Hypertensive Disorders in Pregnancy MCQ

Magnesium sulfate is: Excreted in the urine. Suppresses tendon reflexes in toxicity. Is the drug of choice for eclampsia.

The patient has magnesium sulfate toxicity. The next step is to give calcium gluconate, the antidote for magnesium toxicity. Discontinuing MgSO4 is necessary but giving the antidote is crucial. Dexamethasone is for fetal lung maturity. Oxygen is supportive. Measuring serum magnesium levels confirms toxicity but treatment should not be delayed.

Regarding pre-eclampsia: Proteinuria is no longer required for diagnosis. Fetal growth restriction is a known complication. The risk of HELLP syndrome is associated with, but not directly proportional to, the severity of blood pressure. Antihypertensive treatment improves *maternal*, but not consistently fetal, outcomes. Aspirin reduces the risk of pre-eclampsia in high-risk women.

This patient is at increased risk of pre-eclampsia due to her age and multiparity. Low-dose aspirin is recommended for prophylaxis in women at high risk of pre-eclampsia, and is most effective when started before 16 weeks of gestation. Increasing calcium supplementation is not a standard recommendation for pre-eclampsia prophylaxis in this scenario. There’s no indication for high-dose folic acid or increased iron. Micronized progesterone is used for recurrent miscarriage, not pre-eclampsia.

Magnesium sulfate is: Excreted by the kidneys, the drug of choice for eclampsia, and its toxicity is treated with calcium gluconate. It *can* be used with nifedipine. Toxicity causes *respiratory depression*, not tachypnea.

The patient’s history of recurrent miscarriages and hypertension suggests antiphospholipid syndrome (APS). The lupus anticoagulant test helps diagnose APS. HbA1C and OGTT are for diabetes. TORCH screening is for infections. TSH is for thyroid disease.

The first sign of magnesium toxicity is absence of knee jerk reflexes. Other signs include: Absence of ankle clonus (not the *first* sign), absent urine output (later sign), respiratory rate 15/min (respiratory depression is a sign of toxicity, but less than 16 is not usually the first indicator), and absence of biceps jerk.

The patient has severe pre-eclampsia with signs of end-organ involvement (headache, vomiting, visual disturbances, right hypochondrial pain) and ankle clonus. The most appropriate next step is IV magnesium sulfate for seizure prophylaxis. CTG is important for fetal monitoring. Immediate delivery may be necessary but not before stabilizing the patient and preventing seizures. Diazepam is not the first-line agent for eclampsia prevention. Oxygen is supportive but does not address the primary concern.

The patient has eclampsia (pre-eclampsia with seizures). The most appropriate next step is to give IV magnesium sulfate 4g bolus to control the seizure and prevent recurrence. Infusion of 0.9% saline is important but secondary. IV labetalol is for hypertensive control, not seizure management. IV diazepam may stop the current seizure, but magnesium sulfate is the drug of choice for eclampsia. Delivery (EM-I-SCS) is indicated but only *after* stabilizing the patient and controlling the seizure.

The patient has eclampsia. The next management step is to give magnesium sulfate (MgSO4) to prevent further seizures. Delivery is important but after stabilizing the patient. IV diazepam can stop the *current* seizure, but MgSO4 prevents recurrent eclampsia. Reducing BP is important but MgSO4 is the priority. Coagulation profile is part of the workup, but seizure prevention comes first.

The patient has severe pre-eclampsia with epigastric pain and headache, indicating increased risk for maternal complications. The best management is delivery, and with an unfavorable cervix, Cesarean section is often the most expedient option. Oral nifedipine is for blood pressure control but does not address the need for delivery. Diazepam is not the primary treatment. Prostaglandin pessary is for cervical ripening, but the patient needs prompt delivery. Observation in the ICU is for *postpartum* management, not the active management of severe pre-eclampsia. (RCOG Green-top Guideline No. 10(a), 2019)

A blood pressure of 160/110 mmHg indicates severe hypertension. IV labetalol is a first-line antihypertensive medication for severe pre-eclampsia. IV magnesium sulfate is used for seizure prophylaxis. Diclofenac sodium suppositories and IM dexamethasone are not used. Sublingual nifedipine can be used for acute hypertension, but IV labetalol is preferred in this scenario.

The patient has severe pre-eclampsia. The most appropriate next step is IV magnesium sulfate to prevent seizures. Immediate Cesarean section is not the first step. IV hydralazine is for blood pressure control but not seizure prevention. Steroids are for fetal lung maturity, not acute management. Ultrasound is not the priority.

Features of magnesium sulfate toxicity include: Reduced urine output, respiratory depression, slurred speech. Bradycardia is a later sign. Uterine overstimulation is not a feature of magnesium toxicity; it is used to prevent seizures.

The patient has hypertension in pregnancy. To assess the severity, the most appropriate investigation is urine albumin (proteinuria). Low platelet count, serum creatinine, and elevated liver enzymes are also important in assessing severity, but are not listed. Serum C3 is not used to assess the *severity* of pre-eclampsia. Ultrasound is important for fetal well-being, but urine albumin assesses *maternal* severity.

Losartan and enalapril are contraindicated in pregnancy. Labetalol is a safe and effective antihypertensive in pregnancy, especially in women with chronic hypertension. Hydrochlorothiazide can be used, but is not the first-line agent in this case. Nifedipine is also safe, but labetalol is often preferred for chronic hypertension in pregnancy, especially with renal disease.

The first sign of magnesium toxicity is loss of deep tendon reflexes. Other signs of magnesium toxicity occur sequentially: Reduced urine output, respiratory depression, altered level of consciousness, and bradycardia are later signs.

The patient has hypertension and swelling, suggesting pre-eclampsia. The most important next step is to carry out investigations to confirm the diagnosis and assess the severity. Bed rest and reassessment, oral nifedipine, and induction may be considered later, but only after proper evaluation. Emergency Cesarean is not indicated at this stage.

Features of magnesium toxicity include: Respiratory depression, slurred speech. Acute renal failure and hyperstimulation of the uterus are not features of magnesium toxicity.

The patient has eclampsia. The most beneficial drug is magnesium sulfate to prevent further seizures. Dexamethasone is used for fetal lung maturity. Hydralazine and nifedipine are antihypertensives. Diazepam can stop a seizure, but magnesium sulfate is superior in preventing recurrent eclamptic seizures.

The patient has severe pre-eclampsia. The most appropriate initial step is to administer a bolus dose of 4 g of magnesium sulfate for seizure prophylaxis. Intravenous hydralazine or oral labetalol are used to control blood pressure. Catheterization is often needed, but MgSO4 is the priority. Emergency Cesarean section may be needed but not before stabilizing the patient.

Low-dose aspirin is recommended to reduce the risk of pre-eclampsia in women with specific risk factors. These include: Pre-existing diabetes mellitus. A past history of SLE. Increased umbilical artery Doppler resistance. High parity and previous first-trimester miscarriage are not established indications for low-dose aspirin for pre-eclampsia prevention.