia

Intra-uterine growth retardation

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39
Q

Describe the placenta

A

Maternal unit:
Blood supply gives rise to spiral arteries
Spiral arteries supply maternal blood spaces
Drainage from venous system

From the foetal side:
Formation of chorionic villi
Branch and become vascularised

Invasion of fetal circulatory system into chorionic villi that provide the large surface area for exchange between mother and fetus

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40
Q

How does nutrient exchange across the placenta occur?

A

Diffusion
Facilitated diffusion
Active transport

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41
Q

How is oxygen exchanged?

A

diffusional gradient (high maternal O2 tension, low fetal O2 tension)

42
Q

How is glucose exchanged?

A

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

43
Q

How is water exchanged?

A

placenta main site of exchange, though some crosses amnion-chorion. Majority by diffusion, though some local hydrostatic gradients.

44
Q

How are electrolytes exchanged?

A

large traffic of sodium and other electrolytes across the placenta – combination of diffusion and active energy-dependent co-transport.

45
Q

How is calcium exchanged?

A

actively transported against a concentration gradient by magnesium ATPase calcium pump.

46
Q

How are amino acids exchanged?

A

reduced maternal urea excretion and active transport of amino acids to fetus

47
Q

What are the changes observed in the mother’s cardiac system?

A

Maternal cardiac output increases 30% during first trimester (stroke vol & rate)

Maternal peripheral resistance decreases up to 30%

Maternal blood volume increases to 40% (near term (20-30% erythrocytes, 30-60% plasma)

48
Q

What are the changes observed in the mother’s respiratory system?

A

Pulmonary ventilation increases 40%

49
Q

How much glucose and oxygen does the placenta consume?

A

Placenta consumes 40-60% glucose and O2 supplied

50
Q

What are the features of fetal blood O2?

A

But although fetal O2 tension is low, O2 content and saturation are similar to maternal blood.

Embryonic and fetal hemoglobins: greater affinity for O2 than maternal hemoglobin.

51
Q

What are the stages of maturation for the circulatory system?

A

Placenta acts as site of gas exchange for fetus

Ventricles act in parallel rather than series

Vascular shunts bypass pulmonary & hepatic circulation -> close at birth to give the circulatory system we are familiar with

52
Q

What are the stages of maturation for the respiratory system?

A

Primitive air sacs form in lungs around 20 weeks, vascularization from 28 weeks

Surfactant production begins around week 20, upregulated towards term

Fetus spends 1-4h/day making rapid respiratory movements during REM sleep, practice for breathing reflex for once it leaves the uterus. Also important in development of diaphragm.

53
Q

What are the stages of maturation for the GI system?

A

Endocrine pancreas functional from start of 2T, insulin from mid-2T

Liver glycogen progressively deposited – accelerates towards term

Large amounts of amniotic fluid swallowed –debris and bile acids form meconium

54
Q

What. is meconium?

A

First stool which is delivered just after birth

55
Q

What are the stages of maturation for the nervous system?

A

Fetal movements begin late 1T, detectable by mother from ~14 weeks

Stress responses from 18 weeks, thalamus-cortex connections form by 24 weeks

Fetus does not show conscious wakefulness – mostly in slow-wave or REM sleep

56
Q

What initiates the final maturation process of the organ systems?

A

Orchestrated by increase in foetal corticosteroids towards the end of pregnancy

57
Q

What are the aims of labour?

A

Safe expulsion of the fetus at the correct time

Expulsion of the placenta and fetal membranes

Resolution/healing to permit future reproductive events

58
Q

What characteristics does labour have?

A

Labour has the characteristics of a pro-inflammatory reaction
Immune cell infiltration
Inflammatory cytokine and prostaglandin secretion

59
Q

What is important in the timing and sequence of labour?

A

Prostaglandins

60
Q

What are the stages of parturition?

A

Phase 1: Quiescence
Phase 2: Activation
Phase 3: Stimualtion
Phase 4: Involution

61
Q

What is phase 1?

A

Prelude to parturition

Contractile unresponsiveness, cervical softening

62
Q

What is phase 2?

A

Preparation for labour

Uterine preparedness for labour

Cervical ripening

63
Q

What is phase 3?

A

Process of labour

Uterine contraction

Cervical dilation

Foetal and placental expulsion

64
Q

What is phase 4?

A

Uterine involution

Cervical repair

Breast feeding

65
Q

What is the first stage of labour?

A

Contractions start,

Cervix dilation

66
Q

What can the first stage of labour be broken into?

A

Latent Phase:
Slow dilation of the cervix to 2-3cm

Active Phase:
Rapid dilation of the cervix to 10cm

67
Q

What is the second stage of labour?

A

Delivery of the fetus

68
Q

What are the features of delivery?

A

Commences at full dilation of the cervix (10cm)

Maximal myometrial contractions

69
Q

What is the third stage of labour?

A

Delivery of the placenta
Explusion of placenta and fetal membranes
Post-partum repair

70
Q

What is the timings for labour?

A

Prolonged first stage

Second and third - around an hour

Between 8 and 18 hours for first delivery

Between 5 and 12 for subsewuent

71
Q

What is the role of the cervix?

A

Cervix has a critical role in retaining the fetus in the uterus.

72
Q

What features of the cervix allow it to function?

A

High connective tissue content:
Provides rigidity
Stretch resistant

Bundles of collagen fibres embedded in a proteo-glycan matrix

Changes to collagen bundle structure underlie softening, but mechanism unclear.

73
Q

When does cervical softening begin?

A

Softening – begins in first trimester

Measurable changes in compliance but retains cervical competence

74
Q

When does cervical ripening occur?

A

Ripening – weeks and days before birth
Monocyte infiltration and IL-6 and IL-8 secretion
Hylaluron deposition

75
Q

What is cervical dilation?

A

Dilation – increased elasticity
Increased hyaluronidase expression -> HA breakdown
MatrixMetalloProteinases decrease collagen content

76
Q

What is postpartum repair characterised by?

A

Recovery of tissue integrity and competency

77
Q

What do we currently think the trigger for labour is ?

A

Fetus determines timing of parturition through changes in fetal HPA axis

CRH levels rise exponentially towards the end of pregnancy

Decline in CRH binding protein levels, so CRH bioavailability increases

78
Q

What is the role of Corticotrophin-releasing hormone in labour?

A

Promotes fetal ACTH and cortisol release

Increasing cortisol drives placental production of CRH -> Positive feedback

Stimulates DHEAS production by the fetal adrenal cortex -> substrate for estrogen production

79
Q

What are levels of progesterone through pregnancy?

A

High progesterone through pregnancy maintains uterine relaxation

80
Q

What happens to the progesterone:oestrogen ratio around the time of birth?

A

Serum estrogen:progesterone ratio may shift in favour of estrogen – this is unclear in humans

81
Q

What changes in O and P signalling occurs as delivery approaches?

A

As term approaches, switch from PR-A isoforms (activating) to PR-B and PR-C (repressive) isoforms

expressed in the uterus -> functional prog. withdrawal

High levels of P but the receptor changes blind the uterus to the increasing levels

Rise in Estrogen Receptor - Uterus is sensitised to the action of oestrogen

Alpha expression

82
Q

What is oxytocin?

A

Nonapeptide (9aa) hormone synthesized mainly in the utero-placental tissues and pituitary.

83
Q

What happens to uterine oxytocin during labour?

A

Uterine oxytocin production increases sharply at onset of labour

Expression increase is driven by increase in oestrogen levels.

Release promoted by stretch receptors as the foetus bares down on the cervix, stretching it -> Ferguson reflex

84
Q

How does Oxytocin signal?

A

Signals through G-coupled oxytocin receptor (OTR / OXTR)

85
Q

What happens re the OXRT pre-labour?

A

Pre-labour: progesterone inhibits OXTR expression -> uterus relaxed

86
Q

What allows for an increase in OXTR expression?

A

Rise in estrogen promotes large increase in uterine OXTR expression

87
Q

What are the functions of oxytocin?

A

Increases connectivity of myocytes in myometrium (syncytium)
Destabilise membrane potentials to lower threshold for contraction
Enhances liberation of intracellular Ca2+ ion stores

88
Q

What does oxytocin work in conjunction with?

A

Prostaglandins

89
Q

What are the primary PGs synthesised during labour?

A

PGE2, PGF2alpha and PGI2

90
Q

How do rising oestrogen levels drive PG action?

A
  1. Rising estrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis
  2. Estrogen stimulation of oxytocin receptor expression promotes PG release.
91
Q

What is PGE2 involved with?

A

cervix re-modelling

Promotes leukocyte infiltration into the cervix, IL-8 release and collagen bundle re-modelling

92
Q

What is PGF2 alpha involved with?

A

myometrial contractions

Destabilises membrane potentials and promotes connectivity of myocytes (with Oxytocin)

93
Q

What is PGI2 involved with?

A

myometrium

Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segnment

94
Q

What are other factors important for cervix remodelling?

A

peptide hormone relaxin and nitric oxide (NO) implicated in cervix re-modelling

95
Q

What is the integrated hypothesis for the regulation of labour?

A

CRH by foetal pituitary

Cortisol by foetal adrenals

Placenta also produces CRH and DHEAS which is converted to oestrogen

Oestrogen acts on myometrium promoting the expression of the oxytocin receptor

Uterus becomes sensitive to produce the pituitary production of maternal oxytocin and that triggers contractions

Oestrogen promotes local production of oxytocin which stimulates contractions and prostaglandin production

PGs mediate myometrial contractions and help to soften the cervix to ensure dilation can occur

96
Q

What happens in the non-labouring state?

A

Progesterone inhibits the production of these oxytocin receptors that keeps the myometrium quiescent

Stops contractions occurring prematurely

97
Q

How do the myometrial contractions work?

A

Myometrial muscle cells form a syncytium (extensive gap junctions)

Contractions start from the fundus, spread down upper segment

Muscle contractions are brachystatic –fibres do not return to full length on relaxation

This causes lower segment and cervix to be pulled up forming birth canal

98
Q

What happens to foetal positioning towards the end of term?

A

Head engages with pelvic space 34-38wks

Pressure on fetus causes chin to press against chest (flexion)

99
Q

How is the foetus expelled?

A

Fetus rotates (belly to mother’s spine

Head expelled first after cervix dilates

Shoulders delivered sequentially (upper first) followed by torso.

100
Q

What occurs to allow for placental expulsion?

A

Rapid shrinkage of the uterus after fetal delivery causes area of contact of placenta with endometrium to shrink

Uterine shrinkage also causes folding of fetal membranes – peel off the endometrium

Clamping of the umbilical cord after birth stops fetal blood flow to placenta -> villi collapse

Hematoma formation between decidua and placenta

Contractions expel placenta and fetal tissues

101
Q

How is the uterus repaired?

A

Uterus remains contracted after delivery to facilitate uterine vessel thrombosis.

Uterine involution and cervix repair restore non-pregnant state

Shielding uterus from commensural bacteria

Restore endometrial cyclicity in response to hormones

Year 2 Development (9 decks)

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