Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 711: All of the following are scenarios in which it would have been appropriate to administer RhoGam to this patient in the past, except:

A. After a spontaneous first-trimester abortion (Correct Answer)
B. After treatment for ectopic pregnancy
C. Within 3 days of delivering an Rh-positive fetus
D. At the time of amniocentesis

Explanation: The administration of Anti-D immunoglobulin (RhoGam) is critical in preventing Rh isoimmunization in Rh-negative, unsensitized mothers. **Explanation of the Correct Answer (A):** The correct answer is **A** because a **spontaneous** first-trimester abortion (miscarriage) occurring before 12 weeks of gestation carries a negligible risk of feto-maternal hemorrhage (FMH) sufficient to cause sensitization. Current clinical guidelines (such as ACOG) state that RhoGam is **not mandatory** for spontaneous abortions before 12 weeks, although it is still required for induced abortions or any instrumental evacuation (D&C) in the first trimester. **Analysis of Incorrect Options:** * **B. Ectopic Pregnancy:** Even in the first trimester, an ectopic pregnancy (ruptured or treated) is considered a high-risk event for FMH. Anti-D (50 mcg or 300 mcg) must be administered. * **C. Within 3 days of delivering an Rh-positive fetus:** This is the standard postpartum prophylaxis. 300 mcg of Anti-D should be given within 72 hours of delivery to neutralize up to 30 mL of fetal whole blood. * **D. Amniocentesis:** Any invasive prenatal procedure (amniocentesis, CVS, or cordocentesis) can cause fetal blood to enter the maternal circulation, necessitating RhoGam administration. **NEET-PG High-Yield Pearls:** 1. **Standard Dose:** 300 mcg (1500 IU) is the standard dose; 50 mcg is sufficient for first-trimester events (except ectopic pregnancy where 300 mcg is often preferred). 2. **Routine Prophylaxis:** Administered at **28 weeks** gestation to all Rh-negative unsensitized women. 3. **Kleihauer-Betke Test:** Used to quantify the volume of FMH to determine if additional doses of RhoGam are needed beyond the standard 300 mcg. 4. **Indirect Coombs Test (ICT):** Must be negative (unsensitized) before administering RhoGam. If ICT is positive, the mother is already sensitized, and RhoGam is ineffective.

Question 712: What is the surest sign of intrauterine fetal death?

A. Small sized fetus
B. Overriding of cranial bones
C. Spalding's sign
D. Gas in the aorta (Correct Answer)

Explanation: **Explanation:** Intrauterine Fetal Death (IUFD) is diagnosed through various radiological and clinical signs. The **surest (most specific and earliest) sign** of fetal death is the presence of **gas in the fetal heart or great vessels (Aorta)**, known as **Robert’s Sign**. 1. **Why "Gas in the Aorta" is correct:** Robert’s Sign occurs due to the release of gases (mainly nitrogen) from the decomposition of fetal blood. It can appear on an X-ray or ultrasound as early as **6 to 12 hours** after death. Because gas cannot exist within the circulatory system of a living fetus, its presence is a pathognomonic and definitive indicator of fetal demise. 2. **Analysis of Incorrect Options:** * **Small sized fetus:** This is non-specific. A small fetus may indicate Intrauterine Growth Restriction (IUGR) or incorrect dating rather than death. * **Overriding of cranial bones (Spalding’s Sign):** While a classic sign, it is **not the surest**. It occurs due to the liquefaction of the brain and loss of intracranial pressure, causing the vault bones to collapse. Crucially, it takes **4 to 7 days** to develop and can be a false positive in a living fetus during labor (due to molding). * **Spalding's Sign:** (See above). It is a late sign compared to Robert's Sign. **High-Yield Clinical Pearls for NEET-PG:** * **Robert’s Sign:** Gas in fetal vessels (Earliest sign, ~12 hours). * **Spalding’s Sign:** Overriding of skull bones (Late sign, >4 days). * **Deuel’s Halo Sign:** Edema of the fetal scalp causing a "halo" appearance (due to fluid accumulation in subcutaneous tissues). * **Curvature of the Spine:** Excessive angulation of the fetal spine due to loss of muscle tone. * **Gold Standard:** The investigation of choice for IUFD today is **Ultrasonography**, demonstrating the absence of fetal cardiac activity.

Question 713: What is the most common cause of thrombocytopenia in pregnancy?

A. Immune thrombocytopenia
B. Incidental thrombocytopenia
C. Idiopathic thrombocytopenia
D. Benign gestational thrombocytopenia (Correct Answer)

Explanation: **Explanation:** **Gestational Thrombocytopenia** (also known as incidental thrombocytopenia of pregnancy) is the most common cause of a low platelet count during pregnancy, accounting for approximately **70–80% of cases**. It is a diagnosis of exclusion characterized by a mild decrease in platelets (typically >70,000/µL, but most often >100,000/µL) occurring in the mid-to-late second or third trimester. The underlying mechanism is thought to be a combination of hemodilution (increased plasma volume) and accelerated platelet consumption in the placenta. It is "benign" because it does not affect the fetus (no fetal thrombocytopenia) and resolves spontaneously within 1–2 months postpartum. **Analysis of Incorrect Options:** * **Option A & C (Immune/Idiopathic Thrombocytopenia):** ITP is the most common cause of isolated thrombocytopenia in the **first trimester**. Unlike gestational thrombocytopenia, ITP can cause severe thrombocytopenia (<50,000/µL) and carries a risk of neonatal thrombocytopenia as IgG antibodies can cross the placenta. * **Option B (Incidental Thrombocytopenia):** While this is a synonym for gestational thrombocytopenia, "Benign Gestational Thrombocytopenia" is the more specific clinical terminology used in standard textbooks (like Williams Obstetrics) to describe this physiological variant. **NEET-PG High-Yield Pearls:** * **Platelet Cut-off:** Gestational thrombocytopenia rarely drops below 70,000/µL. If platelets are <50,000/µL, suspect ITP or preeclampsia/HELLP syndrome. * **Management:** No specific treatment is required for gestational thrombocytopenia; it is not a contraindication to regional anesthesia (epidural) if platelets are >70,000–80,000/µL. * **Second most common cause:** Preeclampsia/HELLP syndrome (approx. 20% of cases).

Question 714: All are true regarding symmetric IUGR except?

A. Obstetric cause like utero-placental insufficiency (Correct Answer)
B. Ponderal index > 2
C. Problem occurring in first trimester
D. Brain growth (head circumference) spared

Explanation: **Explanation:** Intrauterine Growth Restriction (IUGR) is classified into two types: **Symmetric (Type I)** and **Asymmetric (Type II)**. Understanding the distinction is high-yield for NEET-PG. **Why Option A is the correct answer (The False Statement):** Symmetric IUGR is typically caused by **intrinsic factors** that affect the fetus from early pregnancy, such as chromosomal abnormalities (e.g., Trisomies), intrauterine infections (TORCH), or severe maternal malnutrition. In contrast, **utero-placental insufficiency** is the hallmark cause of **Asymmetric IUGR**, where growth slows down later in pregnancy (third trimester) due to a lack of nutrients. **Analysis of other options:** * **Option B (Ponderal Index > 2):** In symmetric IUGR, both weight and length are proportionately reduced. Therefore, the Ponderal Index (Weight/Length³) remains **normal (>2)**. In asymmetric IUGR, the fetus is "wasted," leading to a low Ponderal Index (<2). * **Option C (First Trimester):** Symmetric IUGR results from an insult during the **hyperplastic phase** of cellular growth (early pregnancy), leading to a decrease in the total number of cells. * **Option D (Brain growth spared):** This is a characteristic of **Asymmetric IUGR** (Brain-sparing effect). In **Symmetric IUGR**, there is no brain-sparing; the head circumference, abdominal circumference, and femur length are all proportionately small. **Clinical Pearls for NEET-PG:** * **Symmetric IUGR:** Early onset, decreased cell *number*, normal HC/AC ratio, Ponderal Index >2, poor prognosis. * **Asymmetric IUGR:** Late onset (3rd trimester), decreased cell *size*, increased HC/AC ratio (Head > Abdomen), Ponderal Index <2, better prognosis with postnatal catch-up growth. * **Most common cause of IUGR overall:** Utero-placental insufficiency (Asymmetric).

Question 715: Which of the following can cause an elevated Mean Corpuscular Volume (MCV) in pregnancy?

A. Megaloblastic anemia
B. Alcohol use
C. Hypothyroidism
D. All of the above (Correct Answer)

Explanation: **Explanation:** The **Mean Corpuscular Volume (MCV)** measures the average size of a red blood cell. In pregnancy, while a slight physiological increase in MCV occurs due to increased erythropoiesis, a significant elevation (Macrocytosis, MCV >100 fL) indicates underlying pathology. **Why "All of the above" is correct:** 1. **Megaloblastic Anemia:** This is the most common cause of macrocytosis in pregnancy, primarily due to **Folic Acid deficiency** (increased fetal demand) or, less commonly, Vitamin B12 deficiency. Deficiency impairs DNA synthesis, leading to large, immature RBCs. 2. **Alcohol Use:** Alcohol has a direct toxic effect on the bone marrow and interferes with folate metabolism, leading to macrocytic changes even in the absence of liver disease. 3. **Hypothyroidism:** Thyroid hormones are essential for erythropoiesis. Hypothyroidism slows down cell division in the bone marrow, resulting in the release of larger, macrocytic cells. **Clinical Pearls for NEET-PG:** * **Physiological Anemia of Pregnancy:** This is a **normocytic normochromic** anemia caused by a disproportionate increase in plasma volume (50%) compared to RBC mass (20-30%), leading to hemodilution. * **Iron Deficiency Anemia (IDA):** The most common cause of anemia in pregnancy globally; it typically presents with **decreased MCV** (Microcytic). * **High-Yield Lab Finding:** In megaloblastic anemia, look for **hypersegmented neutrophils** on a peripheral smear. * **Prophylaxis:** The WHO/Government of India (IFA tablets) recommends 60mg elemental iron and 500mcg folic acid daily for pregnant women to prevent these conditions.

Question 716: What is the dose of Anti-D immunoglobulin given to an Rh-negative patient with ectopic pregnancy in the first trimester?

A. 10mcg
B. 25mcg
C. 40mcg
D. 50mcg (Correct Answer)

Explanation: **Explanation:** The correct answer is **50 mcg (Option D)**. Rh-isoimmunization occurs when an Rh-negative mother is exposed to Rh-positive fetal red blood cells, leading to the production of anti-D antibodies. In the first trimester (up to 12–13 weeks), the total fetal blood volume is very small. Therefore, a "mini-dose" of **50 mcg** of Anti-D immunoglobulin is sufficient to neutralize the potential feto-maternal hemorrhage (FMH) associated with conditions like ectopic pregnancy, threatened abortion, or induced abortion. **Analysis of Options:** * **10 mcg, 25 mcg, 40 mcg (Options A, B, C):** These doses are sub-therapeutic and do not follow standard clinical guidelines (ACOG/RCOG/FOGSI) for the prevention of Rh-sensitization. * **50 mcg (Option D):** This is the standard "mini-dose" recommended for first-trimester sensitizing events. It can neutralize up to 2.5–5 ml of Rh-positive whole blood. **High-Yield Clinical Pearls for NEET-PG:** * **Standard Dose:** After 12 weeks of gestation or following full-term delivery, the standard dose is **300 mcg**, which neutralizes **30 ml** of fetal whole blood (or 15 ml of packed RBCs). * **Timing:** Anti-D should ideally be administered within **72 hours** of the sensitizing event. * **Kleihauer-Betke (KB) Test:** Used to quantify the volume of FMH to determine if additional doses of Anti-D are required beyond the standard 300 mcg in the third trimester or postpartum. * **Routine Prophylaxis:** In an unsensitized Rh-negative woman, 300 mcg is routinely given at **28 weeks** of gestation.

Question 717: Antenatal corticosteroids to reduce neonatal respiratory distress syndrome is most effective:

A. When given between 28 and 34 weeks of gestation (Correct Answer)
B. When given every week
C. When given within 48 hours of delivery
D. When given less than 28 weeks of gestation

Explanation: **Explanation:** The primary goal of antenatal corticosteroids (ACS) is to accelerate fetal lung maturity by stimulating the production of surfactant by Type II pneumocytes. **Why Option A is correct:** The maximum benefit of ACS in reducing the incidence and severity of Respiratory Distress Syndrome (RDS), Intraventricular Hemorrhage (IVH), and Necrotizing Enterocolitis (NEC) is seen when administered between **24 and 34 weeks** of gestation. While the question specifies 28–34 weeks, this remains the most effective window as the fetal lungs are in the saccular stage of development and highly responsive to steroids. **Why other options are incorrect:** * **Option B:** Weekly administration (serial courses) is contraindicated. It does not provide additional respiratory benefit and is associated with decreased birth weight and reduced head circumference. * **Option C:** While the maximum effect occurs if delivery happens between 24 hours and 7 days after the first dose, "within 48 hours" is too narrow a window. The treatment is most effective when the full course is completed at least 24 hours before delivery. * **Option D:** Before 24–26 weeks (pre-viable or periviable period), the lungs are in the canalicular stage with minimal surfactant-producing capacity, making steroids less effective, though they are still considered from 23 weeks in certain guidelines. **NEET-PG High-Yield Pearls:** * **Standard Regimen:** Betamethasone (12 mg IM, 2 doses, 24 hours apart) or Dexamethasone (6 mg IM, 4 doses, 12 hours apart). * **Betamethasone** is generally preferred due to better reduction in IVH. * **Rescue Dose:** A single repeat course can be given if the initial course was >7 days ago and the gestational age is <34 weeks. * **Late Preterm:** Recent guidelines (ACOG) now suggest considering ACS up to **36 weeks 6 days** in women at high risk of imminent preterm birth who have not received a prior course.

Question 718: Fetal pulmonary maturity can be evaluated by phospholipids' activity in amniotic fluid. In which of the following pregnancies does the fetus have the least chance of developing respiratory distress syndrome (RDS)?

A. Normal pregnancy: amniotic fluid L/S ratio is 1.8:1, phosphatidyl glycerol (PG) is absent
B. Diabetic pregnancy: amniotic fluid L/S ratio is 2:1, PG is absent
C. Diabetic pregnancy: amniotic fluid L/S ratio is 2:1, PG is present (Correct Answer)
D. All of the above

Explanation: **Explanation:** Fetal lung maturity is determined by the production of surfactants, primarily phospholipids, which reduce surface tension in the alveoli. The two most critical markers are the **Lecithin/Sphingomyelin (L/S) ratio** and the presence of **Phosphatidylglycerol (PG)**. 1. **Why Option C is Correct:** In a normal pregnancy, an **L/S ratio ≥ 2:1** typically indicates maturity. However, in **diabetic pregnancies**, hyperinsulinemia in the fetus can inhibit the action of surfactant proteins, leading to RDS even with an L/S ratio of 2:1. Therefore, the presence of **Phosphatidylglycerol (PG)** is the most reliable "final marker" of maturity. PG appears late (around 35–36 weeks) and its presence provides the highest assurance that RDS will not occur, regardless of the diabetic status. 2. **Why Other Options are Incorrect:** * **Option A:** An L/S ratio of 1.8:1 is below the maturity threshold (2:1), and the absence of PG indicates an immature lung profile, posing a high risk for RDS. * **Option B:** In a diabetic mother, an L/S ratio of 2:1 without PG is notoriously unreliable. Insulin acts as an antagonist to cortisol-induced lung maturation, often leading to "false positive" L/S ratios where the lungs remain functionally immature. **High-Yield Clinical Pearls for NEET-PG:** * **L/S Ratio:** Lecithin increases as the lungs mature, while Sphingomyelin remains constant. A ratio of **2:1** is the standard cutoff for maturity in non-diabetic patients. * **Phosphatidylglycerol (PG):** It is not affected by blood or meconium contamination in the sample, making it a robust marker. * **Amniotic Fluid Index (AFI):** The sample for these tests is obtained via **amniocentesis**. * **Corticosteroids:** Dexamethasone or Betamethasone is administered to the mother to accelerate surfactant production if preterm delivery is anticipated.

Question 719: Golden coloured amniotic fluid is typically seen in which of the following conditions?

A. Rh incompatibility (Correct Answer)
B. Fetal death
C. Intrauterine Growth Restriction (IUGR)
D. Fetal distress with IUGR

Explanation: **Explanation:** The color of amniotic fluid is a significant clinical indicator of fetal well-being. **Golden-colored amniotic fluid** is a classic diagnostic sign of **Rh isoimmunization (Rh incompatibility)**. **1. Why Rh Incompatibility is correct:** In Rh isoimmunization, maternal antibodies cross the placenta and cause hemolysis of fetal red blood cells. This massive breakdown of hemoglobin leads to the production of **unconjugated bilirubin**. This bilirubin is excreted into the fetal urine and subsequently into the amniotic fluid, imparting a characteristic golden-yellow hue. **2. Why other options are incorrect:** * **Fetal death (Option B):** In cases of Intrauterine Fetal Death (IUFD), the amniotic fluid typically appears **dark brown or "tobacco juice"** colored due to the presence of decomposed blood and macerated fetal tissues. * **Intrauterine Growth Restriction (Option C):** Simple IUGR does not typically change the color of the fluid unless accompanied by distress. * **Fetal distress with IUGR (Option D):** Fetal distress leads to the passage of meconium. This results in **greenish** amniotic fluid (meconium-stained). If the meconium is old, it may appear greenish-yellow (saffron). **Clinical Pearls for NEET-PG:** * **Normal:** Colorless or pale straw-colored (near term). * **Green (Meconium):** Fetal distress (acute). * **Golden:** Rh incompatibility (due to bilirubin). * **Greenish-Yellow (Saffron):** Post-maturity. * **Dark Red/Port Wine:** Abruptio placentae (due to concealed hemorrhage). * **Dark Brown (Tobacco juice):** I.U.F.D.

Question 720: Which of the following conditions is associated with increased AFP levels?

A. Down's syndrome
B. Molar pregnancy
C. Overestimated gestational age
D. Congenital nephrosis (Correct Answer)

Explanation: **Explanation:** Alpha-fetoprotein (AFP) is a glycoprotein synthesized by the fetal yolk sac and liver. It is excreted into the fetal urine and subsequently enters the maternal circulation. Levels of Maternal Serum AFP (MSAFP) are a crucial screening tool between 15–20 weeks of gestation. **Why Congenital Nephrosis is Correct:** In **Congenital Nephrosis (Finnish type)**, there is a defect in the glomerular filtration barrier (specifically the protein nephrin). This leads to massive proteinuria in utero. Since AFP is a protein, it leaks into the amniotic fluid in large quantities and subsequently into the maternal serum, resulting in **markedly elevated AFP levels**. **Analysis of Incorrect Options:** * **Down’s Syndrome (Trisomy 21):** This is associated with **decreased** AFP levels (along with decreased Estriol and increased hCG/Inhibin-A). * **Molar Pregnancy:** Gestational trophoblastic disease is associated with **decreased** AFP levels because there is no functional fetal liver or yolk sac to produce it. * **Overestimated Gestational Age:** AFP levels rise naturally as pregnancy progresses. If the gestational age is overestimated (e.g., the patient is actually 14 weeks but thought to be 18 weeks), the AFP will appear **falsely low** for the perceived date. Conversely, *underestimated* age causes high AFP. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of elevated MSAFP:** Underestimated gestational age (dating error). * **Other causes of increased AFP:** Neural Tube Defects (Anencephaly, Spina Bifida), Abdominal wall defects (Omphalocele, Gastroschisis), Multiple gestations, and Fetal demise. * **Mnemonic for Low AFP:** "**D**own **M**e **Q**uickly" (**D**own syndrome, **M**olar pregnancy, **Q**uestionable/Overestimated dates).

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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