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

Pregnancy, Parturition and Late Fetal Development Flashcards

1
Q

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

A
  • damage to kidneys, liver, brain and other organs
  • possible progression to eclampsia (seizures, loss of consciousness)
  • placental abruption (separation of the placenta from the endometrium)
  • HELLP syndrome
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2
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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3
Q

What are the sub-types of pre-eclampsia?

A
  • early onset (<34 weeks)
  • late onset (>34 weeks)
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4
Q

How do you characterise HELLP syndrome?

A
  • haemolysis
  • elevated liver enzymes
  • low platelets
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5
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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6
Q

What is early onset pre-eclampsia?

A
  • <34 weeks
  • associated with fetal and maternal symptoms
  • changes in the placental structure
  • reduced placental diffusion
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7
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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8
Q

What form of nutrition is the early embryo dependent on?

A

histiotrophic

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9
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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10
Q

When is the embryo reliant on histiotrophic nutrition?

A

the first trimester

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11
Q

When does the embryo swap to haemotrophic support?

A

at the start of the second trimester

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12
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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13
Q

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

A

12 weeks gestation

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14
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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15
Q

What is the role of chorionic villi?

A

provide substantial surface area for exchange

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16
Q

How many stages are there in chorionic villi development?

A

3

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17
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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18
Q

What is the secondary stage of chorionic villi development?

A

growth of the fetal mesoderm into the primary villi

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19
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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20
Q

Describe the microstructure of the terminal chorionic villus?

A
  • convoluted knot of vessels
  • vessel dilation
  • slows blood flow to enhance exchange between fetal and maternal blood
  • whole structure covered in trophoblast
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21
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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22
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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23
Q

What is the function of spiral arteries?

A

provide the maternal blood supply to the endometrium

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24
Q

What are extra-villus trophoblasts?

A

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

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25
Q

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

A

they become endovascular EVT cells

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26
Q

What do endovascular EVT cells do?

A
  • breaks down the endothelium and smooth muscle
  • coats the vessels to form a new endothelial layer
27
Q

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

A

conversion

28
Q

What is the purpose of conversion?

A

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

29
Q

What do the spiral arteries supply?

A

the intervillus spaces/maternal blood spaces with blood

30
Q

How is pre-eclampsia diagnosed?

A
  • persistant hypertension
  • proteinuria
  • urine analysis
  • umbilical artery (Doppler Velocimetry)
31
Q

How can pre-eclampsia be excluded?

A

placenta growth factor test

32
Q

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

A
  • reduced fetal growth
  • preterm birth
  • pregnancy loss/stillbirth
33
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
34
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.
35
Q

What is Placental Growth Factor (PLGF)?

A

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

36
Q

What is Flt1 (soluble VEGFR1)?

A

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

37
Q

What is the Flt1and 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.
38
Q

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

A
  • PLGF levels
  • Flt-1/PLGF levels
39
Q

What is the benefit of PLGF?

A
  • triage test

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

40
Q

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

A
  • positive test (highly abnormal)
  • increased risk of preterm delivery
41
Q

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

A
  • positive test (abnormal)
  • increased risk of preterm delivery
42
Q

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

A
  • negative test (normal)
  • unlikely to progress to delivery within 14 days of test
43
Q

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

A

24-36weeks and 6days

44
Q

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

A

rules out pre-eclampsia

45
Q

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

A

increased risk of pre-eclampsia

46
Q

How can pre-eclampsia be resolved?

A

only by the delivery of the placenta

47
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
48
Q

What happens in failed spiral artery remodelling?

A
  • smooth muscle remains
  • immune cells become embedded in vessel walls
  • vessels occluded by RBCs
49
Q

What are the consequences of failed spiral artery remodelling?

A
  • vulnerable to intimal hyperplasia and atherosis
  • perturbed flow
  • local hypoxia
  • free radical damage
  • inefficient substrate movement into intervillous space
  • residual contractile capacity disturbing blood flow to intravillous space
50
Q

What is released by a healthy placenta?

A
  • PLGF and VEGF
  • bind to receptors on endothelial surface
  • promote vasodilation, anticoagulation and healthy maternal endothelial cells
51
Q

What is released by a PE placenta?

A
  • sFlt-1
  • mops up PGLF and VEGF, stopping them from binding to endothelial cells
  • endothelial cells become dysfunctional
52
Q

What are extracellular vesicles?

A
  • tiny lipid-bilayer laminated vesicles released by almost all cell types
  • contain mRNA, proteins and microRNA which can influence behaviour of cells locally and at a e
53
Q

What are the changes in extracellular vesicles seen in pre-eclampsia?

A
  • increased in maternal circulation
  • increase in endothelial-derived extracellular vesicles
  • decrease in placenta-derived endothelial vesicles
54
Q

What is the role of extracellular vesicles?

A
  • autocrine, endocrine and paracrine cell signalling
  • homeostasis
55
Q

What is the possible mechanism of EVs causing pre-eclampsia?

A
  • placental ischaemia induces apoptosis of trophopblasts and EV release
  • EVs enter maternal circulation
  • EVs cause endothelial cell dysfunction, inflammation and hypercoagulation
56
Q

What can cause later onset PE?

A
  • existing genetic predisposition to cardiovascular disease manifesting during pregnancy
  • little evidence of issues with spiral artey remodelling
  • normal placental perfusion
57
Q

What is SGA?

A
  • fetal weight <10th percentile
  • severe SGA is <3rd percentile
58
Q

What are the three classifications of SGA?

A
  • small throughout pregnancy but otherwise healthy
  • interuterine growth restriction (IUGR)/ fetal growth srestriction (FGR)
  • non-placental growth restriction
59
Q

What is IUGR/FGR?

A
  • normal early growth but slows later in pregnancy
  • clinical features of malnutrition and growth restriction, irrespective of weight percentile
60
Q

What are the two types of IUGR?

A

Symmetric and asymmetric

61
Q

What are the features of symmetric IUGR?

A
  • early gestational insult
  • genetic disorder or infection of fetus
  • everything reduced in proportion
  • reduced cell number, normal size
  • less features of malnutrition
  • poor prognosis
  • less common
62
Q

What are the features of asymmetric IUGR?

A
  • later gestational injury
  • utero-placental deficiency
  • head normal, rest of body is smaller
  • normal cell number, reduced size
  • more features of malnutrition
  • good prognosis
  • more common
63
Q

What are the implications of IUGR/FGR?

A
  • fetal cardiac hypertrophy
  • remodelling of fetal vessels due to chronic vasoconstriction
  • poor maturation of lungs leading to bronchopulmonary dysplasia
  • long term motor defects and cognitive impairments
64
Q

What happens during spiral artery remodelling?

A
  • EVT cell invasion triggers chemokine release from endothelial cells
  • leads to recruitment of immune cells
  • immune cells invade spiral artery walls which disrupts them
  • EVT cells replace broken down vessel walls with fibrinoid matrix

BRS YR2 (67 decks)

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