Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 811: What is the utero-placental blood flow at term?

A. 300-500 ml/min
B. 500-700 ml/min (Correct Answer)
C. 700-900 ml/min
D. 900-1100 ml/min

Explanation: **Explanation:** The correct answer is **B. 500-700 ml/min**. **1. Understanding the Correct Answer:** During pregnancy, the cardiovascular system undergoes significant remodeling to meet the metabolic demands of the growing fetus. The uterine blood flow increases dramatically from approximately 50 ml/min in the non-pregnant state to **500–700 ml/min at term**. This represents about **10–15% of the total maternal cardiac output**. This increase is achieved through the massive vasodilation of the spiral arteries (mediated by trophoblastic invasion) and a decrease in vascular resistance, ensuring adequate oxygen and nutrient exchange across the placenta. **2. Analysis of Incorrect Options:** * **Option A (300-500 ml/min):** This range represents uterine blood flow during the mid-trimester. It is insufficient for the metabolic requirements of a full-term fetus. * **Options C & D (700-1100 ml/min):** While some textbooks may cite upper limits near 750-800 ml/min in twin pregnancies or exceptionally large placentas, 500-700 ml/min is the standard physiological range for a singleton pregnancy at term used in most standard textbooks (like Williams Obstetrics). **3. High-Yield Clinical Pearls for NEET-PG:** * **Distribution:** At term, approximately 80% of the uterine blood flow goes to the placenta (intervillous space), while the remaining 20% supplies the myometrium. * **Regulation:** Uterine blood flow is **not autoregulated**; it is dependent on maternal systemic blood pressure. Therefore, maternal hypotension (e.g., from spinal anesthesia or supine hypotension syndrome) can lead to immediate fetal hypoxia. * **Resistance:** The uterine artery Doppler shows a **low-resistance flow** pattern in normal pregnancy. Persistence of a "diastolic notch" after 24 weeks is a predictor of pre-eclampsia and IUGR.

Question 812: The following CTG indicates:

A. Fetal head compression
B. Cord compression (Correct Answer)
C. Normal tracing
D. Fetal anemia

Explanation: ***Cord compression*** - **Variable decelerations** are the hallmark of cord compression, appearing as abrupt drops in FHR with **variable timing** relative to contractions. - These decelerations have a characteristic **"V" or "W" shape** and can occur before, during, or after contractions due to intermittent cord occlusion. *Fetal head compression* - Causes **early decelerations** that mirror uterine contractions, starting with contraction onset and returning to baseline as contractions end. - These decelerations are **gradual** (≥30 seconds from onset to nadir) and have a **smooth, uniform shape** that matches contraction intensity. *Normal tracing* - A normal CTG shows **baseline FHR of 110-160 bpm**, **moderate variability** (6-25 bpm), and **no decelerations**. - May include **accelerations** with fetal movement, indicating good fetal oxygenation and neurological function. *Fetal anemia* - Produces a **sinusoidal pattern** with smooth, wave-like oscillations of the baseline FHR resembling a sine wave. - This pattern shows **absent variability** and **no accelerations**, typically associated with severe fetal compromise or Rh isoimmunization.

Question 813: Intrauterine growth restriction (IUGR) is caused by all except:

A. Rh incompatibility (Correct Answer)
B. Smoking
C. Diabetes Mellitus (DM)
D. Chronic Renal Failure (CRF)

Explanation: **Explanation:** **Intrauterine Growth Restriction (IUGR)** refers to a condition where a fetus fails to reach its biological growth potential due to maternal, fetal, or placental factors. **Why Rh Incompatibility is the Correct Answer:** Rh incompatibility typically leads to **fetal hydrops** and **macrosomia** (fetal overgrowth) rather than growth restriction. In this condition, maternal antibodies cause fetal hemolysis, leading to severe anemia. The fetus compensates with extramedullary hematopoiesis, resulting in hepatosplenomegaly and generalized edema (anasarca). Consequently, the fetus appears larger and heavier, making Rh incompatibility a cause of "Large for Gestational Age" (LGA) rather than IUGR. **Analysis of Incorrect Options:** * **Smoking:** Nicotine and carbon monoxide cause vasoconstriction and increase carboxyhemoglobin levels, leading to chronic fetal hypoxia and placental insufficiency—a classic cause of IUGR. * **Diabetes Mellitus (DM):** While gestational diabetes often causes macrosomia, **pre-gestational diabetes** (especially classes D, F, and R with vasculopathy) leads to placental dysfunction and is a significant risk factor for IUGR. * **Chronic Renal Failure (CRF):** Maternal renal disease is associated with chronic hypertension and impaired uterine blood flow, which restricted nutrient delivery to the fetus, leading to IUGR. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of IUGR:** Placental insufficiency (often secondary to maternal hypertension). * **Symmetrical IUGR:** Usually due to early insults like chromosomal anomalies (Trisomy 18) or TORCH infections. * **Asymmetrical IUGR:** Usually due to late-onset factors like Preeclampsia (shows "Head Sparing" effect). * **Ponderal Index:** Used to differentiate between symmetrical and asymmetrical IUGR.

Question 814: In pregnant diabetic patients, intrauterine fetal mortality increases after which week of gestation?

A. 30th week
B. 40th week (Correct Answer)
C. 36th week
D. 25th week

Explanation: **Explanation:** In diabetic pregnancies, the risk of **unexplained intrauterine fetal death (IUFD)** increases significantly as the pregnancy approaches and passes term. The physiological basis for this is multifactorial, involving fetal hyperinsulinemia, which increases fetal metabolic rate and oxygen consumption. This leads to relative fetal hypoxia and acidosis. Additionally, placental insufficiency and vasculopathy associated with diabetes further compromise fetal oxygenation. **Why Option B (40th week) is correct:** Statistically, the incidence of stillbirth in diabetic patients rises sharply after the **36th week**, but the risk becomes most pronounced and clinically significant as the patient reaches the **40th week (term)**. To prevent this, current obstetric guidelines generally recommend delivery between 39 weeks 0 days and 39 weeks 6 days for well-controlled gestational diabetes (GDM), and often earlier (37–38 weeks) for pre-gestational or poorly controlled diabetes. **Why other options are incorrect:** * **Option A (30th week) & D (25th week):** While complications like congenital anomalies or miscarriage occur early, sudden "unexplained" late-trimester deaths are rare at these stages unless there is severe ketoacidosis or extreme vascular disease. * **Option C (36th week):** While the risk *begins* to climb here, it is not the peak threshold for mortality compared to the 40th week. Most protocols initiate intensive fetal surveillance (NST/BPP) starting at 32–36 weeks to mitigate this risk. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of IUFD in Diabetes:** Poor glycemic control leading to chronic fetal hypoxia. * **Target HbA1c:** Ideally <6.0% pre-conception to reduce the risk of congenital malformations (most common: Ventricular Septal Defect; most specific: Caudal Regression Syndrome). * **Delivery Timing:** If diabetes is poorly controlled or there is vascular complication, delivery is considered at 37–38 weeks. If well-controlled on diet/meds, delivery is recommended at 39 weeks to avoid the mortality spike seen at 40 weeks.

Question 815: Which of the following treatments is not indicated in ectopic pregnancy?

A. Salpingectomy
B. Salpingo-oophorectomy (Correct Answer)
C. Salpingostomy
D. Resection of involved segment

Explanation: The management of ectopic pregnancy focuses on removing the conceptus while preserving as much reproductive function as possible. **Explanation of the Correct Answer:** **Salpingo-oophorectomy (Option B)** involves the removal of both the fallopian tube and the ovary. This is **not indicated** because the ovary is rarely involved in a tubal ectopic pregnancy. Preserving the ovary is crucial for maintaining hormonal function and future fertility. Even in cases of ruptured tubal pregnancy with significant hemorrhage, the ovary has a separate blood supply (ovarian artery) and can almost always be salvaged. **Analysis of Incorrect Options:** * **Salpingectomy (Option A):** This is the standard surgical treatment for a ruptured ectopic pregnancy or when the tube is severely damaged. It involves the total removal of the affected fallopian tube. * **Salpingostomy (Option C):** This is a conservative surgical procedure where a longitudinal incision is made on the tube to remove the products of conception, leaving the tube intact. It is preferred in hemodynamically stable patients who desire future fertility. * **Resection of involved segment (Option D):** This is specifically indicated for **isthmic ectopic pregnancies**. Since the isthmus is narrow, salpingostomy can lead to scarring and occlusion; therefore, segmental resection followed by delayed re-anastomosis is often preferred. **NEET-PG High-Yield Pearls:** * **Most common site:** Ampulla of the fallopian tube. * **Most common site for rupture:** Isthmus (due to its narrow lumen). * **Gold Standard Diagnosis:** Transvaginal Ultrasound (TVUS) + Quantitative β-hCG (Discriminatory zone: 1500–2000 mIU/mL). * **Medical Management:** Methotrexate is the drug of choice if the patient is stable, the mass is <3.5–4 cm, and there is no fetal cardiac activity.

Question 816: Which congenital infection in a fetus carries minimal teratogenic risk?

A. HIV (Correct Answer)
B. Rubella
C. Varicella
D. CMV

Explanation: **Explanation:** The core concept in this question is the distinction between **teratogenicity** (structural malformations during organogenesis) and **vertical transmission** (infection of the fetus). **Why HIV is the correct answer:** While HIV carries a significant risk of vertical transmission (mother-to-child transmission) during pregnancy, labor, or breastfeeding, it is **not considered a teratogen**. HIV does not disrupt embryogenesis or cause specific structural birth defects. The primary concern with HIV in pregnancy is the risk of the infant developing neonatal HIV/AIDS, which is managed with Antiretroviral Therapy (ART) and elective cesarean sections, rather than structural anomalies. **Why the other options are incorrect:** * **Rubella (Option B):** Highly teratogenic. **Congenital Rubella Syndrome (CRS)** presents with the classic triad of cataracts, sensorineural deafness, and cardiac defects (PDA), especially if contracted in the first trimester. * **Varicella (Option C):** Causes **Congenital Varicella Syndrome** if contracted between 8–20 weeks of gestation. It is characterized by skin scarring (cicatrices), limb hypoplasia, and chorioretinitis. * **CMV (Option D):** The most common congenital infection. It is a potent teratogen causing microcephaly, periventricular calcifications, and sensorineural hearing loss. **High-Yield NEET-PG Pearls:** * **Highest risk of transmission:** HIV transmission risk is highest during **delivery** (intrapartum), whereas Rubella risk is highest in the **first trimester**. * **Zika Virus:** Another high-yield teratogen to remember, specifically associated with **microcephaly** and "fetal brain disruption sequence." * **Rule of Thumb:** Most "TORCH" infections are teratogenic; HIV and Hepatitis B are notable exceptions that cause neonatal infection without structural malformations.

Question 817: What is the normal fetal heart rate between 37-40 weeks of gestation?

A. 80 - 120 beats per minute
B. 120 - 160 beats per minute (Correct Answer)
C. 140 - 180 beats per minute
D. 160 - 200 beats per minute

Explanation: **Explanation:** The baseline fetal heart rate (FHR) is the mean rate rounded to increments of 5 beats per minute (bpm) during a 10-minute segment, excluding periodic changes and periods of marked variability. At term (37–40 weeks), the normal baseline FHR is **110–160 bpm** (often simplified in exams as **120–160 bpm**). This rate is governed by the balance between the sympathetic and parasympathetic nervous systems. As the fetus matures, the parasympathetic (vagal) tone increases, causing the baseline heart rate to gradually decrease from approximately 160 bpm in early pregnancy to the term range. **Analysis of Options:** * **Option A (80–120 bpm):** This range is too low. A baseline below 110 bpm is defined as **fetal bradycardia**, which may indicate fetal distress, cord compression, or maternal hypotension. * **Option C (140–180 bpm) & D (160–200 bpm):** These ranges are too high. A baseline above 160 bpm is defined as **fetal tachycardia**. Common causes include maternal fever, intrauterine infection (chorioamnionitis), fetal hypoxia, or maternal hyperthyroidism. **High-Yield Clinical Pearls for NEET-PG:** * **Fetal Bradycardia:** Baseline <110 bpm for >10 minutes. * **Fetal Tachycardia:** Baseline >160 bpm for >10 minutes. * **Beat-to-Beat Variability:** The most reliable indicator of fetal well-being (Normal: 6–25 bpm). * **Early Decelerations:** Usually benign; caused by fetal head compression (vagal response). * **Late Decelerations:** Always pathological; indicate uteroplacental insufficiency.

Question 818: What is the classical definition of recurrent pregnancy loss?

A. Two or more consecutive pregnancy losses before 20 weeks' gestation or with a fetal weight less than 500 g
B. Three or more consecutive pregnancy losses before 20 weeks' gestation or with a fetal weight less than 500 g (Correct Answer)
C. Four or more consecutive pregnancy losses before 20 weeks' gestation or with a fetal weight less than 500 g
D. Five or more consecutive pregnancy losses before 20 weeks' gestation or with a fetal weight less than 500 g

Explanation: **Explanation:** The definition of Recurrent Pregnancy Loss (RPL) varies slightly between international societies, but the **classical definition** (traditionally used in textbooks like Williams Obstetrics and frequently tested in NEET-PG) is **three or more consecutive pregnancy losses** occurring before 20 weeks of gestation or with a fetal weight less than 500 g. 1. **Why Option B is Correct:** This definition follows the traditional clinical criteria. It emphasizes "consecutive" losses to distinguish it from sporadic miscarriages, which are common in the general population. The 20-week/500g threshold marks the boundary between spontaneous abortion and preterm birth/stillbirth. 2. **Why Other Options are Incorrect:** * **Option A (Two losses):** While the **ASRM (American Society for Reproductive Medicine)** and **ESRE (European Society of Human Reproduction and Embryology)** now recommend evaluation after **two** losses (consecutive or non-consecutive) to initiate early intervention, this is considered the *modern* or *clinical* definition rather than the "classical" one. * **Options C & D:** These are incorrect as they exceed the established diagnostic thresholds used in any major clinical guideline. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Cause:** Genetic factors (chromosomal abnormalities) are the most common cause of sporadic loss, but **Antiphospholipid Syndrome (APLS)** is the most important treatable *acquired* cause of RPL. * **Parental Karyotyping:** Indicated in couples with RPL to rule out balanced reciprocal or Robertsonian translocations (found in 2-5% of couples). * **Uterine Factors:** Septate uterus is the most common Mullerian anomaly associated with RPL. * **Prognosis:** Even after 3 losses, the chance of a successful future pregnancy is approximately 60-70% without specific treatment, depending on the etiology.

Question 819: A 30-year-old class D diabetic is concerned about pregnancy. She can be assured that which of the following risks is the same for her as for the general population?

A. Preeclampsia and eclampsia
B. Infection
C. Fetal cystic fibrosis (Correct Answer)
D. Postpartum hemorrhage after vaginal delivery

Explanation: **Explanation:** The core concept here is distinguishing between **maternal/fetal complications directly influenced by maternal hyperglycemia** and **unrelated genetic conditions.** **Why Fetal Cystic Fibrosis is the Correct Answer:** Cystic Fibrosis (CF) is an **autosomal recessive genetic disorder** caused by mutations in the CFTR gene. Its inheritance depends solely on the carrier status of the parents. Maternal diabetes (pre-gestational or gestational) does not alter the genetic makeup of the gametes or the risk of Mendelian inheritance. Therefore, the risk remains identical to that of the general population. **Why the Other Options are Incorrect:** * **Preeclampsia and Eclampsia:** Diabetic patients (especially Class D with underlying vasculopathy) have a **3–4 times higher risk** of hypertensive disorders due to endothelial dysfunction and underlying renal involvement. * **Infection:** Hyperglycemia impairs leukocyte function (chemotaxis and phagocytosis), making diabetic mothers more prone to **monilial vulvovaginitis, urinary tract infections (UTIs), and puerperal sepsis.** * **Postpartum Hemorrhage (PPH):** Diabetes is associated with **fetal macrosomia**, which leads to overdistension of the uterus. This increases the risk of **uterine atony**, the leading cause of PPH. **High-Yield NEET-PG Pearls:** * **White’s Classification:** Class D refers to diabetes with onset before age 10, duration >20 years, or the presence of benign retinopathy. * **Most Common Fetal Anomaly in Diabetes:** Cardiac defects (specifically **Ventricular Septal Defect**). * **Most Specific Fetal Anomaly:** **Caudal Regression Syndrome** (Sacral Agenesis). * **HbA1c Goal:** Ideally **<6.0–6.5%** preconception to minimize the risk of congenital malformations.

Question 820: The Twin Peak sign is characteristic of which of the following conditions?

A. Dichorionic Diamniotic twins (Correct Answer)
B. Monochorionic Diamniotic twins
C. Monochorionic Monoamniotic twins
D. Conjoined twins

Explanation: ### Explanation The **Twin Peak sign**, also known as the **Lambda (λ) sign**, is a pathognomonic ultrasonographic marker used to determine chorionicity in multiple pregnancies. **1. Why Option A is Correct:** In **Dichorionic Diamniotic (DCDA)** twins, each fetus has its own placenta. When these two placentas are adjacent or fused, a triangular projection of placental tissue grows into the base of the inter-twin membrane. This creates a thick, "lambda-shaped" appearance at the junction. It is most reliably seen during the first trimester (10–14 weeks). **2. Why the Other Options are Incorrect:** * **Option B (MCDA):** In Monochorionic Diamniotic twins, there is only one placenta. The inter-twin membrane is composed of only two layers of amnion (without intervening chorion), resulting in a very thin junction known as the **"T-sign."** * **Option C (MCMA):** In Monochorionic Monoamniotic twins, there is no intervening membrane at all between the fetuses; therefore, neither the Lambda nor the T-sign is present. * **Option D (Conjoined Twins):** These are a rare complication of monoamniotic pregnancies where the embryonic disc fails to divide completely. Diagnosis is based on fused fetal body parts, not membrane characteristics. **3. High-Yield Clinical Pearls for NEET-PG:** * **Chorionicity** is the most important factor determining the prognosis and management of twin pregnancies. * **Lambda Sign (λ):** DCDA twins (Thick membrane >2mm). * **T-Sign:** MCDA twins (Thin membrane <2mm). * **Best time for ultrasound:** 10–14 weeks (accuracy decreases as the pregnancy progresses and the placenta compresses the membrane). * **Vanishing Twin Syndrome:** More common in DCDA pregnancies. * **TTTS (Twin-to-Twin Transfusion Syndrome):** Only occurs in Monochorionic pregnancies.

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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