Lecture 20: 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, and
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!
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
What is the purpose of the haematological change?
During delivery loss of 500mL roughly of blood. The hypervolaemia accounts for this. Haemtocrit retuns slowly
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 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: 30days
- 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!!!
How are lymphocytes (B and T cells) altered during pregnancy?
- The lymphocyte count doesn’t change, but there is a bias in the type of T Helper (CD4) cells and the cytokines they produce
- Shift towards the Th2 cytokines
- Th2 Cytokines: drive the IS towards an Antibody mediated response
- Th2 Cytokines: drive the immune system towards a cell mediated response (cytotoxic T cell → transplant rejection)
What does the Decidua contain in regards to an immune system?
A vast amount!
- Almost no B cells
- About 10% of the leucocytes are T cells
- 70% are specialise uterine-NK cells.
- Natural Killer Cells: in the peripheral blood can act by antibody-dependent cell mediated cytotoxicity
- BUT uNK cells lack CD16 the receptor required to affect ADCC by bnding to ABs, which aren’t there bc not produced by B cells
- So not killer cells, instead uNK appear to produce growth factors that promote vascular development.
Spontaneous Miscarriage is often due to?
Genetic anomiles in embryo that aren’t compatible with life are removed by nature
This happens in 1/4 pregnancies.
Less then the prevelance of recurrent miscarriages!
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
