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BRS YR2 > Pregnancy, Parturition and Late Fetal Development > Flashcards

Pregnancy, Parturition and Late Fetal Development Flashcards

1
Q

What cannabinoid receptors does the fallopian tubes express?

A

CB1

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2
Q

What does reduced CB1 receptors indicate?

A

an ectopic pregnancy

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3
Q

When are endocannabinoid levels high?

A

during an ectopic pregnancy

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4
Q

How do components like THC impact the fallopian tube?

A
  • peturb embryo transport

- disrupt the embryo environment

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5
Q

How do components like THC disrupt the embryo environment?

A

by altering the balance of endocannabinoids in the fallopian tube

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6
Q

Which animal is a good model for humans during pregnancy?

A

the sheep

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7
Q

How common is pre-eclampsia?

A

in around 2-4% of pregnancies in the USA and Europe

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8
Q

What is the mortality of pre-eclampsia?

A

50,000-60,000 deaths/year

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9
Q

What are the risks of PE to the mother during pregnancy?

A
  • damage to: kidneys, liver, brain…
  • possible progression to eclampsia (seizures, loss of consciousness)
  • placental abruption (separation of the placenta from the endometrium)
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10
Q

What maternal risk factors may pre-dispose to developing PE?

A
  • history/family history of pre-eclampsia
  • BMI >30
  • Age > 40, and <20
  • pregnancy (multiple)
  • sub-fertility
  • gestational diabetes
  • PCOS
  • diabetes
  • autoimmune disease
  • non-natural cycle IVF
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11
Q

What are the sub-types of pre-eclampsia?

A
  • early onset (<34 weeks)

- late onset (>34 weeks)

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12
Q

How do you characterise HELLP syndrome?

A
  • haemolysis
  • elevated liver enzymes
  • low platelets
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13
Q

What is the main diagnostic tests done for pre-eclampsia?

A
  • Urine Analysis

- Umbilical Artery Doppler velocimetry

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14
Q

What are the main characteristics of pre-eclampsia?

A
  • > 20 weeks gestation
  • sudden, persistant hypertension
  • protein uria
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15
Q

What are the characteristics of pre-eclampsia?

A
  • reduced fetal movement
  • reduced amniotic fluid volume
  • oedema (not discriminatory)
  • new onset hypertension (>140/90)
  • > 20 weeks gestation
  • headache
  • abdominal pain
  • visual disturbances
  • seizures
  • breathlessness
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16
Q

What is early onset pre-eclampsia?

A
  • <34 weeks
  • associated with fetal and maternal symptoms
  • changes in the placental structure
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17
Q

What is late onset pre-eclampsia?

A
  • > 34 weeks
  • more common (90%)
  • maternal symptoms
  • fetus generally OK
  • less overt/no placental changes
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18
Q

What is a placental abruption?

A

seperation of the placenta from the endometrium

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19
Q

What form of nutrition is the early embryo dependent on?

A

histiotrophic

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20
Q

What is histiotrophic nutrition?

A
  • the derivation of nutrients from the breakdown of surrounding (endometrial) tissues and maternal capillaries
  • uterine milk from uterine glands
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21
Q

When is the embryo reliant on histiotrophic nutrition?

A

the first trimester

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22
Q

When does the embryo swap to haemotrophic support?

A

at the start of the second trimester

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23
Q

What is haemotrophic nutrition?

A

derive its nutrients from maternal blood through a haemochorial-type placenta where maternal blood directly contacts the fetal membrane

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24
Q

When does the activation of the haemochorial-type placenta happen?

A

12 weeks gestation

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25
Q

What happens in the early implantation stage in terms of the origin of the placenta?

A
  • syncytiotrophoblast invades the surrounding endometrial tissue
  • secretions of uterine glands and maternal capillary breakdown allows syncytiotrophoblast access to maternal blood
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26
Q

What is the function of the amniotic sac?

A

surrounds and cushions the foetus for it’s development through the second and third trimesters

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27
Q

What causes the amniotic sac to expand?

A

secretions from the amnion cells

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28
Q

What are the key fetal membranes?

A
  • amnion
  • chorion
  • allantosis
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29
Q

What is a connecting stalk?

A
  • extra-embryonic tissue

- grows from the embryo to connect the conceptus with the chorion

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30
Q

What does the extensive invasion by the syncytiotrophoblasts form?

A

trophoblastic lacunae

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31
Q

What is trophoblastic lacunae?

A

large spaces filled with maternal blood formed by the breakdown of maternal capillaries and uterine glands
(intervillous/maternal blood spaces)

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32
Q

What is the role of the fetal membranes?

A
  • extra-embryonic tissues

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

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33
Q

What is the amnion?

A
  • inner-fetal membrane

- forms a closed, avascular sac with the developing embryo at one end

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34
Q

Where does the amnion arise from?

A

epiblast (but does not contribute to fetal tissues)

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35
Q

When does the amnion begin to secrete amniotic fluid?

A

5th week

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36
Q

What is the chorion?

A
  • outer fetal membrane

- high vascularised

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37
Q

What does the chorion arise from?

A
  • yolk sac derivatives

- trophoblast

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38
Q

What arises from the chorion?

A

chorionic villi

- outgrowth of cytotrophoblast from the chorion that form the basis of the fetal side of the placenta

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39
Q

What happens when the amniotic sac expands?

A
  • forces the amnion to come into contact with the chorion

- they fuze, forming the amniotic sac

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40
Q

What are the 2 layers that make up the amniotic sac?

A
  • amnion (inside)

- chorion (outside)

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41
Q

What is the allantois?

A
  • outgrowth of the yolk sac

- grows along the connecting stalk from the embryo to chorion

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42
Q

What arises from the allanosis?

A
  • coated in mesoderm and vascularizes

- forms the umbilical cord

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43
Q

What happens to the cytotrophoblasts when the placenta is developing?

A
  • provides the cells to form syncitiotrophoblasts
  • form finger-like projections through the synciotrophoblast layer into the maternal endometrium (primary chorionic villi)
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44
Q

What are primary chorionic villi?

A

finger-like extensions of the chorionic cytotrophoblast, which then undergoes branching

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45
Q

What is the role of chorionic villi?

A

provide substantial surface area for exchange

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46
Q

How many stages are there in chorionic villi development?

A

3

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47
Q

What is the primary stage of chorionic villi development?

A

outgrowth of the cytotrophoblast and the branching of these extensions

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48
Q

What is the secondary stage of chorionic villi development?

A

growth of the fetal mesoderm into the primary villi

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49
Q

What is the tertiary stage of chorionic villi development?

A

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

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50
Q

Describe the microstructure of the terminal chorionic villus?

A
  • convoluted knot of vessels
  • vessel dilation
  • slows blood flow to enhance exchange
  • whole structure covered in trophoblast
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51
Q

What is the structure of the chorionic villi during early pregnancy?

A
  • diameter: 150-200 micrometers

- trophoblast thickness: 10 micrometer (between capillaries and maternal blood)

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52
Q

What is the structure of the chorionic villi during late pregnancy?

A
  • diameter: thin-40 micrometers

- trophoblast thickness: 1-2 micrometer (between capillaries and maternal blood)

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53
Q

Describe the maternal blood supply to the endometrium?

A
  • uterine artery > arcuate arteries
  • arcuate arteries > radial arteries
  • radial arteries > basal arteries
  • basal artery > spiral arteries during menstrual cycle endometrial thickening
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54
Q

Where are radial arteries found?

A

myometrium and endometrium

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55
Q

What is the function of spiral arteries?

A

provide the maternal blood supply to the endometrium

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56
Q

What are extra-villus trophoblasts?

A

cells coating the villi that invade down into the maternal spiral arteries

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57
Q

What happens when extra-villus trophoblasts grow into the spiral arteries?

A

they become endovascular EVT cells

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58
Q

What do endovascular EVT cells do?

A
  • breaks down the endothelium and smooth muscle

- coats the vessels to form a new endothelial layer

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59
Q

What term is used to describe the process of endovascular EVT cells replacing the endothelium of the vessels?

A

conversion

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60
Q

What is the purpose of conversion?

A

turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow

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61
Q

What do the spiral arteries supply?

A

the intervillus spaces/maternal blood spaces with blood

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62
Q

How does oxygen cross the placenta?

A

diffusional gradient

  • high maternal oxygen tension
  • low fetal oxygen tension
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63
Q

How does glucose cross the placenta?

A
  • facilitated diffusion by transporters on the maternal side and fetal trophoblast cells
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64
Q

How does water cross the placenta?

A
  • main site of exchange is placenta
  • some exchange crosses the amnion-chorion
  • majority by diffusion
  • some local hydrostatic gradients
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65
Q

How do electrolytes cross the placenta?

A

large traffic of sodium and other electrolyes

- diffusion and active energy-dependent co-transport

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66
Q

How does calcium cross the placenta?

A

actively transported against a concentration gradient by Mg ATPase calcium pump

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67
Q

How do amino acids cross the placenta?

A
  • reduced maternal urea excretion

- active transport of amino acids to the fetus

68
Q

What are the physiological changes seen in the mother in regards to oxygen exchange?

A
  • increased cardiac output (30%), by increasing stroke volume and rate
  • peripheral resistance decreases by 30%
  • pulmonary ventilation increases by 40%
  • blood volume increases by 40%
69
Q

How is the placenta/fetus adapted to enhance oxygen exchange?

A
  • placenta consumes 40-60% of oxygen and glucose supplied
  • oxygen content and saturation are similar to mternal blood
  • embryonic and fetal haemoglobin has a greater affinity for oxygen than maternal haemoglobin
70
Q

How is pre-eclampsia diagnosed?

A
  • persistant hypertension
  • proteinuria
  • urine analysis
  • umbilical artery (Doppler Velocimetry)
71
Q

How can pre-eclampsia be excluded?

A

placenta growth factor test

72
Q

What are the risks of PE to the fetus during pregnancy?

A
  • reduced fetal growth
  • preterm birth
  • pregnancy loss/stillbirth
  • Placental abruption (separation of the placenta from the endometrium)
73
Q

What happens in the development of a normal placenta?

A
  • EVT invasion of maternal spiral arteries leads to endothelial and smooth muscle breakdown.
  • EVT become endothelial EVT and spiral arteries become high capacity
74
Q

What happens in the development of a placenta with a risk of pre-eclampsia?

A
  • EVT invasion of maternal spiral arteries is limited to decidual layer.
  • Spiral arteries are not extensively remodelled, thus placental perfusion is restricted.
75
Q

What is Placental Growth Factor (PLGF)?

A

VEGF related, pro-angiogenic factor released in large amounts by the placenta.

76
Q

What is Fit1 (soluble VEGFR1)?

A

Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.

77
Q

What is the Flt1 (souble VEGFR1) and PLGF levels seen in pre-eclampsia?

A
  • excess production of Flt-1 by distressed placenta

- reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.

78
Q

What can be used to predict the onset of pre-eclampsia?

A
  • PLGR levels

- Flt-1/PLGR levels

79
Q

What is the benefit of PLGR?

A
  • triage test

- rules out pre-eclampsia in the next 14 days in women 20-36weeks and 6days

80
Q

What does a PLGR result of <12 pg/ml mean?

A
  • positive test (highly abnormal)

- increased risk of preterm delivery

81
Q

What does a PLGR result of >12 pg/ml and <100 pg/ml mean?

A
  • positive test (abnormal)

- increased risk of preterm delivery

82
Q

What does a PLGR result of >100 pg/ml mean?

A
  • negative test (normal)

- unlikely to progress to delivery within 14 days of test

83
Q

When is a Flt-1/PlGF ratio test done?

A

24-36weeks and 6days

84
Q

What does a Flt-1/PlGF ratio of <38 mean?

A

rules out pre-eclampsia

85
Q

What does a Flt-1/PlGF ratio of >38 mean?

A

increased risk of pre-eclampsia

86
Q

How can pre-eclampsia be resolved?

A

only by the delivery of the placenta

87
Q

What is the management plan if <34 weeks?

A
  • preferable to try and maintain the pregnancy if possible for benefit of the fetus
  • anti-hypertensive therapies
  • corticosteroids to promote fetal lung development before delivery
88
Q

What is the management plan if >37 weeks?

A

delivery is preferable

89
Q

What are the 3 main approaches to prevent pre-eclampsia?

A
  • weight loss (esp if BMI>35)
  • exercise throughout the pregnancy
  • low dose aspirin (from 11-14weeks for high risk groups), may delay not prevent
90
Q

What are the long term impacts of pre-eclampsia on maternal health?

A

elevated risk of:

  • CVD
  • T2DM
  • renal disease
  • 1/8 risk of pre-eclampsia in next pregnancy
91
Q

How does the circulatory system mature in late fetal development?

A
  • placenta acts as a site of gas exchange for the fetus
  • ventricles act in parallel rather than series
  • vascular shunts bypass pulmonary and hepatic circulation (close at birth)
92
Q

How does the respiratory system mature in late fetal development?

A
  • primitive air sacs form in the lungs (at 20 weeks)
  • vascularization at 28 weeks
  • surfactant production begins around week 20, upregulated towards term
  • the fetus spends 1-4hours/day making rapid respiratory movements during REM sleep
93
Q

How does the GI system mature in late fetal development?

A
  • endocrine pancreas functional from start of the second trimester
  • insulin from the middle of the second trimester
  • liver glycogen is progressively deposited, accelerates towards DD
  • large amounts of amniotic fluid swallowed (debris and bile acids form meconium)
94
Q

How does the nervous system mature in late fetal development?

A
  • fetal movements start in the late first T, detectable by the mother from 14 weeks
  • stress response from 18 weeks
  • thalamus-cortex connections form by 24 weeks
  • fetus does not show conscious wakefulness (slow wave / REM sleep)
95
Q

What is thought to cause the further maturation of the organs?

A

increased corticosteroids

96
Q

What is the purpose of labour?

A
  • safe expulsion of the fetus at the correct time
  • explusion of the placenta and fetal membranes
  • resolution/healing to permit future reproductive events
97
Q

What are the characteristics of labour?

A

pro-inflammatory reaction:

  • immune cell infiltration
  • inflammatory cytokine and prostaglandin secretion
98
Q

How many phases are there to labour?

A

4

99
Q

What are the 4 phases of labour?

A

1 - prelude to parturition
2 - preparation for labour
3 - processes of labour
4 - parturient recovery

100
Q

What happens in the first phase of labour?

A
  • contractile unresponsiveness

- cervical softening

101
Q

When does the first phase of labour happen?

A

late 1st trimester and onwards

102
Q

What happens in the second phase of labour?

A
  • uterine preparedness for labour

- cervical ripening

103
Q

What happens in the third phase of labour?

A
  • uterine contraction
  • cervical dilation
  • fetal and placenta expulsion
    (3 stages of labour)
104
Q

What happens in the fourth phase of labour?

A
  • uterine involution
  • cervical repair
  • breast feeding
105
Q

What is the first stage of labour?

A
  • contractions start

- cervix dilates

106
Q

What can the first stage of labour be split into?

A
  • latent phase

- active phase

107
Q

What happens in the latent phase of the first stage of labour?

A

slow dilation of the cervix to 2-3cm

108
Q

What happens in the active phase of the first stage of labour?

A

rapid dilation of the cervix to 10cm

109
Q

What is the second stage of labour?

A
  • delivery of the fetus
  • commences at full dilation of the cervix (10cm)
  • maximal myometrial contractions
110
Q

What is the third stage of labour?

A
  • expulsion of the placenta and fetal membranes

- post-partum repair

111
Q

What is the role of the cervix?

A

retains the fetus in the uterus

112
Q

What are the characteristics of the cervix?

A
  • high connective tissue content (rigidity and resistance to stretch)
  • bundles of collagen fibres embedded in a proteo-glycan matrix
113
Q

What changes happen to the cervix during labour/delivery?

A

changes to the collagen bundle structure to soften the cervix to allow dilation

114
Q

When does cervical softening start?

A

begins in the 1st trimester

115
Q

What happens in cervical softening?

A
  • changes in compliance

- retains cervical competence

116
Q

When does cervical ripening occur?

A

weeks and days before birth

117
Q

What happens in cervical ripening?

A
  • monocyte infiltration (macrophages and neutrophils)
  • IL-6 and IL-8 secretion
  • hylaluron deposition
118
Q

What happens in cervical dilation?

A
  • increased elasticity
  • increased hyaluronidase expression (HA breakdown)
  • MMPs decrease collagen content
119
Q

What happens in cervical post-partum repair?

A

recovery of tissue integrity and competency

120
Q

What causes the initiation of labour?

A

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

121
Q

Why is it believed that the fetus determines the timing of parturition?

A
  • CRH levels rise exponentially towards the end of pregnancy
  • decline in CRH binding protein levels
  • increased bioavailability of CRH
122
Q

When does CRH exponetially increase in the fetus?

A

30 days before pregnancy

123
Q

What is the impact of CRH 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 by the placenta)
124
Q

What are progesterone levels during pregnancy?

A

high progesterone throughout the pregnancy to promote uterine relaxation

125
Q

Is there a shift in the estrogen:progesterone ratio at birth?

A
  • may
  • to favour estrogen
  • unsure as to why
126
Q

What are the changes seen to progesterone receptors as term approaches?

A 
swap from:
- PR-A isoforms (activating)
to:
- PR-B
- PR-C (repressive) isoforms
127
Q

What is the result of these changes seen to progesterone receptors as term approaches?

A
  • functional progesterone is withdrawn

- uterus becomes blinded to progesterone action

128
Q

What are the changes seen to estrogen receptors as term approaches?

A

increased estrogen receptor alpha expression

129
Q

What is the result of these changes seen to estrogen receptors as term approaches?

A

uterus is sensitised to estrogen action

130
Q

What is thought to cause these changes in the estrogen/progesteron receptors?

A

likely: local changes in the E:P ratio in uterine tissues

131
Q

What is oxytocin?

A

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

132
Q

When is oxytocin produced during pregnancy?

A

at the onset of labour

133
Q

What is thought to trigger the release of oxytocin?

A
  • increased estrogen levels

- stretch receptors (Ferguson reflex)

134
Q

What is the Ferguson reflex?

A
  • stretch receptors in the cervix and vagina
  • hypothalamus by posterior pituitary
  • triggers the release of oxytocin by the posterior pituitary
135
Q

What does oxytocin use to signal?

A

G-coupled oxytocin receptor (OTR/OXTR)

136
Q

What happens to oxytocin expression/signalling pre-labour?

A

progesterone inhibits OXTR expression so that the uterus can relax

137
Q

What happens to oxytocin expression/signalling labour?

A

rise in estrogen promotes a large increase in uterine OXTR expression

138
Q

What is the function of oxytocin?

A
  • increases the connectivity of myocytes in the myometrium (syncytium)
  • destabilise membrane potentials to lower the threshold for contraction
  • enhances the liberation of intracellular Ca2+ ion stores
139
Q

What are the primary prostaglandins that are synthesized during labour?

A
  • PGE2
  • PGF2alpha
  • PGI2
140
Q

What drives the action of prostaglandins?

A
  • rising estrogen activates phospholipidase A2 enzyme, generating more arachidonic acid for PG synthesis
  • estrogen stimulation of oxytocin receptor expression promotes PG release
141
Q

What is the role of PGE2?

A
  • cervix re-modelling
  • promotes leukocyte infiltration into the cervix
  • IL-8 release
  • collagen bundle re-modelling
142
Q

What is the role of PGF2 alpha?

A
  • myometrial contractions

- destabilises membrane potentials and promotes connectivity of myocytes (with oxytocin)

143
Q

What is the role of PGI2?

A

promotes myometrium smooth muscle relaxation and relaxation of the lower uterine segment

144
Q

What are the factors that also may be involved in cervix remodelling?

A
  • relaxin

- nitric oxide

145
Q

What is DHEAS converted to in the placenta?

A

Estrogen

146
Q

What does oxytocin from the fetus and the mothers pituitary glad stimulate?

A
  • stimulates the uterus to contract

- stimulates the placenta to make prostaglandins

147
Q

What is the effect of prostaglandins?

A

stimulate more vigorous contractions of the uterus

148
Q

What would progesterone limit if present during labour?

A

the increased expression of oxytocin receptors on the uterus, preventing contractions

149
Q

Which part of the uterus drives myometrial contractions?

A

the fundus, and spread down the upper segment

150
Q

Which parts of the uterus are passive?

A
  • lower segment

- cervix

151
Q

What muscle cells are present in fundus and upper segment of the uterus?

A

myometrial muscle cells

152
Q

What do the myometrial muscles form?

A

syncytium - extensive gap junctions

153
Q

What forms the birth canal?

A

the lower segment and the cervix being pulled up

154
Q

What causes the passive part of the uterus to be pulled up?

A
  • brachystatic muscle contractions

- fibres do not return to full length on relaxation

155
Q

What is required before delivery can proceed?

A
  • birth canal formed

- dilation of the cervix

156
Q

What signals the start of delivery?

A

the head engages with the pelvic space at 34-38 weeks

157
Q

What happens when the fetus’ head engages with the pelvic space?

A

there is pressure on the fetus causing chin to press against the chest (flexion)

158
Q

What happens to the fetus’s position as delivery progresses?

A

fetus rotates (belly to mothers spine)

159
Q

What is expelled first when the cervix dilates?

A

head

160
Q

What is delivered after the head?

A
  • shoulders delivered sequentially

- followed by torso

161
Q

What process happens after the expulsion of the fetus?

A

placental expulsion and repair

162
Q

What does the rapid shrinkage of the uterus after delivery cause?

A
  • reduction in the area of contact of the placenta to the endometrium
  • folding of fetal membranes (peel off the endometrium)
163
Q

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

A

stops fetal blood flow to the placenta, and villi collapse

164
Q

What expels the placenta and fetal tissues?

A

contractions

165
Q

What is the effect of the placenta villi collapse?

A

hematoma formation between decidua and placenta

166
Q

What happens after the delivery of the placenta?

A

the uterus remains contracted after delivery to facilitate uterine vessel thrombosis

167
Q

Why does the uterus and cervix return back to non-pregnant state?

A
  • shields the uterus from commensal bacteria

- restores endometrial cyclicity in response to hormones

BRS YR2 (70 decks)

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