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DEVELOPMENT AND AGEING phase 1b > 1b Disorders of Pregnancy > Flashcards

1b Disorders of Pregnancy Flashcards

1
Q

What are the intervillous lacunae?

A

They are maternal blood spaces which re supplied by the maternal blood supply

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2
Q

Describe how the fetal demands on the placenta change through pregnancy?

A

They increase - The branching of the chorionic villi increases with progression through pregnancy to increase the surface area for exchange

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3
Q

What is the term given to describe early embryo nutrition?

A

Histiotrophic

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4
Q

What is histiotrophic nutrition?

A

Nutrition which is reliant on uterine gland secretions and breakdown of endometrial tissues

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5
Q

Describe the change which occurs in the type of nutrition at the start of the second trimester?

A

switches to haemotrophic support at the start of the second trimester

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6
Q

How is haemotrophic nutrition achieved?

A

Haemochorial type placenta where maternal blood is in direct contact with the fetal membranes = choronic villi

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7
Q

What are the chorionic Villi?

A

Finger-like extensions of the chorionic cytotrophoblasts, which then undergo branching

They provide substancial surface area or branching

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8
Q

What are the three stages of chorionic villi development?

A

Primary: Outgroths of the cytotrophoblast and branching of these extensions

Secondary: growth of the fetal 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

What cells are the chorionic villi formed from?

A

cytotrophoblast cells - they grown into the chorion, and then undergo vascularisation and branching

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10
Q

Describe the structure of the terminal villus microstructure?

A

Convoluted knot of vessels and vessel dilation - this slows blood flow enabling exchange between maternal and fetal blood

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11
Q

What is the whole terminal villus coated in?

A

Trophoblast cells

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12
Q

What happens to the terminal villus microstructure between early and late 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.

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13
Q

What do the spiral arteries do?

A

They provide the maternal blood supply to the endometrium

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14
Q

What is the name given to the cells which coat the villi?

A

Extra-villus trophoblasts

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15
Q

What happens to the EVT’s during spiral artery remodelling?

A

Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT.

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16
Q

What happens to the endothelium and smooth muscle of the spiral arteries when they are remodelling?

A

Endothelium and smooth muscle is broken down – EVT coats inside of vessels

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17
Q

What is the process of conversion?

A

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

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18
Q

What does EVT cell invasion trigger?

A

EVT cell invasion triggers endothelial cells to release chemokines, recruiting immune cells.

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19
Q

What happens when the EVT cells invade the spiral artery walls?

A

they break down the normal vessel and ECM, and replace it with a new matrix which is known as fibrinoid

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20
Q

What is meant by failed conversion?

A

Failed conversion: smooth muscle remains, immune cells become embedded in vessel wall and vessels occluded by RBCs, immune cells

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21
Q

When spiral arteries fail to remodel, what are the consequences of the retained smooth muscle?

A

Retained smooth musclemay allow residual contractile capacity -> perturb blood delivery to the intravillous space.

Restricts blood flow into the maternal blood spaces

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22
Q

What changes are unconverted spiral arteries vulnerable to?

A

Unconverted spiral arteries are vulnerable to pathological change including intimal hyperplasia and atherosis -> this can lead to pertubed flow and local hypoxia, free radical damage and the inefficient delivery of substances into the intervillous spaces

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23
Q

Aside from spiral arteries, where can atherosis also occur as a result of failed spiral artery remodelling?

A

Atherosis can also occur in basal (non-spiral) arteries that would not normally be targeted by trophoblast.

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24
Q

What is pre-eclampsia?

A

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

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25
Q

What are the diagnostic features of PE?

A

reduced fetal movments / amniotic fluid volume

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26
Q

What are the 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)

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27
Q

What is the main risk of PE?

A

Can escalate to Eclampsia - severe neuronal seizures which can lead to maternal death

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28
Q

What are the two subtypes of Pre-Eclampsia?

A

Early onset <34 weeks

Late onset > 34 Weeks

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29
Q

What are the features of early onset Pre-Eclampsia? (to do with the placenta)

A

Associated with fetal and maternal symptoms

Changes in placental structure

Reduced placental perfusion

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30
Q

What are the features of late onset Pre-Eclampsia?

A

Mostly maternal symptoms

Fetus generally OK

Less overt/no placental changes

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31
Q

What are the risk factors of Pre-Eclampsia?

A
  1. Previous pregnancy with pre-eclampsia
  2. BMI >30 (esp >35)
  3. Family history
  4. Increased maternal age (>40) and possibly low maternal age (<20?)
  5. Gestational hypertension or previous hypertension
  6. Pre-existing conditions: diabetes, PCOS, renal disease, subfertility,
  7. Autoimmune disease (anti-phospholipid antibodies)
  8. Non-natural cycle IVF?
32
Q

What are the risks to the mother with PE?

A
  1. damage to kidneys, liver, brain and other organ systems
  2. Possible progression to eclampsia (seizures, loss of consciousness)
  3. HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets
  4. Placental abruption (separation of the placenta from the endometrium)
33
Q

What is HELLP syndrome?

A

HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets

34
Q

What is placental abruption?

A

Placental abruption (separation of the placenta from the endometrium)

35
Q

What are the risks to the foetus with pre-eclampsia?

A

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

36
Q

Describe the placental defects underpinning PE?

A

EVT invasion of maternal spiral arteries is limited to decidual layer.

Spiral arteries are not extensively remodelled,

Placental perfusion is restricted.

placental ischaemia

37
Q

Why is there limited EVT invasion in PE?

A

In PE, cells failure to undergo switch to become invasive, therefore only a shallow conversion occurs

38
Q

What is PLGF?

A

Placental Growth Factor - VEGF related, pro-angiogenic factor which is released in large amounts from the placenta

39
Q

What is Flt1?

A

Soluble receptor for VEGF = VEGFR1

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

40
Q

Describe the pathology associated with Flt1 and PLGF in PE?

A

PE: excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.

41
Q

Describe the pre-eclamsia 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.

42
Q

What does the binding of PLGF to Flt1 cause?

A

promotion of the healthy endothelium = anti-coagulant and vasodilatory factors

43
Q

What is stage 1 of PE called?

A

Abnormal placentation (1st and 2nd trimester)

44
Q

What is stage 2 of PE called?

A

Maternal syndrome - 3rd trimster

45
Q

What are the systemic dysfunctions which might arise from PE?

A

Proteinuria

Hypertension

Visual Disturbances / Headache / Seizures

HELLP syndrome

46
Q

What can be used to predict the onset of PE?

A

PLGF alone or sFlt-1/PLGF ratio

47
Q

Describe what the results of PLGF alone show?

A

PlGF < 12 pg/ml = TEST POSITIVE = HIGHLY ABNORMAL

PLGF >12 AND <100 = TEST POSITIVE = ABNORMAL

PLGF > 100 = TEST NEGATIVE = NORMAL

48
Q

What is the interpretation of a positive test for PLGF result in?

A

Increased risk for preterm delivery

49
Q

What does a negative test for PLGF levels result in?

A

Unlikely to progress to delivery within 14 days

50
Q

What level of sFlt-1/PLGF ratio allows you to rule out pre-eclampsia?

A

when it is less than 38

51
Q

What level of sFlt-1/PLGF ratio results in an increased risk of pre-eclampsia?

A

When it is greater than 38

52
Q

What are extracellular vesicles?

A

Tiny lipid-bilayer laminated vesicles released by almost all cell types which contain diverse cargos, including mRNAs, proteins and microRNAs which influence cell behaviour

53
Q

What are 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

54
Q

Possible mechanism for EVs and 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

55
Q

What causes later onset PE?

A

maternal genetic pre-disposition to cardiovascular disease, which manifests during the ‘stress-test’ of pregnancy.

56
Q

How is PE resolved?

A

Through the delivery of the placenta

57
Q

What is the preferable management for PE when the mother is <34 into term?

A

preferable to try and maintain the pregnancy if possible for benefit of the fetus

58
Q

What is the ideal management for PE when the mother is >37 into term?

A

Delivery

59
Q

What are the conservative management strategies for PE?

A

Regular (daily?) monitoring
Anti-hypertensive therapies.
Magnesium sulphate to counter-act seizures
Corticosteroids for <34 weeks to promote fetal lung development before delivery.

60
Q

What medications are the mothers given with PE?

A

Corticosteroids to promote fetal lung development

61
Q

What are the three main approaches in the prevention of PE

A
  1. Reduce BMI
  2. Exercise throughout pregnancy
  3. Lose dose aspirin for high risk groups
62
Q

What are the long term health impacts of PE?

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)

63
Q

What is SGA?

A

Small for Gestational Age - when the fetal weight is <10th centile

64
Q

What is the requirements for severe SGA?

A

when the fetal weight is less than the 3rd centile

65
Q

What are the three subclassifications for SGA?

A

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

66
Q

What is the definition of IUGR?

A

IUGR is a clinical definition of fetuses/neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of weight percentile.

67
Q

If a baby shows features of malnutrition not growth restriction, what condition do they have?

A

IUGR, not SGA

68
Q

What condition will a baby have if they have a birth weight less than the 10th centile, but no features of malnutrition?

A

SGA

69
Q

What is symmetrical IUGR?

A

When the baby and all aspects of the baby are proportionatly smaller eg head is smaller and so is the body

70
Q

What is the cause of symmetrical IUGR?

A

Starts early, consequence of genetic abnormalities or potential substance misuse

71
Q

What is asymmetric IUGR?

A

Head sparing = when the rest of the body is smaller, except the head

72
Q

What causes asymmetric IUGR?

A

Utero-placental insufficiency eg more of a nutritional defect

73
Q

What happens to the cell number and size in asymmetric IUGR?

A

normal cell number, but reduced cell size

74
Q

What happens to the cell number and size in symmetric IUGR?

A

Cell Number = reduced
Cell Size = normal

75
Q

What are the main 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

DEVELOPMENT AND AGEING phase 1b (4 decks)

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