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BRS Y2 > disorders of pregnancy and parturition > Flashcards

disorders of pregnancy and parturition Flashcards

1
Q

early embryro nutrition vs 2nd trimester nutrition (fetal demands on placenta increases with pregnancy)

A

histiotrophic- relies on uterine gland secretion and breakdown of endometrial tissue

2: haemotrophic

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2
Q

how does haemotrophic support work

A

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

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2
Q

how does histiotrophic nutrition work

A

relies on uterine gland secretion and breakdown of endometrial tissue

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3
Q

why is there increased branching of chorionic villi with progression through pregnancy

A

increase area for exchange (higher O2 demand)

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4
Q

3 phases of chorionic villi developmenet

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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5
Q

what is the microstructure of terminal villus

A

Convoluted knot of vessels and vessel dilation
->Slows blood flow enabling exchange between maternal and fetal blood

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6
Q

what is the terminal villus microstructure covered in

A

trophoblast

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7
Q

changes in microstructure of terminal villus from early to late pregnancy in terms of

A

Early pregnancy:
150-200µm diameter,
approx. 10µm trophoblast thickness between capillaries and maternal blood.

Late pregnancy:
villi thinner in diameter- 40µm,
1-2µm trophoblast thin(ner) separation from maternal blood.

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8
Q

spiral artery re-modelling steps and what does it convert spiral arteries into? -brief

A
  1. Extra-villus trophoblast (EVT) cells coating the villi invade down into the maternal spiral arteries, forming endovascular EVT.
  2. Endothelium and smooth muscle is broken down – EVT coats inside of vessels

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

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9
Q

purpose of spiral arteries

A

provide maternal blood supply to endometrium

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10
Q

how does spiral artery remodelling occur? depth

A

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

2.Immune cells invade spiral artery walls + disrupt vessel walls.

3.EVT cells secrete: break down normal vessel wall ECM + replace with a new matrix (fibrinoid)

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

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11
Q

consequence of failed spiral artery re-remodelling

A

1.Unconverted spiral arteries are vulnerable to pathological change ie. atherosis-thickening of the arterial wall due to the accumulation of lipids and inflammatory cells

  1. disrupted flow and local hypoxia, free radical damage and inefficient delivery of substrates into the intervillous space.
  2. Retained smooth musclemay allow residual contractile capacity -> turbulent blood delivery to the intravillous space.

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

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12
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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13
Q

signs and symptoms of pre-eclampsia

A

Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases
OHAVS=
-Oedema common but not discriminatory for PE
-Headache
-Abdominal pain
-Visual disturbances, -Seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)

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14
Q

early onset pre-eclampsia

A

<34 weeks
-fetal and maternal symptoms
-Changes in placental structure
-Reduced placental perfusion

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15
Q

late onset pre-eclampsia

A

> 34 weeks
-More common
-Mostly maternal symptoms
-Fetus generally OK
-no placental changes

16
Q

PE- risk to mother

A

-damage to kidneys, liver, brain
-Poss progress to eclampsia (seizures, loss of consciousness)
-HELLP syndrome: Hemolysis, Elevated Liver Enzymes, Low Platelets
-Placental abruption (separation of the placenta from the endometrium)

17
Q

what is placental abruption

A

(separation of the placenta from the endometrium)

18
Q

PE- risk to fetus

A

-Pre-term delivery
-Reduced fetal growth (IUGR/FGR)
-Fetal death

19
Q

Placental defects underpinning PE- in regards to EVT, spiral artery remodelling etc

A

1.PE (esp early onset):

2.EVT invasion of maternal spiral arteries is limited to decidual/endometrial layer. (cannot reach myometrium)

3.Spiral arteries not extensively remodelled,

4.Placental perfusion restricted.
5.Placental ischaemia

20
Q

what is PLGF

A

Placental Growth Factor:
VEGF related, pro-angiogenic factor released in large amounts by the placenta.

21
Q

what is Flt1

A

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

22
Q

what is PE in terms of Flt-1

A

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

23
Q

healthy placenta vs pre-eclampsia placenta in terms of PLGF/VEGF/

A

Healthy placenta releases PLGF and VEGF, which bind to endothelial receptors, promoting vasodilation, anti-coagulation, and maintaining maternal endothelial health.

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.

In preeclampsia, the placenta releases sFLT1, which blocks PLGF and VEGF from binding to endothelial receptors, leading to endothelial dysfunction. (procoagulant and vasoconstricting)

24
Q

Extracellular vesicles- what are they, where are they released, what do they contain?

A

EVs are tiny (nano-meter scale) lipd-bilayer laminted vesicles.

released by almost all cell types

Contain mRNAs, proteins and microRNAs (miRNAs) etc. + influence cell behaviour (locally and at distance)

25
Q

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

26
Q

Extracellular vesicles (EVs) and PE- possible mechanism

A

-Placental ischaemia induces trophoblast cell apoptosis and EV release
-These enter the maternal circulation
-Act on endothelial cells-> induce dysfunction, inflammation and hypercoagulation
-Collectively contribute to pre-eclampsia

27
Q

what does EV in severe PE do in terms of relaxation and eNOS production

A

inhibit vasorelaxation of aorta

inhibit production of eNOS in endothelial cells

28
Q

PLGR levels can be used to test for Pre-Eclampsia
how to interpret results—

A

PLGF <12pg/ml= test positive. Highly abnormal. increased risk for preterm delivery

PLGF 12-100= test positive. Abnormal. increased risk for preterm delivery

PLGF 100+= test negative. Normal. unlikely to progress to delivery within 14 days of test

29
Q

sFlt-1/PlGR ratio can be used to test for Pre-Eclampsia
how to interpret results

A

24-36 weeks +6 days:
sFlt-1/PLGR ratio <38
=rule out pre-eclampsia

> 38= increased risk of pre-eclampsia

30
Q

what is small for gestational age

A

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

Severe SGA: 3rd centile or less

31
Q

3 sub classification 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)

32
Q

symmetric vs asymmetric IUGR characteristics

A

symmetric
-early onset
-25% incident
-proportionally reduced
- less cell number
-difference between head and chest circumference <3cm
-features of malnutrition is less pronounced

asymmetric
-later gestation onset
-75%
-abdominal circumference decreased
-cell size reduced
-reduction in weight
-difference between head and chest circumference 3cm+
-features of malnutrition is more pronounced.

33
Q

implications of FGR/IUGR

A

fetus:
cardiac hypertrophy/chronic vasoconstriction

poor lung maturation-> bronchopulmonary dysplasia

LT motor defects and cognitive impairments

BRS Y2 (60 decks)

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