Maternal-Fetal Medicine — MCQs

A 32-week pregnant woman, who was HBsAg positive during her first pregnancy 8 years ago, presents with normal LFT, HBsAg positive, HBeAg negative, and HBV DNA of 90,000 copies/ml. Her first child received hepatitis B immunoglobulin and vaccination shortly after birth and is currently HBsAg negative. Which of the following statements is true regarding this current scenario?

Q140Medium

A 30 weeks pregnant multigravida presents with hypertension, proteinuria, and pedal edema. Which antihypertensive medication is appropriate for managing the blood pressure in this patient?

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 131: Which of the following is/are NOT a fetal complication of uncontrolled diabetes during pregnancy?

A. Stillbirth
B. Chromosomal anomaly
C. Neural tube defect (NTD)
D. Intrauterine growth restriction (IUGR) (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Intrauterine growth restriction (IUGR)**. In uncontrolled maternal diabetes, the primary fetal growth complication is **Macrosomia** (birth weight >4kg), not IUGR. This occurs due to the **Pedersen Hypothesis**: maternal hyperglycemia leads to fetal hyperglycemia, which stimulates the fetal pancreas to secrete excess **insulin**. Since fetal insulin acts as a potent growth hormone, it causes excessive fat deposition and organomegaly. IUGR is typically seen in diabetic pregnancies only if there is underlying **maternal vascular disease** (e.g., White’s Class F or R), which impairs placental perfusion. **Why other options are incorrect:** * **A. Stillbirth:** Uncontrolled diabetes increases the risk of unexplained late-trimester stillbirth, often attributed to fetal acidemia and hyperglycemia-induced hypoxia. * **B. Chromosomal anomaly:** Diabetes is a **teratogen**, causing structural malformations, but it does **not** cause chromosomal numerical or structural abnormalities (like Trisomy 21). *Note: While technically not caused by diabetes, in the context of this standard MCQ, IUGR is the "more" correct answer as diabetes is classically associated with overgrowth.* * **C. Neural tube defect (NTD):** Hyperglycemia during organogenesis (first 8 weeks) is highly teratogenic. NTDs are 10 times more common in diabetic pregnancies. **High-Yield Clinical Pearls for NEET-PG:** * **Most common malformation:** Cardiac defects (specifically Ventricular Septal Defect). * **Most specific malformation:** Caudal Regression Syndrome (Sacral Agenesis). * **Most common neonatal metabolic complication:** Hypoglycemia (due to persistent fetal hyperinsulinemia after the cord is cut). * **Other complications:** Polyhydramnios, Hypocalcemia, Hyperbilirubinemia, and Respiratory Distress Syndrome (insulin inhibits surfactant production).

Question 132: Brain sparing effect on Doppler is seen in which fetal vessel?

A. Umbilical artery
B. Fetal Middle Cerebral Artery (MCA) (Correct Answer)
C. Fetal ductus venosus
D. Uterine artery

Explanation: **Explanation:** The **Brain Sparing Effect** is a compensatory hemodynamic mechanism seen in fetuses experiencing chronic hypoxia, most commonly due to Fetal Growth Restriction (FGR) or placental insufficiency. **1. Why the Middle Cerebral Artery (MCA) is correct:** Under normal conditions, the fetal MCA is a high-resistance vessel with low diastolic flow. When hypoxia occurs, the fetus redistributes its cardiac output to prioritize vital organs (brain, heart, and adrenals). This leads to **vasodilation** of the MCA to increase blood flow to the brain. On Doppler, this manifests as **increased end-diastolic flow** and a **decreased Pulsatility Index (PI)**. This shift from high to low resistance is the hallmark of the "Brain Sparing Effect." **2. Why the other options are incorrect:** * **Umbilical Artery:** In placental insufficiency, resistance in the umbilical artery *increases* (reduced, absent, or reversed end-diastolic flow). It reflects placental status, not the compensatory "sparing" of the brain. * **Ductus Venosus:** This is a late marker of fetal cardiac decompensation. Changes here (like an absent or reversed 'a' wave) indicate right heart strain and are an ominous sign, occurring after the brain-sparing effect has already failed. * **Uterine Artery:** This reflects maternal blood flow to the placenta. High resistance or "notching" in the uterine artery indicates impaired trophoblastic invasion and a risk for preeclampsia/FGR, but it does not represent fetal redistribution. **High-Yield Clinical Pearls for NEET-PG:** * **Cerebro-Placental Ratio (CPR):** Calculated as MCA-PI / Umbilical Artery-PI. A CPR < 1 is an early and sensitive marker of fetal hypoxia. * **Sequence of Doppler changes:** Umbilical Artery (Increased resistance) → MCA (Vasodilation/Brain Sparing) → Ductus Venosus (Reversed 'a' wave). * **Management:** While brain sparing is a protective mechanism, its presence indicates significant stress and necessitates close monitoring or delivery.

Question 133: Which of the following is true regarding early deceleration in a cardiotocography (CTG)?

A. It is due to increased vagal tone in the fetus. (Correct Answer)
B. It is due to fetal hypoxia.
C. It is due to raised blood pressure in the mother.
D. It is due to cord compression.

Explanation: ### Explanation **1. Why Option A is Correct:** Early decelerations are characterized by a gradual decrease and return of the fetal heart rate (FHR) that coincides with the peak of a uterine contraction (the "mirror image" pattern). The underlying mechanism is **fetal head compression**. When the fetal head is compressed during a contraction, it leads to an increase in intracranial pressure, which stimulates the **vagus nerve**. This increased vagal tone results in a transient slowing of the heart rate. Because it is a physiological reflex rather than a sign of distress, early decelerations are considered benign. **2. Why the Other Options are Incorrect:** * **Option B (Fetal Hypoxia):** This is associated with **Late Decelerations**. Late decelerations occur due to uteroplacental insufficiency, where reduced blood flow during contractions leads to fetal hypoxia and metabolic acidosis. * **Option C (Raised Maternal BP):** Maternal hypertension (e.g., Preeclampsia) is a risk factor for uteroplacental insufficiency, which would more likely cause *late* decelerations, not early ones. * **Option D (Cord Compression):** This is the hallmark cause of **Variable Decelerations**. These are abrupt in onset and vary in shape and timing relative to contractions. **3. High-Yield Clinical Pearls for NEET-PG:** * **Early Deceleration:** "Mirror image" of contraction; Nadir of FHR matches Peak of contraction; Cause: **Head compression** (Vagal). * **Late Deceleration:** Nadir of FHR occurs *after* the peak of contraction; Cause: **Uteroplacental insufficiency** (Hypoxia). * **Variable Deceleration:** Most common type; V-shaped; Cause: **Umbilical cord compression**. * **Sinusoidal Pattern:** Associated with severe **fetal anemia** (e.g., Rh isoimmunization) or fetal hemorrhage. * **Management:** Early decelerations require no active intervention; they are not indicative of fetal compromise.

Question 134: Which of the following is NOT a fetal heart tracing finding in maternal carbon monoxide poisoning?

A. Elevated baseline
B. Absence of accelerations
C. Marked beat-to-beat variability (Correct Answer)
D. Decreased beat-to-beat variability

Explanation: **Explanation:** Maternal carbon monoxide (CO) poisoning leads to fetal hypoxia through two primary mechanisms: the formation of **carboxyhemoglobin (COHb)**, which reduces the oxygen-carrying capacity of blood, and a **leftward shift of the oxyhemoglobin dissociation curve**, which prevents the release of oxygen to fetal tissues. **Why "Marked beat-to-beat variability" is the correct answer:** Fetal hypoxia typically leads to a **depression** of the fetal central nervous system (CNS). In cases of CO poisoning, the resulting hypoxia and acidosis cause a **decrease** in variability, not an increase. Marked (saltatory) variability is usually associated with acute umbilical cord compression or early hypoxia, but it is not a characteristic finding of the profound, systemic cellular hypoxia caused by CO poisoning. **Analysis of incorrect options:** * **Elevated baseline (Tachycardia):** This is an early compensatory response to fetal hypoxia as the fetus attempts to increase cardiac output to maintain tissue perfusion. * **Absence of accelerations:** Accelerations signify a healthy, reactive CNS. In CO poisoning, the hypoxic state leads to a non-reactive stress test (NST). * **Decreased beat-to-beat variability:** This is a hallmark finding of fetal acidemia and CNS depression resulting from prolonged or severe CO exposure. **Clinical Pearls for NEET-PG:** * **Affinity:** CO has an affinity for hemoglobin **200–250 times** greater than oxygen. * **Fetal Impact:** Fetal COHb levels are typically **10–15% higher** than maternal levels because fetal hemoglobin has an even higher affinity for CO, and clearance is slower. * **Treatment:** The definitive treatment is **100% normobaric oxygen** for the mother. Hyperbaric oxygen (HBO) is indicated if the mother is unconscious, has neurological symptoms, or has a COHb level >20%.

Question 135: Absent stomach bubble on antenatal ultrasonography is an important finding for the antenatal diagnosis of?

A. Congenital heart disease in the fetus
B. Esophageal atresia in the fetus (Correct Answer)
C. Omphalocele in the fetus
D. Spina bifida in the fetus

Explanation: **Explanation:** The presence of a fluid-filled **stomach bubble** on antenatal ultrasonography is a marker of a functional upper gastrointestinal tract. Fetal swallowing of amniotic fluid begins around 10–12 weeks; this fluid then passes through the esophagus into the stomach. **1. Why Esophageal Atresia is correct:** In **Esophageal Atresia (EA)**, there is a physical discontinuity of the esophagus. If there is no distal tracheoesophageal fistula (TEF), or if the fistula is too narrow, the swallowed amniotic fluid cannot reach the stomach. This results in an **absent or persistently small stomach bubble**. This finding is often associated with **polyhydramnios**, as the fetus cannot effectively recirculate amniotic fluid. Note: In 90% of cases (Type C EA with distal TEF), a small stomach bubble may still be seen due to air/fluid entering from the trachea. **2. Why other options are incorrect:** * **Congenital heart disease:** Typically diagnosed via fetal echocardiography (e.g., four-chamber view abnormalities). It does not directly affect the presence of the stomach bubble. * **Omphalocele:** This is a ventral wall defect where bowel loops (and sometimes the liver) herniate into the umbilical cord. While the stomach may be displaced into the sac, it is usually visible. * **Spina bifida:** A neural tube defect diagnosed by visualizing spinal dysraphism or cranial signs (Lemon/Banana signs). It does not interfere with swallowing. **Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Absent Stomach Bubble:** Esophageal atresia, diaphragmatic hernia (stomach moved into the chest), facial clefts/masses (inability to swallow), or neuromuscular disorders. * **VACTERL Association:** Always screen for Vertebral, Anal, Cardiac, TEF, Renal, and Limb anomalies when EA is suspected. * **Double Bubble Sign:** Distinct from "absent bubble," this indicates **Duodenal Atresia**.

Question 136: Which of the following statements is true regarding Acute Fatty Liver of Pregnancy?

A. Occurs due to LCHAD deficiency (long-chain 3-hydroxyacyl coenzyme A dehydrogenase) (Correct Answer)
B. Characterized by macrovesicular steatosis with periportal sparing
C. Associated with an increase in fibrinogen, ammonia, and SGOT
D. Most cases are asymptomatic

Explanation: **Acute Fatty Liver of Pregnancy (AFLP)** is a rare but life-threatening obstetric emergency occurring in the third trimester. ### **Explanation of the Correct Answer** **Option A** is correct. AFLP is strongly associated with a fetal deficiency of the enzyme **Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD)**. This is an autosomal recessive mitochondrial fatty acid oxidation disorder. When the fetus cannot oxidize long-chain fatty acids, these metabolites accumulate and enter the maternal circulation. The mother’s liver, already stressed by pregnancy, cannot process this excess load, leading to hepatocyte toxicity and failure. ### **Analysis of Incorrect Options** * **Option B:** AFLP is characterized by **microvesicular** steatosis (small fat droplets) that typically involves the **centrilobular** (Zone 3) area, not macrovesicular steatosis with periportal sparing. * **Option C:** AFLP leads to liver failure, resulting in a **decrease** in fibrinogen (due to consumption/coagulopathy) and an **increase** in ammonia and SGOT/SGPT. Hypoglycemia is also a hallmark finding. * **Option D:** AFLP is never asymptomatic; it is a critical illness presenting with nausea, vomiting, abdominal pain, jaundice, and often progresses to multi-organ failure or DIC. ### **High-Yield Clinical Pearls for NEET-PG** * **Swansea Criteria:** Used for clinical diagnosis (includes jaundice, hypoglycemia, elevated urate, and ultrasound findings). * **Gold Standard Diagnosis:** Liver biopsy (though rarely done due to coagulopathy risk). * **Management:** Immediate stabilization and **urgent delivery** regardless of gestational age. * **Key Lab Triad:** Hypoglycemia + Hyperuricemia + Elevated Ammonia. * **Differential:** Unlike HELLP syndrome, AFLP is more likely to cause significant hypoglycemia and prolonged PT/INR.

Question 137: Presence of gas in the great vessels of a fetus indicates which of the following?

A. Fetal distress
B. Postmature fetus
C. Fetal death (Correct Answer)
D. Premature fetus

Explanation: **Explanation:** The presence of gas in the fetal heart or great vessels (aorta and vena cava) is known as **Robert’s Sign**. This is a classic radiological sign of **intrauterine fetal death (IUFD)**. **Why it occurs:** When a fetus dies, the blood undergoes decomposition and fermentation. This process releases gases (primarily nitrogen, along with some oxygen and carbon dioxide) into the circulatory system. On an X-ray or ultrasound, this appears as linear or branching radiolucency within the fetal trunk. It is one of the earliest signs of fetal death, often appearing within 12 to 24 hours after cessation of the fetal heartbeat. **Analysis of Incorrect Options:** * **A. Fetal distress:** This is a clinical state of hypoxia during labor or pregnancy, usually diagnosed via abnormal fetal heart rate patterns or biophysical profile. It does not involve gas formation. * **B & D. Postmature/Premature fetus:** These terms refer to the gestational age of the fetus (post-term vs. pre-term). Neither condition causes spontaneous gas formation in the vessels unless fetal death has occurred. **High-Yield Clinical Pearls for NEET-PG:** * **Robert’s Sign:** Gas in the fetal great vessels (earliest sign, ~12 hours). * **Spalding’s Sign:** Overlapping of fetal skull bones due to liquefaction of the brain and loss of alignment (appears after 4–7 days). * **Deuel’s Halo Sign:** Elevation of the fetal scalp fat due to edema, creating a "halo" appearance. * **Curvature of the Spine:** Excessive angulation or collapse of the fetal spine due to loss of muscle tone. * **Gold Standard:** Today, the definitive diagnosis of IUFD is made via **ultrasound** by demonstrating the absence of fetal cardiac activity.

Question 138: Which of the following conditions is NOT associated with twin pregnancy?

A. Pre-eclampsia
B. Oligohydramnios (Correct Answer)
C. Antepartum hemorrhage
D. Atonic uterus

Explanation: In twin pregnancies, the physiological and mechanical demands on the mother and the fetuses are significantly increased, leading to specific complications. **Why Oligohydramnios is the Correct Answer:** Twin pregnancy is typically associated with **Polyhydramnios** (excess amniotic fluid), not oligohydramnios. This occurs due to increased fetal urine production from two fetuses and is especially common in Monochorionic Diamniotic (MCDA) twins as a component of Twin-to-Twin Transfusion Syndrome (TTTS), where the recipient twin develops polyhydramnios. While oligohydramnios can occur in the "stuck twin" (donor) in TTTS, it is a complication of the *syndrome*, whereas the pregnancy as a whole is classically associated with an increased total liquor volume. **Explanation of Incorrect Options:** * **Pre-eclampsia:** The risk is 2–3 times higher in multifetal gestations due to increased placental mass and higher levels of anti-angiogenic factors (sFlt-1). * **Antepartum Hemorrhage (APH):** There is an increased risk of both **Placenta Previa** (due to the larger surface area of the placenta(s) encroaching on the lower segment) and **Abruptio Placentae** (often following the sudden decompression after the birth of the first twin). * **Atonic Uterus:** Overdistension of the myometrium by multiple fetuses and polyhydramnios leads to poor uterine contractility after delivery, making **Postpartum Hemorrhage (PPH)** a major risk. **NEET-PG High-Yield Pearls:** * **Most common complication:** Anemia (Iron deficiency). * **Most common fetal complication:** Prematurity. * **TTTS:** Occurs only in Monochorionic twins; characterized by "Poly-Oli" sequence (Polyhydramnios in recipient, Oligohydramnios in donor). * **Weight gain:** Recommended weight gain for a normal BMI woman with twins is 17–25 kg.

Question 139: A 32-week pregnant woman, who was HBsAg positive during her first pregnancy 8 years ago, presents with normal LFT, HBsAg positive, HBeAg negative, and HBV DNA of 90,000 copies/ml. Her first child received hepatitis B immunoglobulin and vaccination shortly after birth and is currently HBsAg negative. Which of the following statements is true regarding this current scenario?

A. There is a very high risk of hepatitis B transmission to the baby.
B. Entecavir is safe in pregnancy and should be started as early as possible for the mother.
C. Antiviral therapy against hepatitis B is contraindicated in pregnancy.
D. The patient can be monitored without antivirals, and the baby should receive immunoglobulin and active immunization soon after delivery. (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** The management of Hepatitis B in pregnancy is primarily determined by the **HBV DNA viral load**. According to current guidelines (AASLD/EASL), antiviral therapy is recommended in the third trimester only if the HBV DNA is **>200,000 IU/ml** (or >10^6 copies/ml) to reduce the risk of Mother-to-Child Transmission (MTCT). In this case, the patient’s viral load is **90,000 copies/ml**, which is below the threshold for initiating maternal antiviral therapy. Therefore, the standard protocol is to monitor the mother and ensure the neonate receives **Hepatitis B Immune Globulin (HBIG)** and the **Hepatitis B vaccine** within 12 hours of birth. This "passive-active" immunization is >90% effective in preventing transmission when the maternal viral load is low. **2. Why Other Options are Incorrect:** * **Option A:** The risk of transmission is significantly lower when the mother is **HBeAg negative** and has a low viral load (<200,000 IU/ml), especially with neonatal immunoprophylaxis. * **Option B:** While antivirals are used in pregnancy, **Tenofovir (TDF)** is the drug of choice due to its safety profile and high resistance barrier. **Entecavir** is generally avoided in pregnancy due to potential concerns regarding fetal safety (Category C). * **Option C:** Antiviral therapy is **not contraindicated**; it is specifically indicated for mothers with high viral loads (>200,000 IU/ml) starting at 28–32 weeks gestation. **3. Clinical Pearls for NEET-PG:** * **Drug of Choice:** Tenofovir (TDF) is the preferred antiviral for HBV in pregnancy. * **Threshold for Treatment:** HBV DNA >200,000 IU/ml (approx. 10^6 copies/ml). * **Timing:** Start antivirals at 28–32 weeks of gestation if the threshold is met. * **Breastfeeding:** HBsAg-positive mothers **can breastfeed** safely, even if taking Tenofovir, as the drug concentration in breast milk is minimal. * **Mode of Delivery:** Cesarean section is **not** routinely recommended solely to reduce HBV transmission.

Question 140: A 30 weeks pregnant multigravida presents with hypertension, proteinuria, and pedal edema. Which antihypertensive medication is appropriate for managing the blood pressure in this patient?

A. Guanethidine
B. Labetalol (Correct Answer)
C. Atenolol
D. Captopril

Explanation: **Explanation:** The patient presents with the classic triad of **Preeclampsia** (hypertension, proteinuria, and edema after 20 weeks of gestation). The primary goal of antihypertensive therapy in pregnancy is to prevent maternal cerebrovascular accidents without compromising uteroplacental blood flow. **Why Labetalol is Correct:** **Labetalol** is a combined alpha- and beta-adrenergic blocker. It is considered a **first-line agent** for managing hypertension in pregnancy because it effectively lowers blood pressure while maintaining stroke volume and preserving blood flow to the placenta. It has a rapid onset of action and a well-established safety profile for the fetus. **Why the Other Options are Incorrect:** * **Guanethidine (A):** This is a post-ganglionic sympathetic blocker that is rarely used in modern medicine due to its severe side effect profile, including orthostatic hypotension and interference with uterine blood flow. * **Atenolol (C):** While a beta-blocker, Atenolol is generally avoided in pregnancy (especially long-term use) as it is associated with **fetal growth restriction (IUGR)** and placental necrosis. * **Captopril (D):** ACE inhibitors (and ARBs) are strictly **contraindicated** in the second and third trimesters. They cause significant fetal toxicity, including renal dysgenesis, oligohydramnios, skull hypoplasia, and fetal death. **High-Yield Clinical Pearls for NEET-PG:** * **First-line oral drugs for Chronic HTN/Preeclampsia:** Labetalol (most preferred), Methyldopa (safest over long term), and Nifedipine (long-acting). * **Drugs for Hypertensive Emergency in Pregnancy:** IV Labetalol, IV Hydralazine, or Oral Nifedipine. * **Drug of Choice for Eclampsia seizures:** Magnesium Sulfate ($MgSO_4$)—not an antihypertensive, but essential for seizure prophylaxis. * **Contraindicated drugs:** ACE inhibitors, ARBs, Sodium Nitroprusside (risk of fetal cyanide poisoning), and Diuretics (unless pulmonary edema is present).

Practice by Chapter

Fetal Assessment Techniques

Practice Questions

Hypertensive Disorders in Pregnancy

Practice Questions

Intrauterine Growth Restriction

Practice Questions

Multiple Gestation

Practice Questions

Rh Isoimmunization and Other Blood Group Incompatibilities

Practice Questions

Intrauterine Fetal Therapy

Practice Questions

Prenatal Diagnosis and Genetic Counseling

Practice Questions

Placental Abnormalities

Practice Questions

Preterm Labor and Delivery

Practice Questions

Management of Medical Disorders in Pregnancy

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free