Maternal-Fetal Medicine — MCQs

A 23-year-old primigravida at 33 weeks gestation presented with jaundice for 2 days. On examination, her BP was 140/90 mmHg, serum bilirubin was 5 mg%, Hb was 8 gm%, platelet count was 90,000/cu.mm, TLC was 10,000/cu.mm, and blood sugar was 40 mg/dL. AST and ALT were 85 and 80 IU/L, respectively. What is the probable diagnosis?

Q628Medium

What is a common cause of recurrent second-trimester fetal loss?

Q629Easy

Which drug is used for fetal lung maturity?

Q630Easy

A 31-year-old woman in her second trimester of pregnancy presents with dyspnea on exertion. She has no history of chest pain, cough, or fever, and no known cardiac disease. Physical examination reveals a pulse of 75/min, BP of 110/70 mmHg, and SpO2 of 96%. Chest and cardiovascular examinations are unremarkable. What is the most probable cause of this patient's clinical presentation?

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 621: Single umbilical artery is associated with an increased involvement of which system?

A. Genitourinary system (Correct Answer)
B. Central nervous system
C. Pulmonary system
D. Endocrine system

Explanation: **Explanation:** A **Single Umbilical Artery (SUA)**, or a two-vessel cord, occurs when one of the two umbilical arteries is absent due to primary agenesis or secondary atrophy. It is the most common umbilical cord anomaly, occurring in approximately 0.5–1% of singleton pregnancies. **Why Genitourinary system is correct:** There is a strong embryological association between the development of the umbilical arteries and the primitive urogenital system. When a SUA is identified, the **genitourinary system** is the most frequently affected organ system (up to 30% of associated anomalies). Common defects include renal agenesis, multicystic dysplastic kidney, and ureteropelvic junction obstruction. This is followed closely by cardiovascular malformations. **Why other options are incorrect:** * **Central nervous system (CNS):** While CNS anomalies (like neural tube defects) can occur with SUA, they are statistically less frequent than renal or cardiac defects. * **Pulmonary system:** Lung hypoplasia may occur secondary to renal anomalies (Potter sequence), but primary pulmonary defects are not the most common association. * **Endocrine system:** There is no significant established embryological or clinical link between SUA and primary endocrine system malformations. **High-Yield Clinical Pearls for NEET-PG:** * **Screening:** If SUA is found on a routine scan, a detailed **Targeted Imaging for Fetal Anomalies (TIFFA)** and **Fetal Echocardiography** are mandatory. * **Chromosomal Link:** SUA is associated with an increased risk of **Trisomy 18 (Edwards Syndrome)** and Trisomy 13. * **Growth:** Isolated SUA (no other malformations) is associated with an increased risk of **Intrauterine Growth Restriction (IUGR)** and preterm birth. * **Side Predilection:** The **left** umbilical artery is more commonly absent than the right.

Question 622: In Gestational diabetes mellitus, what is NOT usually seen?

A. Macrosomic baby
B. Malformations like cardiac and neural tube defects (Correct Answer)
C. Shoulder dystocia
D. Polyhydramnios

Explanation: The key to answering this question lies in distinguishing between **Gestational Diabetes Mellitus (GDM)** and **Pregestational (Overt) Diabetes**. ### Why Option B is the Correct Answer Congenital malformations (such as cardiac defects, neural tube defects, and sacral agenesis) occur during **organogenesis**, which takes place in the **first 8 weeks** of gestation. * In **GDM**, hyperglycemia typically develops in the late second or third trimester (after 24 weeks) due to increased insulin resistance from placental hormones (hPL). Since blood glucose is normal during the first trimester, the risk of structural malformations is **not increased** compared to the general population. * In contrast, **Pregestational Diabetes** involves hyperglycemia during conception and early pregnancy, which is highly teratogenic. ### Why the Other Options are Incorrect * **A. Macrosomic baby:** Maternal hyperglycemia leads to fetal hyperglycemia. The fetal pancreas responds by secreting excess insulin (a potent growth hormone), leading to fetal overgrowth (macrosomia). * **C. Shoulder dystocia:** Macrosomia in GDM involves disproportionate fat deposition around the shoulders and abdomen, significantly increasing the risk of the shoulders getting stuck during delivery. * **D. Polyhydramnios:** Fetal hyperglycemia causes osmotic diuresis, leading to fetal polyuria, which increases the volume of amniotic fluid. ### NEET-PG High-Yield Pearls * **Most common malformation in Overt Diabetes:** Ventricular Septal Defect (VSD). * **Most specific malformation in Overt Diabetes:** Caudal Regression Syndrome (Sacral Agenesis). * **Screening for GDM:** Best done at 24–28 weeks using the DIPSI criteria (75g oral glucose; positive if 2-hour value $\geq$ 140 mg/dL). * **Target Blood Sugars in GDM:** Fasting $<95$ mg/dL; 1-hour postprandial $<140$ mg/dL; 2-hour postprandial $<120$ mg/dL.

Question 623: Which of the following statements is FALSE regarding pregnancy with epilepsy?

A. Seizure risk is decreased by 30% in most epileptic women during pregnancy. (Correct Answer)
B. Valproate is associated with adverse fetal outcomes.
C. Antiepileptic drugs (AEDs) can cause malformations in approximately 15% of cases.
D. Monotherapy with antiepileptic drugs is generally preferred during pregnancy.

Explanation: ### Explanation **1. Why Option A is False (The Correct Answer):** In reality, seizure frequency remains **unchanged** in about 50–60% of pregnant women. For the remainder, seizure risk is more likely to **increase** (approx. 20–30%) rather than decrease. This increase is driven by physiological changes such as hemodilution (lowering drug concentration), increased hepatic metabolism, increased renal clearance, and decreased patient compliance due to fear of teratogenicity. **2. Analysis of Other Options:** * **Option B:** Valproate is highly teratogenic. It is associated with the highest risk of major congenital malformations (MCMs), specifically **neural tube defects** (risk ~1–2%), and is linked to lower IQ and neurodevelopmental delays in children. * **Option C:** While the baseline risk of malformations in the general population is 2–3%, the risk in women on AEDs is significantly higher. While 15% represents the higher end of the spectrum (often seen with polytherapy or high-dose valproate), it is a clinically recognized risk factor compared to the general population. * **Option D:** **Monotherapy** at the lowest effective dose is the gold standard. Polytherapy (using multiple AEDs) synergistically increases the risk of structural malformations. **3. NEET-PG High-Yield Clinical Pearls:** * **Pre-conception:** Start **Folic acid (5 mg/day)** at least 3 months prior to conception to reduce NTD risk. * **Drug of Choice:** Levetiracetam or Lamotrigine are generally preferred due to lower teratogenic potential. * **Vitamin K:** Though controversial, some guidelines suggest 10 mg oral Vitamin K daily in the last month of pregnancy for women on enzyme-inducing AEDs (e.g., Phenytoin, Phenobarbital) to prevent neonatal hemorrhagic disease. * **Breastfeeding:** Encouraged, as the benefits outweigh the risks of small amounts of AEDs in breast milk.

Question 624: For antenatal fetal monitoring in a diabetic pregnancy, all of the following are useful except?

A. Non-stress test
B. Biophysical profile
C. Doppler flow study (Correct Answer)
D. Fetal kick count

Explanation: **Explanation:** The primary goal of antenatal fetal monitoring in diabetic pregnancies is to prevent stillbirth caused by **fetal acidemia and hyperglycemia-induced hypoxia**. **Why Doppler flow study is the correct answer:** Umbilical artery Doppler flow studies are primarily used to monitor pregnancies complicated by **Intrauterine Growth Restriction (IUGR)** and **Placental Insufficiency** (e.g., Preeclampsia). In a typical diabetic pregnancy (especially Gestational Diabetes or Type 2), the pathophysiology involves fetal hyperinsulinemia and increased metabolic demand rather than primary placental vascular resistance. Therefore, Doppler studies are **not** routinely recommended for monitoring fetal well-being in diabetic patients unless there is concurrent hypertension or suspected growth restriction. **Why the other options are used:** * **Fetal Kick Count (D):** A simple, cost-effective screening tool for all high-risk pregnancies to assess fetal alertness. * **Non-Stress Test (NST) (A):** The most common surveillance tool used (usually starting at 32–34 weeks) to assess fetal heart rate reactivity, which reflects an intact central nervous system. * **Biophysical Profile (BPP) (B):** Combines NST with ultrasound parameters (breathing, movements, tone, and liquor). It is highly sensitive for detecting acute and chronic fetal hypoxia in diabetic mothers. **High-Yield Clinical Pearls for NEET-PG:** * **Target:** The most common cause of fetal demise in poorly controlled diabetes is **fetal acidemia**. * **Polyhydramnios:** Common in diabetes; if present, BPP is often preferred over NST. * **Timing:** For well-controlled GDM, monitoring usually starts at **32–34 weeks**; if poorly controlled, it may start earlier. * **Doppler Exception:** Use Doppler in diabetics **only** if there is associated **Pre-eclampsia** or **Small for Gestational Age (SGA)** fetus.

Question 625: Which of the following statements regarding monozygotic twins is not true?

A. Ultrasound is more useful in the first half of pregnancy
B. Sex discordance can occur rarely
C. They are always monochorionic (Correct Answer)
D. They are more common following ovulation induction

Explanation: **Explanation:** **1. Why Option C is the Correct Answer (The "False" Statement):** Monozygotic (MZ) twins are not always monochorionic. The chorionicity and amnionicity depend entirely on the **timing of the zygotic split**. If the split occurs early (within the first 3 days post-fertilization, at the morula stage), the twins will be **Dichorionic Diamniotic (DCDA)**, just like dizygotic twins. Approximately 25–30% of monozygotic twins are DCDA. **2. Analysis of Other Options:** * **Option A:** Ultrasound is indeed more useful in the first half (specifically the first trimester) for determining chorionicity. Signs like the **'Lambda' (T-sign)** are most accurate before 14 weeks. * **Option B:** While MZ twins are genetically identical, sex discordance can occur rarely due to **post-zygotic non-disjunction** (e.g., one twin is 46,XY and the other is 45,X Turner syndrome) or in cases of phenotypic discordance in disorders of sexual development. * **Option C:** Assisted Reproductive Technology (ART) and ovulation induction are known risk factors that increase the incidence of monozygotic twinning, likely due to micromanipulation of the zona pellucida. **3. High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of Split":** * 0–3 days: DCDA (25-30%) * 4–8 days: Monochorionic Diamniotic (MCDA) — **Most common (70-75%)** * 8–13 days: Monochorionic Monoamniotic (MCMA) — High risk (1-2%) * >13 days: Conjoined twins (Rare) * **T-sign vs. Lambda sign:** Lambda (λ) sign indicates Dichorionic; T-sign indicates Monochorionic. * **Twin-to-Twin Transfusion Syndrome (TTTS):** Occurs only in monochorionic pregnancies.

Question 626: Anti-D immune globulin is administered to Rh-negative women antenatally at which gestational week?

A. 20 weeks
B. 24 weeks
C. 28 weeks (Correct Answer)
D. 30 weeks

Explanation: **Explanation:** The administration of Anti-D immune globulin (RhoGAM) is a critical preventive measure against Rh isoimmunization in Rh-negative, unsensitized mothers. **Why 28 weeks is correct:** The primary goal of antenatal prophylaxis is to neutralize any fetal Rh-positive red blood cells that may enter the maternal circulation. While the risk of fetomaternal hemorrhage (FMH) is low in the first two trimesters, it increases significantly in the third trimester as the placenta thins. Research shows that the incidence of "silent" sensitization peaks after 28 weeks. Administering Anti-D at **28 weeks** provides protective antibody levels that last for approximately 12 weeks, covering the remainder of the pregnancy until delivery. **Analysis of Incorrect Options:** * **A & B (20 & 24 weeks):** At these stages, the risk of spontaneous FMH is negligible. Administering Anti-D this early would result in sub-therapeutic antibody levels by the time the mother reaches full term, leaving her vulnerable during the period of highest risk. * **D (30 weeks):** While closer to the window, waiting until 30 weeks leaves a two-week "gap" (28–30 weeks) where sensitization could occur. International guidelines (ACOG/RCOG) have standardized 28 weeks to maximize the duration of protection. **High-Yield Clinical Pearls for NEET-PG:** 1. **Standard Dose:** 300 mcg (1500 IU) is the standard dose given at 28 weeks; it covers up to 30 ml of fetal whole blood (or 15 ml of fetal RBCs). 2. **Postpartum Dose:** A second dose must be given within **72 hours of delivery** if the neonate is confirmed Rh-positive. 3. **Indirect Coombs Test (ICT):** Anti-D is only given if the mother is **ICT negative** (unsensitized). If ICT is positive, the mother is already sensitized, and Anti-D is of no use. 4. **First Trimester Events:** For abortions or ectopic pregnancies (<13 weeks), a smaller dose of 50 mcg is typically sufficient.

Question 627: A 23-year-old primigravida at 33 weeks gestation presented with jaundice for 2 days. On examination, her BP was 140/90 mmHg, serum bilirubin was 5 mg%, Hb was 8 gm%, platelet count was 90,000/cu.mm, TLC was 10,000/cu.mm, and blood sugar was 40 mg/dL. AST and ALT were 85 and 80 IU/L, respectively. What is the probable diagnosis?

A. Acute Hepatitis A
B. Acute fatty liver in pregnancy (Correct Answer)
C. HELLP syndrome
D. Acute hepatitis E

Explanation: **Explanation:** The clinical presentation of jaundice, mild hypertension, and significant biochemical abnormalities in the third trimester points toward **Acute Fatty Liver of Pregnancy (AFLP)**. **1. Why Acute Fatty Liver of Pregnancy (AFLP) is correct:** AFLP typically occurs in the third trimester. The hallmark that distinguishes AFLP from other pregnancy-related liver disorders is **profound hypoglycemia** (Blood sugar 40 mg/dL in this case) and signs of liver failure. While the transaminases (AST/ALT) are only modestly elevated (usually <500 IU/L), there is significant hyperbilirubinemia and evidence of multi-organ involvement (thrombocytopenia and anemia). The diagnosis is clinically supported by the **Swansea Criteria**. **2. Why other options are incorrect:** * **HELLP Syndrome:** While HELLP presents with hemolysis, elevated liver enzymes, and low platelets, it is rarely associated with severe hypoglycemia or significant jaundice (bilirubin is usually <1.2 mg/dL unless severe). In this patient, the low blood sugar is the "pathognomonic" differentiator favoring AFLP. * **Acute Hepatitis (A or E):** Viral hepatitis typically presents with much higher transaminase levels (often >1000 IU/L) and lacks the systemic features like hypertension or thrombocytopenia seen here. While Hepatitis E can be severe in pregnancy, the hypoglycemia and mild BP elevation strongly suggest a pregnancy-specific pathology. **Clinical Pearls for NEET-PG:** * **Pathophysiology:** AFLP is associated with a deficiency of the enzyme **Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD)** in the fetus. * **Key Differentiator:** Hypoglycemia + Hyperuricemia + Jaundice in the 3rd trimester = AFLP. * **Management:** Immediate stabilization and **urgent delivery**, regardless of gestational age, as it is a life-threatening emergency. * **Swansea Criteria:** Used for diagnosis (includes vomiting, abdominal pain, polydipsia/polyuria, encephalopathy, elevated bilirubin, hypoglycemia, and elevated urate).

Question 628: What is a common cause of recurrent second-trimester fetal loss?

A. Chromosomal anomaly
B. Intrauterine infection
C. Abnormality of cervix and uterus (Correct Answer)
D. Hormonal imbalance

Explanation: **Explanation:** Recurrent pregnancy loss (RPL) is etiologically distinct depending on the gestational age. **Abnormalities of the cervix and uterus** are the most common causes of recurrent **second-trimester** losses. Specifically, **Cervical Insufficiency** (painless cervical dilation) and structural uterine anomalies (such as a septate or bicornuate uterus) or acquired lesions (like submucosal fibroids or intrauterine synechiae) compromise the structural integrity required to hold a growing fetus, leading to mid-trimester expulsions. **Analysis of Options:** * **A. Chromosomal anomaly:** This is the most common cause of **first-trimester** sporadic and recurrent abortions (approx. 50-60%). Their incidence decreases significantly as pregnancy advances into the second trimester. * **B. Intrauterine infection:** While infections (e.g., TORCH, bacterial vaginosis) can cause sporadic mid-trimester loss or preterm labor, they are rarely responsible for *recurrent* losses. * **D. Hormonal imbalance:** Conditions like Luteal Phase Defect (LPD) or uncontrolled diabetes are primarily associated with implantation failure or early first-trimester losses. **High-Yield Clinical Pearls for NEET-PG:** * **Cervical Insufficiency:** Characterized by painless cervical ripening and spontaneous mid-trimester abortion. The gold standard treatment is **McDonald’s or Shirodkar’s Cerclage**, typically performed at 12–14 weeks. * **Uterine Septum:** The most common uterine anomaly associated with recurrent pregnancy loss. * **Antiphospholipid Syndrome (APS):** The most important *treatable* autoimmune cause of recurrent second-trimester loss due to placental thrombosis. * **Rule of Thumb:** 1st Trimester = Genetic/Chromosomal; 2nd Trimester = Anatomic/Structural.

Question 629: Which drug is used for fetal lung maturity?

A. Dexamethasone (Correct Answer)
B. Folic acid
C. Eclomethasone
D. One

Explanation: **Explanation:** The administration of antenatal corticosteroids is a cornerstone in the management of preterm labor (between 24 and 34 weeks of gestation) to accelerate **fetal lung maturity**. These steroids induce the synthesis and release of **surfactant** by Type II pneumocytes, significantly reducing the incidence of Respiratory Distress Syndrome (RDS), Intraventricular Hemorrhage (IVH), and Necrotizing Enterocolitis (NEC). **Why Dexamethasone is Correct:** Dexamethasone and Betamethasone are the drugs of choice because they lack mineralocorticoid activity, have long half-lives, and, most importantly, **cross the placenta** in their active form. The standard WHO/ACOG regimen for Dexamethasone is **6 mg intramuscularly every 12 hours for 4 doses** (total 24 mg). **Analysis of Incorrect Options:** * **Folic acid:** Used periconceptionally to prevent Neural Tube Defects (NTDs) and to treat megaloblastic anemia; it has no effect on lung surfactant. * **Beclomethasone:** While a corticosteroid, it is primarily used via inhalation for asthma or topically. It is not the standard of care for fetal lung maturity due to different pharmacokinetic profiles compared to Dexamethasone. * **Option D ("One"):** This appears to be a distractor or typographical error and carries no clinical relevance to fetal lung maturity. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Betamethasone (12 mg IM, 2 doses, 24 hours apart) is often preferred over Dexamethasone in some guidelines due to a lower risk of cystic periventricular leukomalacia, though both are equally effective for RDS. * **Timing:** Maximum benefit is seen if delivery occurs **24 hours to 7 days** after the first dose. * **Rescue Dose:** A single "rescue course" can be considered if the initial course was given >7 days ago and the patient is still <34 weeks with a fresh risk of preterm delivery.

Question 630: A 31-year-old woman in her second trimester of pregnancy presents with dyspnea on exertion. She has no history of chest pain, cough, or fever, and no known cardiac disease. Physical examination reveals a pulse of 75/min, BP of 110/70 mmHg, and SpO2 of 96%. Chest and cardiovascular examinations are unremarkable. What is the most probable cause of this patient's clinical presentation?

A. Asthma
B. Pulmonary embolism
C. Physiological dyspnea of pregnancy (Correct Answer)
D. Left heart failure

Explanation: **Explanation:** **Physiological dyspnea of pregnancy** is the most likely diagnosis. It affects approximately 60–75% of pregnant women, typically beginning in the first or second trimester. The underlying mechanism is primarily hormonal: increased levels of **progesterone** act as a direct respiratory stimulant, increasing the sensitivity of the respiratory center to CO2. This leads to **hyperventilation** (increased tidal volume), which results in a physiological state of mild respiratory alkalosis. Clinically, the patient remains comfortable at rest, and physical examination (vitals, chest auscultation) is characteristically normal. **Why other options are incorrect:** * **Asthma:** Usually presents with a history of atopy, cough, wheezing, or chest tightness. Physical exam would typically reveal expiratory wheeze. * **Pulmonary Embolism (PE):** While pregnancy is a hypercoagulable state, PE usually presents with sudden-onset dyspnea, tachycardia, tachypnea, and often pleuritic chest pain or hypoxia (SpO2 <95%). * **Left Heart Failure:** This would present with orthopnea, paroxysmal nocturnal dyspnea, and clinical signs like pulmonary crackles (rales), an S3 gallop, or peripheral edema. **High-Yield Clinical Pearls for NEET-PG:** * **Respiratory Changes:** Pregnancy increases **Tidal Volume** (by 40%) and **Minute Ventilation**, but **Functional Residual Capacity (FRC)** and **Residual Volume** decrease due to the elevating diaphragm. * **ABG Profile:** Normal pregnancy shows a compensated **respiratory alkalosis** (pH 7.40–7.45, pCO2 27–32 mmHg). * **Vital Signs:** A respiratory rate >20/min or SpO2 <95% is **never** physiological in pregnancy and warrants investigation for pathology.

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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