Maternal-Fetal Medicine Practice Questions

Q: What is the most common cause of maternal mortality?

Hemorrhage. **Explanation:** **Hemorrhage (Option C)** is the leading cause of maternal mortality worldwide and in India, accounting for approximately 25–30% of maternal deaths. Among hemorrhages, **Postpartum Hemorrhage (PPH)** is the most significant contributor. The primary physiological reason is the high blood flow to the gravid uterus (approx. 600–700 mL/min); if the uterus fails to contract effectively after delivery (Atonic PPH), massive blood loss can occur within minutes, leading to hypovolemic shock and death. **Why other options are incorrect:** * **Sepsis (Option A):** While a major cause of mortality, particularly in settings with poor hygiene or prolonged labor, it usually ranks behind hemorrhage and hypertensive disorders. * **Eclampsia (Option B):** Hypertensive disorders of pregnancy are the second most common cause of maternal death globally. While life-threatening, the incidence of death is statistically lower than that caused by acute hemorrhage. * **Obstructed Labor (Option D):** This is an indirect cause that leads to mortality via secondary complications like uterine rupture, hemorrhage, or sepsis, rather than being the most frequent direct cause itself. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of PPH:** Uterine Atony (80% of cases). * **Active Management of Third Stage of Labor (AMTSL):** The most important intervention to reduce maternal mortality. * **Global vs. India:** Hemorrhage remains #1 in both. However, always check for "Indirect causes"—globally, non-obstetric causes (like cardiac disease or malaria) are rising in proportion. * **Maternal Mortality Ratio (MMR):** Defined as maternal deaths per 100,000 live births.

Q: What is a cause of oligohydramnios?

Renal agenesis. **Explanation:** The volume of amniotic fluid is a dynamic balance between production and removal. From the second trimester onwards, **fetal urine production** becomes the primary source of amniotic fluid, while fetal swallowing is the main route of removal. **Why Renal Agenesis is Correct:** In **Renal Agenesis** (Potter’s Syndrome), the kidneys fail to develop, leading to a total absence of fetal urine production. This results in severe **oligohydramnios** (Amniotic Fluid Index <5 cm or Single Deepest Pocket <2 cm). Without adequate fluid, the fetus suffers from pulmonary hypoplasia and limb deformities due to uterine compression. **Why the Other Options are Incorrect:** * **Esophageal and Duodenal Atresia:** These are gastrointestinal obstructions that prevent the fetus from swallowing amniotic fluid. Since the fluid is produced but not removed, these conditions lead to **polyhydramnios**. * **Diabetes:** Maternal diabetes (especially gestational or poorly controlled) causes fetal hyperglycemia, leading to osmotic diuresis (increased fetal urination). This results in **polyhydramnios**. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Oligohydramnios is defined as an AFI < 5 cm or a Single Deepest Pocket (SDP) < 2 cm. * **Common Causes:** Renal anomalies (agenesis, posterior urethral valves), Premature Rupture of Membranes (PROM), Uteroplacental insufficiency (IUGR), and Post-term pregnancy. * **Drug-induced:** ACE inhibitors and NSAIDs (Indomethacin) can cause oligohydramnios by reducing fetal renal blood flow. * **Potter’s Sequence:** Remember the triad of Renal agenesis → Oligohydramnios → Pulmonary hypoplasia (the most common cause of death).

Q: What is the risk of vertical transmission of HIV without intervention during pregnancy and breastfeeding?

15% to 30%. **Explanation:** The risk of vertical transmission (Mother-to-Child Transmission - MTCT) of HIV occurs at three stages: in utero, during labor/delivery, and through breastfeeding. In the absence of any medical intervention (no Antiretroviral Therapy, vaginal delivery, and breastfeeding), the cumulative risk is approximately **15% to 30%**. If breastfeeding continues into the second year, the risk can further increase to 35-45%. * **Why Option A is correct:** Without intervention, the transmission rate is roughly divided as: 5-10% during pregnancy, 10-15% during labor (the period of highest risk per hour), and 5-15% through prolonged breastfeeding. This totals the 15-30% range commonly cited in standard textbooks like Williams Obstetrics. * **Why Options B, C, and D are incorrect:** These figures represent risks *with* some level of intervention. For instance, **Option D (2%)** is the target risk level when a mother is on effective HAART with an undetectable viral load and avoids breastfeeding. Options B and C represent partial interventions (e.g., Zidovudine monotherapy without viral suppression). **High-Yield Clinical Pearls for NEET-PG:** * **Most common timing:** The majority of transmission occurs **intranatally** (during labor and delivery) due to "micro-transfusions" and contact with infected vaginal secretions. * **Gold Standard Goal:** With modern HAART, elective Cesarean Section (if viral load >1000 copies/mL), and avoidance of breastfeeding, the risk can be reduced to **<1-2%**. * **Breastfeeding:** In India, the current WHO/NACO guideline suggests that "Exclusive Breastfeeding" for the first 6 months is recommended even for HIV-positive mothers if they are on ART, as the benefits of nutrition and immunity outweigh the risk of HIV in resource-limited settings. * **Prophylaxis:** Nevirapine is the drug of choice for infant prophylaxis in the immediate postnatal period.

Q: Patients with organic heart disease in pregnancy most commonly die during which period?

Soon following delivery. **Explanation:** The correct answer is **Soon following delivery** (Option C). The period immediately following the delivery of the placenta is the most critical for a woman with organic heart disease. This is due to a phenomenon known as **"Autotransfusion."** When the placenta is delivered, the compression of the inferior vena cava is relieved, and the blood previously circulating in the uteroplacental unit (approx. 500-800 mL) is shifted back into the maternal systemic circulation. This sudden increase in venous return leads to a massive surge in cardiac output (up to 60-80% above baseline), which can overwhelm a compromised heart, leading to acute pulmonary edema and heart failure. **Analysis of Incorrect Options:** * **A. 20-24 weeks:** While cardiac output begins to rise significantly during the second trimester, it reaches its peak plateau between **28-32 weeks**. This is a period of high risk, but not the most common time for mortality compared to the immediate postpartum surge. * **B. First stage of labor:** Cardiac output increases during labor due to pain, anxiety, and uterine contractions (each contraction pushes ~300-500 mL of blood into circulation), but the peak hemodynamic stress occurs after the fetus is expelled. * **D. Two weeks postpartum:** By this time, hemodynamic stability is usually restored as the excess fluid has been diuresed. **High-Yield Clinical Pearls for NEET-PG:** * **Maximum Risk Periods:** 1. Immediately postpartum (highest risk), 2. During labor, 3. 28-32 weeks of gestation. * **Management:** To prevent heart failure during the third stage, avoid ergometrine (causes vasoconstriction) and use slow IV infusion of oxytocin. * **Positioning:** Encourage the left lateral position to minimize caval compression. * **Vaginal vs. C-Section:** Vaginal delivery with an assisted second stage (forceps/ventouse) to cut short maternal bearing down is preferred over elective Cesarean section.

Q: The risk of fetal varicella syndrome is maximum when the mother is infected between which gestational periods?

13 to 20 weeks. **Explanation:** The risk of **Congenital Varicella Syndrome (CVS)** is directly linked to the gestational age at the time of primary maternal infection. While maternal infection can occur at any time, the period of maximum vulnerability for the fetus is between **13 and 20 weeks** of gestation. 1. **Why 13 to 20 weeks is correct:** During this window, the fetal immune system is immature, and the virus can cross the placenta to cause multi-organ damage. Studies indicate the risk of CVS is approximately **2%** during this period. The hallmark features include cicatricial skin scarring (in a dermatomal distribution), limb hypoplasia, chorioretinitis, and microcephaly. 2. **Why other options are incorrect:** * **6 to 12 weeks (Options A & B):** While infection can occur, the risk of CVS is lower (approximately 0.4% to 1%) compared to the second trimester peak. * **20 to 28 weeks (Option D):** After 20 weeks, the risk of CVS becomes negligible as the fetus develops better immunological defenses, though the virus may remain latent and manifest as childhood herpes zoster. **High-Yield Clinical Pearls for NEET-PG:** * **Maximum Risk Period:** 13–20 weeks (2% risk). * **Varicella Zoster Immunoglobulin (VZIG):** Should be administered to non-immune pregnant women within **10 days** of exposure to prevent or attenuate maternal disease. * **Neonatal Varicella:** If the mother develops a rash **5 days before to 2 days after delivery**, the neonate is at high risk for severe disseminated disease due to lack of transplacental antibodies; the neonate must receive VZIG immediately. * **Treatment:** Oral Acyclovir is the drug of choice for maternal infection to reduce maternal complications (pneumonia).

Q: An ultrasound shows a twin pregnancy. Which of the following is a feature of dizygotic twins?

Separate chorion and amnion. **Explanation:** **1. Why Option B is Correct:** Dizygotic (fraternal) twins result from the fertilization of **two separate ova by two separate sperm**. Because each zygote undergoes its own independent process of implantation and development, each fetus develops its own placenta, its own outer membrane (chorion), and its own inner sac (amnion). Therefore, dizygotic twins are **always Dichorionic-Diamniotic (DCDA)**. **2. Why the Other Options are Incorrect:** * **Option A (Separate amnion and same chorion):** This describes Monochorionic-Diamniotic (MCDA) twins. This configuration is unique to **monozygotic** (identical) twins where the zygote splits between days 4 and 8 post-fertilization. Dizygotic twins can never share a chorion. * **Option C (Always different sex):** This is a common misconception. Since two separate sperm are involved, the sex of each twin is independent. They can be the same sex (approx. 50% of the time) or different sexes. Only "different sex" twins are guaranteed to be dizygotic, but dizygotic twins are not "always" different sex. **3. NEET-PG High-Yield Pearls:** * **Zygosity vs. Chorionicity:** All dizygotic twins are DCDA. Monozygotic twins can be DCDA, MCDA, or MCMA depending on the timing of the split. * **The "Lambda" vs. "T" Sign:** On ultrasound, a thick membrane with the **Lambda (λ) sign** (or twin-peak sign) indicates DCDA (Dizygotic or early-split Monozygotic). A thin membrane with a **T-sign** indicates MCDA. * **Incidence:** The rate of monozygotic twins is constant worldwide (~1 in 250), whereas the rate of dizygotic twins varies by race (highest in Nigerians, lowest in Japanese), maternal age, and use of assisted reproductive technology (ART).

Q: Which of the following is NOT a complication of Rh incompatibility?

Oligohydramnios. **Explanation:** Rh isoimmunization occurs when a Rh-negative mother carries a Rh-positive fetus, leading to the production of maternal antibodies that cross the placenta and cause fetal hemolysis. **Why Oligohydramnios is the correct answer:** In Rh incompatibility, fetal hemolysis leads to **anemia**. To compensate, the fetus increases cardiac output, leading to hyperdynamic circulation and eventual heart failure (Hydrops fetalis). A key physiological response to fetal anemia is increased hepatic and splenic erythropoiesis, which causes organomegaly and portal hypertension. Crucially, fetal anemia leads to **Polyhydramnios**, not oligohydramnios. This occurs due to increased fetal cardiac output resulting in increased renal perfusion and fetal urine production, as well as placental edema interfering with fluid exchange. **Analysis of other options:** * **APH & PPH:** Rh isoimmunization is associated with a **large, boggy, and edematous placenta** (Placentomegaly). This increases the risk of placental abruption (leading to APH) and uterine atony after delivery due to overdistension (leading to PPH). * **Pregnancy-induced hypertension (PIH):** The enlarged, "hyperplacentosis" state seen in severe Rh isoimmunization is a known risk factor for the early onset of preeclampsia (Mirror Syndrome). **NEET-PG High-Yield Pearls:** * **Mirror Syndrome (Ballantyne’s Syndrome):** A rare condition where maternal edema "mirrors" fetal and placental hydrops; it is often associated with severe Rh isoimmunization. * **First sign of Hydrops on USG:** Increased thickness of the placenta (>4 cm). * **Most sensitive non-invasive test for fetal anemia:** Peak Systolic Velocity of the Middle Cerebral Artery (MCA-PSV) via Doppler.

Q: Which of the following statements regarding alpha-fetoprotein is true?

Its major source in fetal life is the yolk sac.. **Explanation:** **Alpha-fetoprotein (AFP)** is a glycoprotein produced during fetal development that serves as the fetal analog of albumin. 1. **Why Option A is Correct:** In early embryonic life, AFP is primarily synthesized by the **yolk sac**. As gestation progresses, the **fetal liver** becomes the predominant source of production. Small amounts are also produced by the fetal gastrointestinal tract. 2. **Why Options B, C, and D are Incorrect:** * **Option B:** AFP is a tumor marker for **Hepatocellular carcinoma** and **Germ cell tumors** (specifically Yolk Sac Tumors/Endodermal Sinus Tumors). It is *not* typically associated with Wilms' tumor (Nephroblastoma). * **Option C:** In fetal serum, AFP levels peak at the end of the **first trimester (approx. 12–14 weeks)**. In maternal serum (MSAFP), levels peak later, around **30–32 weeks**. Screening for neural tube defects is ideally done between **15–20 weeks**. * **Option D:** The biological half-life of AFP is approximately **3 to 5 days**. This is clinically significant when monitoring the clearance of the marker after surgical resection of a tumor. **High-Yield Clinical Pearls for NEET-PG:** * **Elevated MSAFP:** Associated with Neural Tube Defects (NTDs), abdominal wall defects (Omphalocele, Gastroschisis), multiple gestations, and fetal demise. * **Decreased MSAFP:** Associated with **Down Syndrome (Trisomy 21)**, Trisomy 18, gestational trophoblastic disease, and maternal obesity. * **Amniotic Fluid Acetylcholinesterase (AChE):** This is a more specific test than AFP for confirming the diagnosis of an open neural tube defect.

Question 1

What is the most common cause of maternal mortality?

Accepted Answer

Hemorrhage

Answer

Sepsis

Answer

Eclampsia

Answer

Obstructed labor

Question 2

What is a cause of oligohydramnios?

Accepted Answer

Renal agenesis

Answer

Esophageal atresia

Answer

Duodenal atresia

Answer

Diabetes

Question 3

What is the risk of vertical transmission of HIV without intervention during pregnancy and breastfeeding?

Accepted Answer

15% to 30%

Answer

5% to 10%

Answer

10% to 15%

Answer

2% to 5%

Question 4

Patients with organic heart disease in pregnancy most commonly die during which period?

Accepted Answer

Soon following delivery

Answer

20-24 weeks of pregnancy

Answer

First stage of labor

Answer

Two weeks postpartum

Question 5

The risk of fetal varicella syndrome is maximum when the mother is infected between which gestational periods?

Accepted Answer

13 to 20 weeks

Answer

6 to 10 weeks

Answer

8 to 12 weeks

Answer

20 to 28 weeks

Question 6

An ultrasound shows a twin pregnancy. Which of the following is a feature of dizygotic twins?

Accepted Answer

Separate chorion and amnion

Answer

Separate amnion and same chorion

Answer

Always different sex

Answer

None of the above

Question 7

Which of the following complications is seen in pregnancy?

Accepted Answer

Hypertension complicating pregnancy

Answer

Diabetes complicating pregnancy

Answer

Placenta previa complicating pregnancy

Answer

Preterm delivery

Question 8

A 21-week pregnant patient presents with fever and chills, and a diagnosis of Malaria is made. What is the next line of management?

Accepted Answer

Start antimalarial treatment immediately and continue the pregnancy.

Answer

Wait until term and start treatment for malaria.

Answer

Terminate the pregnancy and treat the patient for malaria.

Answer

Treat only if it is falciparum malaria; otherwise, wait until term.

Question 9

Which of the following is NOT a complication of Rh incompatibility?

Accepted Answer

Oligohydramnios

Answer

Antepartum hemorrhage (APH)

Answer

Postpartum hemorrhage (PPH)

Answer

Pregnancy-induced hypertension

Question 10

Which of the following statements regarding alpha-fetoprotein is true?

Accepted Answer

Its major source in fetal life is the yolk sac.

Answer

It is commonly increased in Wilms' tumor.

Answer

Maximum levels are observed around the 20th week of gestation.

Answer

Its half-life is 5-7 days.

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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