What is the pathophysiology of Pregnancy induced hypertension?

The symptoms of PIH affect almost all organs. The vasculature spasm may be caused by increased cardiac output that injures the endothelial cells of the arteries and the action prostaglandins (notably decreased prostacyclin and thrombexane). In PIH there is a reduced responsiveness to blood pressure changes. Vasoconstriction occurs and blood pressure increases dramatically. With elevated blood pressure, the cardiac system becomes overwhelmed and the heart is forced to pump against rising peripheral resistance. This in turn reduces the blood supply to the organs, specifically to the kidneys, pancreas, liver, brain and placenta. Poor placental perfusion results to inadequate nutrient and oxygen supply to the fetus. Ischemia in the pancreas may cause epigastric pain and an elevated amylase-creatinine ratio. Spasm of the arteries in the retina leads to vision changes. And if retinal hemorrhages occur, it can result to blindness.

Vasospasm in the kidney increases blood flow resistance. Degenerative changes develop in the kidney glomeruli because of back pressure. This leads to increased permeability of the glomerular membrane, allowing the serum protein to escape in the urine. The degenerative changes also result in lowered glomerular filtration rate; in turn there is a decrease in urine output and clearance of creatinine. And because of tubular reabsorption of sodium along with fluid retention, subsequent edema develops. Which is then further increased because as more protein is lost, the osmotic pressure in the circulation drops and fluid diffuses from the circulatory system into the denser interstitial spaces to equalize pressure. Extreme edema can lead to cerebral and pulmonary edema and seizures (as seen in eclampsia).