Maternal-Fetal Medicine Practice Questions

Q: A 30-week pregnant woman presents for an antenatal check-up complaining of mild dyspnea and palpitations. On examination, pedal edema is present. An ejection systolic murmur is noted. ECG shows sinus tachycardia, left axis deviation, and occasional premature ventricular beats. Echocardiogram reveals a small pleural effusion and mild mitral regurgitation. No other relevant findings are present. What is the next line of treatment?

No treatment needed. **Explanation:** The correct answer is **C. No treatment needed**. This question tests the ability to distinguish between physiological cardiovascular changes in pregnancy and pathological heart disease. During pregnancy, blood volume increases by 40–50%, leading to a hyperdynamic circulation. The findings described in the clinical vignette are **normal physiological adaptations** at 30 weeks: * **Symptoms:** Mild dyspnea and palpitations are common due to the enlarging uterus and increased cardiac output. * **Physical Signs:** Dependent pedal edema occurs due to IVC compression. An **ejection systolic murmur** (Grade I/II) is heard in up to 90% of pregnant women due to increased flow across the pulmonary and aortic valves. * **ECG Changes:** Left axis deviation occurs as the diaphragm elevates and shifts the heart's position. Sinus tachycardia and isolated PVCs are common. * **Echocardiogram:** Mild mitral or tricuspid regurgitation and trace pericardial/pleural effusions can be seen due to volume overload and are not necessarily indicative of failure. **Why incorrect options are wrong:** * **Option A:** Diuretics are not indicated as the edema is physiological, not due to congestive heart failure. * **Option B:** Endocarditis prophylaxis is no longer recommended for physiological murmurs or uncomplicated vaginal/cesarean deliveries. * **Option D:** Termination is contraindicated. These findings do not meet the criteria for NYHA Class III/IV heart failure or life-threatening conditions (like Eisenmenger syndrome or severe MS). **Clinical Pearls for NEET-PG:** * **Diastolic murmurs** in pregnancy are **always pathological** and require investigation. * The most common heart disease in pregnancy in India is **Rheumatic Heart Disease (Mitral Stenosis)**. * Cardiac output peaks at **30–34 weeks** and immediately **post-partum** (due to autotransfusion). These are the periods of maximum risk for heart failure.

Q: A patient at 36 weeks of gestation presents with abdominal pain, uterine tenderness, and vaginal bleeding. Her vital signs are stable, and fetal heart tracing is regular. Which of the following steps is NOT required?

Tocolysis to arrest labor. ### Explanation The clinical presentation of abdominal pain, uterine tenderness, and vaginal bleeding in the third trimester is a classic triad for **Abruptio Placentae** (premature separation of the placenta). **1. Why Tocolysis (Option D) is NOT required:** In the management of placental abruption, **tocolysis is strictly contraindicated**. The primary goal is delivery, as the retroplacental clot acts as a uterine irritant, often leading to labor anyway. Attempting to arrest labor with tocolytics in the presence of abruption can lead to worsening hemorrhage, concealment of bleeding, and delay in definitive management, potentially resulting in maternal shock or fetal demise. **2. Why the other options are part of management:** * **Amniotomy/Prostaglandins (Option A):** Vaginal delivery is the preferred route if the fetus is stable. Amniotomy (rupturing membranes) is a priority as it reduces intrauterine pressure, decreases the entry of thromboplastin into maternal circulation (reducing DIC risk), and often accelerates labor. * **Blood Products (Option B):** Abruption is an obstetric emergency with a high risk of sudden, massive hemorrhage and Consumptive Coagulopathy (DIC). Cross-matching and arranging blood products is a mandatory safety step. * **IV Crystalloids/Colloids (Option C):** Aggressive fluid resuscitation is essential to maintain maternal hemodynamic stability and ensure adequate placental perfusion. **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, giving it a bluish/purplish appearance. * **Management Rule:** If the fetus is alive and stable, aim for vaginal delivery (Amniotomy + Oxytocin). If there is fetal distress or maternal instability, proceed to immediate Cesarean Section.

Q: A G1 P0 patient presents with blood pressure of 160/102 mmHg, 3+ proteinuria, and right upper quadrant discomfort at 36 weeks gestation. Following induction of labor, she delivers vaginally and experiences 1500mL blood loss. Her serum creatinine rises from 0.98 mg/dL pre-delivery to 1.42 mg/dL post-delivery. What is the most likely diagnosis?

Acute tubular necrosis. ### Explanation **Correct Answer: D. Acute tubular necrosis (ATN)** The patient presents with **Severe Preeclampsia** (BP 160/102, 3+ proteinuria, RUQ pain) complicated by a massive **Postpartum Hemorrhage (PPH)** of 1500 mL. The core clinical event is the sudden rise in serum creatinine (from 0.98 to 1.42 mg/dL) following significant blood loss. In the context of obstetric hemorrhage and hypovolemia, the most common cause of acute kidney injury (AKI) is **Acute Tubular Necrosis**. The ischemic insult to the renal tubules caused by profound hypotension (from PPH) leads to the rise in creatinine. **Why other options are incorrect:** * **A. Severe preeclampsia:** While the patient meets the criteria for severe preeclampsia, this is the *underlying condition*, not the specific diagnosis for the post-delivery renal deterioration. * **B. Postpartum hemorrhage:** This is the *precipitating event* (the cause), but it does not describe the resulting renal pathology. * **C. Subcapsular liver hematoma:** Although RUQ pain in preeclampsia suggests liver involvement (Glisson’s capsule stretch), it does not explain the acute rise in creatinine following delivery and blood loss. **Clinical Pearls for NEET-PG:** * **Renal Failure in Pregnancy:** The most common cause of AKI in the third trimester is preeclampsia/HELLP syndrome, but the most common cause of *ischemic* AKI (ATN) is obstetric hemorrhage (Abruptio placentae or PPH). * **Creatinine Norms:** Remember that normal serum creatinine in pregnancy is lower (0.4–0.8 mg/dL) due to increased GFR. A value of 1.42 mg/dL represents significant renal impairment. * **Management:** The priority in ATN is fluid resuscitation and maintaining renal perfusion. Most cases are reversible if the primary cause is managed.

Q: At what gestational age are the weight of the placenta and fetus approximately equal?

17 weeks. **Explanation:** The relationship between fetal weight and placental weight changes dynamically throughout pregnancy. In early gestation, the placenta develops more rapidly than the fetus to establish the nutritional and gas-exchange infrastructure required for later growth. **1. Why 17 Weeks is Correct:** During the first trimester and early second trimester, the placenta is actually heavier than the fetus. As the fetus enters the period of rapid somatic growth, the weights eventually converge. At approximately **17 weeks of gestation**, the weight of the placenta and the fetus are roughly equal (approx. 150–180 grams each). After this point, fetal weight increases exponentially, while placental growth slows down. **2. Analysis of Incorrect Options:** * **14 weeks:** At this stage, the placenta is significantly heavier than the fetus. The fetus weighs roughly 40-50g, while the placenta is nearly double that. * **16 weeks:** The fetus is approaching the placental weight but is still slightly lighter. * **21 weeks:** By this time, the fetus has clearly overtaken the placenta in weight. By the end of the second trimester, the fetus is roughly twice as heavy as the placenta. **3. High-Yield Facts for NEET-PG:** * **Placental-Fetal Weight Ratio:** At term (40 weeks), the ratio is approximately **1:6**. The average placenta weighs ~500g, while the average fetus weighs ~3000-3500g. * **Placental Growth:** The placenta reaches its maximum thickness at 16–20 weeks and continues to increase in circumference until term. * **Clinical Significance:** A high placental-to-fetal weight ratio (large placenta, small baby) is often seen in conditions like maternal diabetes, fetal hydrops, or syphilis. A low ratio (small placenta) is associated with placental insufficiency and Fetal Growth Restriction (FGR).

Q: Which of the following is NOT a direct cause of maternal mortality?

Heart disease. **Explanation:** In maternal mortality statistics, causes are classified into two categories: **Direct** and **Indirect**. **Why Heart Disease is the Correct Answer:** Heart disease is classified as an **Indirect Obstetric Cause**. Indirect deaths result from pre-existing disease or disease that developed during pregnancy, which was not due to direct obstetric causes but was aggravated by the physiological effects of pregnancy. While heart disease is a leading cause of maternal death globally, it does not arise from obstetric complications themselves. **Why the Other Options are Incorrect:** Direct obstetric causes are those resulting from obstetric complications of the pregnant state (pregnancy, labor, and puerperium). * **Hemorrhage (A):** The leading cause of maternal mortality worldwide (specifically Postpartum Hemorrhage). It is a direct result of the birthing process. * **Sepsis (B):** Puerperal sepsis is a direct complication arising from infections of the genital tract during or after delivery. * **Hypertension (C):** Preeclampsia and Eclampsia are pregnancy-specific conditions and are major direct contributors to maternal morbidity and mortality. **High-Yield NEET-PG Pearls:** * **Most common cause of maternal mortality (World & India):** Hemorrhage (specifically PPH). * **Most common indirect cause of maternal mortality:** Anemia (in developing countries) and Heart Disease (increasingly in developed regions). * **Maternal Mortality Ratio (MMR):** Calculated per 100,000 live births. * **The "Big Three" Direct Causes:** Hemorrhage, Hypertension (Sepsis/Eclampsia), and Sepsis.

Q: A woman has had two previous anencephalic babies. What is the risk of having a third one?

10%. **Explanation:** Neural Tube Defects (NTDs), such as anencephaly and spina bifida, follow a **multifactorial inheritance** pattern. This means they result from a combination of multiple genetic predispositions and environmental factors (like folic acid deficiency). In multifactorial inheritance, the recurrence risk increases significantly with each previously affected sibling. * **Why 10% is correct:** In the general population, the risk of NTD is approximately 0.1–0.2%. After **one** affected child, the recurrence risk rises to **2–5%**. After **two** affected children, the risk increases further to approximately **10%**. This is a classic high-yield statistic for postgraduate exams. **Analysis of Incorrect Options:** * **0%:** Incorrect, as genetic and environmental predispositions persist in subsequent pregnancies. * **25%:** This risk is characteristic of **Autosomal Recessive** disorders (e.g., Thalassemia). While some rare syndromes involving NTDs exist, isolated anencephaly does not follow this pattern. * **50%:** This risk is characteristic of **Autosomal Dominant** disorders (if one parent is affected). **Clinical Pearls for NEET-PG:** 1. **Prevention:** For a woman with a previous history of NTD, the recommended dose of **Folic Acid is 4 mg/day**, started at least 1 month (ideally 3 months) prior to conception and continued through the first trimester. 2. **Low-risk prophylaxis:** For women without a history, the standard dose is **400 mcg (0.4 mg)/day**. 3. **Screening:** Maternal Serum Alpha-Fetoprotein (MSAFP) is elevated in open NTDs. Diagnosis is confirmed via targeted ultrasound (Level II scan) at 18–20 weeks.

Q: The fetus, which is foreign to the mother, is not rejected due to which of the following reasons?

All of the above. The survival of the fetus (a semi-allograft) within the maternal environment is a phenomenon known as **immunological privilege**. This is achieved through a multi-factorial mechanism involving anatomical, hormonal, and cellular barriers. ### **Explanation of Options:** * **A. Immunosuppressive effect of placental hormones:** High local concentrations of **Progesterone** and **hCG** at the maternal-fetal interface suppress maternal T-cell activity and promote a shift from a pro-inflammatory (Th1) to an anti-inflammatory (**Th2**) cytokine profile. * **B. Absence of HLA molecules in villous trophoblast:** The syncytiotrophoblast (which is in direct contact with maternal blood) does not express classical **HLA Class I (A, B)** or **Class II** molecules. This prevents recognition and destruction by maternal cytotoxic T-cells. Instead, they express **HLA-G**, which inhibits Natural Killer (NK) cell activity. * **C. Production of blocking antibodies:** Maternal B-cells produce non-complement-fixing antibodies (asymmetric IgG) that bind to fetal antigens, "masking" them from maternal immune recognition without causing damage. ### **Clinical Pearls for NEET-PG:** * **The Th2 Shift:** Pregnancy is a Th2-dominant state. This explains why Th1-mediated autoimmune diseases (like Rheumatoid Arthritis) often improve during pregnancy, while Th2-mediated ones (like SLE) may flare. * **HLA-G:** This is a non-classical Class I MHC molecule unique to the extravillous trophoblast. It is the "shield" that protects the fetus from NK cell-mediated lysis. * **Indoleamine 2,3-dioxygenase (IDO):** An enzyme produced by the placenta that depletes tryptophan, effectively "starving" and inactivating maternal T-cells. * **Fas-L Expression:** Trophoblasts express Fas-ligand, which induces apoptosis in any maternal activated T-cells that attempt to attack the placenta.

Question 1

A 30-week pregnant woman presents for an antenatal check-up complaining of mild dyspnea and palpitations. On examination, pedal edema is present. An ejection systolic murmur is noted. ECG shows sinus tachycardia, left axis deviation, and occasional premature ventricular beats. Echocardiogram reveals a small pleural effusion and mild mitral regurgitation. No other relevant findings are present. What is the next line of treatment?

Accepted Answer

No treatment needed

Answer

Start diuretics

Answer

Start endocarditis prophylaxis

Answer

Terminate pregnancy as features are diagnostic of heart failure

Question 2

A patient at 36 weeks of gestation presents with abdominal pain, uterine tenderness, and vaginal bleeding. Her vital signs are stable, and fetal heart tracing is regular. Which of the following steps is NOT required?

Accepted Answer

Tocolysis to arrest labor

Answer

Amniotomy or prostaglandins to induce labor

Answer

Arrange for blood products

Answer

Intravenous crystalloids and colloids

Question 3

A G1 P0 patient presents with blood pressure of 160/102 mmHg, 3+ proteinuria, and right upper quadrant discomfort at 36 weeks gestation. Following induction of labor, she delivers vaginally and experiences 1500mL blood loss. Her serum creatinine rises from 0.98 mg/dL pre-delivery to 1.42 mg/dL post-delivery. What is the most likely diagnosis?

Accepted Answer

Acute tubular necrosis

Answer

Severe preeclampsia

Answer

Postpartum hemorrhage

Answer

Subcapsular liver hematoma

Question 4

A 36-year-old multigravida at 34 weeks gestation, with a history of two previous lower segment caesarean sections (LSCS), presents with an unstable lie. What is the most likely diagnosis in this case?

Accepted Answer

Placenta previa

Answer

Oligohydramnios

Answer

Pelvic tumor

Answer

Uterine anomalies

Question 5

All of the following are cardiac contraindications to pregnancy, EXCEPT?

Accepted Answer

Wolff-Parkinson-White (WPW) syndrome

Answer

Eisenmenger's syndrome

Answer

Pulmonary hypertension

Answer

Coarctation of aorta

Question 6

At what gestational age are the weight of the placenta and fetus approximately equal?

Accepted Answer

17 weeks

Answer

14 weeks

Answer

16 weeks

Answer

21 weeks

Question 7

Which of the following is NOT a direct cause of maternal mortality?

Accepted Answer

Heart disease

Answer

Hemorrhage

Answer

Sepsis

Answer

Hypertension

Question 8

A 28-year-old woman (Gravida 2, Para 1, Abortus 0) at 36 weeks of gestation has a history of a prior stillbirth at 37 weeks. What is the optimal timing for delivery in this current pregnancy?

Accepted Answer

39 weeks of gestation

Answer

Immediately

Answer

37 weeks of gestation

Answer

38 weeks of gestation

Question 9

A woman has had two previous anencephalic babies. What is the risk of having a third one?

Accepted Answer

10%

Answer

0%

Answer

25%

Answer

50%

Question 10

The fetus, which is foreign to the mother, is not rejected due to which of the following reasons?

Accepted Answer

All of the above

Answer

Immunosuppressive effect of placental hormones

Answer

Absence of HLA molecules in villous trophoblast

Answer

Production of blocking antibodies

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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