Maternal-Fetal Medicine Practice Questions

Q: Which one of the following medical disorders leads to delayed fetal lung maturity?

Diabetes. **Explanation:** The correct answer is **Diabetes**. Fetal lung maturity is primarily determined by the production of pulmonary surfactant (phospholipids like lecithin). In pregnancies complicated by maternal diabetes, maternal hyperglycemia leads to **fetal hyperinsulinemia**. High levels of fetal insulin act as a potent antagonist to the action of cortisol on the type II pneumocytes. This inhibits the synthesis of surfactant proteins and phospholipids, specifically delaying the appearance of **Phosphatidylglycerol (PG)**. Consequently, infants of diabetic mothers are at a higher risk of Respiratory Distress Syndrome (RDS) even at relatively mature gestational ages. **Analysis of Incorrect Options:** * **Heart Disease:** Chronic maternal hypoxia or circulatory compromise (as seen in heart disease) acts as a form of chronic fetal stress. Stress triggers the premature release of endogenous fetal glucocorticoids, which actually **accelerates** lung maturity. * **Thalassemia Minor:** This is generally an asymptomatic carrier state and does not significantly alter the intrauterine environment or fetal hormonal milieu to delay lung maturation. * **Epilepsy:** While the medications used (anti-epileptics) may have teratogenic risks, the disorder itself does not interfere with the biochemical pathways of surfactant production. **High-Yield Clinical Pearls for NEET-PG:** * **Accelerated Lung Maturity:** Seen in conditions causing **chronic placental insufficiency** or fetal stress (e.g., Preeclampsia, Chronic Hypertension, IUGR, Premature Rupture of Membranes, and Maternal Smoking). * **Delayed Lung Maturity:** Primarily associated with **Diabetes Mellitus** and **Rh Isoimmunization**. * **Gold Standard:** The presence of **Phosphatidylglycerol (PG)** in amniotic fluid is the most reliable indicator of lung maturity in diabetic pregnancies, as the L/S ratio can sometimes be falsely reassuring.

Q: Maternal serum alpha-fetoprotein concentration is elevated in all of the following conditions except:

Fetal Down's syndrome. **Explanation:** Maternal Serum Alpha-Fetoprotein (MSAFP) is a glycoprotein produced initially by the yolk sac and later by the fetal liver. It serves as a crucial biomarker in prenatal screening and oncology. **Why Fetal Down’s Syndrome is the Correct Answer:** In pregnancies affected by **Down’s Syndrome (Trisomy 21)**, the MSAFP levels are characteristically **decreased** (usually <0.5 MoM), not elevated. This is often accompanied by low unconjugated estriol (uE3) and elevated levels of Beta-hCG and Inhibin-A (the "Quadruple Test" pattern). The exact mechanism for decreased AFP in Down's syndrome is thought to be related to reduced fetal liver synthesis or delayed maturity of the liver. **Why the other options are incorrect:** * **Hepatoma (Hepatocellular Carcinoma) & Hepatoblastoma:** AFP is a classic tumor marker for primary liver malignancies. It is re-expressed by malignant hepatocytes, leading to significantly elevated serum levels. * **Endodermal Sinus Tumor (Yolk Sac Tumor):** This is a highly malignant germ cell tumor. Since the yolk sac is the primary embryological producer of AFP, these tumors secrete high amounts of AFP, making it a specific marker for diagnosis and monitoring recurrence. **High-Yield Clinical Pearls for NEET-PG:** * **Causes of Elevated MSAFP:** Neural tube defects (Anencephaly, Spina bifida), abdominal wall defects (Omphalocele, Gastroschisis), multiple gestations, and fetal demise. * **Most Common Cause of Elevated MSAFP:** Underestimation of gestational age (wrong dates). * **Causes of Low MSAFP:** Down’s syndrome, Trisomy 18 (Edwards syndrome), gestational trophoblastic disease, and maternal obesity. * **Rule of Thumb:** If the question mentions "Open" defects (NTD), think **High AFP**; if it mentions "Chromosomal" defects (Down's), think **Low AFP**.

Q: Which of the following statements regarding asymptomatic bacteriuria in pregnancy is true?

It increases the chance of premature infant.. **Explanation:** **Asymptomatic Bacteriuria (ASB)** is defined as the presence of $>10^5$ colony-forming units (CFU)/mL of a single uropathogen in a midstream clean-catch urine specimen from an individual without symptoms of a urinary tract infection (UTI). **Why Option D is Correct:** ASB in pregnancy is a significant risk factor for adverse obstetric outcomes. The inflammatory response triggered by the infection can lead to the release of prostaglandins and cytokines, which stimulate uterine contractions and cervical ripening. This significantly increases the risk of **preterm labor, premature birth, and low birth weight (LBW)** infants. **Analysis of Incorrect Options:** * **Option A:** While the condition is by definition "asymptomatic," the statement is a tautology and does not address the clinical significance or management goals required by the question context. * **Option B:** While approximately 20–40% of untreated ASB cases progress to **acute pyelonephritis**, it is incorrect to say it *always* progresses in all cases. However, the risk is high enough to mandate universal screening. * **Option C:** Treatment primarily prevents maternal complications (pyelonephritis) and prematurity. It does **not** prevent congenital "abnormalities" (structural malformations) in the fetus, as ASB is not a known teratogen. **High-Yield Clinical Pearls for NEET-PG:** * **Most common organism:** *Escherichia coli* (70–80%). * **Screening:** All pregnant women should be screened via **urine culture** at the first prenatal visit (ideally between 12–16 weeks). * **Treatment:** Essential even if asymptomatic. Common drugs include Nitrofurantoin (avoid near term), Amoxicillin, or Cephalexin. * **Goal:** Treatment reduces the risk of pyelonephritis from 30% to <3%.

Q: In placenta previa, conservative treatment is not done in which of the following cases?

All of the above. **Explanation:** The primary goal of conservative management in placenta previa (known as the **MacAfee and Johnson regimen**) is to prolong pregnancy until fetal maturity is reached (ideally 37 weeks) without compromising maternal safety. This approach is only indicated if the mother is hemodynamically stable, the bleeding has stopped, and the fetus is premature but alive. **Why "All of the Above" is correct:** Conservative management is contraindicated when the risks of continuing the pregnancy outweigh the benefits of fetal maturation. * **Active Labor (Option A):** Once labor starts, the cervix begins to efface and dilate, which inevitably causes massive separation of the placenta and life-threatening hemorrhage. Delivery is mandatory. * **Anencephaly (Option B):** If there is a major lethal congenital anomaly (like anencephaly), there is no clinical benefit in "waiting for maturity" or risking maternal hemorrhage for a fetus that cannot survive. * **Dead baby and severe placenta previa (Option C):** In the presence of intrauterine fetal death (IUFD), the objective of conservative management (fetal maturity) is lost. Furthermore, severe placenta previa (Type III or IV) necessitates delivery (usually by Cesarean section) to prevent maternal exsanguination, regardless of fetal status. **High-Yield Clinical Pearls for NEET-PG:** * **MacAfee Regimen Criteria:** Pregnancy <37 weeks, bleeding is not life-threatening, mother is stable, and the fetus is alive with no gross anomalies. * **Ideal Delivery Timing:** In stable cases of placenta previa, elective delivery is usually planned at **37 weeks**. * **Vaginal Examination:** Digital vaginal examination is **strictly contraindicated** (can cause torrential hemorrhage) unless performed as a "Double Setup Examination" in the operating theater. * **Investigation of Choice:** Transvaginal Ultrasound (TVS) is the gold standard for diagnosing placental localization.

Q: What is the most common congenital malformation seen in infants of diabetic mothers?

Cardiac defect. **Explanation:** Infants of diabetic mothers (IDM) are at a 3–4 fold increased risk of congenital malformations due to the teratogenic effects of maternal hyperglycemia during organogenesis. **1. Why Cardiac Defects are Correct:** Congenital Heart Diseases (CHDs) are the **most common** malformations seen in IDMs. Among these, **Ventricular Septal Defect (VSD)** and **Transposition of the Great Arteries (TGA)** are the most frequent. It is important to distinguish this from the *most specific* malformation (Caudal Regression Syndrome). Hyperglycemia leads to oxidative stress and altered gene expression during the critical period of heart development (3rd to 8th week). **2. Why other options are incorrect:** * **Renal defects:** While renal anomalies (like renal agenesis or hydronephrosis) occur more frequently in IDMs than in the general population, they are statistically less common than cardiac defects. * **Liver and Lung defects:** These are not primary structural malformations associated with diabetic embryopathy. However, IDMs often face functional lung issues, such as **Respiratory Distress Syndrome (RDS)**, due to hyperinsulinemia delaying surfactant production, but this is a developmental delay rather than a structural malformation. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Malformation:** Cardiac defects (VSD > TGA). * **Most Specific Malformation:** Caudal Regression Syndrome (Sacral Agenesis). * **Most Common Echo finding:** Asymmetric Septal Hypertrophy (usually transient/resolves after birth). * **Neural Tube Defects (NTDs):** These are the second most common malformations in IDMs. * **HbA1c Correlation:** The risk of malformations is directly proportional to the maternal HbA1c levels during the first trimester.

Q: Which of the following is NOT associated with an increased risk of thromboembolism in pregnancy?

Blood group O. **Explanation:** Pregnancy is a naturally prothrombotic state due to an increase in clotting factors (I, VII, VIII, IX, X) and a decrease in protein S levels. Understanding the specific risk factors for Venous Thromboembolism (VTE) is crucial for NEET-PG. **Why Blood Group O is the Correct Answer:** Individuals with **Non-O blood groups (A, B, and AB)** have a significantly higher risk (approx. 2–4 times) of thromboembolism compared to those with Blood Group O. This is because Non-O individuals have higher plasma concentrations of **von Willebrand factor (vWF)** and **Factor VIII**, which are stabilized by the A and B antigens. Therefore, Blood Group O is actually "protective" against VTE rather than a risk factor. **Analysis of Other Options:** * **Anemia:** Severe anemia (especially sickle cell disease or acute blood loss requiring transfusion) is associated with an increased risk of VTE due to hyperkinetic circulation and potential endothelial injury. * **Rising Parity:** The risk of VTE increases with parity. Women who are **multiparous (Parity ≥3)** are at a higher risk compared to primigravida women. * **Antithrombin (AT) Deficiency:** This is the **most thrombophilic** of the hereditary thrombophilias. While Factor V Leiden is the most common, AT deficiency carries the highest absolute risk of a thromboembolic event during pregnancy. **High-Yield Clinical Pearls for NEET-PG:** * **Most common VTE in pregnancy:** Deep Vein Thrombosis (DVT), usually occurring in the **left leg** (80%) due to compression of the left common iliac vein by the right axial artery (May-Thurner phenomenon). * **Highest risk period:** The **postpartum period** (especially the first 6 weeks) carries a higher daily risk of VTE than pregnancy itself. * **Gold Standard Diagnosis:** Compression Duplex Ultrasound for DVT; CT Pulmonary Angiography (CTPA) or V/Q scan for Pulmonary Embolism.

Q: What is the indication for amnioinfusion?

Oligohydramnios. **Explanation:** **Amnioinfusion** is the technique of infusing a liquid (usually normal saline or Ringer’s lactate) into the amniotic cavity. **Why Option A is Correct:** The primary indication for amnioinfusion is **Oligohydramnios**, particularly when it leads to **variable decelerations** during labor. In oligohydramnios, the lack of cushioning fluid causes the umbilical cord to be compressed by fetal parts or the uterine wall. Amnioinfusion restores the fluid volume, relieves cord compression, and improves fetal oxygenation. It is also used prophylactically in cases of Preterm Premature Rupture of Membranes (PPROM) to prevent pulmonary hypoplasia. **Why Other Options are Incorrect:** * **B. Suspected renal anomalies:** While renal anomalies (like Potter’s syndrome) cause oligohydramnios, amnioinfusion is not a treatment for the anomaly itself. It may be used as a diagnostic tool (diagnostic amnioinfusion) to improve ultrasound visualization, but it is not the primary therapeutic indication. * **C. To facilitate labor:** Amnioinfusion does not shorten the duration of labor or improve uterine contractions; its role is strictly fetal protection. * **D. Fetal distress:** While it treats fetal distress caused specifically by *cord compression* (variable decelerations), it is contraindicated in cases of acute fetal distress due to other causes (like placental abruption) where immediate delivery is required. **High-Yield NEET-PG Pearls:** 1. **Indications:** Relief of variable decelerations (most common), dilution of thick meconium (though controversial now), and diagnostic visualization. 2. **Route:** Transvaginal (via IUPC) during labor or Transabdominal (ultrasound-guided). 3. **Fluid used:** Room temperature Normal Saline or Ringer's Lactate. 4. **Contraindications:** Amnionitis, Polyhydramnios, Placental Abruption, and Uterine Hypertonicity.

Question 1

Which statement concerning polyhydramnios is true?

Accepted Answer

Complications include placental abruption, uterine dysfunction, and postpartum hemorrhage.

Answer

Acute polyhydramnios always leads to labor prior to 28 weeks.

Answer

The incidence of associated malformations is approximately 3%.

Answer

Maternal edema, especially of the lower extremities and vulva, is rare.

Question 2

Which one of the following medical disorders leads to delayed fetal lung maturity?

Accepted Answer

Diabetes

Answer

Heart disease

Answer

Thalassemia minor

Answer

Epilepsy

Question 3

Maternal serum alpha-fetoprotein concentration is elevated in all of the following conditions except:

Accepted Answer

Fetal Down's syndrome

Answer

Hepatoma

Answer

Hepatoblastoma

Answer

Endodermal sinus tumor

Question 4

Which of the following cannot be used to lower mother-to-child HIV transmission?

Accepted Answer

Omitting ergometrine

Answer

Elective Cesarean section

Answer

Antiretroviral therapy (ART)

Answer

Intrapartum nevirapine

Question 5

Which of the following statements regarding asymptomatic bacteriuria in pregnancy is true?

Accepted Answer

It increases the chance of premature infant.

Answer

Most cases are usually asymptomatic in pregnancy.

Answer

If untreated, it progresses to pyelonephritis.

Answer

Early and prompt treatment prevents abnormalities in the fetus.

Question 6

In placenta previa, conservative treatment is not done in which of the following cases?

Accepted Answer

All of the above

Answer

Active labor

Answer

Anencephaly

Answer

Dead baby and severe placenta previa

Question 7

What is the most common congenital malformation seen in infants of diabetic mothers?

Accepted Answer

Cardiac defect

Answer

Renal defect

Answer

Liver defect

Answer

Lung defect

Question 8

A pregnant patient in her first trimester presents with an amoebic liver abscess. What is the preferred treatment?

Accepted Answer

Aspiration

Answer

Metronidazole

Answer

Diloxanide furoate

Answer

Chloroquine

Question 9

Which of the following is NOT associated with an increased risk of thromboembolism in pregnancy?

Accepted Answer

Blood group O

Answer

Anemia

Answer

Increased risk with rising parity

Answer

Antithrombin deficiency

Question 10

What is the indication for amnioinfusion?

Accepted Answer

Oligohydramnios

Answer

Suspected renal anomalies

Answer

To facilitate labor

Answer

Fetal distress

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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