Maternal-Fetal Medicine Practice Questions

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: 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: In a pregnant lady with pregnancy-induced hypertension (PIH) experiencing bleeding per vagina, what is the primary factor determining the decision to continue the pregnancy?

Presence of fetal cardiac activity. **Explanation:** The clinical scenario describes a patient with Pregnancy-Induced Hypertension (PIH) presenting with vaginal bleeding, which is highly suggestive of **Abruptio Placentae** (Placental Abruption). In cases of abruption, the management algorithm is primarily dictated by the **fetal viability and maternal stability.** 1. **Why A is correct:** The presence or absence of fetal cardiac activity is the "deciding factor" for the mode and timing of delivery. If the fetus is alive, an emergency Cesarean section is often indicated to save the fetus, provided the mother is stable. If fetal death has occurred (absent cardiac activity), the goal shifts entirely to maternal safety, usually favoring a controlled vaginal delivery to avoid the surgical risks associated with coagulopathy (DIC), which is common in abruption. 2. **Why the other options are incorrect:** * **B & D:** While blood availability and medical facilities are essential for safe management, they are supportive requirements rather than the primary clinical factor that determines whether to continue the pregnancy or terminate it immediately. * **C:** Maternal blood pressure control is a management goal to prevent complications like stroke or eclampsia, but it does not dictate the decision to continue the pregnancy once a life-threatening complication like abruption has begun. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DIC in pregnancy:** Abruptio Placentae. * **Couvelaire Uterus:** A complication of severe abruption where blood extravasates into the myometrium; it is not an absolute indication for hysterectomy unless the uterus is atonic. * **Management Rule:** In abruption with a dead fetus, **Vaginal Delivery** is the treatment of choice. In abruption with a live fetus, **Emergency LSCS** is the treatment of choice.

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.

Q: Uterine height more than corresponding gestational age, with complaints of vomiting and pervaginal bleeding, favors which diagnosis?

Hydatidiform mole. **Explanation:** The clinical triad of **uterine size greater than dates**, **hyperemesis gravidarum** (excessive vomiting), and **painless vaginal bleeding** is a classic presentation of a **Hydatidiform Mole** (Molar Pregnancy). 1. **Why Hydatidiform Mole is correct:** In a molar pregnancy, the abnormal proliferation of trophoblastic tissue and the accumulation of fluid within the chorionic villi (hydropic degeneration) lead to rapid uterine enlargement, often exceeding the expected gestational age. The markedly elevated levels of **hCG** (human chorionic gonadotropin) stimulate the chemoreceptor trigger zone, causing severe vomiting. The bleeding occurs due to the separation of the molar tissue from the decidua. 2. **Why other options are incorrect:** * **Threatened Abortion:** While it presents with bleeding, the uterine size is typically **equal** to the gestational age, and hyperemesis is not a defining feature. * **Placenta Previa:** Presents with painless, bright red bleeding, but usually in the **third trimester**. Uterine size is typically appropriate for dates. * **Abruptio Placentae:** Characterized by painful bleeding and a "woody hard" uterus. While the uterus may be slightly larger due to a concealed retroplacental clot, it lacks the hyperemesis and the characteristic "snowstorm" appearance on ultrasound associated with moles. **High-Yield Clinical Pearls for NEET-PG:** * **USG Finding:** "Snowstorm appearance" or "Bunch of grapes" appearance. * **Ovarian Finding:** Bilateral **Theca Lutein Cysts** (due to high hCG). * **Complication:** Early-onset Preeclampsia (before 20 weeks) is highly suggestive of a molar pregnancy. * **Management:** Suction and Evacuation is the treatment of choice.

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

500-700 ml/min. **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.

Q: A 4-month pregnant lady on regular treatment with valproate asks for advice regarding continuing the drug during pregnancy. What is the best course of action?

Continue valproate and monitor blood levels. **Explanation:** The management of epilepsy during pregnancy is governed by a critical principle: **Never change or stop an effective anti-epileptic drug (AED) once pregnancy is confirmed.** **1. Why Option C is Correct:** By the time a woman realizes she is 4 months pregnant (second trimester), the period of organogenesis (weeks 3–8) is already complete. Valproate is associated with **Neural Tube Defects (NTDs)**, but these occur very early in the first trimester. Switching drugs now will not reverse any potential malformations but will expose the fetus to a new drug and risk breakthrough seizures in the mother. Seizures during pregnancy can cause fetal hypoxia, placental abruption, and miscarriage. Therefore, the safest approach is to continue the current effective dose and monitor serum levels, as physiological changes in pregnancy can alter drug pharmacokinetics. **2. Why Incorrect Options are Wrong:** * **Option A & B:** Switching to Lamotrigine or Carbamazepine at 4 months is futile for preventing teratogenicity. Furthermore, polytherapy or rapid switching increases the risk of "status epilepticus," which is more dangerous to the fetus than the drug itself. * **Option D:** Tapering the dose risks loss of seizure control. The goal is to maintain the lowest effective dose that was controlling seizures prior to pregnancy. **High-Yield Clinical Pearls for NEET-PG:** * **Pre-conception:** If a patient is planning pregnancy, Valproate should be avoided and switched to safer alternatives like **Lamotrigine or Levetiracetam**. * **Folic Acid:** High-dose folic acid (5 mg/day) should be started *before* conception to reduce NTD risk. * **Valproate Syndrome:** Characterized by spina bifida, craniofacial anomalies, and cognitive impairment. * **Vitamin K:** If the mother is on enzyme-inducing AEDs (e.g., Phenytoin, Carbamazepine), Vitamin K is given to the neonate to prevent hemorrhagic disease.

Q: The following CTG indicates:

Cord compression. ***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 1

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 2

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 3

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 4

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 5

In a pregnant lady with pregnancy-induced hypertension (PIH) experiencing bleeding per vagina, what is the primary factor determining the decision to continue the pregnancy?

Accepted Answer

Presence of fetal cardiac activity

Answer

Availability of blood for transfusion

Answer

Maternal blood pressure control

Answer

Availability of adequate medical facilities

Question 6

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

Question 7

Uterine height more than corresponding gestational age, with complaints of vomiting and pervaginal bleeding, favors which diagnosis?

Accepted Answer

Hydatidiform mole

Answer

Threatened abortion

Answer

Placenta previa

Answer

Abruptio placentae

Question 8

What is the utero-placental blood flow at term?

Accepted Answer

500-700 ml/min

Answer

300-500 ml/min

Answer

700-900 ml/min

Answer

900-1100 ml/min

Question 9

A 4-month pregnant lady on regular treatment with valproate asks for advice regarding continuing the drug during pregnancy. What is the best course of action?

Accepted Answer

Continue valproate and monitor blood levels

Answer

Immediately stop valproate and start lamotrigine

Answer

Change to carbamazepine

Answer

Slowly taper the dose of valproate

Question 10

The following CTG indicates:

Accepted Answer

Cord compression

Answer

Fetal head compression

Answer

Normal tracing

Answer

Fetal anemia

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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