BIOM2071 Lecture Notes - Lecture 21: Gestational Trophoblastic Disease, Advanced Maternal Age, Placental Abruption
Document Summary
Pre-existing medical problems (dm, renal disease, hypertension, autoimmune disease) Bp at >k20 with proteinuria or systemic disease: proteinuria: >300mg protein/24hr urine. Consequences: maternal long-term renal, liver, cognitive, cv dysfunction, growth restriction, iugr, placental abruption, preterm, programmed disease for foetus, cerebral palsy, gdm. Pre-eclampsia: 2+ episodes hypertension after k20 and dysfunction of one or more organ systems (proteinuria, renal, haematological, neurological, pulmonary, uteroplacental) Treatment: mg so4 (neuro-protectant reduces risk/severity) As placenta implants, uterine spiral arteries remodel (continues until k22) Inappropriate invasion placental dysfunction: regulated by natural killer cells and extravillous trophoblast cells, poor placental invasion = spiral arteries pulsatile (periods high/low oxygen) and smaller diameter. Consequences of shallow invasion: low o2 concentrations, alters placental development, oxidative stress (malperfusion) apoptosis and release of placental debris and bioactive peptides (induce endothelial dysfunction, contribute to symptoms, inflammation) Placenta releases: soluble fms-like tyrosine kinase-1 (sflt-1) antagonises flt-1. Haemolysis, elevated liver enzymes and low platelet count. Presentation: severe abdomen pain, vomiting and headaches.
