Figure 1030

Pathophysiology of preeclampsia. A major unresolved issue in the pathophysiology of preeclampsia is the mechanism whereby abnormalities in placental modulation of the maternal circulation lead to maternal systemic disease. The current schema, which is a hypothesis, depicts a scenario whereby placental ischemia leads to the release of substances that might be toxic to maternal endothelial cells. The resulting endothelial cell dysfunction also results in increased platelet aggregation. These events lead to the widespread systemic vasospasm, intravascular coagulation and decreased organ flow that are characteristic of preeclampsia. NO—nitric oxide; PDGF—platelet-derived growth factor; PGI2—prostacyclin 2.

Periportal hemorrhagic necrosis Subcapsular hematoma T Aspartate aminotransferase T Alanine aminotransferase

Central nervous sytem

Central nervous sytem

Visual disturbances Seizures

Hyperemia, focal anemia Thrombosis, hemorrhage

Visual disturbances Seizures

Hyperemia, focal anemia Thrombosis, hemorrhage

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