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Y2 DEV and Ageing > disorders of pregnancy and partuition > Flashcards

disorders of pregnancy and partuition Flashcards

1
Q

describe the structure of the placenta

A

maternal unit and foetal side.
maternal unit = maternal blood supply and spiral arteries.
foetal side = chorionic villus and invasion of foetal artery and vein into villi.

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2
Q

what happens to chorionic villi as pregnancy progresses?

A

Branching of chorionic villi increases with progression through pregnancy to increase area for exchange

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3
Q

at how many weeks does the dramatic increase for O2 for a foetus occur?

A

13 wks

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4
Q

what term is used to describe embryo nutrition in the first trimester?

A

histiotrophic

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5
Q

embryo nutrition when histiotrophic is dependent on what?

A

on uterine gland secretions and breakdown of endometrial tissues

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6
Q

what switch regarding embryonic nutrition occurs at the start of the second trimester?

A

histiotrophic to haemotrophic

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7
Q

how is the change from histiotrophic to haemotrophic nutrition achieved?

A

Achieved in humans through a haemochorial-type placenta where maternal blood directly contacts the fetal membranes (chorionic villi).

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8
Q

what are chorionic villi?

A

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

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9
Q

what are the three stages of chorionic villi development?

A

Primary: outgrowth 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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10
Q

the microstructure of a terminal villus is a convoluted knot of vessels and vessel dilation, what does this allow?

A

Slows blood flow enabling exchange between maternal and fetal blood

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11
Q

what is the function of the spiral arteries?

A

Spiral arteries provide the maternal blood supply to the endometrium

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12
Q

what conversion occurs during spiral artery remodelling?

A

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

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13
Q

outline the process of spiral artery remodelling

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

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14
Q

what happens during the failed conversion of spiral arterys?

A

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

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15
Q

in spiral artery remodelling, EVT cell invasion triggers endothelial cells to release chemokines, what is the effect of this?

A

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 knowm as fibrinoid

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16
Q

what are the consequences of failed spiral artery remodelling?

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.

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17
Q

what is pre-eclampsia?

A

Pre-eclampsia is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine.

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18
Q

outline the presentation of 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

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)

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19
Q

what are the two subtypes of pre-eclampsia?

A

early onset <34wks
late onset >34wks

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20
Q

which subtype of pre-eclampsia is more common?

A

late onset

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21
Q

what is the difference in the symptoms seen between early and late stage pre-eclampsia?

A

early associated with fetal and maternal symptoms, late associated with maternal symptoms

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22
Q

which subtype of pre-eclampsia involves reduced placental perfusion

A

early onset PE

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23
Q

What maternal risk factors 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?

24
Q

what are the maternal risks associated with pre-eclampsia?

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)

25
Q

what are the fetal risks associated with pre-eclampsia?

A

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

26
Q

EVT invasion involves which structures?

A

EVT invasion of maternal spiral arteries through decidua and into myometrium.

27
Q

in pre-eclampsia, especcialy early onset, what are the placental defects regarding spiral arteries?

A

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

Spiral arteries are not extensively remodelled,

Placental perfusion is restricted.

28
Q

what is PLGF?

A

placental growth factor

29
Q

PLGF is related to which other growth factor?

A

VEGF - vascular endothelial

30
Q

what type of growth factor is PLGF?

A

pro-angiogenic

31
Q

what is Flt1?

A

souble VEGFR1
Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.

32
Q

what changes in Flt-1 occur due to pre-eclampsia and what affect does this have?

A

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

33
Q

in the healthy placenta what is the effect of PLGF and VEGF?

A

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

34
Q

what is the difference in Flt1 and PLGF action between a healthy placenta and a pre-eclampsia placenta?

A

Pre-eclampsia placenta
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.

35
Q

how can PLGF alone be used to predict pre-eclampsia?

A

triage test ruling out PE in next 14 days in women 20-36wks and 6d

36
Q

what PLGF levels show an increased risk for preterm delivery?

A

<100pg/ml

37
Q

what happens to Flt-1/PLGF ratio in pre-eclampsia?

A

increased

38
Q

what FLt-1/PLGF ratio rules out pre-eclampsia?

A

<38 rules out pre-eclampsia

39
Q

what are extracellular vesicles (EVs)

A

are tiny (nano-meter scale) lipd-bilayer laminted vesicles released by almost all cell types

40
Q

what do EVs contain?

A

Contain diverse cargos, including mRNAs, proteins and microRNAs (miRNAs) and can influence cell behaviour (locally and at distance)

41
Q

what changes in EV number and composition are observed in pre-eclampsia?

A

Overall increase in EVs in the maternal circulation
Increase in endothelial-derived EVs (indicative of maternal circulation defects)
Decrease in placenta-derived Evs

42
Q

what effect can the pro-inflammatory cargoes in PE placenta EVs have?

A

may affect trophoblast invasion, maternal endothelial function

43
Q

how can pre-eclampsia be resolved?

A

can only be resolved by delivery of the placenta

44
Q

at how many weeks would you deliver the placenta if a mother is PE?

A

> 37wks, any more than 34wks is case by case basis

45
Q

other than delivery of the placenta, what else is done in the management of pre-eclampsia

A

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

46
Q

what are the three main approaches to prevent pre-eclampsia?

A

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 onset.

47
Q

what long-term health impacts can pre-eclampsia 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)

48
Q

at what weight does a fetus become small for gestational age (SGA)?

A

Fetal weight: <10th centile (or 2 SD below pop norm)

Severe SGA: 3rd centile or less

49
Q

what are the three subtypes of 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)

50
Q

what is the difference between SGA and interuterine growth restriction?

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.

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.

51
Q

what are the two types of interuterine growth restriction (IUGR)?

A

symmetrical and asymmetrical

52
Q

when does symmetrical IUGR occur?

A

earlier gestation, asymmetrical later

53
Q

what is more common symmetrical or asymmetrical IUGR?

A

asymmetrical

54
Q

what is the underlying aetiology of symmetrical IUGR?

A

genetic disorder of infection intrinsic to foetus

55
Q

what is the underlying aetiology of asymmetrical IUGR?

A

utero-placental insufficiency

56
Q

what are the implications of 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

Y2 DEV and Ageing (3 decks)

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