Disorders of Pregnancy and Parturition Flashcards
What are the 7 diagnostic features of pre-eclampsia?
- New onset hypertension (in a previously normotensive woman) BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic
- Occurring after 20 weeks’ gestation
- Reduced fetal movement and/or amniotic fluid volume (by ultrasound) in 30% cases
- Oedema common but not discriminatory for PE
- Headache (in around 40% of severe PE patients)
- Abdominal pain (in around 15% of severe PE patients)
- Visual disturbances, seizures and breathlessness associated with severe PE and risk of eclampsia (seizures)
What are the sub-types of pre-eclampsia?
Early onset: <34 weeks
Associated with fetal and maternal symptoms
Changes in placental structure
Late onset: >34 weeks More common (90%) Mostly maternal symptoms Fetus generally OK Less overt/no placental changes
What are maternal risk factors?
Previous pregnancy with pre-eclampsia
BMI >30 (esp >35)
Family history
Increased maternal age (>40, <20?)
Gestational hypertension or previous hypertension
Pre-existing conditions: diabetes, PCOS, renal disease, subfertility, autoimmune disease.
Non-natural cycle IVF?
What are risks to the fetus and mother?
Mother:
Damage to kidneys, liver, brain and other organ systems
Possible progression to eclampsia (seizures, loss of consciousness)
Placental abruption (separation of the placenta from the endometrium)
Fetus: reduced fetal growth, preterm birth, pregnancy loss/stillbirth
What placental defects underpin pre-eclampsia?
PE (esp early): EVT invasion of maternal spiral arteries is limited to decidual layer. Spiral arteries are not extensively remodelled, thus placental perfusion is restricted.
What is PLGF and Flt-1?
PLGF: Placental Growth Factor
VEGF related, pro-angiogenic factor released in large amounts by the placenta.
Flt1 (soluble VEGFR1)
Soluble receptor for VEGF-like factors which binds soluble angiogenic factors to limit their bioavailabliltiy.
What is the relationship between PLGF and Flt-1 with pre-eclampsia?
Excess production of Flt-1 by distressed placenta leads to reduction of available pro-angiogenic factors in maternal circulation, resulting in endothelial dysfuction.