Maternal-Fetal Medicine Practice Questions

Q: Which of the following conditions is NOT associated with decreased variability of fetal heart rate?

Fetal movement. **Explanation:** Fetal heart rate (FHR) variability represents the beat-to-beat fluctuations in the baseline heart rate, reflecting a healthy, mature interaction between the sympathetic and parasympathetic nervous systems. **Why Fetal Movement is the Correct Answer:** Fetal movement is associated with **increased** variability and accelerations. When a fetus moves, the sympathetic nervous system is activated, causing a transient rise in heart rate (acceleration). This is a hallmark of fetal well-being and forms the basis of a "Reactive" Non-Stress Test (NST). Therefore, it is not a cause of decreased variability. **Analysis of Incorrect Options:** * **Sleep (Fetal Sleep Cycles):** This is the most common physiological cause of decreased variability. Fetal quiet sleep cycles usually last 20–40 minutes; during this time, the autonomic nervous system is less active, leading to a "flat" or minimally variable tracing. * **Chronic Hypoxia & Acidemia:** These are pathological causes. As the fetus becomes hypoxic or acidotic, the central nervous system (CNS) becomes depressed. This depression impairs the autonomic regulatory centers in the brainstem, leading to a loss of variability. Persistent absent variability combined with late decelerations is a sign of impending fetal compromise. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Variability:** 6 to 25 beats per minute (Moderate). * **Drugs causing decreased variability:** Magnesium sulfate, opioids (morphine, pethidine), diazepam, and atropine. * **Saltatory Pattern:** Variability >25 bpm; often seen during acute hypoxia or umbilical cord compression. * **Sinusoidal Pattern:** A smooth, undulating wave-like pattern (variability is technically absent); classically associated with **severe fetal anemia** (Rh isoimmunization) or fetal hemorrhage.

Q: What is the drug of choice for hypertensive emergencies in pregnancy?

Labetalol. **Explanation:** In the management of hypertensive emergencies in pregnancy (defined as BP ≥160/110 mmHg), the goal is to rapidly lower blood pressure to prevent maternal complications like intracranial hemorrhage without compromising uteroplacental blood flow. **1. Why Labetalol is the Correct Answer:** Labetalol is a non-selective beta-blocker with alpha-1 blocking activity (ratio of 1:7 for IV). It is considered the **first-line drug of choice** because of its rapid onset of action (5–10 minutes), excellent safety profile, and its ability to lower BP without causing significant reflex tachycardia. It maintains stable placental perfusion, making it ideal for acute management. **2. Analysis of Incorrect Options:** * **Methyldopa (A):** While it is the drug of choice for *chronic* hypertension in pregnancy, it is **not** used in emergencies due to its slow onset of action (4–6 hours) and sedative side effects. * **Nitroprusside (B):** It is generally avoided in pregnancy due to the risk of **fetal cyanide toxicity**. It is reserved only for refractory cases where all other agents fail. * **Nicardipine (D):** A calcium channel blocker that is effective, but it is typically considered a second-line or alternative agent to Labetalol and Hydralazine. **High-Yield Clinical Pearls for NEET-PG:** * **First-line agents for Acute Hypertensive Crisis:** IV Labetalol, IV Hydralazine, or Oral Nifedipine (immediate release). * **Contraindication for Labetalol:** Avoid in patients with asthma, heart failure, or bradycardia. * **Target BP:** Aim to lower the MAP by no more than 25% in the first hour, targeting a diastolic BP of 90–100 mmHg. * **ACE Inhibitors/ARBs:** Absolutely contraindicated in pregnancy (Teratogenic; cause fetal renal dysgenesis and oligohydramnios).

Q: Rubin's diagnostic criteria is used for which of the following conditions?

Cervical pregnancy.. **Explanation:** **Rubin’s Criteria** are the established diagnostic benchmarks used to confirm a **Cervical Pregnancy**, a rare but life-threatening form of ectopic pregnancy where the blastocyst implants in the endocervical canal. **Why Cervical Pregnancy is Correct:** According to Rubin (1948), for a diagnosis of cervical pregnancy, the following four histological/anatomical criteria must be met: 1. Cervical glands must be opposite the placental attachment site. 2. The attachment of the placenta to the cervix must be intimate (below the internal os). 3. The whole or a portion of the placenta must be situated below the level of the internal os. 4. Fetal elements must be absent from the uterine cavity. **Analysis of Incorrect Options:** * **Ovarian Pregnancy:** Diagnosed using **Spiegelberg’s Criteria** (e.g., the tube on the affected side must be intact, the gestational sac must occupy the position of the ovary). * **Abdominal Pregnancy:** Diagnosed using **Studdiford’s Criteria** (e.g., normal tubes and ovaries with no evidence of recent pregnancy, no evidence of uteroperitoneal fistula). * **Hydatidiform Mole:** This is a gestational trophoblastic disease diagnosed via ultrasound ("snowstorm appearance") and serum beta-hCG levels, not by Rubin’s criteria. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Characterized by painless vaginal bleeding and a soft, "hourglass" shaped uterus (distended cervix larger than the fundus). * **Management:** Historically required hysterectomy due to profuse bleeding; currently managed conservatively with **Methotrexate** or uterine artery embolization. * **Key Distinction:** Do not confuse Rubin’s Criteria (Cervical Pregnancy) with the **Rubin Test** (Insufflation of fallopian tubes with $CO_2$ to check patency).

Q: During an antenatal check-up, a primigravida is found to be positive for Treponema pallidum infection. She is worried about her child. At which week of gestation does Treponema pallidum infection typically transfer to the fetus?

20th week. **Explanation:** The transmission of *Treponema pallidum* (the causative agent of Syphilis) from the mother to the fetus occurs via the placenta. While the spirochetes can technically cross the placenta as early as the 9th week of gestation, the **pathological effects and established infection typically occur after the 16th to 20th week.** The correct answer is **20th week** because, prior to this period, the fetus is protected by the **Langhans layer** (cytotrophoblast) of the chorion. After the 16th week, this layer begins to atrophy, and by the 20th week, it disappears, making the placenta more permeable to the spirochetes. Furthermore, the fetal immune system only becomes capable of mounting an inflammatory response (which causes the characteristic tissue damage of congenital syphilis) after the 18th–20th week. **Analysis of Incorrect Options:** * **A & B (4th and 8th week):** During the first trimester, the Langhans layer is thick and well-developed, acting as a robust physical barrier against the transmission of large organisms like spirochetes. * **C (16th week):** While the Langhans layer begins to thin at this stage, the most significant risk and the standard teaching for established clinical infection is the 20th week. **Clinical Pearls for NEET-PG:** * **Treatment:** Penicillin G is the only effective treatment for preventing fetal infection and treating the fetus. If the mother is allergic, **desensitization** is mandatory. * **Jarisch-Herxheimer Reaction:** Pregnant women treated for syphilis must be monitored for this reaction, as it can trigger preterm labor or fetal distress. * **Screening:** All pregnant women should be screened at the first prenatal visit using non-treponemal tests (VDRL/RPR). * **Congenital Syphilis:** If untreated, it can lead to abortion, stillbirth, or neonatal features like snuffles, Hutchinson’s teeth, and Mulberry molars.

Q: Magnesium sulfate (MgSO4) is indicated in which of the following conditions?

Severe pre-eclampsia. **Explanation:** **1. Why Severe Pre-eclampsia is Correct:** Magnesium sulfate ($MgSO_4$) is the **drug of choice** for the prevention of seizures in severe pre-eclampsia (prophylaxis) and the control of seizures in eclampsia (treatment). Its primary mechanism involves blocking NMDA receptors in the brain, increasing the seizure threshold, and causing cerebral vasodilation to reduce ischemia. According to the **Pritchard Regimen** or **Zuspan Regimen**, it is initiated to prevent the progression of pre-eclampsia to eclampsia, significantly reducing maternal morbidity. **2. Why Other Options are Incorrect:** * **Gestational Trophoblastic Disease (GTD):** While GTD can cause early-onset hypertension, $MgSO_4$ is not a routine treatment unless the patient develops features of severe pre-eclampsia. * **Gestational Diabetes (GDM):** This is a metabolic disorder of glucose intolerance. Management involves medical nutrition therapy (MNT) or insulin, not anticonvulsants. * **Placenta Previa:** This is a hemorrhagic complication (antepartum hemorrhage). Management focuses on hemodynamic stability and timely delivery, not seizure prophylaxis. **3. NEET-PG High-Yield Pearls:** * **Therapeutic Level:** 4–7 mEq/L. * **Monitoring:** Always check for the presence of **Patellar reflex** (first sign of toxicity is loss of reflex), **Respiratory rate** (>12/min), and **Urine output** (>30 ml/hr or 100 ml/4hr). * **Antidote:** 10 ml of 10% **Calcium Gluconate** IV (administered slowly over 10 minutes). * **Neuroprotection:** $MgSO_4$ is also used for fetal neuroprotection in anticipated preterm deliveries <32 weeks to reduce the risk of cerebral palsy.

Q: What is a common cause of recurrent missed abortion at 10 weeks gestation?

Chromosomal abnormality. **Explanation:** **1. Why Chromosomal Abnormality is Correct:** Chromosomal abnormalities are the most common cause of spontaneous pregnancy loss in the first trimester (up to 12 weeks), accounting for approximately 50–60% of cases. Even in cases of **recurrent** pregnancy loss, genetic factors remain a leading etiology. At 10 weeks gestation, an embryonic demise is most frequently due to **autosomal trisomies** (the most common being Trisomy 16), followed by polyploidy and Monosomy X (Turner syndrome). These defects lead to improper embryonic development, resulting in a missed abortion. **2. Analysis of Incorrect Options:** * **B. Cervical Incompetence:** This typically causes **painless cervical dilatation** leading to mid-trimester (second trimester) losses, usually between 16–24 weeks, rather than early first-trimester missed abortions. * **C. Corpus Luteum Failure:** While progesterone is vital for pregnancy maintenance, the placenta takes over progesterone production (luteal-placental shift) by **7–9 weeks**. Therefore, primary corpus luteum failure is an uncommon cause of loss as late as 10 weeks. * **D. Retroverted Uterus:** This is considered a **normal anatomical variant** in many women and does not increase the risk of miscarriage. It only rarely causes "incarceration of the uterus" in the second trimester, but not missed abortion. **3. NEET-PG High-Yield Pearls:** * **Most common chromosomal cause of abortion:** Autosomal trisomy (Overall). * **Most common specific trisomy:** Trisomy 16. * **Most common single chromosomal anomaly:** Monosomy X (45,X). * **Investigation of choice for Recurrent Pregnancy Loss (RPL):** Parental karyotyping to rule out balanced translocations. * **Definition of RPL (WHO):** 3 or more consecutive pregnancy losses before 20 weeks; however, ASRM defines it as 2 or more losses.

Q: A 25-week pregnant woman presents with hypertension (160/95 mmHg), proteinuria, generalized edema, hyperuricemia, and elevated liver enzymes. Which of the following usually provides definitive therapy for this condition?

Delivery. **Explanation:** The patient presents with classic features of **Preeclampsia with severe features** (BP ≥160/110 mmHg, proteinuria, and biochemical evidence of end-organ dysfunction like elevated liver enzymes and hyperuricemia). **Why Delivery is the Correct Answer:** The underlying pathophysiology of preeclampsia is rooted in **abnormal placentation** and placental ischemia, which triggers systemic endothelial dysfunction. Since the placenta is the source of the pathology, the only **definitive (curative) treatment** is the removal of the placenta, which is achieved through **delivery**. While the timing of delivery depends on gestational age and maternal-fetal stability, it remains the only way to halt the disease progression. **Why Other Options are Incorrect:** * **A. Antihypertensive medical therapy:** Drugs like Labetalol or Hydralazine are used to prevent maternal complications (e.g., stroke) but do not cure the disease or prevent its progression. * **C. Low-dose aspirin:** This is a **preventive** measure started early in pregnancy (before 16 weeks) for high-risk patients; it has no role as a definitive treatment once preeclampsia is established. * **D. Oxygen supplementation:** This is supportive care and does not address the underlying placental pathology. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC)** for seizure prophylaxis in preeclampsia/eclampsia: **Magnesium Sulfate ($MgSO_4$)** (Pritchard Regimen). * **Antidote for $MgSO_4$ toxicity:** Calcium Gluconate (10% solution, 10ml IV). * **Hyperuricemia** (Serum Uric acid >4.5 mg/dL) is a sensitive marker for the severity of preeclampsia and correlates with poor fetal outcomes. * **Definitive Management:** Delivery is indicated regardless of gestational age if there is evidence of HELLP syndrome, eclampsia, or placental abruption.

Q: Which of the following is an impending sign of eclampsia in pregnancy-induced hypertension (PIH)?

Visual symptoms. **Explanation:** The transition from pre-eclampsia to eclampsia is marked by "impending signs" that indicate severe multi-system involvement and cerebral irritability. **1. Why Visual Symptoms are Correct:** Visual disturbances (scotoma, blurring of vision, photophobia, or temporary blindness) are classic **premonitory signs** of eclampsia. They occur due to retinal artery vasospasm, retinal edema, or occipital lobe ischemia (as seen in PRES - Posterior Reversible Encephalopathy Syndrome). These symptoms, along with severe persistent headache and epigastric pain, indicate that a seizure is imminent. **2. Analysis of Incorrect Options:** * **Weight gain (2 lb/week):** While rapid weight gain due to occult edema is a diagnostic feature of pre-eclampsia, it is a non-specific finding and does not necessarily signal an immediate progression to seizures. * **Severe proteinuria (10 g):** According to current ACOG and NHBPEP guidelines, the *degree* of proteinuria is no longer used to classify "severity" or predict eclamptic fits. Massive proteinuria is a sign of renal involvement but not an impending sign of a seizure. * **Pedal Edema:** This is common in normal pregnancies (physiological) and is no longer included in the diagnostic criteria for PIH. It is not a reliable predictor of eclampsia. **Clinical Pearls for NEET-PG:** * **The "Triad" of Impending Eclampsia:** 1. Severe headache (frontal/occipital), 2. Epigastric/Right Upper Quadrant pain (liver capsule stretch), 3. Visual disturbances. * **Hyperreflexia:** Brisk patellar reflex (clonus) is a critical physical sign of neuromuscular irritability preceding a fit. * **Drug of Choice:** Magnesium Sulfate ($MgSO_4$) is the treatment of choice for both prophylaxis and management of eclamptic seizures (Pritchard Regimen).

Q: A 29-week pregnant patient presents with jaundice and severe pre-eclampsia (BP 170/110, urine albumin 3+). Investigations show Hb 7 gm%, platelet count 70,000, TLC 13,000, SGOT 230, bilirubin 2 mg/dL, and INR 2. What is the most likely diagnosis?

HELLP syndrome. **Explanation:** The clinical presentation of severe pre-eclampsia (BP 170/110, proteinuria) combined with biochemical evidence of multi-organ involvement points directly to **HELLP Syndrome** (Hemolysis, Elevated Liver enzymes, Low Platelets). **Why HELLP Syndrome is correct:** The diagnosis is based on the **Tennessee Classification** or **Mississippi Criteria**: * **Hemolysis:** Suggested by low Hb (7 gm%) and jaundice (bilirubin 2 mg/dL). * **Elevated Liver Enzymes:** SGOT (230 U/L) is significantly elevated (typically >70 U/L). * **Low Platelets:** Platelet count is 70,000/mm³ (Thrombocytopenia <100,000/mm³). The elevated INR (2) indicates impaired hepatic synthetic function or incipient DIC, which are known complications of severe HELLP. **Why other options are incorrect:** * **Acute Cholecystitis:** Presents with RUQ pain, fever, and Murphy’s sign; it does not explain severe hypertension, proteinuria, or profound thrombocytopenia. * **Hepatic Rupture:** A catastrophic complication of HELLP/Eclampsia presenting with sudden severe abdominal pain and hypovolemic shock. While possible, HELLP is the primary underlying diagnosis. * **IHCP:** Characterized by intense pruritus (palms/soles) and elevated bile acids. It does not cause hypertension, proteinuria, or hemolysis. **Clinical Pearls for NEET-PG:** * **Treatment of Choice:** Delivery is the definitive management (regardless of gestational age if >34 weeks or if maternal/fetal condition deteriorates). * **Dexamethasone:** Used to increase platelet counts in HELLP, though it doesn't improve maternal outcomes. * **Differential:** Always differentiate from **Acute Fatty Liver of Pregnancy (AFLP)**, where hypoglycemia and markedly prolonged PT/INR are more prominent than in HELLP.

Question 1

Which of the following conditions is NOT associated with decreased variability of fetal heart rate?

Accepted Answer

Fetal movement

Answer

Chronic hypoxia

Answer

Sleep

Answer

Acidemia

Question 2

What is the drug of choice for hypertensive emergencies in pregnancy?

Accepted Answer

Labetalol

Answer

Methyldopa

Answer

Nitroprusside

Answer

Nicardipine

Question 3

Rubin's diagnostic criteria is used for which of the following conditions?

Accepted Answer

Cervical pregnancy.

Answer

Ovarian pregnancy.

Answer

Hydatiform mole.

Answer

Abdominal pregnancy.

Question 4

During an antenatal check-up, a primigravida is found to be positive for Treponema pallidum infection. She is worried about her child. At which week of gestation does Treponema pallidum infection typically transfer to the fetus?

Accepted Answer

20th week

Answer

4th week

Answer

8th week

Answer

16th week

Question 5

Magnesium sulfate (MgSO4) is indicated in which of the following conditions?

Accepted Answer

Severe pre-eclampsia

Answer

Gestational trophoblastic disease

Answer

Gestational diabetes

Answer

Placenta previa

Question 6

What is a common cause of recurrent missed abortion at 10 weeks gestation?

Accepted Answer

Chromosomal abnormality

Answer

Cervical incompetence

Answer

Corpus luteum failure

Answer

Retroverted uterus

Question 7

A 25-week pregnant woman presents with hypertension (160/95 mmHg), proteinuria, generalized edema, hyperuricemia, and elevated liver enzymes. Which of the following usually provides definitive therapy for this condition?

Accepted Answer

Delivery

Answer

Antihypertensive medical therapy

Answer

Low dose aspirin

Answer

Oxygen supplementation

Question 8

Which of the following is an impending sign of eclampsia in pregnancy-induced hypertension (PIH)?

Accepted Answer

Visual symptoms

Answer

Weight gain of 2 lb per week

Answer

Severe proteinuria of 10 g

Answer

Pedal edema

Question 9

On transvaginal sonography (TVS), which of the following cervical shapes indicates a high chance of miscarriage?

Accepted Answer

U-shaped

Answer

T-shaped

Answer

Y-shaped

Answer

O-shaped

Question 10

A 29-week pregnant patient presents with jaundice and severe pre-eclampsia (BP 170/110, urine albumin 3+). Investigations show Hb 7 gm%, platelet count 70,000, TLC 13,000, SGOT 230, bilirubin 2 mg/dL, and INR 2. What is the most likely diagnosis?

Accepted Answer

HELLP syndrome

Answer

Acute Cholecystitis

Answer

Hepatic rupture

Answer

Intrahepatic Cholestasis of Pregnancy (IHCP)

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

On this page

Practice by Chapter

Want unlimited practice?