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BRS Year 2 > Pregnancy, parturition and late foetal development > Flashcards

Pregnancy, parturition and late foetal development Flashcards

1
Q

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 happens between first and second trimester?

A

Rapid increase in rate of growth

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3
Q

what happens in first trimester

A

limited growth due to histiotrophic nutrition

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4
Q

what is the nutrition in second trimester

A

haemotrophic

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5
Q

how is histitrophic nutrition supported in the early implantation of the embryo

A

Syncytiotrophoblast breaks down maternal cells and uses their products to support embryo development
breakdown of maternal capillaries + uterine gland secretions exposes syncytiotrophoblast to maternal blood to derive nutrients from

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6
Q

what is the amnion

A

Derivative of epiblast - extraembryonic structure
First foetal membrane
Forms the amniotic cavity that goes on to become the amniotic sac

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7
Q

two key foetal membranes

A

amnion

chorion

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8
Q

what is the chorion

A

outer membrane surrounding whole conceptus unit

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9
Q

what is the connecting stalk

A

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

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10
Q

What are 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 are 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 foetal membranes and their function

A

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

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13
Q

what happens in the 5th week to amniotic fluid

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

chorion main features

A

Formed from yolk sac derivatives and the trophoblast
highly vascularized
forms chorionic villi

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15
Q

what are chorionic villi (cell and function)

A

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

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16
Q

how is the amniotic sac expanded?

A

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

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17
Q

layers of amniotic sac

A

amnion on the inside

chorion on the outside

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18
Q

what is the allantois

A

yolk sac outgrowth
grows along connecting stalk embryo-chorion
becomes coated in mesoderm and vascularises
FORMS UMBILICAL CORD

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19
Q

what forms the umbilical cord

A

connecting stalk
allantois
plus mesoderm cells

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20
Q

what are cytotrophoblast cells

A

Important in the development of the placenta

form finger-like projections through syncitiotrophoblast layer Into maternal endometrium (primary chorionic villi)

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21
Q

fingerlike projections of cytotrophoblast into endometrium

A

primary chorionic villi

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22
Q

role of chorionic villi

A

Provide substantial surface area for exchange (gases and nutrients)

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23
Q

phases of chorionic villi development

A

primary secondary tertiary

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24
Q

primary phase of chorionic villi development

A

outgrowth of the cytotrophoblast and branching of these extensions

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25
Q

seconary phase of chorionic villi development

A

growth of the fetal mesoderm into the primary villi

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26
Q

tertiary phase of chorionic villi development

A

growth of the umbilical artery and umbilical vein into the villus mesoderm

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27
Q

structure of terminal chorionic villi

A

convoluted blood vessel comes up through the villus, coated in trophoblast cells
Surrounded by maternal blood

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28
Q

what do the knots of terminal chorionic villi allow

A

slows blood flow

enables exchange between maternal and foetal blood

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29
Q

how do the villi change from early to late pregnancy

A

thick to thin

reduced diffusion distance in late pregnancy

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30
Q

blood supply of endometrium

A

UTERINE ARTERY - ARCUATE arteries - RADIAL arteries - BASAL arteries - SPIRAL arteries

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31
Q

maternal blood supply changes in menstrual cycle

A

basal arteries spiralise
if no implantation - regression of spiral As
implantation - stabilise

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32
Q

what is spiral artery remodelling

A

as spiral arteries develop the extra-villi trophoblast cells invade, break down smooth muscle and endothelium of arteries
EVT cells coat inside of spiral arteries

turns spiral artery into low pressure high capacity conduit for maternal blood

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33
Q

what is the process of spiral artery remodelling called

A

conversion

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34
Q

what do issues in conversion cause

A

preeclampsia

intra-uterine growth retardation

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35
Q

structure of placenta

A

maternal arteries and veins supply intervillous space
chorionic villi from foetus act as exchange surface
half moon shape

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36
Q

how does nutrient exchange occur across placenta

A

Diffusion
Facilitated diffusion
Active transport

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37
Q

how is oxygen exchanged across the placenta

A

diffusion gradient

high maternal O2 tension, low foetal

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38
Q

how is glucose exchanged across the placenta

A

facilitated diffusion

by foetal trophoblast cells and maternal transporters

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39
Q

how is water exchanged across the placenta

A

diffusion
some local hydrostatic gradients
some crosses chorion-amnion

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40
Q

how are electrolytes exchanged across the placenta

A

diffusion and active transport

41
Q

how is calcium exchanged across the placenta

A

active transport by magnesium ATPase calcium pump

42
Q

transport of amino acids across placenta

A

reduced maternal urea excretion

active transport

43
Q

changes in maternal cardiac system

A

CO increased
peripheral resistance decreased
blood volume increases - erythrocytes and plasma

44
Q

changes to maternal resp system

A

pulmonary ventilation increases almost half fold

45
Q

features of foetal blood O2

A

foetal O2 tension low
O2 content and sats similar to maternal blood
embryonic/foetal haemoglobins have greater affinity for O2 than maternal haemoglobin

46
Q

how does the circulatory system mature in foetuses

A

placenta is main site of gas exchange
ventricles act in parallel
pulmonary and hepatic circulation bypassed until birth

47
Q

maturation of respiratory system

A

Primitive air sacs form in lungs around 20 weeks, vascularization from 28
Surfactant production begins around week 20, upregulated towards term
foetus makes rapid respiratory movements during REM sleep, practice for breathing reflex for once it leaves the uterus. - important for diaphragm dev.

48
Q

maturation of GI tract

A

endocrine pancreas function from 2nd trimester - insulin mid 2T
liver glycogen progressively deposited – accelerates towards term
Large amounts of amniotic fluid swallowed –debris and bile acids form meconium

49
Q

what is the meconium

A

first stool delivered just after birth

formed from amniotic fluid debris and bile acids

50
Q

maturation of nervous system

A

movement from late 1T
stress response starts at 18wk
no conscious wakefulness - mostly slow wave or REM sleep

51
Q

what initiates final maturation f organ systems

A

increase in foetal corticosteroids

52
Q

aims of labour

A

safe expulsion of foetus
placenta, foetal membranes
healing for future reproduction

53
Q

what chemical has key role in timing and sequence of labour

A

prostaglandins

54
Q

stages of partituition

A

quiescence
activation
stimulation
involution

55
Q

phase 1 of partiution

A

prelude

contractile unresponsiveness, cervical softening

56
Q

phase 2 of partuition

A

Preparation for labour
Uterine preparedness for labour
Cervical ripening

57
Q

phase 3 partiuition

A

Process of labour
Uterine contraction
Cervical dilation
Foetal and placental expulsion

58
Q

phase 4 partiuition

A

Uterine involution
Cervical repair
Breast feeding

59
Q

first stage of labour

A

contractions start

cervical dilation

60
Q

stages of first stage of labour

A

Latent Phase:
Slow dilation of the cervix to 2-3cm
Active Phase:
Rapid dilation of the cervix to 10cm

61
Q

second stage of labour

A

foetus delivery

62
Q

third stage of labour

A

Delivery of the placenta and foetal membranes

Post-partum repair

63
Q

cervix structure and role in labour and pregnancy

A

High connective tissue content:
Provides rigidity
Stretch resistant
Bundles of collagen fibres embedded in a proteoglycan matrix
Changes to collagen bundle structure underlie softening

64
Q

what is the first cervical change and when is it

A

softening - first trimester

65
Q

when does cervical ripening occur

A

weeks/days before birth
monocyte infiltration and IL-6 IL-8 secretion
hylaluron deposition

66
Q

how does cervical dilation occur

A

hyaluronidase enzyme expression increase

hyaluronic acid degrades, matrix metalloproteinases decrease collagen content

67
Q

role of corticotrophin releasing hormone in pregnancy

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

68
Q

what are progesterone levels in pregnancy and why

A

high

maintains uterine relaxation

69
Q

what changes occur in oestrogen and progesterone signalling close to delivery

A

As term approaches, switch from PR-A isoforms (activating) to PR-B and PR-C (repressive) expressed in the uterus -> functional prog. withdrawal

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

Rise in oestrogen alpha receptor - Uterus sensitised to action of oestrogen

70
Q

production of oxytocin in 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 bears down on the cervix, stretching it -> Ferguson reflex

71
Q

what is the ferguson reflex

A

foetus bares down on cervix, stretch receptors cause increased release of oxytocin

72
Q

oxytocin signalling

A

via g-coupled oxytocin receptor

OXTR

73
Q

functions of oxytocin in labour

A

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

74
Q

how does a rise in oestrogen drive prostaglandin action

A

Rising oestrogen activates phospholipase A2 enzyme, generating more arachidonic acid for PG synthesis

oestrogen stimulation of oxytocin receptor OXGR expression promotes PG release

75
Q

PGE2 role in labour

A

cervix re-modelling

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

76
Q

PGF2 alpha role in labour

A

myometrial contractions

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

77
Q

role of PGI2 in labour

A

myometrium

Promotes myometrial smooth muscle relaxation and relaxation of lower uterine segnment

78
Q

regulation of labour process

A

foetal CRH - cortisol
placenta CRH + DHEAS (oestrogen produced)
oestrogen acts on myometrium promoting the expression of OXTR and local production of oxytocin
Uterus becomes sensitive to produce the pituitary production of maternal oxytocin - CONTRACTIONS + prostaglandin synth
PGs ripen and soften cervix

79
Q

process of myometrial contractions

A

Myometrial muscle cells form syncytium (extensive gap junctions)
Contractions start from the fundus, spread down upper segment
Muscle contractions are brachystatic (fibres dont return to full length on relaxation)
therefore Lower segment and cervix pulled up forming birth canal

80
Q

how does foetal head position change towards delivery

A

Head engages with pelvic space 34-38wks

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

81
Q

how is foetus expelled

A 
Fetus rotates (belly to mother’s spine
Head expelled first after cervix dilates
Shoulders delivered sequentially (upper first) followed by torso.
82
Q

what happens after foetal expulsion

A

placenta expulsion
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

83
Q

how does the uterus undergo repair

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

84
Q

how is preeclampsia diagnosed

A

During routine check ups:
Check BP
Urine tests
Blood tests

85
Q

maternal risk factors for preeclampsia

A 
Age
Obesity
First pregnancy
Previous pregnancy with pre-eclampsia/Family history
Gestational hypertension or previous hypertension
PCOS
Renal disease
Diabetes
Subfertility
Autoimmune disease
86
Q

early onset preeclampsia

A

less than 34 wk
foetal and maternal symptoms
changes in placental structure

87
Q

late onset preeclampsia

A

over 34wk
mostly maternal symptoms
less placental structural changes

88
Q

symptoms of preeclampsia

A

high bp when previously normotensive
headaches
proteinuria
upper abdominal pain (less common)

89
Q

risks to foetus in preeclampsia

A

reduced growth
stillbirth
neonatal respiratory distress syndrome
preterm birth

90
Q

risks to mother in preeclampsia

A

HELLP syndrome
pulmonary oedema
eclampsia
placental abruption

91
Q

pathophysiology of preeclampsia

A

failure of normal trophoblast invasion (only in decidual layer)
maladaption of maternal spiral arterioles - placental perfusion restricted

92
Q

factors associated with preeclampsia

A

PLFG - proangiogenic, released in large amounts by placenta

Flt1 (soluble VEGFR1) - receptor for VEGF like factors, limits their bioavailability

93
Q

role of factors in preeclampsia

A

excess Flt1 leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfunction

94
Q

use of PLGR tests alone in PE

A

triage test

rules out PE in the next 14 days

95
Q

use of sFlt1:PLGF ratio in PE

A

under 38 rules out PE

over 38 has increased risk of PE

96
Q

how is PE managed

A

only cured by placenta delivery - if over 37wk, deliver, under 34, keep, in between is case by case
anithypertensives
corticosteroids if under 34wk for lung development before delivery

97
Q

long term impacts of PE

A

Elevated risk of CV disease, t2DM and renal disease

Roughly 1/8 risk of having pre-eclampsia in next pregnancy (greater if early onset)

98
Q

prevention of pre-eclampsia

A

weight loss
exercise - regardless of PE
baby aspirin for high risk groups prevents early onset

BRS Year 2 (67 decks)

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