## Pathophysiology of Preeclampsia **Key Point:** Endothelial dysfunction is the central pathophysiological mechanism that distinguishes preeclampsia from other hypertensive disorders in pregnancy. This dysfunction leads to increased vascular permeability, platelet activation, and multi-organ involvement. ## Mechanism The pathophysiology involves: 1. Abnormal placentation and impaired trophoblastic invasion 2. Release of placental factors (sFlt-1, sEng) that antagonize VEGF and TGF-β 3. Endothelial cell activation and dysfunction 4. Increased vascular permeability and loss of fluid into interstitial space 5. Activation of coagulation cascade and platelet consumption ## Comparison with Other Hypertensive Disorders | Feature | Preeclampsia | Chronic Hypertension | Gestational Hypertension | |---------|--------------|----------------------|-------------------------| | **Endothelial dysfunction** | Present (hallmark) | Absent | Absent | | **Proteinuria** | New-onset (≥0.3 g/24 h) | Pre-existing | Usually absent | | **Platelet count** | Often decreased | Normal | Normal | | **Liver enzymes** | May be elevated | Normal | Normal | | **Onset** | After 20 weeks | Before 20 weeks | After 20 weeks | **High-Yield:** The endothelial dysfunction in preeclampsia is what causes the systemic manifestations (HELLP syndrome, eclampsia, acute kidney injury) that distinguish it from simple hypertension. This is why preeclampsia is a systemic disease, not just a blood pressure problem. **Clinical Pearl:** Endothelial dysfunction explains why some patients with preeclampsia have normal or only mildly elevated blood pressures yet still develop severe complications — the pathology is not primarily about BP elevation but about vascular integrity loss.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.