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Antihypertensive therapy is used to reduce blood pressure and prevent complications like stroke, but it does not treat the underlying placental pathology. Drugs like labetalol or hydralazine are supportive, not curative. BP control alone does not halt disease progression.

Magnesium sulfate prevents seizures but does not reverse the disease process. It is used for neuroprotection and eclampsia prevention, not as a curative measure. The underlying endothelial dysfunction persists unless the placenta is removed.

Corticosteroids are used to accelerate fetal lung maturity in preterm gestations but have no effect on the maternal disease process. They are adjunctive therapy to improve neonatal outcomes, not definitive treatment for preeclampsia.

A BP of 140/90 mmHg meets the minimum threshold for gestational hypertension or mild preeclampsia, but not severe disease. It does not fulfill the criteria for severe features and is managed conservatively unless other symptoms develop.

A BP of 150/100 mmHg is elevated but does not meet the severe range. It may indicate worsening disease but is not diagnostic of severe preeclampsia. Close monitoring is warranted, but it does not trigger immediate intervention.

A BP of 130/80 mmHg is within normal limits for pregnancy. It does not meet any diagnostic criteria for hypertensive disorders in pregnancy. No clinical concern for preeclampsia arises from this value alone.

While mild headaches can occur in normal pregnancy, a severe, persistent headache that does not respond to analgesics is not typical. Normal pregnancy discomforts are usually transient and mild. This presentation exceeds expected physiologic changes.

Dehydration may cause headache, but it is usually associated with other signs like dry mucous membranes, tachycardia, and decreased urine output. It typically responds to hydration and rest. The persistence and severity here suggest a more serious etiology.

Hypoglycemia can cause headache, but it is usually accompanied by symptoms like diaphoresis, tremors, hunger, and confusion. It resolves quickly with glucose intake. The absence of these features and lack of response to acetaminophen makes this unlikely.

Macrosomia is typically associated with maternal diabetes due to fetal hyperinsulinemia and increased glucose transfer. Hypertensive disorders do not cause fetal overgrowth; instead, they restrict growth. In fact, the opposite—low birth weight—is more common in hypertensive pregnancies.

Polyhydramnios is linked to fetal anomalies such as anencephaly or gastrointestinal obstructions, and maternal diabetes. Hypertensive disorders often result in oligohydramnios due to reduced placental perfusion and decreased fetal urine output, not excess amniotic fluid.

Congenital heart defects are primarily associated with teratogenic exposures or genetic syndromes. Hypertension in pregnancy does not directly cause structural cardiac malformations. There is no strong evidence linking maternal hypertension to increased incidence of congenital heart anomalies.

Increased deep tendon reflexes are not associated with magnesium toxicity. In fact, hyperreflexia is seen in early preeclampsia before magnesium is administered. Magnesium causes reflex depression, not enhancement. This choice contradicts the pharmacologic action of magnesium on neuromuscular transmission.

Respiratory rate of 20 breaths/minute is within normal limits. Toxic levels of magnesium depress the respiratory center, leading to bradypnea below 12 breaths/minute. A rate of 20 indicates adequate ventilation and no current compromise. This is not an early sign of toxicity.

Hypertension resistant to medication is not a feature of magnesium toxicity. Magnesium sulfate causes vasodilation and lowers blood pressure. Persistent hypertension may indicate worsening preeclampsia, not magnesium overdose. This reflects disease progression, not drug toxicity.

Spinal anesthesia is contraindicated at platelet counts below 75,000/mm³. At 15,000/mm³, the risk of spinal bleeding and compression is unacceptably high. This choice ignores standard safety thresholds and exposes the patient to irreversible neurologic injury.

Epidural anesthesia is not safe at platelet counts below 75,000/mm³. It carries similar risks to spinal anesthesia, including epidural hematoma and paralysis. The slower onset of epidural also makes it unsuitable for emergent delivery.

No anesthesia is never appropriate, even in emergencies. Cesarean section is a major abdominal surgery requiring pain control and muscle relaxation. Proceeding without anesthesia would cause severe distress and violate ethical standards of care.

Vascular endothelial growth factor is a pro-angiogenic molecule that promotes vascular development and endothelial integrity. In preeclampsia, VEGF is suppressed by sFlt-1, not elevated. Its deficiency contributes to vascular dysfunction, not its presence. This factor is not the pathogenic agent but a target of inhibition.

Placental growth factor is another pro-angiogenic molecule essential for placental vascularization. Like VEGF, it is neutralized by sFlt-1 in preeclampsia. Low levels of PlGF are associated with disease severity, but it is not the causative factor. It is a victim of antagonism, not the driver.

Insulin-like growth factor is involved in fetal growth and placental development but is not directly implicated in the angiogenic imbalance of preeclampsia. It does not interact with VEGF or PlGF pathways. Its role is metabolic, not vascular, making it irrelevant to the anti-angiogenic mechanism.

Blood pressure does not directly determine fetal well-being. Fetal status is assessed via ultrasound, biophysical profile, and non-stress testing. While maternal hypertension may affect placental perfusion, BP alone is not a reliable indicator of fetal compromise.

Pain level is not assessed through blood pressure. Pain may transiently elevate BP, but accurate pain evaluation requires subjective reporting and behavioral cues. BP monitoring is not a validated tool for pain assessment in obstetrics.

Postpartum hemorrhage is influenced by uterine atony, retained placenta, and coagulopathy—not directly by blood pressure. While severe preeclampsia may predispose to bleeding, BP measurement is not a preventive tool for hemorrhage control.