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Development and ageing domain > Disorders of pregnancy & parturition > Flashcards

Disorders of pregnancy & parturition Flashcards

1
Q

Describe the general structure of the placenta

A

Most of the placental tissue is made up of blood vessels: they connect with the baby through the umbilical cord and branch throughout the placenta disc
- The fetal vein and artery connect from the umbilical cord and feed blood into the chorionic villi (finger-like projections of placental tissue)
- The chorionic villi are bathed in the lacunae (intervillous space: enlarged spaces filled with maternal blood)
- The lacunae are supplied by maternal arteries (decidual spiral arteries) and veins

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2
Q

What are the demands on the placenta and foetus and how does this change throughout pregnancy?

A
  • Placenta demands increase: placenta has high energy turnover
  • Foetus demands increase: switch to haemotrophic support
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3
Q

How does the body accommodate for the change in placental demands?

A
  • Progressive branching of the chorionic villi, surface area increases for exchange as the demand on placenta/ mother for oxygen/ nutrients
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4
Q

How does fetal growth change throughout the pregnancy?

A
  1. Embryo-fetal growth during the first trimester is relatively limited:
    - Low fetal demand on the placenta
    - Early embryro nutrition is histiotrophic
    - reliant on uterine gland secretions and breakdown of endometrial tissues
  2. The fetal growth then accelerates:
    - Switch to haemotrophic support at start of 2nd trimester.
    - Fetal demands on placenta increase with pregnancy
    - Achieved in humans through a haemochorial-type placenta where maternal blood directly contacts the fetal membranes (chorionic villi).
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5
Q

Describe the structure of/ around the placenta during the early implantation stage

A
  • Placenta: amniotic cavity, bilaminar embryonic disc
  • Surrounded by cytotrophoblast cells (proliferative cells)
  • The cytotrophoblast cells are further surrounded by the syncytiotrophoblast cells (responsible for outward growth- invade endothelial tissue)
  • Surrounding the ball of cells: maternal capillary and uterine glands (these both get broken down by the syncytiotrophoblast cells)
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6
Q

What are the chorionic villi?

A

Finger-like extensions of the chorionic cytotrophoblast, which then undergo branching (we get growth of the cytotrophobast cells coming off of/ out of chorion)
They provide substantial surface area for exchange

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7
Q

Describe the process by which we have chorionic villi development

A
  1. Primary: outgrowth of the cytotrophoblast and branching of these extensions
  2. Secondary: growth of the fetal mesoderm into the primary villi
  3. Tertiary: growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature.
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8
Q

Describe the structure of the terminal villus microstructure

A
  1. Convoluted knot of vessels and vessel dilation
  2. Slows blood flow enabling exchange between maternal and fetal blood
  3. Whole structure coated with trophoblast
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9
Q

How do the terminal villi change in structure throughout the pregnancy?

A
  • Early pregnancy: 150-200µm diameter, approx. 10µm trophoblast thickness between capillaries and maternal blood.
  • Late pregnancy: villi thin to 40µm, vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood.
  • As the pregnancy progresses, the villi get thinner to lessen the space b/t the foetal blood and maternal blood to increase exchange
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10
Q

What type of arteries supply the foetus with maternal blood?

A

Spiral artery: provide the maternal blood supply to the endometrium

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11
Q

Describe the process of spiral artery re-modelling

A
  1. Extra-villus trophoblast (EVT) cells coating the anchoring villi invade down into the maternal spiral arteries, forming endovascular EVTs
  2. They activate the endothelial cells of the spiral artery and trigger a release of chemoattractants
  3. These recruit surrounding immune cells to also invade the spiral arteries and begin to disrupt vessel walls
  4. EVT cells breakdown normal vessel wall ECM and replace it/ start to deposit new fibrinoid ECM
  5. SMCs also broken down (reduced resistance)
  6. Immune cells leave- the entire vessel is now lined with EVT and fibrinoid ECM

Overall, there is increased diameter of the arteries and so increased blood volume to the foetus

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12
Q

What is meant by “failed conversion” during spiral artery re-modelling?

A

Partial breakdown of ECM & immune cells remain around the arteries

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13
Q

What occurs during failed conversion

A
  1. There is only partial breakdown of the ECM, and the immune cells remain inside the artery
  2. The artery stays spiral: SMC intact (resistance is not decreased), leads to occlusion/ blockage of the vessels
  3. Immune cells become embedded into the vessel walls; RBCs get convoluted
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14
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.
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15
Q

What is pre-eclampsia?

A

“New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
Occurring after 20 weeks’ gestation”

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16
Q

What is a clinical sign of pre-eclampsia?

A

Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases

17
Q

What are some associated symptoms of pre-eclampsia?

A
  • Oedema common but not discriminatory for PE
  • Headache (in around 40% of severe PE patients)
  • Abdominal pain (in around 15% of severe PE patients)
  • Visual disturbances, seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)
18
Q

What is eclampsia?

A

Rare secondary complications of PE (occurs after PE)- severe form of PE

19
Q

What are the 2 subtypes of PE?

A
  1. Early onset: <34 weeks
    Less common
    Associated with fetal and maternal symptoms
    Changes in placental structure
    Reduced placental perfusion (placenta does not work as well as it should)
  2. Late onset: >34 weeks
    More common (80-90% cases)
    Mostly maternal symptoms
    Fetus generally OK
    Less overt/no placental changes (generally working ok)
20
Q

What maternal risk factors pre-dispose to PE?

A
  • Previous pregnancy with pre-eclampsia
  • BMI >30 (esp >35)
  • Family history (some proteins hace genetic markers that can cuase risk)
  • Increased maternal age (>40) and possibly low maternal age (<20?)
  • Gestational hypertension or previous hypertension
  • Pre-existing conditions: diabetes, PCOS, renal disease, subfertility,
  • Autoimmune disease (anti-phospholipid antibodies)
  • Non-natural cycle IVF? (women who have hormonal support)
21
Q

What risks does PE pose to the foetus and the mother?

A

Risks to Mother:
- High bp= damage to kidneys, liver, brain and other organ systems
- Possible progression to eclampsia if left untreated (seizures, loss of consciousness)
- HELLP syndrome: Hemolysis, Elevated Liver Enzymes, - Low Platelets
- Placental abruption (separation of the placenta from the endometrium) foetal detachment= hemorrhage (more abrupt onset can cause placenta dysfunction)

Risks to foetus:
- Pre-term delivery
- Reduced fetal growth (IUGR: inter uterine growth restricition/FGR: foetal growth restriction)
- Fetal death (500,000/year worldwide)

22
Q

Describe the defects seen in PE in relation to the maternal blood supply to the foetus

A

Normally:
- chroionic villi (finger-like projections) enter the site of implantation
- The EVT cells invade the maternal spiral arteries through decidua and go down into the myometrium.
- EVT become endothelial EVT
- Spiral arteries become high capacity

PE:
- EVT cells fail to switch from their proliferative behaviour to invasive
- EVT invasion of maternal spiral arteries is limited to decidual layer (the cells do not get all the way down into myometrium “shallow conversion”
- Spiral arteries are not extensively remodelled (only the shallow beds/ tops are remodelled) vessel remains spiral, SMCs intact; resistance maintained
- Placental perfusion is restricted= placenta distress

23
Q

True or false in PE the spiral arteires fail to remodel and this leads to high blood pressure?

A

FASLE: failure to remodel the spiral arteries is not thought to be what actually causes high bp in PE (but not confirmed)

24
Q

Describe the pathogenesis of PE that leads to high maternal blood pressure

A

Normally:
1. Vascular endothelial growth factors (VEGF) and pro-angiogenic, VEGF- like factors, known as PLGF (placental growth factors) are released in large amounts into maternal circulation by the placenta
2. Also in the maternal circulation, are Flt1 (soluble VEGFR1) soluble receptors for VEGF-like factors which binds soluble angiogenic factors (they are floating/ unbound receptors that bind to PLGFs
3. These growth factors bind receptors on the endothelial surface to release anticoagulant and vasodilatory factors (control bp)

PE:
Placenta distress caused by the restricted perfusion in PE is thought to cause an imbalance between the factors and receptors:
1. Reduction in PLGF and increase in sFlt1 receptors (these receptors act as more of a “sponge” and “mop up” the PLGF to stop them from binding to the endothelial surfaces
2. increased mopping up of (already low levels) of PLGF
3. Reduction of available pro-angiogenic factors in maternal circulation, results in endothelial dysfuction (there is now a release of procoagulant and vasoconstricting factors that trigger HIGH maternal BP)

25
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: maternal genetic pre-disposition to cardiovascular disease, which manifests during the ‘stress-test’ (development of placenta) of pregnancy.
26
Q

What tests can be done to predict the onset of PE?

A
  1. PLGR levels alone: (in PE, PLGR levels are reduced):
    - e.g. Triage test
    - Rules out PE in next 14 days in women 20-36wks and 6d
  2. sFlt-1/PlGF ratio (in PE, PLGR levels are reduced, sFlt-1 are increased; ratio increases with increased risk of PE)
27
Q

What are extracellular vesicles? what is there role?

A
  • EVs are tiny (nano-meter scale) lipd-bilayer laminted vesicles released by almost all cell types
  • Contain diverse cargos, including mRNAs (inhibit protein translation to maintain balance), proteins and microRNAs (miRNAs) and can influence cell behaviour (locally: to neighboring cells and at distance: released in circulation to other organs)
28
Q

What changes are observed in EV number and composition 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
  • Pro-inflammatory cargoes in PE placenta EVs may affect trophoblast invasion (inhibit EVT invasion), maternal endothelial function
29
Q

Describe the management for PE

A

PE can only be resolved by delivery of the placenta (getting the foetus + placenta out)= v. preterm delivery
- If <34 weeks, preferable to try and maintain the pregnancy if possible for benefit of the fetus
-If >37 weeks, delivery preferable
-In between – case by case basis.

  • Regular (daily?) monitoring (bp checks, PLGF checks, ratio test)
  • Anti-hypertensive therapies.
  • Magnesium sulphate to counter-act seizures
    -Corticosteroids for <34 weeks to promote fetal lung development before delivery.
30
Q

What are some steps that can be taken to help prevent PE?

A

Three main approaches:
- Reduce BMI (esp if BMI >35)
- Exercise throughout pregnancy (seems to work independent of BMI)
- Low-dose asprin (from 11-14 weeks) for high risk groups – but may only prevent early onse

31
Q

Wha are the long-term health impacts of PE on the mother

A
  • Elevated risk of cardiovascular disease, type 2 diabetes and renal disease after PE
  • Roughly 1/8 risk of having pre-eclampsia in next pregnancy (greater if early onset)
32
Q

What is meant by “small for gestational age”

A

“Fetal weight: <10th centile (or 2 SD below pop norm)”
- Severe SGA: 3rd centile or less
- Can be subclassified into 3 groups
- often mistaken for FGR (foetal growth resistance)

33
Q

What is a limitation to using PLGF and Fltr levels to predict PE?

A

Only works for pateints b/t 20-36 weeks (normally there is a dramatic decline in the levels of PLGF: reduces dramatically in the last few weeks of pregnancy)

34
Q

What are the 3 groups used to subclassify SGA?

A

SGA= “small for gestational age”
Can be subclassified into 3 groups:
1. Small throughout pregnancy, but otherwise health
2. Early growth normal but slows later in pregnancy (FGR/IUGR)
3. Non-placental growth restriction (genetic, metabolic, infection)

35
Q

What is the difference between SGA vs IUGR/FGR?

A
  1. SGA considers only the fetal/neonatal weight without any consideration of the in-utero growth and physical characteristics at birth.
  2. IUGR is a clinical definition of fetuses/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.
36
Q

What is the difference between symmetrical and asymmetrical IUGR?

A

Symmetrical: whole baby is smaller but everything is reduced in proportion
- more common
- occurs earlier in gestation
- cell number reduced
- cell size normal
- features of malnutrition less pronounced
- poor prognosis (disease progression)

Asymterical: Abdominal circumference- decreased, biparietal diameter, head circumference and femur-length normal
- less common
- later gestation
- cell numer is normal
- cell size reduced
- features of malnutrition more pronounced
- Good prognosis

37
Q

What are the implications of FGR/IUGR?

A
  • Cardiovascular: fetal cardiac hypertrophy, and re-modelling of fetal vessels due to chronic vasoconstriction
  • Respiratory: poor maturation of lungs during fetal life, leading to bronchopulmonary dysplasia and respiratory compromise
  • Neurological: long term motor defects and cognitive impairments
38
Q

What are common causes of FGR/IUGR?

A
  1. Genetic causes
  2. Abnormal maternal immunoloigcal adaptation
  3. Trophoblast invasion defect
  4. Defective decidualization
  5. Abnormal maternal systemic vascular adaptation to pregnancy
  6. Villous placental vulnerability, stress of ageing

Development and ageing domain (2 decks)

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