disorders of pregnancy and parturition Flashcards
early embryro nutrition vs 2nd trimester nutrition (fetal demands on placenta increases with pregnancy)
histiotrophic- relies on uterine gland secretion and breakdown of endometrial tissue
2: haemotrophic
how does haemotrophic support work
Achieved through a haemochorial-type placenta where maternal blood directly contacts the fetal membranes (chorionic villi).
how does histiotrophic nutrition work
relies on uterine gland secretion and breakdown of endometrial tissue
why is there increased branching of chorionic villi with progression through pregnancy
increase area for exchange (higher O2 demand)
3 phases of chorionic villi developmenet
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.
what is the microstructure of terminal villus
Convoluted knot of vessels and vessel dilation
->Slows blood flow enabling exchange between maternal and fetal blood
what is the terminal villus microstructure covered in
trophoblast
changes in microstructure of terminal villus from early to late pregnancy in terms of
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.
spiral artery re-modelling steps and what does it convert spiral arteries into? -brief
- 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
Conversion: turns the spiral artery into a low pressure, high capacity conduit for maternal blood flow.
purpose of spiral arteries
provide maternal blood supply to endometrium
how does spiral artery remodelling occur? depth
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
consequence of failed spiral artery re-remodelling
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
- disrupted flow and local hypoxia, free radical damage and inefficient delivery of substrates into the intervillous space.
- 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.
what is pre-eclampsia
New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
Occurring after 20 weeks’ gestation
signs and symptoms of pre-eclampsia
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)
early onset pre-eclampsia
<34 weeks
-fetal and maternal symptoms
-Changes in placental structure
-Reduced placental perfusion
late onset pre-eclampsia
> 34 weeks
-More common
-Mostly maternal symptoms
-Fetus generally OK
-no placental changes
PE- risk to mother
-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)
what is placental abruption
(separation of the placenta from the endometrium)
PE- risk to fetus
-Pre-term delivery
-Reduced fetal growth (IUGR/FGR)
-Fetal death
Placental defects underpinning PE- in regards to EVT, spiral artery remodelling etc
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
what is PLGF
Placental Growth Factor:
VEGF related, pro-angiogenic factor released in large amounts by the placenta.
what is Flt1
soluble VEGFR1-
Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.
what is PE in terms of Flt-1
excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.
healthy placenta vs pre-eclampsia placenta in terms of PLGF/VEGF/
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)
