Disorders Of Pregnancy Flashcards
What are the two ways of foetal nutrition
Early- histiotrophic
Late-haemotrophic
What is the function of chorionic villi?
How does its branching change over pregnancy?
What do they stem from?
Provides an area for exchange
Grows further into uterine wall and increase branching
Cytotrophoblasts
Explain spinal artery remodelling
What features does the remodelled spiral artery have?
Extra villus trophoblasts (EVT) invade spiral artery
This makes endovascular EVT
Endothelium and smooth muscle is broken down and EVT coats inside of vessels
Endothelium recruits chemokine to help its breakdown
Maternal ECM changes to fibrinoid
= spiral artery becomes low pressure high capacity conduit for blood flow
What are the consequences of failed spiral artery remodelling?
How does this affect nutrient exchange?
Vessels are occluded impeding RBC movement
Inflammatory and immune cells get stuck in spiral artery
Local hypoxia
Free radical damage
= decrease of nutrient exchange
What are the risks of preeclampsia to mother and child?
Mother: progression to eclampsia
HELLP syndrome- hemolysis, elevated liver enzyme, low platelet
Child: pre-term delivery, reduced fetal growth
What is the difference between normal spiral remodelling and preeclampsia spiral remodelling?
What does placental condition does it cause?
PE- EVT doesn’t dig deep low enough into myometrium, only reaches decidual/endometrial layer
= placental ischaemia
What is the role of PLGF and VEGF?
What is the role of Flt1?
What causes pre-eclampsia?
Angiocrine growth factors that placenta releases to promote healthy endothelial cells. They promote vasodilation and anticoagulation
Binds to VEGF to limit its bioavailability (balance maintained) also released by placenta
Insufficient placental growth factor (PLGF)
too much Flt1 due to stress on placenta (due to lack of blood) which mops up PGLF and VEGF and decreases endothelium function = vasoconstriction and coagulation = high BP
What are Extracellular vesicles?
How do preeclamptic extracellular vesicles differ to normal?
Vesicles released as a result of trophoblasts apoptosis causing proinflammation and procoagulation of endothelium
There are less placental but more endothelial vesicles
But they carry different things eg different RNA or genes
What is small for gestational age? What are the 3 groups?
Fetal weight lower than 10 percentile
Small throughout pregnancy but healthy
Early growth normal but slows later in pregnancy (FGR/IUGR)
Non-placental growth restriction (genetic, metabolic)
What are implications of FGR/IUGR (foetal growth restriction/intrauterine growth restriction)?
Poor lung maturation
Long term motor defects
Cardiac hypertrophy
What are the differences between early preeclampsia and late preeclampsia?
Early- not as common but more dangerous
Late- most cases but not as dangeroys
What are the differences between asymmetrical and symmetrical IUGR?
Assymetrical: later onset, more common, head bigger than body, better prognsosis, cause by placental defects
Symmetrical: early onset, less common, small overall, caused by genetic disorder, poor prognosis
