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Pathology - Preeclampsia Syndrome
Preeclampsia syndrome is characterized for a first term pregnancy as a systolic pressure greater than 140 or diastolic pressure greater than 90 after 20 weeks’ gestation plus the presence of proteinuria. mother hypertension is a significant cause of mother and newborn morbidity and mortality. Risk factors include obesity, African American ethnicity, and first pregnancy. The pathophysiology is hypothesized to include an early stage in which there is incomplete invasion of maternal uterine arteries by the trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that induce endothelial injury in the mother. Subsequent problems develop on a range of severity and can span numerous organ systems. Platelet aggregation and activation cause release of thromboxane A2 leading to vasospasm that drives high blood pressure. In severe circumstances platelet depletion can occur. Increased endothelial permeability leads to protein leak, which in this case is evidenced by proteinuria and pitting edema in the extremities. Pulmonary edema is observed in this case generating rales and shortness of breath.
In severe situations, hemolysis and vascular blockage may also occur, for example, in the liver or brain. The state of eclampsia is defined if the mother suffers tonic–clonic seizures and is associated with bad outcomes. Initial treatment involves blood pressure medication but timely delivery of the fetus is important if signs of severe preeclampsia develop; birth is usually curative.
Preeclampsia syndrome is characterized for a first term pregnancy as a systolic pressure greater than 140 or diastolic pressure greater than 90 after 20 weeks’ gestation plus the presence of proteinuria. mother hypertension is a significant cause of mother and newborn morbidity and mortality. Risk factors include obesity, African American ethnicity, and first pregnancy. The pathophysiology is hypothesized to include an early stage in which there is incomplete invasion of maternal uterine arteries by the trophoblast during implantation. Later in pregnancy this leads to oxidative stress in the placenta, which produces inflammatory chemicals that induce endothelial injury in the mother. Subsequent problems develop on a range of severity and can span numerous organ systems. Platelet aggregation and activation cause release of thromboxane A2 leading to vasospasm that drives high blood pressure. In severe circumstances platelet depletion can occur. Increased endothelial permeability leads to protein leak, which in this case is evidenced by proteinuria and pitting edema in the extremities. Pulmonary edema is observed in this case generating rales and shortness of breath.
In severe situations, hemolysis and vascular blockage may also occur, for example, in the liver or brain. The state of eclampsia is defined if the mother suffers tonic–clonic seizures and is associated with bad outcomes. Initial treatment involves blood pressure medication but timely delivery of the fetus is important if signs of severe preeclampsia develop; birth is usually curative.
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