Maternal-Fetal Medicine Practice Questions

Q: All the following are signs of intrauterine fetal death except?

Hegar's sign. **Explanation:** The correct answer is **Hegar’s sign** because it is a sign of **early pregnancy**, not fetal death. **1. Why Hegar’s sign is the correct answer:** Hegar’s sign is a clinical indicator of pregnancy typically elicited between **6–10 weeks of gestation**. It refers to the softening of the uterine isthmus, allowing the fingers of the examiner to seemingly meet during a bimanual examination. Since it is a physiological change of a progressing early pregnancy, it has no diagnostic value in identifying intrauterine fetal death (IUFD). **2. Analysis of Radiological Signs of IUFD (Incorrect Options):** The other options represent classic radiological signs seen on X-ray (though now largely replaced by Ultrasound) following fetal demise: * **Spalding’s sign:** Overlapping of the fetal skull bones due to liquefaction of the brain and loss of intra-cranial pressure. It usually appears 4–7 days after death. * **Robert’s sign:** The presence of gas (usually nitrogen) in the fetal heart and large vessels. It is often the earliest radiological sign, appearing within 12 hours of death. * **Halo sign (Deuel’s sign):** Elevation of the fetal scalp fat due to edema, creating a "halo" appearance around the skull. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Real-time **Ultrasonography** (demonstrating absence of fetal cardiac activity) is the definitive investigation for IUFD. * **Deuel’s Sign vs. Spalding’s:** Spalding’s involves bone; Deuel’s involves soft tissue (scalp edema). * **Other signs:** **Rolander’s sign** (excessive curvature of the fetal spine) is also associated with IUFD.

Q: What is the recommended time for termination of pregnancy in a female with type 1 diabetes controlled with insulin?

37+ weeks. **Explanation:** The management of a pregnant woman with Type 1 Diabetes Mellitus (T1DM) requires a delicate balance between ensuring fetal lung maturity and preventing the risk of late-gestational complications, such as stillbirth and macrosomia. **Why 37+ weeks is correct:** In women with pre-gestational diabetes (Type 1 or Type 2) that is well-controlled with insulin, the current clinical guidelines (ACOG and FIGO) recommend delivery between **37 weeks 0 days and 38 weeks 6 days**. Delivery during the early term period (37+ weeks) is preferred because the risk of intrauterine fetal death (IUFD) increases significantly after 39 weeks due to placental insufficiency and metabolic complications, while fetal lung maturity is generally achieved by this stage. **Why the other options are incorrect:** * **A. 40 weeks:** Waiting until the due date (full term) is avoided in insulin-dependent diabetics due to the high risk of placental aging, sudden fetal demise, and shoulder dystocia from macrosomia. * **B. 32 weeks & D. 34 weeks:** These represent preterm deliveries. Unless there is an acute maternal or fetal indication (e.g., severe preeclampsia, non-reassuring fetal heart rate, or vasculopathy), delivery this early is avoided to prevent complications of prematurity like Respiratory Distress Syndrome (RDS). **High-Yield Clinical Pearls for NEET-PG:** * **Poorly Controlled Diabetes:** If there is poor glycemic control or vascular complications (nephropathy/retinopathy), delivery is often considered earlier, between **34 0/7 and 36 6/7 weeks**. * **Gestational Diabetes (GDM):** If controlled on diet, delivery can wait until **39–40+6 weeks**. If controlled on drugs/insulin, deliver at **39+ weeks**. * **Steroid Cover:** If delivery is planned before 37 weeks, antenatal corticosteroids are indicated to accelerate lung maturity, though they require strict insulin adjustment due to hyperglycemia.

Q: All of the following may be observed in a normal pregnancy except?

Increase in blood viscosity. **Explanation:** The correct answer is **C. Increase in blood viscosity**. In a normal pregnancy, blood viscosity actually **decreases**. This is due to the disproportionate increase in plasma volume (approx. 40-50%) compared to the increase in red cell mass (approx. 20-30%). This "hemodilution" results in a lower hematocrit and reduced blood viscosity, which ensures better perfusion of the placental bed and reduces cardiac afterload. **Analysis of Options:** * **A. Fall in serum iron concentration:** Despite an increase in total red cell mass, the demand for iron by the fetus and the expanding maternal blood volume exceeds dietary intake. This leads to a physiological fall in serum iron levels. * **B. Increase in serum iron binding capacity (TIBC):** In response to lower iron stores and increased demand, the liver increases the production of Transferrin. Consequently, the Total Iron Binding Capacity (TIBC) rises during pregnancy. * **D. Increase in blood oxygen carrying capacity:** Although there is "physiological anemia" due to hemodilution, the absolute number of red blood cells and the total hemoglobin mass increase. Therefore, the total oxygen-carrying capacity of the blood is higher than in the non-pregnant state to meet fetal demands. **High-Yield Clinical Pearls for NEET-PG:** * **Plasma Volume vs. RBC Mass:** Plasma volume starts increasing at 6 weeks and peaks at 32-34 weeks. * **Physiological Anemia:** Defined by the WHO as Hb < 11 g/dL in pregnancy. * **Cardiac Output:** Increases by 30-50%, peaking by the end of the second trimester. * **Hypercoagulability:** Pregnancy is a pro-thrombotic state (increased Factors VII, VIII, IX, X, and Fibrinogen), but viscosity remains low due to hemodilution.

Q: Which of the following is NOT a cause of intrauterine growth retardation?

Gestational diabetes. **Explanation** Intrauterine Growth Retardation (IUGR) occurs when there is a restriction in the delivery of oxygen and nutrients to the fetus, leading to a failure to reach its biological growth potential. **Why Gestational Diabetes (GDM) is the correct answer:** In GDM, maternal hyperglycemia leads to fetal hyperglycemia. This stimulates the fetal pancreas to secrete excess insulin (**fetal hyperinsulinemia**). Since insulin is a potent anabolic hormone (growth promoter), it typically results in **fetal macrosomia** (large for gestational age) rather than growth retardation. *Note: IUGR in diabetes is only seen in long-standing Pre-gestational Diabetes with established vasculopathy (White’s Class D, F, R).* **Analysis of incorrect options:** * **Severe Anemia:** Leads to reduced oxygen-carrying capacity of maternal blood, causing chronic fetal hypoxia and subsequent growth restriction. * **Pregnancy-Induced Hypertension (PIH):** This is the most common cause of IUGR. It causes vasospasm and pathological changes in the placental spiral arteries, leading to **uteroplacental insufficiency**. * **Maternal Heart Disease:** Conditions (especially cyanotic heart disease) result in chronic maternal hypoxemia and reduced cardiac output, limiting nutrient transfer to the fetus. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of IUGR:** Uteroplacental insufficiency (often due to PIH). * **Symmetrical IUGR:** Usually due to early insults like chromosomal anomalies or TORCH infections (Ponderal index is normal). * **Asymmetrical IUGR:** Usually due to placental insufficiency (Head sparing effect; Ponderal index is low). * **GDM Complications:** Macrosomia, shoulder dystocia, neonatal hypoglycemia, and polyhydramnios.

Q: Which of the following has been proved to be effective in the management of preeclampsia?

Magnesium. **Explanation:** The correct answer is **Magnesium (Magnesium Sulfate/MgSO₄)**. In the context of preeclampsia, Magnesium Sulfate is the **drug of choice** for the prevention and treatment of seizures (eclampsia). Its primary mechanism involves blocking NMDA receptors in the brain, raising the seizure threshold, and causing cerebral vasodilation to reduce ischemia. Large-scale clinical trials, such as the **Magpie Trial**, conclusively proved that MgSO₄ reduces the risk of eclampsia by more than 50% in women with severe preeclampsia. **Analysis of Incorrect Options:** * **Zinc:** While some studies have explored the role of trace elements in pregnancy, there is no robust clinical evidence to suggest that zinc supplementation is effective in managing or treating preeclampsia. * **Calcium:** Calcium supplementation (1.5–2g/day) is recommended by the WHO for the **prevention** of preeclampsia in populations with low dietary calcium intake. However, it is not used for the **management** (treatment) of the condition once it has developed. **NEET-PG High-Yield Pearls:** * **Therapeutic Level of MgSO₄:** 4–7 mEq/L (or 4.8–8.4 mg/dL). * **Toxicity Sequence:** Loss of patellar reflex (8–10 mEq/L) → Respiratory depression (12 mEq/L) → Cardiac arrest (>25 mEq/L). * **Antidote:** 10 ml of 10% **Calcium Gluconate** IV (administered over 10 minutes). * **Monitoring:** Before each dose, ensure: Respiratory rate >12/min, Patellar reflex present, and Urine output >30 ml/hr (as MgSO₄ is excreted solely by the kidneys).

Q: A woman with no history of prenatal care is about to deliver a baby. She has no history of amniotic rupture, and ultrasound showed severe oligohydramnios. Which of the following conditions can be a cause of oligohydramnios?

Renal agenesis. **Explanation:** The volume of amniotic fluid is a dynamic balance between production and clearance. From the second trimester onwards, **fetal urine** becomes the primary source of amniotic fluid, while fetal swallowing is the main route of clearance. **1. Why Renal Agenesis is Correct:** In cases of bilateral renal agenesis (Potter’s Syndrome), the fetus fails to produce urine. Since fetal micturition is the major contributor to the amniotic pool after 16 weeks of gestation, its absence leads to **severe oligohydramnios**. This lack of fluid often results in pulmonary hypoplasia and characteristic facial deformities due to uterine pressure. **2. Why the Incorrect Options are Wrong:** * **Anencephaly:** This neural tube defect causes **polyhydramnios**. The mechanism is twofold: a lack of the swallowing reflex and the transudation of fluid from the exposed meninges into the amniotic sac. * **Duodenal Atresia:** This is a classic cause of **polyhydramnios**. The structural obstruction in the gastrointestinal tract prevents the fetus from effectively swallowing and absorbing amniotic fluid. * **Trisomy 18 (Edwards Syndrome):** While chromosomal anomalies can vary, Trisomy 18 is more frequently associated with **polyhydramnios** due to associated GI tract malformations or impaired swallowing. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Oligohydramnios is defined as an Amniotic Fluid Index (AFI) **< 5 cm** or a Single Deepest Pocket (SDP) **< 2 cm**. * **Common Causes:** Renal anomalies (agenesis, posterior urethral valves), Placental insufficiency (IUGR), and Premature Rupture of Membranes (PROM). * **Potter Sequence:** Remember the mnemonic **P-O-T-T-E-R**: **P**ulmonary hypoplasia, **O**ligohydramnios, **T**wisted face (Potter facies), **T**wisted skin, **E**xtremity defects, **R**enal failure.

Q: What is the most common fetal response to acute hypoxia?

Bradycardia. **Explanation:** The fetal response to acute hypoxia is fundamentally different from that of an adult. In the fetus, the primary mechanism for managing a sudden drop in oxygen is the **Chemoreceptor Reflex**. **1. Why Bradycardia is Correct:** When acute hypoxia occurs (e.g., cord prolapse or placental abruption), fetal chemoreceptors (located in the carotid and aortic bodies) are stimulated. This triggers a powerful **vagal (parasympathetic) response**, leading to a rapid decrease in fetal heart rate (bradycardia). This is a protective, energy-conserving mechanism that reduces myocardial oxygen consumption and allows for better diastolic filling, ensuring that the limited oxygen available is diverted to vital organs like the brain, heart, and adrenals (the "diving reflex"). **2. Why the other options are incorrect:** * **Tachycardia:** While mild or chronic hypoxia may initially cause a sympathetic surge (tachycardia) to increase cardiac output, **acute** and severe hypoxia characteristically results in bradycardia due to the dominant vagal reflex. * **Tachypnea:** The fetus does not breathe air in utero. While fetal breathing movements (FBM) exist, they actually **decrease or cease** during hypoxia to conserve energy. * **Arrhythmia:** While hypoxia can lead to myocardial irritability, it does not consistently produce a specific arrhythmia other than sinus bradycardia or late decelerations. **Clinical Pearls for NEET-PG:** * **Late Decelerations:** These are the hallmark of uteroplacental insufficiency and are caused by the same chemoreceptor-mediated vagal response to hypoxia. * **The "Rule of 3s" for Bradycardia:** A fetal heart rate 3 minutes is a medical emergency requiring immediate intrauterine resuscitation or delivery. * **Primary Fetal Energy Source:** The fetus relies on anaerobic glycolysis during periods of hypoxia, leading to the accumulation of lactic acid and metabolic acidosis.

Q: A 26-week gestation pregnant woman with G2P1L1, carrying monochorionic twins, undergoes a routine obstetric scan. The scan reveals oligohydramnios in one fetus and polyhydramnios in the other. What is the most suspected condition?

Twin-to-twin transfusion syndrome (TTTS). ### Explanation **Correct Answer: B. Twin-to-twin transfusion syndrome (TTTS)** **Why it is correct:** TTTS is a serious complication unique to **monochorionic (MC)** pregnancies, occurring in approximately 10–15% of cases. It is caused by unbalanced blood flow through deep **arteriovenous (AV) anastomoses** in the shared placenta. * **The Donor Twin:** Becomes hypovolemic, leading to decreased renal perfusion and **oligohydramnios** (stuck twin). * **The Recipient Twin:** Becomes hypervolemic, leading to polyuria and **polyhydramnios**. The diagnostic hallmark of TTTS is the **"Oli-Poly Sequence"** (Deepest Vertical Pocket 8cm in the other). **Why the other options are incorrect:** * **A. Normal reproductive outcome:** A significant discrepancy in liquor volume in MC twins is never normal and indicates a high risk of fetal morbidity/mortality. * **C. Twin reversed arterial perfusion sequence (TRAP):** This involves an "acardiac twin" perfused by a "pump twin" via large artery-to-artery anastomoses. While it occurs in MC twins, the primary finding is a malformed fetus without a functioning heart, not just liquor discrepancy. * **D. Discordant twins:** This refers to a significant weight difference (usually >20-25%) between twins. While TTTS twins are often discordant, discordancy can occur in dichorionic twins due to placental insufficiency without the Oli-Poly sequence. **High-Yield NEET-PG Pearls:** * **Staging:** TTTS is staged using the **Quintero Staging System** (Stage I: Oli-Poly; Stage II: Absent bladder in donor; Stage III: Abnormal Dopplers; Stage IV: Hydrops; Stage V: Death). * **Treatment of Choice:** Fetoscopic **Laser ablation** of placental anastomoses (Solomon technique) is the gold standard. * **Screening:** Monochorionic twins should be monitored via ultrasound every **2 weeks** starting from 16 weeks to detect TTTS early.

Question 1

All the following are signs of intrauterine fetal death except?

Accepted Answer

Hegar's sign

Answer

Spalding's sign

Answer

Robe's sign

Answer

Halo sign

Question 2

What is the recommended time for termination of pregnancy in a female with type 1 diabetes controlled with insulin?

Accepted Answer

37+ weeks

Answer

40 weeks

Answer

32 weeks

Answer

34 weeks

Question 3

All of the following may be observed in a normal pregnancy except?

Accepted Answer

Increase in blood viscosity

Answer

Fall in serum iron concentration

Answer

Increase in serum iron binding capacity

Answer

Increase in blood oxygen carrying capacity

Question 4

Which of the following is NOT a cause of intrauterine growth retardation?

Accepted Answer

Gestational diabetes

Answer

Severe anemia

Answer

Pregnancy-induced hypertension

Answer

Maternal heart disease

Question 5

Which of the following has been proved to be effective in the management of preeclampsia?

Accepted Answer

Magnesium

Answer

Zinc

Answer

Calcium

Answer

None of the above

Question 6

Which of the following parameters is NOT used for the diagnosis of Intrauterine Growth Restriction (IUGR) on ultrasonography?

Accepted Answer

Abdominal circumference

Answer

Elevated S/D ratio

Answer

Decreased placental Doppler ratio

Answer

Reduction in fetal facial fat stores

Question 7

A woman with no history of prenatal care is about to deliver a baby. She has no history of amniotic rupture, and ultrasound showed severe oligohydramnios. Which of the following conditions can be a cause of oligohydramnios?

Accepted Answer

Renal agenesis

Answer

Anencephaly

Answer

Trisomy 18

Answer

Duodenal atresia

Question 8

A 21-year-old healthy woman, who is in week 34 of a normal pregnancy, complains of itching with burning pain in the perianal region for the past 4 months. She noted a small amount of bright red blood on toilet paper last week. Which of the following underlying conditions is most likely to be present in this patient?

Accepted Answer

External hemorrhoid

Answer

Filariasis

Answer

Polyarteritis nodosa

Answer

Micronodular cirrhosis

Question 9

What is the most common fetal response to acute hypoxia?

Accepted Answer

Bradycardia

Answer

Tachycardia

Answer

Tachypnea

Answer

Arrhythmia

Question 10

A 26-week gestation pregnant woman with G2P1L1, carrying monochorionic twins, undergoes a routine obstetric scan. The scan reveals oligohydramnios in one fetus and polyhydramnios in the other. What is the most suspected condition?

Accepted Answer

Twin-to-twin transfusion syndrome (TTTS)

Answer

Normal reproductive outcome

Answer

Twin reversed arterial perfusion sequence (TRAP)

Answer

Discordant twins

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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