Maternal-Fetal Medicine — MCQs

A 20-year-old woman, gravida 3, para 2, has a screening ultrasound at 18 weeks' gestation that shows hydrops fetalis but no malformations. The woman's two previous pregnancies ended at term in live births. The current pregnancy results in a live birth at 36 weeks. Physical examination shows marked hydrops of the neonate and placenta. Laboratory studies show a cord blood hemoglobin level of 9.2 g/dL and total bilirubin concentration of 20.2 mg/dL. Which of the following laboratory findings is most likely to be present in this case?

Q185Easy

Supine hypotension syndrome occurs in which condition?

Q186Easy

Which of the following conditions is the most frequent cause of spontaneous abortion in the first trimester of pregnancy?

Q187Medium

When should a pregnant woman with a prosthetic valve be switched to heparin?

Q188Easy

Late deceleration in fetal heart rate monitoring is suggestive of:

Q189Medium

You are called to the operating room for a patient found to have an abdominal pregnancy with an 18-week fetus and placenta attached to the omentum during surgery for suspected appendicitis. What is the best course of action?

Q190Easy

All of the following are risk factors for IUGR except?

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 181: The Kleihaeur-Betke test is performed to detect:

A. Cephalopelvic disproportion
B. Fetomaternal hemorrhage (Correct Answer)
C. Karyotype of a normal fetus
D. Fetal infections

Explanation: ### Explanation **Correct Answer: B. Fetomaternal hemorrhage** The **Kleihaeur-Betke (KB) test** is the gold standard for quantifying the volume of **fetomaternal hemorrhage (FMH)**. The test relies on the physiological principle that **Fetal Hemoglobin (HbF)** is resistant to acid elution, whereas Adult Hemoglobin (HbA) is not. When a maternal blood smear is exposed to an acid bath, the adult red blood cells lose their hemoglobin and appear as "ghost cells." In contrast, fetal red blood cells retain their hemoglobin and appear dark pink/red under a microscope. By counting the ratio of fetal cells to maternal cells, clinicians can calculate the volume of fetal blood that has entered the maternal circulation. This is critical for determining the required dose of **Anti-D immunoglobulin (RhoGAM)** in Rh-negative mothers to prevent isoimmunization. **Why other options are incorrect:** * **A. Cephalopelvic disproportion:** This is a clinical or radiological diagnosis based on the relationship between the fetal head size and the maternal pelvic dimensions; it does not involve blood cell analysis. * **C. Karyotype of a normal fetus:** Fetal karyotyping requires genetic material obtained via amniocentesis or chorionic villus sampling (CVS), not an acid elution test of maternal blood. * **D. Fetal infections:** These are typically diagnosed via maternal serology (TORCH profile), PCR of amniotic fluid, or ultrasound markers. **High-Yield Clinical Pearls for NEET-PG:** * **Formula for Anti-D Dose:** Volume of FMH (mL) = (Fetal cells counted / Total cells counted) × 5000 mL. * **Standard Dose:** One 300 µg vial of Anti-D covers **30 mL of fetal whole blood** (or 15 mL of fetal packed RBCs). * **Indications:** Perform a KB test after trauma, placental abruption, or unexplained fetal death in Rh-negative women to ensure adequate immunoprophylaxis. * **Screening:** The **Rosette test** is often used as a qualitative screen; if positive, the KB test is performed for quantification.

Question 182: Abruptio placentae is a form of antepartum hemorrhage. Which among the following is the clinical classification system for abruptio placentae?

A. Macafee regimen
B. Johnson regimen
C. Apt test
D. Page classification (Correct Answer)

Explanation: **Explanation:** **Abruptio placentae** refers to the premature separation of a normally situated placenta from the uterine wall after 28 weeks of gestation. The **Page classification** is the standard clinical grading system used to assess the severity of abruption based on clinical signs and symptoms: * **Grade 0:** Asymptomatic; diagnosed retrospectively by finding a retroplacental clot after delivery. * **Grade 1 (Mild):** Vaginal bleeding is slight; no signs of maternal shock or fetal distress. * **Grade 2 (Moderate):** Increased bleeding; uterine tenderness and tetany are present. Fetal distress (tachycardia or late decelerations) is common. * **Grade 3 (Severe):** Severe bleeding (may be concealed); uterus is board-like and painful. Maternal shock is present, and fetal death is typical. This is further divided into 3A (without coagulopathy) and 3B (with coagulopathy/DIC). **Analysis of Incorrect Options:** * **Macafee and Johnson Regimen:** This is the protocol for the **expectant management of Placenta Previa**, aimed at prolonging pregnancy until fetal lung maturity is achieved (usually up to 37 weeks). * **Apt Test:** A biochemical test used to differentiate between **maternal and fetal blood**. It is specifically used in cases of suspected **Vasa Previa**, where fetal vessels rupture. **High-Yield Clinical Pearls for NEET-PG:** * **Most common risk factor:** Hypertension (Pregnancy-induced or chronic). * **Classic presentation:** Painful vaginal bleeding with a "woody hard" or "board-like" uterus. * **Couvelaire Uterus:** A complication of severe abruption where blood extravasates into the myometrium, giving the uterus a bluish/purplish mottled appearance. * **Most common cause of DIC in pregnancy:** Abruptio placentae.

Question 183: In Erythroblastosis fetalis, why is the first child typically spared?

A. The immune response during a second exposure is rapid.
B. Sensitization of Rh-negative mothers by a Rh-positive fetus generally occurs at birth. (Correct Answer)
C. Small amounts of fetal blood leak into the maternal circulation at the time of delivery.
D. Mothers develop significant titers of anti-Rh agglutinins during the postpartum period.

Explanation: ### Explanation **Core Concept: Rh Isoimmunization** Erythroblastosis fetalis (Hemolytic Disease of the Fetus and Newborn) occurs when an Rh-negative mother carries an Rh-positive fetus. The first child is typically spared because the maternal and fetal circulations are separated by the placental barrier during a normal pregnancy. Significant **feto-maternal hemorrhage (FMH)**—the mixing of fetal red blood cells into maternal circulation—usually occurs only during the **third stage of labor (delivery)** or during invasive procedures (e.g., amniocentesis). By the time the mother’s immune system recognizes the Rh-D antigen and produces antibodies, the first baby has already been delivered. The primary immune response produces **IgM antibodies**, which are too large to cross the placenta. It is only in subsequent pregnancies that the "memory" response produces **IgG antibodies**, which cross the placenta and cause hemolysis. **Analysis of Options:** * **Option B (Correct):** Sensitization (the initial trigger of the immune system) generally occurs at the time of birth, meaning the first baby is out of the womb before maternal antibodies can cause harm. * **Option A:** This describes the *anamnestic response* (secondary exposure), which explains why the *second* child is affected, not why the first is spared. * **Option C:** While true that blood leaks at delivery, this is the *mechanism* of sensitization, but Option B more directly addresses the timing that spares the first child. * **Option D:** While titers do develop postpartum, this is a consequence of sensitization, not the primary reason for the first child's safety. **High-Yield NEET-PG Pearls:** * **Critical Volume:** As little as **0.1 mL** of Rh-positive fetal blood can sensitize an Rh-negative mother. * **Prophylaxis:** Administer **Anti-D Gamma Globulin (300 mcg)** at 28 weeks and within 72 hours of delivery to prevent sensitization. * **Kleihauer-Betke Test:** Used to quantify the amount of fetal-maternal hemorrhage to calculate the required dose of Anti-D. * **Exception:** The first child may be affected if the mother was previously sensitized by a mismatched blood transfusion or an earlier miscarriage/ectopic pregnancy.

Question 184: A 20-year-old woman, gravida 3, para 2, has a screening ultrasound at 18 weeks' gestation that shows hydrops fetalis but no malformations. The woman's two previous pregnancies ended at term in live births. The current pregnancy results in a live birth at 36 weeks. Physical examination shows marked hydrops of the neonate and placenta. Laboratory studies show a cord blood hemoglobin level of 9.2 g/dL and total bilirubin concentration of 20.2 mg/dL. Which of the following laboratory findings is most likely to be present in this case?

A. Diminished glucocerebrosidase activity in fetal cells
B. Elevated maternal serum alpha-fetoprotein level
C. Positive Coombs test result on cord blood (Correct Answer)
D. Positive maternal hepatitis B surface antigen

Explanation: ### Explanation The clinical presentation of **Hydrops Fetalis** (generalized fetal edema involving at least two compartments) combined with severe neonatal anemia (Hb 9.2 g/dL) and profound hyperbilirubinemia (20.2 mg/dL) in a multiparous woman strongly suggests **Immune Hydrops** due to **Rh Isoimmunization**. **1. Why the Correct Answer is Right:** In Rh isoimmunization, maternal IgG antibodies (formed during previous pregnancies) cross the placenta and attack fetal Rh-positive red blood cells. This leads to **immune-mediated hemolysis**, resulting in anemia, extramedullary hematopoiesis, and congestive heart failure (hydrops). A **Positive Direct Coombs Test** on cord blood confirms the presence of maternal antibodies (anti-D) coated on the surface of the neonate's erythrocytes, confirming the diagnosis of hemolytic disease of the newborn (HDN). **2. Why the Other Options are Wrong:** * **A. Diminished glucocerebrosidase activity:** This is characteristic of Gaucher disease. While some lysosomal storage diseases can cause hydrops, they are rare and would not typically present with such acute neonatal hemolysis and hyperbilirubinemia. * **B. Elevated maternal serum alpha-fetoprotein (MSAFP):** MSAFP is a screening tool for neural tube defects and abdominal wall defects. While it can be elevated in hydrops, it is non-specific and does not explain the underlying hemolytic process. * **D. Positive maternal HBsAg:** Maternal Hepatitis B infection is associated with vertical transmission but does not cause immune hydrops or acute neonatal hemolysis. **3. Clinical Pearls for NEET-PG:** * **Immune Hydrops:** Most commonly due to RhD incompatibility. It typically affects the **second and subsequent** pregnancies. * **Non-Immune Hydrops:** Now more common than immune hydrops due to Rhogam prophylaxis. Causes include chromosomal anomalies (Turner syndrome), parvovirus B19 infection, and alpha-thalassemia (Hb Bart’s). * **Critical Titer:** An indirect Coombs test (ICT) titer of **1:16** is generally considered the critical threshold for monitoring fetal well-being via Middle Cerebral Artery (MCA) Doppler.

Question 185: Supine hypotension syndrome occurs in which condition?

A. Obesity
B. Ascites
C. Early pregnancy
D. Advanced pregnancy (Correct Answer)

Explanation: ### Explanation **Supine Hypotension Syndrome** (also known as Aortocaval Compression Syndrome) occurs primarily in **advanced pregnancy** (usually after 20 weeks of gestation). #### Why Advanced Pregnancy is Correct: The underlying mechanism is the **mechanical compression** of the **Inferior Vena Cava (IVC)** and the abdominal aorta by the gravid uterus when the woman lies in a supine position. 1. **Venous Return:** Compression of the IVC leads to a significant decrease in venous return to the heart (preload). 2. **Cardiac Output:** Reduced preload results in decreased stroke volume and cardiac output. 3. **Hypotension:** This manifests as a drop in maternal blood pressure, leading to symptoms like dizziness, nausea, pallor, and syncope. It can also cause fetal distress due to reduced placental perfusion. #### Why Other Options are Incorrect: * **Early Pregnancy:** The uterus is still a pelvic organ or not large enough to exert significant pressure on the retroperitoneal vessels. * **Obesity & Ascites:** While these conditions increase intra-abdominal pressure, they rarely cause the acute, posture-dependent vascular collapse seen in pregnancy. The gravid uterus is a unique, solid, and heavy mass that specifically targets the IVC when supine. #### NEET-PG High-Yield Pearls: * **Management:** The immediate treatment is the **Left Lateral Position**, which shifts the uterus off the IVC, restoring venous return. * **Aortic Compression:** While IVC compression causes maternal hypotension, compression of the **Aorta** can lead to "Poseiro Effect" (fetal hypoxemia without maternal hypotension). * **Clinical Tip:** During CPR in a pregnant woman, manual **Left Uterine Displacement (LUD)** is a critical step to ensure effective chest compressions.

Question 186: Which of the following conditions is the most frequent cause of spontaneous abortion in the first trimester of pregnancy?

A. Abruptio placentae
B. Chorioamnionitis
C. Chromosomal abnormalities (Correct Answer)
D. Placenta previa

Explanation: **Explanation:** **1. Why Chromosomal Abnormalities is Correct:** Chromosomal abnormalities are the single most common cause of spontaneous abortion, accounting for approximately **50-60%** of all first-trimester miscarriages. Among these, **Autosomal Trisomies** are the most frequent (Trisomy 16 being the most common specific trisomy), followed by Monosomy X (Turner Syndrome) and Polyploidy. These genetic errors usually occur de novo during gametogenesis or early fertilization, leading to non-viable embryos that the body naturally expels. **2. Why Other Options are Incorrect:** * **Abruptio Placentae (A):** This is the premature separation of the placenta, typically occurring in the **third trimester**. It is a cause of antepartum hemorrhage and fetal distress, not first-trimester spontaneous abortion. * **Chorioamnionitis (B):** This is an intra-amniotic infection usually associated with prolonged rupture of membranes. While it can cause mid-trimester loss or preterm labor, it is not the leading cause of early first-trimester miscarriage. * **Placenta Previa (D):** This refers to the placenta covering the internal os. Like abruption, it is a cause of **late-pregnancy bleeding** (antepartum hemorrhage) and does not cause first-trimester spontaneous abortion. **3. NEET-PG High-Yield Pearls:** * **Most common Trisomy in miscarriages:** Trisomy 16. * **Most common single chromosomal anomaly:** Monosomy X (45, X). * **Second most common cause of miscarriage:** Maternal endocrine factors (e.g., Luteal Phase Defect, uncontrolled Diabetes). * **Recurrent Pregnancy Loss (RPL):** Defined as $\geq$ 2 consecutive spontaneous abortions; the most common treatable cause is Antiphospholipid Antibody Syndrome (APS).

Question 187: When should a pregnant woman with a prosthetic valve be switched to heparin?

A. 28 weeks gestation
B. 32 weeks gestation
C. 36 weeks gestation (Correct Answer)
D. Postpartum

Explanation: **Explanation:** The management of anticoagulation in pregnant women with prosthetic heart valves is a high-stakes clinical scenario. The primary goal is to balance the risk of maternal valve thrombosis with the risk of fetal hemorrhage and teratogenicity. **Why 36 weeks is the correct answer:** Warfarin (Oral Anticoagulant) is highly effective at preventing maternal valve thrombosis but crosses the placenta. If a patient is on Warfarin during labor, the fetus—which has an immature liver and low levels of clotting factors—is at high risk of **intracranial hemorrhage** during the birth process. Therefore, Warfarin must be discontinued and replaced with **Unfractionated Heparin (UFH)** or **Low Molecular Weight Heparin (LMWH)** at **36 weeks gestation**. Heparin does not cross the placenta, ensuring the fetus has normal coagulation status by the time labor begins. **Analysis of Incorrect Options:** * **28 & 32 weeks (A & B):** Switching this early unnecessarily increases the risk of maternal valve thrombosis. Warfarin is superior to Heparin for maternal protection; thus, it is continued as long as safely possible until near-term. * **Postpartum (D):** Waiting until after delivery is dangerous. If the patient goes into labor while on Warfarin, the risk of fetal death due to hemorrhage is extremely high. **High-Yield Clinical Pearls for NEET-PG:** * **Warfarin Embryopathy:** Occurs if Warfarin is used between **6–12 weeks** (features: nasal hypoplasia, stippled epiphyses). * **The "Switch" Protocol:** * **<6 weeks:** Warfarin. * **6–12 weeks:** Switch to Heparin (to avoid embryopathy). * **13–36 weeks:** Warfarin (safest for the mother). * **>36 weeks:** Switch to Heparin (to avoid fetal hemorrhage during delivery). * **Labor Management:** UFH is typically stopped 4–6 hours before delivery; LMWH is stopped 24 hours before. Warfarin is usually restarted 6–12 hours after an uncomplicated delivery.

Question 188: Late deceleration in fetal heart rate monitoring is suggestive of:

A. Fetal hypoxia (Correct Answer)
B. Head compression
C. Cord compression
D. Fetal death

Explanation: **Explanation:** **Late decelerations** are characterized by a gradual decrease in fetal heart rate (FHR) that begins *after* the peak of the uterine contraction and returns to baseline only after the contraction has ended. This pattern is a hallmark sign of **uteroplacental insufficiency**. During a contraction, uterine blood flow decreases; if the placental reserve is already low, the fetus experiences a drop in $PO_2$ below the critical threshold. This triggers chemoreceptors, leading to a vagal response and myocardial depression, resulting in **fetal hypoxia** and metabolic acidosis. **Analysis of Incorrect Options:** * **B. Head Compression:** This causes **Early Decelerations**. The pressure on the fetal head increases vagal tone, causing a heart rate dip that mirrors the contraction (the nadir of the FHR coincides with the peak of the contraction). It is considered physiological. * **C. Cord Compression:** This leads to **Variable Decelerations**. These are abrupt in onset and offset and vary in timing relative to contractions. They are the most common type of deceleration seen in labor. * **D. Fetal Death:** While hypoxia can lead to death, late decelerations are a sign of a struggling, live fetus. Fetal death is confirmed by the absence of cardiac activity on ultrasound or Doppler. **High-Yield Clinical Pearls for NEET-PG:** * **VEAL CHOP Mnemonic:** **V**ariable = **C**ord; **E**arly = **H**ead; **A**ccelerations = **O**k (Oxygenated); **L**ate = **P**lacenta. * Late decelerations are categorized as **Category III** (Abnormal) if associated with absent variability, requiring immediate resuscitation or delivery. * The first step in management is "intrauterine resuscitation": Left lateral position, oxygen, IV fluids, and stopping oxytocin.

Question 189: You are called to the operating room for a patient found to have an abdominal pregnancy with an 18-week fetus and placenta attached to the omentum during surgery for suspected appendicitis. What is the best course of action?

A. Removal of both fetus and placenta
B. Laparoscopic ligation of the umbilical cord
C. Removal of the fetus only (Correct Answer)
D. Closely follow until viability and then deliver by laparotomy

Explanation: **Explanation:** The management of abdominal pregnancy is a high-stakes scenario in maternal-fetal medicine. The primary challenge is the **placenta**, which lacks the contractile myometrium of the uterus to control bleeding after separation. **1. Why "Removal of the fetus only" is correct:** In abdominal pregnancies, the placenta often attaches to highly vascular organs (like the omentum, bowel, or major vessels). Attempting to detach the placenta can lead to **uncontrollable, life-threatening hemorrhage**. The standard recommendation is to ligate the umbilical cord close to the placenta and leave the placenta *in situ*. It is then allowed to undergo spontaneous resorption, which can be monitored using serial β-hCG levels and ultrasound. Methotrexate may occasionally be used to accelerate this process. **2. Why the other options are incorrect:** * **Option A:** Removing the placenta is contraindicated unless it is attached to a simple, pedicled structure (like the omentum) that can be easily ligated and removed entirely. However, as a general rule for exams, "leaving the placenta" is the safest answer to prevent surgical catastrophe. * **Option B:** While the cord is ligated, the fetus must be removed to prevent infection, lithopedion formation, or further complications. * **Option D:** Abdominal pregnancy carries a very high risk of maternal mortality and fetal anomalies (due to oligohydramnios). Expectant management until viability is rarely recommended and is extremely hazardous. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Often suggested by "easily palpable fetal parts" and an "empty uterus" on ultrasound. * **Management of Placenta:** If left behind, the patient is at risk for bowel obstruction and infection. * **Most common site:** The Pouch of Douglas. * **Key Rule:** Never attempt to peel the placenta off a vital organ.

Question 190: All of the following are risk factors for IUGR except?

A. Maternal diabetes (Correct Answer)
B. Severe Anemia
C. Placental infarcts
D. In utero infection

Explanation: **Explanation:** The correct answer is **Maternal Diabetes**. In the context of pregnancy, maternal diabetes (especially Gestational Diabetes or Type 2 Diabetes without vascular complications) is typically associated with **fetal macrosomia** (birth weight >4000g) rather than Intrauterine Growth Restriction (IUGR). This occurs because maternal hyperglycemia leads to fetal hyperglycemia, which stimulates the fetal pancreas to produce excess insulin. Since insulin is a potent growth-promoting hormone, it results in excessive fetal fat deposition and organomegaly. **Analysis of other options:** * **Severe Anemia:** Maternal hemoglobin <7 g/dL leads to chronic fetal hypoxia and reduced oxygen delivery to the placenta, which is a well-established cause of IUGR. * **Placental Infarcts:** These represent areas of placental tissue death, reducing the functional surface area for nutrient and gas exchange (placental insufficiency), directly leading to growth restriction. * **In utero infection:** TORCH infections (especially CMV and Rubella) cause IUGR by reducing cell proliferation and causing direct fetal tissue damage. **High-Yield Clinical Pearls for NEET-PG:** * **The Exception:** While diabetes usually causes macrosomia, **Pre-gestational Diabetes with vascular complications** (White’s Classification Class R, F, or H) can cause IUGR due to compromised uterine blood flow. * **Symmetrical vs. Asymmetrical IUGR:** Infections and chromosomal anomalies usually cause *Symmetrical IUGR* (early onset), while placental insufficiency (like infarcts or preeclampsia) causes *Asymmetrical IUGR* (late onset, "head-sparing"). * **Ponderal Index:** Used to differentiate types of IUGR; it is low in asymmetrical IUGR.

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

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