PATHOPHYSIOLOGY OF PREECLAMPSIA

Pathophysiology of preeclampsia is poorly understood, Factors may include poorly

developed uterine placental spiral arterioles (which decrease uteroplacental blood flow
during late pregnancy), a genetic abnormality on chromosome 13, immunologic
abnormalities, and placental ischemia or infarction. Lipid peroxidation of cell
membranes induced by free radicals may contribute to preeclampsia. That’s why the
first in the flow chart is the unknown etiology of the pre-eclampsia, the book based
research said that it might be a genetic factors, environmental factors or immulogical
factors. Etiology means the cause, set of causes, or manner of causation of a disease
or condition. After the causation there goes the inadequate placentation or the poor
growth of the placenta. The physiological vascular remodeling of spiral arteries by
trophoblasts does not occur in preeclampsia. At the cellular level, cytotrophoblasts
undergo pseudovasculogenesis by switching their adhesion molecules to mimic those of
vascular cells. In preeclampsia, this process does not occur appropriately, and therefore
invasion into the spiral arteries is incomplete. By the way, the cytotrophoblast is the
inner layer of the trophoblast responsible for the pathway of the fetal-maternal gas
exchange. Various pathways including deficient heme oxygenase expression, genetic
factors, oxidative stress, immune factors such as angiotensin receptor autoantibodies or
altered natural killer cell signaling and, more recently deficient catechol-O-methyl
transferase or deficient corin enzymes have been all proposed to have key roles in
inducing placental disease. Still the constrictive properties of the arteries remained. And
yet it leads to vasoconstriction or the constriction of blood vessels, which increases
blood pressure. The maternal syndrome and clinical features of preeclampsia are
unified by the presence of systemic endothelial dysfunction and microangiopathy that
targets and/or damages the glomerular endothelium. If the glomeryular endothelium is
damaged the filtration capacity of the body fails that creates the presence of the
proteinuria. In healthy person, urine contains very little protein, an excess protein in the
urine is indicative of illness. Then an observable swelling from fluid accumulates in body
tissues which we called the edema.
 UNKNOWN ETIOLOGY

INADEQUATE
PLACENTATION

UTERINE SPIRAL ARTERIES ARE

POORLY INVADED BY
CYTOTROPHOBLAST

UTERINE SPIRAL ARTERIES

CYTOTROPHOBLAST
ARE POORLY INVADED BY
FAILED TO REPLACE
CYTOTROPHOBLAST
TUNICA MEDIA
ENDOTHELIAL
INCOMPLETE DYSFUCNTION
PSEUDOVASCULARIZATION

GLOMERULAR
DECREASED PLACENTAL ENDOTHELIUM IS
PERFUSION DAMAGED

VASOCONSTRICTION FILTRATION CAPACITY

CONSTRICTIVE
PROPERTIES OF THE FAILS
ARTERIES REMAINED

INCREASE BLOOD
PRESSURE PROTEINURIA

EDEMA