Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs

Question 651: A 32-year-old woman is at 34 weeks of gestation. The uterine size is less than her weeks of gestation, and ultrasound reveals oligohydramnios with an AFI of 2.1 cm. Which of the following agents is responsible for this condition?

A. Angiotensin converting enzyme (ACE) inhibitor (Correct Answer)
B. Lithium exposure
C. Phenytoin (Dilantin)
D. Oral hypoglycemic agent

Explanation: **Explanation:** The correct answer is **A. Angiotensin converting enzyme (ACE) inhibitor.** **Mechanism of Action:** ACE inhibitors (e.g., Enalapril, Lisinopril) are contraindicated in the second and third trimesters of pregnancy. They interfere with the fetal Renin-Angiotensin-Aldosterone System (RAAS), which is essential for maintaining fetal renal perfusion and blood pressure. Inhibition leads to **fetal renal tubular dysgenesis**, resulting in decreased fetal urine production. Since fetal urine is the primary constituent of amniotic fluid in the latter half of pregnancy, its reduction leads to **severe oligohydramnios**. This can further cause the "Potter sequence" (pulmonary hypoplasia, limb contractures, and cranial deformities). **Analysis of Incorrect Options:** * **B. Lithium:** Primarily associated with cardiac malformations, specifically **Ebstein’s anomaly** (atrialization of the right ventricle), when used in the first trimester. It does not typically cause oligohydramnios. * **C. Phenytoin:** Associated with **Fetal Hydantoin Syndrome**, characterized by craniofacial abnormalities (cleft lip/palate), hypoplastic nails/phalanges, and growth restriction, but not specifically oligohydramnios. * **D. Oral Hypoglycemic Agents:** Poorly controlled maternal diabetes (or certain drugs) is more commonly associated with **polyhydramnios** due to fetal osmotic diuresis, rather than oligohydramnios. **High-Yield Clinical Pearls for NEET-PG:** * **ACE Inhibitors/ARBs:** Category D drugs. Key complications: Renal agenesis, oligohydramnios, and hypocalvaria (hypoplasia of skull bones). * **Amniotic Fluid Index (AFI):** Oligohydramnios is defined as an AFI < 5 cm or a Single Deepest Pocket (SDP) < 2 cm. * **Drug of Choice for Hypertension in Pregnancy:** Labetalol (Alpha + Beta blocker), Methyldopa (Centrally acting), or Nifedipine (CCB). ACE inhibitors are strictly avoided.

Question 652: A hemodynamically stable patient with early pregnancy presents with an adnexal mass of 2.5 x 3 cms and a beta-hCG titre of 1500 mIU/ml, with no intrauterine gestational sac. What is the suitable modality of treatment?

A. Progesterone therapy
B. Medical management (Correct Answer)
C. Laparoscopic surgery
D. Laparotomy

Explanation: ### Explanation The clinical presentation of a stable patient with an adnexal mass, no intrauterine gestational sac, and a beta-hCG of 1500 mIU/ml is diagnostic of an **unruptured ectopic pregnancy**. **Why Medical Management is Correct:** Medical management with **Methotrexate** is the treatment of choice for patients who are hemodynamically stable and meet specific criteria. The standard indications for medical management (as per ACOG/RCOG guidelines) include: 1. **Hemodynamic stability** (no signs of rupture/hemoperitoneum). 2. **Beta-hCG levels < 5000 mIU/ml** (Success rate is highest when < 3000). 3. **Adnexal mass size < 3.5 or 4 cm**. 4. **Absence of fetal cardiac activity** on ultrasound. This patient fits all criteria (Mass 3 cm, hCG 1500 mIU/ml), making medical management the most conservative and appropriate first-line approach. **Why Other Options are Incorrect:** * **A. Progesterone therapy:** Used for luteal phase support or threatened abortion; it has no role in treating an ectopic pregnancy. * **C. Laparoscopic surgery:** This is the gold standard for **surgical** management (Salpingectomy/Salpingostomy). It is indicated if the patient is unstable, the mass is > 4 cm, hCG is > 5000, or medical therapy fails. * **D. Laparotomy:** Reserved for hemodynamically unstable patients with massive hemoperitoneum or when laparoscopy is unavailable/contraindicated. **NEET-PG High-Yield Pearls:** * **Most common site of Ectopic Pregnancy:** Ampulla of the Fallopian tube. * **Most common site of Rupture:** Isthmus (due to its narrow lumen). * **Discriminatory Zone:** The beta-hCG level (usually 1500–2000 mIU/ml) at which an intrauterine sac should be visible on Transvaginal Sonography (TVS). * **Methotrexate Mechanism:** A folic acid antagonist that inhibits Dihydrofolate Reductase, stopping the proliferation of trophoblastic cells.

Question 653: A patient treated for infertility was diagnosed with a twin pregnancy at 6 weeks gestation. On her follow-up ultrasound at 12 weeks, there was a single developing live fetus. What is the further management?

A. Advise MTP as the second twin is at increased risk of abortion.
B. Continue pregnancy like a normal singleton pregnancy. (Correct Answer)
C. Watch for coagulation defect in the mother.
D. Chorionic villous sampling.

Explanation: This question addresses the phenomenon of the **"Vanishing Twin Syndrome,"** where one fetus in a multi-gestational pregnancy spontaneously regresses or is resorbed in the first trimester. ### **Explanation** **1. Why Option B is Correct:** When a twin is lost during the **first trimester** (typically before 12–14 weeks), the fetal tissue is usually resorbed completely or forms a small *fetus papyraceous*. In such early cases, there is no significant risk to the surviving twin or the mother. The pregnancy should be managed as a **routine singleton pregnancy**, and the prognosis for the surviving fetus is excellent, comparable to a pregnancy that started as a singleton. **2. Why Other Options are Incorrect:** * **Option A (MTP):** There is no medical indication for termination. The surviving fetus is not at an increased risk of miscarriage or anomalies due to the early loss of its co-twin. * **Option C (Coagulation Defect):** Consumptive coagulopathy (DIC) is a concern only if fetal demise occurs in the **second or third trimester** (usually after 20 weeks) and the dead fetus is retained for more than 3–4 weeks. It does not occur with first-trimester losses. * **Option D (CVS):** Vanishing twin syndrome is not an indication for invasive genetic testing unless other specific risk factors are present. ### **Clinical Pearls for NEET-PG** * **Vanishing Twin Syndrome:** Occurs in up to 20–30% of pregnancies conceived via IVF. * **Second/Third Trimester Loss:** If a twin dies later in pregnancy, the risks increase significantly: * **Monochorionic twins:** High risk of neurological damage or death to the survivor due to acute hemodynamic shifts through vascular anastomoses. * **Dichorionic twins:** Risk is primarily related to preterm labor; the survivor is generally safe from embolic/hemodynamic events. * **Biochemical Note:** A vanishing twin can cause transiently elevated Maternal Serum Alpha-Fetoprotein (MSAFP) levels, leading to false-positive screening for neural tube defects.

Question 654: Hypothyroidism in pregnancy is least likely associated with which of the following complications?

A. Recurrent abortions
B. Polyhydramnios (Correct Answer)
C. Pregnancy induced hypertension (PIH)
D. Prematurity

Explanation: **Explanation:** Hypothyroidism during pregnancy is a high-yield topic in NEET-PG, as thyroid hormones are critical for both maternal health and fetal neurodevelopment. **Why Polyhydramnios is the Correct Answer:** Polyhydramnios (excess amniotic fluid) is **not** typically associated with hypothyroidism. In fact, severe hypothyroidism is more frequently associated with **Oligohydramnios** (decreased amniotic fluid), often secondary to placental insufficiency and intrauterine growth restriction (IUGR). Polyhydramnios is classically associated with maternal **Diabetes Mellitus**, fetal structural anomalies (like esophageal atresia), or multiple gestations. **Analysis of Incorrect Options:** * **A. Recurrent abortions:** Thyroid hormones are essential for maintaining early pregnancy. Untreated hypothyroidism leads to a higher risk of first-trimester miscarriage and recurrent pregnancy loss due to impaired luteal function and placental development. * **B. Pregnancy-Induced Hypertension (PIH):** There is a strong correlation between hypothyroidism and hypertensive disorders of pregnancy. The lack of thyroxine increases peripheral vascular resistance and leads to endothelial dysfunction, predisposing the mother to Preeclampsia/PIH. * **D. Prematurity:** Hypothyroidism is a known risk factor for preterm labor and premature rupture of membranes (PROM), often due to the associated complications like PIH or placental abruption. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Levothyroxine is the mainstay of treatment. * **Dosage Adjustment:** Requirements typically **increase by 30–50%** during pregnancy, starting as early as the 4th–6th week. * **Target TSH:** The goal is to keep TSH in the lower half of the trimester-specific reference range (usually <2.5 mIU/L). * **Fetal Impact:** The fetus depends entirely on maternal T4 until the **12th week** of gestation. Untreated maternal hypothyroidism is a leading cause of impaired cognitive development and **Cretinism** in the offspring.

Question 655: The separation of a normally situated placenta in a case of multiple pregnancy may be due to the following, except:

A. Increased incidence of toxaemia
B. Sudden escape of liquor following rupture of membranes
C. Deficiency of vitamin B12
D. Deficiency of folic acid (Correct Answer)

Explanation: **Explanation:** The question asks for the factor **not** associated with placental abruption (abruptio placentae) in multiple pregnancies. **Why Folic Acid Deficiency is the Correct Answer:** Historically, folic acid deficiency was thought to be linked to placental abruption due to its role in DNA synthesis and vascular integrity. However, modern evidence-based obstetrics has established that **folic acid deficiency is not a causative factor** for abruption. While folic acid is crucial for preventing Neural Tube Defects (NTDs), its deficiency does not trigger the retroplacental hemorrhage seen in abruption. **Analysis of Incorrect Options:** * **A. Increased incidence of toxaemia:** Multiple pregnancies have a significantly higher risk of Pre-eclampsia (Toxaemia). Hypertension is the most common pathological cause of placental abruption due to degenerative changes in maternal arterioles. * **B. Sudden escape of liquor:** In twin pregnancies, the sudden decompression of the uterus (following the rupture of membranes of the first twin or polyhydramnios) causes a rapid decrease in intrauterine surface area. This mechanical "shearing force" leads to the separation of the placenta. * **C. Deficiency of Vitamin B12:** Hyperhomocysteinemia (often caused by B12 or B6 deficiency) is a recognized risk factor for placental vasculopathy and abruption. While less common than hypertension, it remains a documented etiological factor. **NEET-PG High-Yield Pearls:** * **Most common cause of Abruption:** Maternal Hypertension (Preeclampsia/Chronic HTN). * **Most common cause of DIC in Obstetrics:** Abruptio Placentae. * **Couvelaire Uterus:** Also known as uteroplacental apoplexy; it is a complication of severe concealed abruption where blood extravasates into the myometrium. * **Multiple Pregnancy Risk:** The risk of abruption is highest immediately after the delivery of the first twin.

Question 656: Regarding intrahepatic cholestasis of pregnancy, all are true except?

A. More common in multifetal gestation.
B. Disappears after delivery.
C. Mutation of ABCB4 gene is implicated to cause.
D. Usually onset is in early trimester. (Correct Answer)

Explanation: **Explanation:** Intrahepatic Cholestasis of Pregnancy (ICP) is the most common pregnancy-specific liver disease, characterized by pruritus (typically on palms and soles) and elevated serum bile acids. **Why Option D is the Correct Answer (The False Statement):** ICP typically manifests in the **late second or third trimester** (usually after 28 weeks). This is because the levels of estrogen and progesterone, which inhibit the bile salt export pump, reach their peak during the later stages of pregnancy. Onset in the early trimester is extremely rare and should prompt investigation for alternative liver pathology. **Analysis of Other Options:** * **Option A:** ICP is significantly **more common in multifetal gestations** (twins/triplets) due to the higher circulating levels of placental hormones compared to singleton pregnancies. * **Option B:** The condition is reversible; symptoms and biochemical abnormalities typically **disappear rapidly after delivery** (usually within 2–4 weeks) once the hormonal trigger (the placenta) is removed. * **Option C:** Genetic predisposition plays a major role. Mutations in the **ABCB4 (MDR3) gene**, which encodes the hepatocyte phospholipid transporter, are strongly implicated in the pathogenesis of ICP. **NEET-PG High-Yield Pearls:** * **Primary Symptom:** Pruritus without a rash, worse at night, starting on palms and soles. * **Diagnostic Gold Standard:** Elevated **Total Serum Bile Acids (TSBA)** >10 µmol/L. * **Fetal Risks:** Increased risk of meconium-stained amniotic fluid, preterm labor, and **sudden intrauterine fetal death (IUFD)**, especially if bile acids exceed 100 µmol/L. * **Management:** **Ursodeoxycholic acid (UDCA)** is the drug of choice to improve maternal symptoms and biochemical markers. Delivery is usually recommended by 37–38 weeks to prevent stillbirth.

Question 657: Which of the following is a true statement regarding renal changes in preeclampsia?

A. Increased GFR
B. Glomeruloendotheliosis (Correct Answer)
C. Increased renal blood flow
D. Persistent after delivery

Explanation: **Explanation:** **1. Why Glomeruloendotheliosis is Correct:** Glomeruloendotheliosis is the **pathognomonic** renal lesion of preeclampsia. It is characterized by the swelling of glomerular endothelial cells and the deposit of fibrinoid material under the basement membrane, which leads to the narrowing of the capillary lumens. This endothelial dysfunction is driven by anti-angiogenic factors (like sFlt-1) released from the placenta, which neutralize Vascular Endothelial Growth Factor (VEGF) required for maintaining glomerular health. **2. Why Other Options are Incorrect:** * **A & C (Increased GFR and Renal Blood Flow):** In a normal pregnancy, GFR and renal blood flow increase by nearly 50%. However, in **preeclampsia**, the narrowing of glomerular capillaries (due to endotheliosis) and vasospasm lead to a **decrease** in both GFR and renal blood flow. This explains the rise in serum creatinine and uric acid seen in severe cases. * **D (Persistent after delivery):** Unlike chronic kidney disease, the renal changes in preeclampsia are typically **reversible**. Glomeruloendotheliosis usually resolves within weeks postpartum as the placental triggers are removed. **3. High-Yield Clinical Pearls for NEET-PG:** * **Proteinuria:** Defined as ≥300 mg/24 hours or a protein:creatinine ratio ≥0.3. It is a direct clinical consequence of the damaged glomerular barrier. * **Hyperuricemia:** An elevated serum uric acid level is often one of the earliest laboratory markers of preeclampsia, reflecting decreased renal clearance. * **Podocyturia:** The shedding of podocytes in urine is a specific marker currently being researched for early diagnosis.

Question 658: Which of the following is NOT a prognostic indicator of pregnancy-induced hypertension?

A. Low platelets
B. Serum sodium (Correct Answer)
C. Elevated liver enzymes
D. Serum uric acid

Explanation: In Pregnancy-Induced Hypertension (PIH) and Preeclampsia, prognosis is determined by the degree of multi-organ involvement resulting from widespread endothelial dysfunction and vasospasm. **Why Serum Sodium is the Correct Answer:** Serum sodium levels (Option B) are generally **not** used as a prognostic indicator in PIH. While severe preeclampsia can occasionally lead to hyponatremia due to high levels of ADH or fluid overload, it is not a standard marker for predicting disease severity, fetal outcome, or the risk of eclampsia. **Explanation of Incorrect Options (Prognostic Indicators):** * **Low Platelets (Option A):** Thrombocytopenia (<100,000/mm³) indicates microangiopathic hemolytic anemia and is a hallmark of HELLP syndrome. It signifies severe disease and an increased risk of maternal hemorrhage. * **Elevated Liver Enzymes (Option B):** Rising AST and ALT levels indicate hepatic ischemia or periportal necrosis. This is a critical prognostic sign of worsening preeclampsia and potential liver rupture. * **Serum Uric Acid (Option D):** This is one of the **earliest and most reliable markers** of preeclampsia. Hyperuricemia (>4.5–6 mg/dL) results from decreased renal clearance and correlates strongly with the severity of placental lesions and poor fetal outcomes (IUGR). **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Proteinuria:** 24-hour urine collection (>300 mg) or Protein:Creatinine ratio (≥0.3). * **Serum Uric Acid:** Best marker for differentiating Preeclampsia from Chronic Hypertension. * **Serum Creatinine:** Levels >1.1 mg/dL indicate severe features (renal dysfunction). * **Definitive Treatment:** Delivery of the fetus and placenta is the only cure for PIH.

Question 659: Oligohydramnios is seen in all except:

A. Renal agenesis
B. Rh incompatibility (Correct Answer)
C. IUGR
D. Postmaturity

Explanation: **Explanation:** Amniotic fluid volume is primarily maintained by a balance between fetal urine production (the main source) and fetal swallowing (the main clearance). **Oligohydramnios** occurs when there is a decrease in production or an increase in loss/clearance. **Why Rh Incompatibility is the correct answer:** Rh isoimmunization typically leads to **Polyhydramnios**, not oligohydramnios. In severe Rh incompatibility, fetal anemia leads to high-output cardiac failure. This causes increased hydrostatic pressure and decreased oncotic pressure, resulting in fetal hydrops. The increased cardiac output leads to increased renal perfusion and excessive fetal urination, causing an increase in amniotic fluid volume. **Analysis of incorrect options:** * **Renal Agenesis (Potter’s Syndrome):** Since fetal urine is the primary source of amniotic fluid from the second trimester onwards, the absence of kidneys leads to severe, early-onset oligohydramnios. * **IUGR (Intrauterine Growth Restriction):** In placental insufficiency, the fetus redistributes blood flow to vital organs (brain-sparing effect) at the expense of the kidneys. Decreased renal perfusion leads to decreased urine output and oligohydramnios. * **Postmaturity:** After 40–42 weeks, placental function declines and the fetal glomerular filtration rate (GFR) naturally decreases, leading to a progressive reduction in amniotic fluid. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Amniotic Fluid Index (AFI) < 5 cm or Single Deepest Pocket (SDP) < 2 cm. * **Most common cause of Oligohydramnios:** Premature Rupture of Membranes (PROM). * **Most common cause of Polyhydramnios:** Idiopathic (followed by Maternal Diabetes). * **Potter’s Sequence:** Oligohydramnios → Pulmonary hypoplasia, flattened facies, and limb deformities.

Question 660: Nonimmune hydrops fetalis is seen in all of the following conditions except?

A. Alpha-thalassemia
B. Parvovirus B19
C. Rh-incompatibility (Correct Answer)
D. All

Explanation: ### Explanation Hydrops fetalis is defined as the abnormal accumulation of fluid in two or more fetal compartments (e.g., ascites, pleural effusion, pericardial effusion, or skin edema). It is categorized into two types: **Immune** and **Non-immune**. **1. Why Rh-incompatibility is the correct answer:** Rh-incompatibility is the classic cause of **Immune Hydrops Fetalis**. It occurs when an Rh-negative mother is sensitized to Rh-positive fetal red blood cells, leading to the production of IgG antibodies. These antibodies cross the placenta and cause immune-mediated hemolysis of fetal RBCs, resulting in severe anemia and subsequent heart failure. **2. Why the other options are incorrect (Causes of Non-immune Hydrops):** Non-immune hydrops (NIHF) accounts for nearly 90% of cases today due to the success of Rh-immunoglobulin prophylaxis. * **Alpha-thalassemia (Hb Bart’s):** This is the most common hematological cause of NIHF. The absence of alpha-globin chains leads to high-affinity hemoglobin that does not release oxygen to tissues, causing severe tissue hypoxia and high-output cardiac failure. * **Parvovirus B19:** This is the most common infectious cause of NIHF. The virus infects and destroys fetal erythroid progenitor cells, leading to aplastic anemia and hydrops. **Clinical Pearls for NEET-PG:** * **Most common cause of NIHF overall:** Cardiovascular anomalies (e.g., structural defects or arrhythmias). * **Most common chromosomal cause:** Turner Syndrome (45, XO) – often associated with cystic hygromas. * **Diagnosis:** Ultrasound is the gold standard; look for "Mirror Syndrome" (maternal edema mimicking fetal hydrops). * **Management of Rh-isoimmunization:** Monitored via MCA-PSV (Middle Cerebral Artery Peak Systolic Velocity) doppler to detect fetal anemia.

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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