Maternal-Fetal Medicine Practice Questions

Q: Which is the most common complication in monoamniotic twins?

Intertwining. **Explanation:** Monoamniotic-monochorionic (MoMo) twins occur when the zygote divides late, between **8 to 12 days** post-fertilization. Because both fetuses reside in a single amniotic sac without a dividing membrane, they are at unique risk for specific complications. **1. Why "Intertwining" is correct:** **Cord entanglement (Intertwining)** is the most common and characteristic complication of monoamniotic twins, occurring in nearly **100% of cases** in utero. As the fetuses move within the single sac, their umbilical cords inevitably twist around each other. While not always fatal, it can lead to sudden cord occlusion and fetal demise, which is why these pregnancies are managed with intensive monitoring and elective Cesarean delivery (usually at 32–34 weeks). **2. Analysis of Incorrect Options:** * **Discordance (A):** While growth discordance occurs in twins, it is more classically associated with Twin-to-Twin Transfusion Syndrome (TTTS) in diamniotic-monochorionic twins. * **Cord entanglement (B):** In many textbooks and exams, "Intertwining" and "Cord entanglement" are used interchangeably; however, "Intertwining" is the preferred clinical term for the specific phenomenon of the two cords wrapping around one another. * **Conjoined twins (C):** This is a rare complication occurring only if the zygote divides even later (**after 13 days**). While specific to monoamniotic gestations, it is far less common than cord intertwining. **High-Yield Clinical Pearls for NEET-PG:** * **Timing of Division:** 0–72 hours (Di-Di), 4–8 days (Mo-Di), 8–12 days (Mo-Mo), >13 days (Conjoined). * **Management:** MoMo twins require inpatient monitoring from 24–28 weeks and delivery via **LSCS by 32–34 weeks** to prevent late-term fetal death from cord accidents. * **The "T-sign" vs. "Lambda sign":** MoMo twins show **neither**; there is no dividing membrane at all.

Q: What is the approximate recurrence risk for neural tube defects (NTDs) in a subsequent pregnancy, given that the first baby was born with an NTD?

4%. **Explanation:** Neural tube defects (NTDs) follow a **multifactorial inheritance** pattern, meaning they result from a combination of genetic predisposition and environmental factors (most notably folic acid deficiency). **1. Why 4% is correct:** In the general population, the incidence of NTDs is approximately 0.1–0.2% (1 in 1,000). However, once a couple has one child with an NTD (anencephaly, spina bifida, or encephalocele), the risk of recurrence in a subsequent pregnancy increases significantly to approximately **3–5%** (standardized as **4%** for examination purposes). If two previous siblings are affected, the risk rises further to about 10%. **2. Why the other options are incorrect:** * **A (2%):** This underestimates the risk. While recurrence risks vary by geography, 3–5% is the globally accepted range for a single prior affected pregnancy. * **C (10%):** This is the approximate recurrence risk only after **two** previously affected siblings. * **D (20%):** This risk is too high for multifactorial inheritance and would be more characteristic of a high-penetrance autosomal dominant condition. **High-Yield Clinical Pearls for NEET-PG:** * **Prevention:** For the general population, the recommended dose of Folic Acid is **400 mcg (0.4 mg)/day** starting 1 month prior to conception. * **Secondary Prevention (High Risk):** For women with a **previous child with NTD**, the dose is increased to **4 mg/day** (10 times the standard dose). * **Screening:** Maternal Serum Alpha-Fetoprotein (MSAFP) is elevated in open NTDs. The best time for screening is **15–20 weeks** (ideal: 16–18 weeks). * **Diagnosis:** Targeted Level II Ultrasound is the gold standard for detecting structural defects.

Q: Placental enlargement is seen in which of the following infections?

Plasmodium. **Explanation:** **Correct Answer: D. Plasmodium** **Why Plasmodium is correct:** Placental enlargement (placentomegaly) in malaria, particularly *Plasmodium falciparum*, is a hallmark of **Placental Malaria**. The underlying mechanism involves the sequestration of parasitized red blood cells in the intervillous spaces. This triggers a robust maternal inflammatory response, leading to massive infiltration of monocytes and macrophages (intervillositis), fibrin deposition, and basement membrane thickening. These pathological changes significantly increase placental weight and thickness, often correlating with adverse outcomes like intrauterine growth restriction (IUGR) and low birth weight. **Analysis of Incorrect Options:** * **A, B, and C (Toxoplasma, CMV, Parvovirus):** While these infections are part of the TORCH spectrum and can occasionally cause placental edema or "hydrops-like" changes, they are primarily associated with **placental calcifications** (especially CMV and Toxoplasma) or specific fetal effects (e.g., Parvovirus causing fetal anemia and hydrops). In the context of standard PG-level examinations, *Plasmodium* is the classic infectious cause cited for significant placental hypertrophy and weight increase. **High-Yield Clinical Pearls for NEET-PG:** * **Definition of Placentomegaly:** A placental thickness >4 cm in the second/third trimester or a weight >600g at term. * **Other Causes of Placentomegaly:** * **Maternal:** Diabetes Mellitus (most common non-infectious cause), Severe Anemia. * **Fetal:** Rh-Isoimmunization (Hydrops Fetalis), Twin-to-Twin Transfusion Syndrome (recipient), Chromosomal anomalies (Triploidy). * **Tumors:** Chorioangioma. * **Malaria Fact:** Placental malaria is more common and severe in **primigravidae** due to the lack of specific immunity against VAR2CSA-expressing parasites that bind to chondroitin sulfate A in the placenta.

Question 1

A 30-year-old woman at 28 weeks gestation with gestational diabetes managed with insulin presents with decreased fetal movement. Fetal monitoring shows category II tracing. Umbilical artery Doppler shows absent end-diastolic flow. Her glucose control has been suboptimal (HbA1c 7.8%). Maternal blood pressure is normal. Synthesize the pathophysiologic relationship between her metabolic condition and the Doppler findings to determine the primary mechanism.

Accepted Answer

Uteroplacental insufficiency from diabetes-induced vasculopathy affecting spiral arteries

Answer

Placental hypertrophy from fetal macrosomia compressing umbilical cord

Answer

Fetal polycythemia from chronic hypoxia increasing blood viscosity

Answer

Maternal ketoacidosis causing direct fetal myocardial depression

Answer

Maternal hyperglycemia causing fetal hyperinsulinemia and increased oxygen consumption

Question 2

Which is the most common complication in monoamniotic twins?

Accepted Answer

Intertwining

Answer

Discordance

Answer

Cord entanglement

Answer

Conjoined twins

Question 3

What is the approximate recurrence risk for neural tube defects (NTDs) in a subsequent pregnancy, given that the first baby was born with an NTD?

Accepted Answer

4%

Answer

2%

Answer

10%

Answer

20%

Question 4

Placental enlargement is seen in which of the following infections?

Accepted Answer

Plasmodium

Answer

Toxoplasma

Answer

Cytomegalovirus (CMV)

Answer

Parvovirus

Question 5

Hemolytic disease of the newborn is least common with which blood group female?

Accepted Answer

O

Answer

A

Answer

B

Answer

AB

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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