Physiology of Pregnancy II Flashcards
So we know that in Response to maternal HR and SV increasing, which increases CO, mothers undergo a compensatory decrease in peripheral Vascular Resistance. If this doesn’t occur?
Her BP will sky rocket, and she’ll likely develop preeclampsia
Most of the CV and Haemodynamic adaptations for pregnancy occur within ___ weeks gestation?
9
Oestrogen and Cardiovascular changes???
- Can reduce vascular resistance mainly in reproductive tissues.
- Can alter the ratio of type I/type III collagen in the vessel wall, to increase compliancy
- High levels of oestrogen are not reached until 9 weeks (is produced by the fetus) when fetal adrenals induce synthesis.
So there’s actually very little eostrogen (eostrdial) in the maternal circulation prior to 9 weeks gest. when all the CV changes are happening!! Kind of rules this out!
Progesterone and CV changes???
- P4 may induce vascular relaxation (mainly in the uterus) as is a SM relaxant, in the uteroplacental circulation, but doesn’t seem to have a systemic effect.
- Also P4 levels aren’t elevated till ~10weeks
Angiotensin System and CV changes??
- Angiotensin II is a vasoconstrictor which causes the arterioles to contract → increases BP.
- It’s levels increase in pregnancy
- Uteroplacental Unit: produces large amounts of Renin-angiotensin System (RAS) (placenta and decidua can produce all the components, have all the receptors,)
- But A-II effects seem to be blunted in pregnancy, response to RAS decreased
Nitric Oxide and CV changes?
- Produced by vascular endothelial cells by NO synthetase in response to shear stress of blood flowing over the vessel surface.
- Half life of 6secs and causes arterial wall relaxation and dilation
Activity of NO synthetase in some tissues is increased in pregnacy, so probably quite important!
Budding vesicles (syncytial nuclear aggregates) off the placenta into the maternal blood, get trapped in mat. pulmonary capillary bed.
These vesicles (on steroids) are carrying huge loads of protein and DNA, way of conveying information, via many complex signals.
What do these vesicles do to change CV?
When vesicles from normal placenta are added to endothelial cells; they prevent the activation of endothelial cells by potent chemical and pathological activators.
In preeclampsia, the endothelial cells get activated, and this occurs in maternal endothelial cells weeks before the presentation of clinical symptoms.
Is this part of how he placenta tells mum to relax?
Effect of placental EVs on vascular functionin vivo with pregnant mice??
When non-pregnant mice were given vesicles, the blood vessels don’t even know the vesicles are there, “unchanged”
But if you look at the pregnant mice that were given vesicles, they showed endothelium depenedent-vasodilation of resistance vessels in the mesentry.
Is this the fetus’s way of telling mum they are there, and enforcing change so the pregnancy can occur?
There are also Haematological changes that occur in the mother in response to pregnancy:…
- Increased Blood Volume: the Plasma volume and blood volume both increase in human pregnancy but at different rates
- There the haematocrit declines in pregnancy as plasma volume increases at a higher rate then Blood cell mass from 35-47% to 30-40%
- By 30 weeks there’s a 1250ml increase and then remains stable
Non Pregnant: 4L
Pregnant: 6L
Why do we need to now about the changes that occur in the mother during pregnancy?
So that when we are checking her we compare her results against ‘pregnancy norms’ not non-pregnant ones!
Some of the haematologcal adaptions happen earlier in mum. When does this happen and what does it tell us?
- Also cyclic changes in blood/plasma volume during the menstrual cycle
- At 8-10 weeks gestation there’s a 10% increase in plasma volume, this is similar to the menstrual cycle.
- So the plasma expansion of gestation occurs after the changes to the CV system; the Blood vol. increases doesn’t cause the CV changes (which has a massive effect really early on)
During delivery there is blood-loss, how can this occur in the 1st place?
- During delivery there’s substantial blood loss, 500mls for a single vaginal deivery
- 1L for twins or caesarean section
- If this happen to us we would go into hypovolaemic shock
- The hypovolaemia modifies this response; pregnant women can handle this large amount of blood loss, then they slowly loss the rest of the excess post-partum but diuresis and a slow loss of RBC over time
- The haematocrit slowly returns to normal!
The fetus is gnetically half paternal and half maternal!
“Tissue-transplant”
How cant the mothers immune system deal with this?
- For 9 months we have all been “a semi-allograft”, and survived within intimate contact with the maternal immune system.
- Prior to pregnancy sperm must survive the female genital tract. Although sperm are completely foreign to the mother, repeated acts of coitus don’t seem to trigger the maternal immune system (that removes excess sperm) to build up a resistance!
- In fact repeated exposure appears to protect against ecclampsia!
- We know Nulliparity are more likely to develop pre-eclampsia, could this be due to less tolerance build up?
- Seminal Plasma has been found to be immune suppressive and can reduce many IS compenents
How does mum actually allow the baby to be inside her,=?
We cannot completely “turn off” mums immune system during pregnancy as this will leave baby exposed to any pathogens (Fetal IS not developed)
Places like valves, corneas and testis are immune tolerable, as they aren’t vascularised. But the uterus is vascularised.
So the thought is that there’s a specific IS ‘tolerance’ to the fetus.
- Womens incidence of listerosis, leprosy and common colds are higher in pregnancy (but is this just due to being run down??)
How does mums immune system cell count change during pregnancy?
When does neutrophil count peak and why?
- White cell count rises due to the expansion of the neutrophil population, which rises in the luteal phase of m.cycle and doesn’t drop throughout pregnancy.
- Neutrophil count peaks: 30weeks and then at labour
- NPs thought to be important in preparing the cervix for labour (part of the innate immune response, killling bacteria)
**also have changes in the lymphocytes!!!
Recurrent miscarriages are?
When a women has three or more spontaneous miscarriages with the same partner.
More prevalent then spontaneous miscarriages :(
This makes us think there’s more then just genetic abnomalities gone wrong as it’s occuring at a great rate.
If you’re going to have an immune response to the fetus, where is it most likely to occur?
The placenta
Especially the Decidua Basalis, where the embryo is implanting and eating into the uterus.
Women with recurrant miscarriage had tissue that showed 36 Tcells/mm2
Women with normal pregnancies had tissue with 15 T cells/mm2
What is concerning about T-cell Aggregates?
T-cell by themselves are of little harm, but once primed and stimulated by Antigen-Presenting Cells they can pick up an Immune Response → Potential risk of Miscarriage.
Antigen-Presenting Cells:
- Macrophages
- Dedritic cells
This could be a reason for recurrent miscarriage!
How does the skin appearance change during pregnancy?
- Pigmentation in skin, nipples and areola
- Linea Nigra development
- Chloasma (excess pigmentation) may develop in the neck and face; will regress after pregnancy
- 50% get Striae Gravidarum: streak marks due to loss of elasticity
These pigmentation changes occur due to an increased secretion of melanocyte stimulating hormone.
MSH is very elevated from the 2nd month of pregnancy
