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BRS Flashcards (Y2) > Disorders Of Pregnancy And Parturition > Flashcards

Disorders Of Pregnancy And Parturition Flashcards

1
Q

Describe the changes in chorionic villi branching through pregnancy

A

Branching increases to increase area for exchange as foetal (oxygen) demands increase through pregnancy

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2
Q

Describe embryo-foetal growth during the first semester and its placental demands

A

Relatively limited growth
Low foetal demand on placenta

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3
Q

Describe embryo nutrition in the first trimester

A

Histiotrophic - reliant on uterine gland secretions and breakdown of endometrial tissues

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4
Q

Foetal nutrition switches to what at the start of the second trimester and how is this achieved?

A

Haemotrophic support
Achieved through a haemochorial-type placenta where maternal blood directly contacts the foetal membranes (chorionic villi)

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5
Q

Label this image

A
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6
Q

What is the initial function of cytotrophoblast cells?

A

Proliferation cells
Initially divide to form more syncytiotrophoblasts (invasive cells)

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7
Q

What are chorionic villi and what is their function?

A

Finger-like extensions of the chorionic cytotrophoblast, which then undergo branching
Provide substantial surface area for exchange

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8
Q

What are the three phases of chorionic villi development?

A

Primary - outgrowth of the cytotrophoblast and branching of these extensions
Secondary - growth of the foetal mesoderm into the primary villi
Tertiary - growth of the umbilical artery and umbilical vein into the villus mesoderm, providing vasculature

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9
Q

Label this image

A
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10
Q

Describe the terminal villus microstructure and how it’s adapted for its function

A

Convoluted knot of vessels
Vessel dilation
Slows blood flow enabling exchange between maternal and fetal blood
Whole structure coated with trophoblast

(Trophoblasts missing in image)

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11
Q

How does the villi structure change between early and late pregnancy?

A

Early: 150-200µm diameter, approx. 10µm trophoblast thickness between capillaries and maternal blood
Late: villi thin to 40µm, vessels move within villi to leave only 1-2µm trophoblast separation from maternal blood

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12
Q

What are the arteries that supply the maternal blood to the endometrium called?

A

Spiral arteries

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13
Q

Describe the processes of spinal artery re-modelling?

A
  • 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
  • EVT cell invasion triggers ECs to release chemokines - immune cell recruitment
  • Immune cells invade spiral artery walls and begin to disrupt vessel walls
  • EVT cells break down vessel ECM and replace with a new matrix (fibrinoid)
  • Conversion - turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow
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14
Q

What happens in failed conversion of spiral arteries?

A

Smooth muscle remains
Immune cells become embedded in vessel wall
Vessel is occluded by RBCs

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15
Q

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

A

Unconverted arteries are vulnerable to pathological change including intimal hyperplasia and atherosis (immune cell plaques)
Can lead to perturbed flow, local hypoxia, free radical damage and inefficient substrate delivery into intervillous space
Retained smooth muscle may allow residual contractile capacity - perturb blood delivery to intervillous space

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16
Q

Does atherosis only occur in spiral arteries?

A

No can, also occur in basal (non-spiral) arteries - not normally targeted by trophoblast

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17
Q

Describe the epidemiology of pre-eclampsia

A

2-4% of pregnancies in USA and Europe
More common in African and Asia (8-16%?)
Around 10% (Africa) and up to 25% (South America) of maternal deaths are associated with gestational hypertensive disorders (including PE)
Estimated to cause 50,000-60,000 maternal deaths per years

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18
Q

Is the precise underlying cause of pre-eclampsia known?

A

No

19
Q

How is PE diagnosed?

A
  • New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
  • Occurring after 20 weeks’ gestation
  • Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases
  • 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)
20
Q

What are the two subtypes of PE and what are the differences between them?

A

Early onset (<34 weeks)
- Foetal and maternal symptoms
- Changes in placental structure
- Reduced placental perfusion
Late onset (>34 weeks)
- Mostly maternal symptoms
- Foetus generally ok
- Less overt/no placental changes

21
Q

Which subtype of PE is more common?

A

Late onset - 80-90% of cases

22
Q

What maternal risks pre-dispose to PE?

A
  • Previous pregnancy with pre-eclampsia
  • BMI >30 (esp >35)
  • Family history
  • 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?
23
Q

What are the risk to the mother in PE?

A
  • Damage to kidneys, liver, brain and other organ systems
  • Possible progression to eclampsia (seizures, loss of consciousness)
  • HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets
  • Placental abruption (separation of the placenta from the endometrium)
24
Q

What are the risks to the foetus in PE?

A

Pre-term delivery
Reduced foetal growth (IUGR/FGR)
Foetal death (500,000/year worldwide)

25
Q

Compare spiral artery re-modelling in normal conditions vs PE

A

Normal:
- EVT invasion of maternal spiral arteries through decidua and into myometrium
- EVT become endothelial EVT
- Spiral arteries become high capacity
PE (esp. early onset):
- EVT invasion of maternal spiral arteries is limited to decidual layer (proliferative trophoblasts > invasive)
- Spiral arteries are not extensively remodelled
- Placental perfusion is restricted

26
Q

What does VEGF stand for?

A

Vascular endothelial growth factor

27
Q

What is Placental Growth Factor (PLGF)?

A

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

28
Q

What is sFLT1?

A

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

Also have has a surface bound form (on endothelial surface)

29
Q

What role do PLGF and VEGF play in a healthy placenta?

A

Healthy placenta releases PLGF and VEGF into the maternal circulation
Growth factors bind receptors on the endothelial surface to promote vasodilation, anti-coagulation and ‘healthy’ maternal endothelial cells

30
Q

What role does sFLT1 play in a pre-eclampsia placenta?

A

Placenta releases sFLT1, which acts as a sponge – mopping up PLGF and VEGF (pro-angiogenic factors in maternal circulation) and stopping them binding to the endothelial surface receptors
In the absence of these signals, the endothelial cells become dysfunctional

31
Q

Summarise the pathophysiology of PE

A
32
Q

What factor/ratio can be used to predict onset of PE?

A

PLGF levels alone (Triage test) or Flt-1/PLGF ratio
Up to 36 weeks as levels change naturally in late stage

33
Q

What are extracellular vesicles (EVs)?

A

EVs are tiny lipid-bilayer laminated 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)

34
Q

Outline the changes 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 cargos in PE placenta EVs may affect trophoblast invasion and maternal endothelial function

35
Q

What causes later onset PE?

A

Underlying mechanisms are poorly understood
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’ of pregnancy

36
Q

How is PE managed?

A

PE can only be resolved by delivery of the placenta:
- 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
Anti-hypertensive therapies
Magnesium sulphate to counter-act seizures
Corticosteroids for <34 weeks to promote fetal lung development before delivery

37
Q

What are the three main approaches to prevention of PE?

A

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

38
Q

What long-term health impacts may PE have 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)

39
Q

How is Small for Gestational Age (SGA) defined?

A

Fetal weight: <10th centile (or 2 SD below pop norm)
Severe SGA: 3rd centile or less

40
Q

SGA can be subclassified into which three groups?

A

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

41
Q

Outline the differences between SGA and IUGR/FGR?

A
  • SGA considers only the fetal/neonatal weight without any consideration of the in-utero growth and physical characteristics at birth
  • IUGR is a clinical definition of fetuses/neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of weight percentile
  • Baby may be IUGR without being SGA if they show features of malnutrition 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
42
Q

Compare the characteristics of symmetric vs asymmetric IUGR

A
43
Q

What are the implications of FGR/IUGR for the baby?

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

44
Q

Describe potential links between PE and FGR/IUGR?

A

BRS Flashcards (Y2) (79 decks)

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