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dev/age > 1B disorders of pregnancy + parturition > Flashcards

1B disorders of pregnancy + parturition Flashcards

1
Q

How much does the embryo grow in the first trimester?

A

Its growth is relatively limited in the first trimester, and there is low foetal demand on the placenta

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2
Q

Why is there low foetal demand on the placenta in the first trimester?

A

Early embryo nutrition is histiotrophic

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3
Q

What does histiotrophic nutrition mean?

A

It’s reliant on uterine gland secretions (uterine milk) and the breakdown of endometrial tissues and maternal capillaries (to derive nutrients from maternal blood)

The syncitiotrophoblasts that invade the maternal endometrium do this breakdown to fuel the embryo development

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4
Q

As we go from first to second trimester, how does the growth rate of the embryo change?

A

There is significant increase in rate of foetal growth

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5
Q

What kind of nutritional support does the embryo change to (since histiotrophic can’t support it anymore)?

A

Haemotrophic support at the start of the 2nd trimester (around 12th week of gestation)

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6
Q

What is haemotrophic support?

A

Foetus starts to derive nutrients from maternal blood

Achieved because human placenta is a haemochorial-type placenta where maternal blood is in direct contact with the foetal chorion (membrane)

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7
Q

Describe what happens in the early implantation stage using the image below

A
  • Syncitiotrophoblasts (grey) are invading surrounding endometrium to break down cells to provide nutrients to support embryo
  • Uterine gland secretions
  • Maternal capillary breakdown to bathe embryo in maternal blood which gives nutrients too
  • Amnion- derivative of epiblast which is the first of the foetal membranes and forms amniotic cavity
  • Amniotic cavity expands to become amniotic sac which surrounds and cushions foetus in 2nd and 3rd trimesters
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8
Q

Describe what happens in this next stage of development after a few days

A
  • Invasion of syncitiotrophoblasts is more extensive
  • Amnion’s amniotic cells are secreting secretions into space in the middle which will start to expand
  • Yolk sac formed from hypoblast
  • Chorion is another key foetal membrane- outer membrane surrounding whole conceptus unit
  • Connecting stalk forms
  • Trophoblastic lacunae form
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9
Q

What does the connecting stalk do?

A

Links developing embryo unit to chorion

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10
Q

What are 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

Describe the placental structure

A
  • The maternal unit is on the bottom side with the maternal blood supply made up of spiral arteries
    • The spiral arteries supply the intervillous spaces, some of which drains from the maternal vein system
  • On foetal side, we get chorionic villi formation which invade the trophoblasts, become branched and vascularised
    • Foetal circulatory system invade into chorionic villi which provides large SA between maternal blood and foetal chorionic villi
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12
Q

What is the chorionic villi important for?

A
  • Provides substantial SA for exchange of gases and nutrients
  • They’re finger-like projections of the chorionic cytotrophoblast that then undergo branching
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13
Q

What are the 3 phases of chorionic villi development?

A
  • Primary
  • Secondary
  • Tertiary
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14
Q

What happens in the primary stage of chorionic villi development?

A

Outgrowth of the cytotrophoblast and branching of these extensions

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15
Q

What happens in the secondary stage of chorionic villi development?

A

Growth of the foetal mesoderm into the primary villi

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16
Q

What happens in the tertiary stage of chorionic villi development?

A

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

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17
Q

Describe the blood network around each villus

A
  • There is a convoluted knot of vessels that are dilated around each villus
  • This slows down the blood flow to enable exchange between maternal and foetal blood
  • They’re surrounded by maternal blood in the lacunae
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18
Q

How does the villus change from early to late pregnancy?

A
  • Early pregnancy- it’s 150-200μm in diameter with 10μm trophoblast thickness between capillaries and maternal blood
  • Late pregnancy- villi thin to 40μm and vessels within villi move to leave only 1-2μm trophoblast separation from maternal blood to allow diffusion distance to decrease between maternal and foetal circulation
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19
Q

What is spiral artery remodelling?

A
  • Spiral arteries provide the maternal blood supply to the endometrium
  • Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT
  • Endothelium and smooth muscle is broken down- EVT coats inside of vessels

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

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20
Q

How does spiral artery re-modelling occur?

A
  • EVT cell invasion triggers endothelial cells to release chemokines, recruiting immune cells.
  • Immune cells invade spiral artery walls and begin to disrupt vessel walls.
  • EVT cells secrete break down normal vessel wall extracellular matrix and replace with a new matrix known as fibrinoid
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21
Q

What is failed conversion?

A

Smooth muscle remains, immune cells become embedded in vessel wall and vessels occluded by RBCs

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22
Q

What are the consequences of failed spiral artery re-modelling?

A
  • Unconverted spiral arteries are vulnerable to pathological change including intimal hyperplasia and atherosis
  • This can lead to perturbed flow and local hypoxia, free radical damage and inefficient delivery of substrates into the intervillous space.
  • Retained smooth musclemay allow residual contractile capacity -> perturb blood delivery to the intravillous space.
  • Atherosis can also occur in basal (non-spiral) arteries that would not normally be targeted by trophoblast.
23
Q

How do we diagnose preeclampsia?

A
  • New onset hypertension (in previously normotensive woman)
    • BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
    • Occurring after 20 weeks’ gestation
  • Oedema common but not discriminatory for PE
  • Headache (in 40% of severe PE)
  • Abdominal pain (in around 15% of severe PE patients)
24
Q

What happens in more severe cases of PE?

A
  • Visual disturbances
  • Breathlessness
  • Risk of eclampsia (seizures)
25
Q

What happens to foetal movement and amniotic fluid in PE?

A

Reduction of one or both (by ultrasound) in 30% cases

26
Q

What are the 2 subtypes of PE?

A
  • Early onset (<34 weeks)
  • Late onset (>34 weeks)
27
Q

What is early onset PE associated with?

A
  • Foetal and maternal symptoms
  • Changes in placental structure
  • Reduced placental perfusion
28
Q

What is late onset PE associated with?

A
  • Most maternal symptoms
  • Foetus generally OK
  • More common- 90%
  • Less overt/no placental changes
29
Q

What are the risks of PE to the mother?

A
  • Damage to kidneys, liver, brain and other organ systems
  • Possible progression to eclampsia (seizures, loss of consciousness)
  • HELLP syndrome:
    • Haemolysis
    • Elevated Liver Enzymes
    • Low Platelets
  • Placental abruption (separation of the placenta from the endometrium)
30
Q

What risk does PE pose to the foetus?

A
  • Reduced foetal growth
  • Preterm birth
  • Pregnancy loss/stillbirth
31
Q

What happens normally in placental development in terms of maternal spiral arteries?

A
  • EVT cell invasion of maternal spiral arteries leads to endothelial and smooth muscle breakdown
  • EVT becomes endothelial and spiral arteries become high capacity
32
Q

What placental defects underpin PE?

A
  • EVT invasion of maternal spiral arteries is limited to decidual layer
  • Spiral arteries aren’t extensively remodelled, thus placental perfusion is restricted
33
Q

What is PlGF?

A
  • Placental growth factor
  • VEGF related
  • Pro-angiogenic factor release in large amounts by placenta
34
Q

What is Flt1?

A
  • Soluble VEGFR1
  • Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailability
35
Q

What happens to Flt1 in PE?

A

Excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors like PlGF and VEGF in maternal circulation, resulting in endothelial dysfunction

36
Q

What happens to PLGF and VEGF in a healthy placenta?

A

Releases PLGF and VEGF into the maternal circulation. These growth factors bind receptors on the endothelial surface to promote vasodilation, anti-coagulation and ‘healthy’ maternal endothelial cells.

37
Q

What happens to the GFs in PE placenta?

A

Releases sFLT1, which acts as a sponge – mopping up PLGF and VEGF and stopping them binding to the endothelial surface receptors. In the absence of these signals, the endothelial cells become dysfunctional.

38
Q

Aside from GFs in PE, what else is prevalent?

A

Extracellular vesicles (EVs)

39
Q

What are EVs?

A
  • EVs are tiny (nano-meter scale) lipd-bilayer laminted vesicles released by almost all cell types
  • Contain diverse cargos, including mRNAs, proteins and microRNAs (miRNAs) and can influence cell behaviour (locally and at distance)
40
Q

What changes in EV are observed in PE?

A
  • Overall increase in EVs in the maternal circulation
  • Increase in endothelial-derived EVs (indicative of maternal circulation defects)
  • Decrease in placenta-derived EVs
41
Q

What is a possible mechanism of how EVs can cause PE?

A
  • Placental ischaemia induces trophoblast cell apoptosis and EV release
  • These enter the maternal circulation
  • Act on endothelial cells to induce dysfunction, inflammation and hypercoagulation
  • Collectively these may contribute to pre-eclampsia
42
Q

What does these graphs show?

A
  • EVs from severely pre-eclamptic patients inhibit vasorelaxation of mouse aorta explants vs normotensive EVs
  • inhibit production of eNOS by human endothelial cells
43
Q

What causes later onset PE?

A
  • Although >80% PE cases are late onset, the underlying mechanisms are poorly understood
  • In late onset PE there is little no evidence of reduced spiral artery conversion
  • Placental perfusion is normal (possibly increased?)
  • Current theory: existing maternal genetic pre-disposition to cardiovascular disease, which manifests during the ‘stress-test’ of pregnancy.
44
Q

What 2 ways can we detect PE with?

A
  • PlGF levels alone
  • Flt1/PIGR ratio
45
Q

What test is the PlGF alone?

A
  • e.g. Triage test
  • Rules out PE in next 14 days in women 20-36 weeks and 6 days
46
Q

What does a Flt1/PlGF ratio table look like?

A
47
Q

What is SGA?

A

Small for Gestational Age

48
Q

What classifies as SGA?

A
  • Foetal weight: <10th centile (or 2SD below pop norm)
  • Severe SGA: 3rd centile or less
49
Q

What three classes can SGA be subclassified into?

A
  • Small throughout pregnancy, but otherwise healthy
  • Early growth normal but slows later in pregnancy (FGR/IUGR)
  • Non-placental growth restriction (genetic, metabolic, infection)
50
Q

What is IUGR/FGR?

A

Interuterine Growth Restriction (Foetal Growth Restriction)

51
Q

What is the distinction between SGA and IUGR/FGR?

A
  • SGA considers only the foetal/neonatal weight without any consideration of the in-utero growth and physical characteristics at birth.
  • IUGR is a clinical definition of foetuses/neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of weight percentile.
  • Thus a baby may be IUGR without being SGA if the show features of malnutrion but and growth restriction at birth
  • Similarly, a baby with a birth weight less than the 10th percentile will be SGA , not IUGR if there are no features of malnutrition.
52
Q

What are the characteristics of symmetric vs asymmetric IUGR?

A
53
Q

What are the implications of FGR/IUGR?

A
  • Cardiovascular: foetal cardiac hypertrophy, and re-modelling of foetal vessels due to chronic vasoconstriction
  • Respiratory: poor maturation of lungs during foetal life, leading to bronchopulmonary dysplasia and respiratory compromise
  • Neurological: long term motor defects and cognitive impairments
54
Q

What are the common causes integrating PE and FGR/IUGR?

A

dev/age (4 decks)

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