Which vascular change best explains the defective placentation seen in pre-eclampsia?

• A Physiological conversion of spiral arteries into low-resistance uteroplacental vessels extending into the decidua only
• B Hyperplastic arteriolosclerosis with onion-skin thickening of myometrial arteries
• C Failure of trophoblast invasion with retained musculoelastic media of spiral arteries, sometimes with fibrinoid necrosis called acute atherosis ✓
• D Thrombotic occlusion of radial arteries with recanalisation channels

Explanation

In normal pregnancy, endovascular trophoblast replaces the endothelium and musculoelastic media of spiral arteries, converting them into flaccid low-resistance vessels. In pre-eclampsia this transformation is incomplete, the muscular layer persists, vessels remain responsive to vasoconstrictors, and fibrinoid necrosis with lipid-laden macrophages (acute atherosis) may appear. Option A describes partial conversion limited to the decidua, which is itself part of the defect rather than an alternative answer. Hyperplastic arteriolosclerosis belongs to malignant hypertension, not placentation failure.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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