A 28-year-old primigravida at 32 weeks gestation presents with BP 158/102 mmHg, proteinuria 2.4 g/24h, and new-onset thrombocytopenia (platelets 92,000/µL). AST is elevated at 98 U/L. Which mechanism best explains the thrombocytopenia in this setting?
- A Microangiopathic platelet consumption at sites of endothelial injury and fibrin deposition ✓
- B Platelet sequestration in an enlarged spleen due to portal hypertension
- C Immune-mediated destruction via anti-platelet IgG antibodies
- D Decreased thrombopoietin synthesis due to hepatic dysfunction
Correct answer: A. Microangiopathic platelet consumption at sites of endothelial injury and fibrin deposition
Explanation
In HELLP syndrome/severe pre-eclampsia, endothelial dysfunction leads to platelet activation and consumption at sites of microangiopathic damage — fibrin strands trap and lyse platelets, causing thrombocytopenia without splenomegaly or immune mechanisms. Portal hypertension and anti-platelet antibodies characterise ITP and liver cirrhosis respectively, while thrombopoietin deficiency is a different pathophysiology not typical of pre-eclampsia.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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