A 32-year-old primigravida at 28 weeks of gestation presents with blood pressure 160/110 mmHg, proteinuria 2+ on dipstick, and mild epigastric discomfort. Regarding the pathophysiology and management of preeclampsia, all of the following are true EXCEPT:

Explanation

## Pathophysiology and Management of Preeclampsia ### Endothelial Dysfunction Mechanism **Key Point:** Preeclampsia is characterized by endothelial dysfunction caused by an imbalance between vasodilatory prostacyclin and vasoconstrictory thromboxane A₂, leading to vasoconstriction and platelet aggregation [cite:Park 26e Ch 24]. ### Magnesium Sulphate in Severe Preeclampsia **High-Yield:** Magnesium sulphate is the gold standard anticonvulsant for seizure prophylaxis and treatment of eclampsia in preeclampsia. It is superior to phenytoin and diazepam and reduces the risk of eclampsia by approximately 50% [cite:ACOG Guidelines on Hypertension in Pregnancy]. ### Antihypertensive Agents: Hydralazine vs Nifedipine **Clinical Pearl:** This is a common misconception. **Nifedipine (immediate-release sublingual) has a FASTER and MORE PREDICTABLE onset (5–10 minutes) compared to hydralazine (10–20 minutes)**. Nifedipine is now preferred for acute severe hypertension in pregnancy because of its rapid onset, predictable effect, and lower risk of maternal hypotension and fetal compromise [cite:ACOG Guidelines on Hypertension in Pregnancy]. | Agent | Onset | Duration | Advantage | Disadvantage | |-------|-------|----------|-----------|---------------| | Hydralazine IV | 10–20 min | 3–4 hours | Proven safety record | Unpredictable response, reflex tachycardia | | Nifedipine (immediate-release) | 5–10 min | 4–6 hours | Rapid, predictable | Sublingual route less reliable than oral | | Labetalol IV | 5–10 min | 3–4 hours | Combined α/β blockade | Contraindicated in asthma | **Warning:** Hydralazine is NOT faster than nifedipine — this is a frequently tested misconception in NEET PG. ### sFlt-1 and Placental Ischemia **High-Yield:** Placental ischemia and hypoxia trigger increased production of soluble fms-like tyrosine kinase-1 (sFlt-1), an antiangiogenic factor that antagonizes vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). This leads to endothelial dysfunction, proteinuria, and hypertension [cite:Harrison 21e Ch 414]. ### Summary Table: Preeclampsia Pathophysiology | Feature | Mechanism | Clinical Consequence | |---------|-----------|---------------------| | sFlt-1 elevation | Placental ischemia | Endothelial dysfunction, proteinuria | | Prostacyclin ↓ / TXA₂ ↑ | Endothelial injury | Vasoconstriction, platelet aggregation | | Magnesium sulphate use | NMDA antagonism, stabilizes cell membranes | Seizure prophylaxis | | Nifedipine (preferred acute agent) | Rapid calcium channel blockade | Fast BP reduction without reflex tachycardia |