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DEVELOPMENT AND AGEING > 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
What are the diagnostic features of PE?
reduced fetal movments / amniotic fluid volume
26
What are the associated symptoms of pre-eclampsia?
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)
27
What is the main risk of PE?
Can escalate to Eclampsia - severe neuronal seizures which can lead to maternal death
28
What are the two subtypes of Pre-Eclampsia?
Early onset <34 weeks Late onset > 34 Weeks
29
What are the features of early onset Pre-Eclampsia?
Associated with fetal and maternal symptoms Changes in placental structure Reduced placental perfusion
30
What are the features of late onset Pre-Eclampsia?
Mostly maternal symptoms Fetus generally OK Less overt/no placental changes
31
What are the risk factors of Pre-Eclampsia?
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
What are the risks to the mother with PE?
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
What is HELLP syndrome?
HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets
34
What is placental abruption?
Placental abruption (separation of the placenta from the endometrium)
35
What are the risks to the foetus with pre-eclampsia?
Pre-term delivery Reduced fetal growth (IUGR/FGR) Fetal death (500,000/year worldwide)
36
Describe the placental defects underpinning PE?
EVT invasion of maternal spiral arteries is limited to decidual layer. Spiral arteries are not extensively remodelled, Placental perfusion is restricted.
37
Why is there limited EVT invasion in PE?
In PE, cells failure to undergo switch to become invasive, therefore only a shallow conversion occurs
38
What is PLGF?
Placental Growth Factor - VEGF related, pro-angiogenic factor which is released in large amounts from the placenta
39
What is Flt1?
Soluble receptor for VEGF = VEGFR1 Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.
40
Describe the pathology associated with Flt1 and PLGF in PE?
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
Describe the pre-eclamsia placents?
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
What does the binding of PLGF to Flt1 cause?
promotion of the healthy endothelium = anti-coagulant and vasodilatory factors
43
What is stage 1 of PE called?
Abnormal placentation (1st and 2nd trimester)
44
What is stage 2 of PE called?
Maternal syndrome - 3rd trimster
45
What are the systemic dysfunctions which might arise from PE?
Proteinuria Hypertension Visual Disturbances / Headache / Seizures HELLP syndrome
46
What can be used to predict the onset of PE?
PLGF alone or sFlt-1/PLGF ratio
47
Describe what the results of PLGF alone show?
PlGF < 12 pg/ml = TEST POSITIVE = HIGHLY ABNORMAL PLGF >12 AND <100 = TEST POSITIVE = ABNORMAL PLGF > 100 = TEST NEGATIVE = NORMAL
48
What is the interpretation of a positive test for PLGF result in?
Increased risk for preterm delivery
49
What does a negative test for PLGF levels result in?
Unlikely to progress to delivery within 14 days
50
What level of sFlt-1/PLGF ratio allows you to rule out pre-eclampsia?
when it is less than 38
51
What level of sFlt-1/PLGF ratio results in an increased risk of pre-eclampsia?
When it is greater than 38
52
What are extracellular vesicles?
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
What are the changes observed in EV number and composition in PE?
Overall increase in EVs in the maternal circulation Increase in endothelial-derived EVs (indicative of maternal circulation defects) Decrease in placenta-derived Evs
54
What do pro-inflammatory cargos in PE placenta EV's affect?
trophoblast invasion and maternal endothelial function
55
What causes later onset PE?
maternal genetic pre-disposition to cardiovascular disease, which manifests during the ‘stress-test’ of pregnancy.
56
How is PE resolved?
Through the delivery of the placenta
57
What is the preferable management for PE when the mother is <34 into term?
preferable to try and maintain the pregnancy if possible for benefit of the fetus
58
What is the ideal management for PE when the mother is >37 into term?
Delivery
59
What are the conservative management strategies for PE?
Regular (daily?) monitoring Anti-hypertensive therapies. Magnesium sulphate to counter-act seizures  Corticosteroids for <34 weeks to promote fetal lung development before delivery.
60
What medications are the mothers given with PE?
Corticosteroids to promote fetal lung development
61
What are the three main approaches in the prevention of PE
1. Reduce BMI 2. Exercise throughout pregnancy 3. Lose dose aspirin for high risk groups
62
What are the long term health impacts of PE?
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
What is SGA?
Small for Gestational Age - when the fetal weight is <10th centile
64
What is the requirements for severe SGA?
when the fetal weight is less than the 3rd centile
65
What are the three subclassifications for SGA?
Small throughout pregnancy, but otherwise health Early growth normal but slows later in pregnancy (FGR/IUGR) Non-placental growth restriction (genetic, metabolic, infection)
66
What is the definition of IUGR?
IUGR is a clinical definition of fetuses/neonates with clinical features of malnutrition and in-utero growth restriction, irrespective of weight percentile.
67
If a baby shows features of malnutrition not growth restriction, what condition do they have?
IUGR, not SGA
68
What condition will a baby have if they have a birth weight less than the 10th centile, but no features of malnutrition?
SGA
69
What is symmetrical IUGR?
When the baby and all aspects of the baby are proportionatly smaller eg head is smaller and so is the body
70
What is the cause of symmetrical IUGR?
Starts early, consequence of genetic abnormalities or potential substance misuse
71
What is asymmetric IUGR?
Head sparing = when the rest of the body is smaller, except the head
72
What causes asymmetric IUGR?
Utero-placental insufficiency eg more of a nutritional defect
73
What happens to the cell number and size in asymmetric IUGR?
normal cell number, but reduced cell size
74
What happens to the cell number and size in symmetric IUGR?
Cell Number = reduced Cell Size = normal
75
What are the main implications of FGR/IUGR?
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

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