Maternal-Fetal Medicine — MCQs
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In pregnancy, what is the drug of choice for initial treatment of immune thrombocytopenic purpura?
A 36-year-old primigravida develops peripheral edema late in the second trimester. On physical examination, her blood pressure is 155/95 mm Hg. Urinalysis shows 2+ proteinuria, but no blood, glucose, or ketones. At 36 weeks, she gives birth to a normal viable but low-birth-weight infant. Her blood pressure returns to normal, and she no longer has proteinuria. Which of the following pathologic findings is most likely to be found on examination of the placenta?
What is the approximate percentage of water in amniotic fluid?
Which of the following is NOT true regarding the management of suspected myocardial infarction in pregnancy?
Placenta previa is associated with all of the following conditions except?
Which of the following statements about acute fatty liver of pregnancy is true?
What is a true statement about symmetrical IUGR compared to asymmetrical IUGR?
A pregnant woman in her 1st trimester is given spiramycin, but she does not complete the course. The baby is born with hydrocephalus and infection. Which organism is the most likely cause of this infection?
Risk of damage to the fetus by maternal rubella is maximum if the mother gets infected in which period of pregnancy?
Which of the following statements related to the therapy of iron deficiency anemia is incorrect?
Maternal-Fetal Medicine Indian Medical PG Practice Questions and MCQs
Question 611: In pregnancy, what is the drug of choice for initial treatment of immune thrombocytopenic purpura?
- A. Azathioprine
- B. Intravenous immunoglobulins
- C. Systemic corticosteroids (Correct Answer)
- D. Laparoscopic splenectomy
Explanation: **Explanation:** Immune Thrombocytopenic Purpura (ITP) in pregnancy is an autoimmune condition where IgG antibodies are directed against platelet glycoproteins, leading to their destruction. Treatment is generally indicated when the platelet count falls below **30,000/µL** or if the patient is symptomatic (bleeding). **Why Systemic Corticosteroids are the Correct Choice:** Oral corticosteroids (e.g., Prednisolone) are the **first-line/initial treatment** for ITP in pregnancy. They work by decreasing the clearance of antibody-coated platelets by splenic macrophages and suppressing the production of autoantibodies. They are preferred due to their efficacy, ease of administration, and relatively low cost. **Analysis of Incorrect Options:** * **A. Azathioprine:** This is a second-line immunosuppressant used only in refractory cases. It is generally avoided as an initial agent due to its delayed onset of action. * **B. Intravenous Immunoglobulins (IVIG):** While highly effective, IVIG is reserved for patients who do not respond to steroids, those requiring a rapid increase in platelet count (e.g., before delivery or surgery), or when steroids are contraindicated. * **D. Laparoscopic Splenectomy:** This is a second-line surgical intervention. If necessary, it is ideally performed during the **second trimester** to avoid miscarriage (1st trimester) or technical difficulty due to the enlarged uterus (3rd trimester). **NEET-PG High-Yield Pearls:** * **Target Platelet Count:** Aim for >30,000/µL during pregnancy and >50,000/µL near delivery (>80,000/µL for regional anesthesia). * **Fetal Risk:** Maternal ITP antibodies (IgG) can cross the placenta, causing **neonatal thrombocytopenia** in 10-15% of cases. * **Mode of Delivery:** ITP itself is not an indication for Cesarean section; the mode of delivery is based on obstetric indications. * **Contraindication:** Fetal scalp blood sampling and vacuum extraction should be avoided if fetal thrombocytopenia is suspected.
Question 612: A 36-year-old primigravida develops peripheral edema late in the second trimester. On physical examination, her blood pressure is 155/95 mm Hg. Urinalysis shows 2+ proteinuria, but no blood, glucose, or ketones. At 36 weeks, she gives birth to a normal viable but low-birth-weight infant. Her blood pressure returns to normal, and she no longer has proteinuria. Which of the following pathologic findings is most likely to be found on examination of the placenta?
- A. Chorioamnionitis
- B. Chronic villitis
- C. Hydropic villi
- D. Multiple infarcts (Correct Answer)
Explanation: ### Explanation **Diagnosis: Preeclampsia** The patient presents with the classic triad of **Preeclampsia**: hypertension (≥140/90 mm Hg) and proteinuria (2+) developing after 20 weeks of gestation in a primigravida, which resolves postpartum. **Why "Multiple Infarcts" is correct:** The underlying pathology of preeclampsia is **abnormal cytotrophoblast invasion** of the spiral arteries. Instead of transforming into high-capacitance, low-resistance vessels, the spiral arteries remain narrow and muscular. This leads to **placental hypoperfusion and ischemia**. Grossly and microscopically, this manifests as **multiple placental infarcts**, retroplacental hemorrhages, and "villous agglutination." Chronic ischemia results in uteroplacental insufficiency, explaining the **low-birth-weight (IUGR)** infant seen in this case. **Why other options are incorrect:** * **A. Chorioamnionitis:** This is an ascending bacterial infection (usually following prolonged rupture of membranes) characterized by fever, maternal tachycardia, and fetal tachycardia. It shows neutrophil infiltration of the fetal membranes, not infarcts. * **B. Chronic villitis:** Often associated with TORCH infections (e.g., CMV, Syphilis). It involves lymphocytic infiltration of the villi rather than ischemic changes related to maternal hypertension. * **C. Hydropic villi:** This is a hallmark of **Gestational Trophoblastic Disease** (Molar pregnancy). While partial moles can present with hypertension, they occur earlier in pregnancy and involve fetal parts with "Swiss-cheese" cystic villi. **Clinical Pearls for NEET-PG:** * **Definitive Treatment:** Delivery of the fetus and placenta. * **Microscopic hallmark:** **Acute Atherosis** (fibrinoid necrosis of the vessel wall with lipid-laden macrophages) in the spiral arteries. * **Placental weight:** In preeclampsia, the placenta is often small for gestational age due to chronic ischemia.
Question 613: What is the approximate percentage of water in amniotic fluid?
- A. 42%
- B. 64%
- C. 76%
- D. 99% (Correct Answer)
Explanation: **Explanation:** Amniotic fluid is the protective liquid contained within the amniotic sac, serving as a vital environment for fetal growth and development. In the early stages of pregnancy, it is primarily an ultrafiltrate of maternal plasma, but as the fetus develops, fetal urine becomes the major contributor. **Why 99% is correct:** Amniotic fluid is highly aqueous. Chemically, it consists of approximately **98% to 99% water** and only **1% to 2% solids**. These solids include organic and inorganic substances such as proteins, lipids, carbohydrates (glucose), electrolytes (sodium, potassium), urea, creatinine, and fetal cells (vernix caseosa and lanugo). The high water content is essential for maintaining fetal temperature, allowing symmetrical musculoskeletal development, and protecting the fetus and umbilical cord from mechanical compression. **Why the other options are incorrect:** * **Options A (42%), B (64%), and C (76%):** These percentages are significantly lower than the actual water content. Such low values would imply a highly viscous, protein-rich, or cellular fluid, which would be physiologically incompatible with the functions of amniotic fluid, such as fetal lung "breathing" movements and free fetal movement. **High-Yield NEET-PG Pearls:** * **Specific Gravity:** The specific gravity of amniotic fluid is low, typically ranging from **1.008 to 1.010**. * **Osmolality:** As pregnancy advances, the fluid becomes **hypotonic** to maternal plasma due to the increasing contribution of dilute fetal urine. * **Volume Milestones:** The volume reaches its peak of approximately **800 ml at 34 weeks** of gestation, then gradually decreases to about 600 ml at term (40 weeks) and further reduces post-term. * **pH:** It is slightly alkaline, with a pH of approximately **7.0 to 7.5**. This is clinically useful in the "Nitrazine test" to confirm the rupture of membranes.
Question 614: Which of the following is NOT true regarding the management of suspected myocardial infarction in pregnancy?
- A. Immediate delivery is indicated. (Correct Answer)
- B. The patient should be started on a beta-blocker.
- C. Daily low-dose aspirin should be given to the patient.
- D. Troponin levels are helpful in the diagnosis of MI in pregnancy.
Explanation: **Explanation:** The management of acute myocardial infarction (MI) in pregnancy follows the same life-saving principles as in non-pregnant adults, with the primary goal being maternal stabilization. **Why Option A is the correct answer (False statement):** Immediate delivery is **not** indicated in the management of acute MI. In fact, delivery (whether vaginal or cesarean) during the acute phase of an MI is associated with extremely high maternal mortality due to the massive hemodynamic shifts (increased cardiac output and stroke volume) that occur during labor and the immediate postpartum period. The goal is to stabilize the mother medically and delay delivery for at least **2–3 weeks** after the MI, if possible, to allow the myocardium to heal. **Analysis of other options:** * **Option B:** Beta-blockers (e.g., Metoprolol) are standard of care to reduce myocardial oxygen demand and are generally safe in pregnancy, though fetal growth should be monitored. * **Option C:** Low-dose aspirin is indicated for its antiplatelet effects and is considered safe throughout pregnancy. * **Option D:** Cardiac Troponins (I and T) are highly specific and are **not** elevated by normal pregnancy or labor. They remain the gold standard for diagnosing MI in pregnant patients. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** While atherosclerosis is common, **Spontaneous Coronary Artery Dissection (SCAD)** is a uniquely frequent cause of MI in the peripartum period. * **Positioning:** Always manage the patient in the **left lateral decubitus** position to prevent aortocaval compression. * **Thrombolysis:** If PCI (Percutaneous Coronary Intervention) is unavailable, thrombolytics can be used as they do not cross the placenta, though the risk of maternal hemorrhage (e.g., placental abruption) is increased.
Question 615: Placenta previa is associated with all of the following conditions except?
- A. Large placenta
- B. Previous Cesarean section scar
- C. Primigravida (Correct Answer)
- D. Previous placenta previa
Explanation: **Explanation:** Placenta previa occurs when the placenta implants in the lower uterine segment, partially or completely covering the internal os. The underlying pathophysiology usually involves either **delayed implantation** of the blastocyst or a **large placental surface area** seeking a rich blood supply. **Why Primigravida is the correct answer:** Primigravida (a woman pregnant for the first time) is actually a **protective factor** rather than a risk factor. Placenta previa is significantly more common in **multiparous** women. With each pregnancy, the upper uterine segment may undergo scarring or reduced vascularity, encouraging the placenta to implant in the lower, "fresher" uterine segment (the "Dropping Down" theory). **Analysis of Incorrect Options:** * **Large Placenta:** Conditions that increase placental surface area (e.g., multiple gestations, Rh isoimmunization, or diabetes) increase the likelihood that the placental edge will reach the internal os. * **Previous Cesarean Section:** This is the **most significant risk factor**. The scar tissue in the lower segment alters vascularity and predisposes to abnormal implantation (including placenta accreta spectrum). The risk increases linearly with the number of previous C-sections. * **Previous Placenta Previa:** A history of previa increases the recurrence risk by 4–8% in subsequent pregnancies. **NEET-PG High-Yield Pearls:** * **Most common symptom:** Painless, causeless, recurrent bright red vaginal bleeding (Warning hemorrhage). * **Investigation of choice:** Transvaginal Ultrasound (TVUS) is the gold standard (safer and more accurate than transabdominal). * **Stallworthy’s Sign:** A posterior placenta previa can prevent the engagement of the fetal head; pressing the head down causes fetal bradycardia. * **Contraindication:** **Digital vaginal examination** is strictly contraindicated unless performed in an "Operation Theatre" set up for immediate Cesarean (Double Setup Examination).
Question 616: Which of the following statements about acute fatty liver of pregnancy is true?
- A. It is the most common cause of acute liver failure during pregnancy. (Correct Answer)
- B. It typically manifests in the early weeks of pregnancy.
- C. Hepatic dysfunction persists postpartum.
- D. Some patients develop transient diabetes mellitus in the postpartum period.
Explanation: **Explanation:** **Acute Fatty Liver of Pregnancy (AFLP)** is a rare but life-threatening obstetric emergency characterized by the microvesicular fatty infiltration of hepatocytes. **1. Why Option A is Correct:** AFLP is recognized as the **most common cause of acute liver failure** specific to pregnancy. It typically occurs due to a defect in mitochondrial fatty acid oxidation—specifically a deficiency in the enzyme **Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD)** in the fetus. This leads to the accumulation of long-chain fatty acids in the maternal circulation, overwhelming the liver and leading to rapid hepatic failure. **2. Why the Other Options are Incorrect:** * **Option B:** AFLP typically manifests in the **third trimester** (usually between 30–38 weeks) or the immediate postpartum period, not early pregnancy. * **Option C:** The definitive treatment for AFLP is **immediate delivery**. Once the fetus (the source of fatty acid metabolites) is delivered, hepatic function usually begins to improve rapidly, and the liver typically recovers completely without chronic sequelae. * **Option D:** Patients with AFLP are prone to **transient Diabetes Insipidus** (not Diabetes Mellitus) in the postpartum period. This occurs because hepatic dysfunction leads to decreased clearance of vasopressinase (an enzyme produced by the placenta), resulting in the degradation of ADH. **High-Yield Clinical Pearls for NEET-PG:** * **Swansea Criteria:** Used for the clinical diagnosis of AFLP. * **Hallmark Lab Finding:** Profound **hypoglycemia** (due to liver failure) and hyperuricemia. * **Association:** Strongly associated with **Preeclampsia** (seen in ~50% of cases). * **Management:** Intensive care stabilization followed by **prompt delivery**, regardless of gestational age.
Question 617: What is a true statement about symmetrical IUGR compared to asymmetrical IUGR?
- A. Worse prognosis (Correct Answer)
- B. Late onset
- C. Brain sparing effect
- D. More common
Explanation: **Explanation:** Intrauterine Growth Restriction (IUGR) is classified into two types based on the timing of the insult and the fetal growth pattern. **1. Why Option A is Correct:** **Symmetrical IUGR** (Type I) occurs due to an early insult during the **hyperplastic phase** of cellular growth (e.g., chromosomal anomalies, early TORCH infections). This results in a global reduction in the number of cells in all organs. Because the damage occurs early and affects the total cell count of the brain and body equally, the fetus has a limited capacity for catch-up growth, leading to a **worse prognosis** and higher risk of long-term neurodevelopmental deficits compared to asymmetrical IUGR. **2. Why Other Options are Incorrect:** * **B. Late onset:** Symmetrical IUGR is typically **early-onset** (before 32 weeks). Late-onset growth restriction is characteristic of asymmetrical IUGR, usually caused by placental insufficiency. * **C. Brain sparing effect:** This is a hallmark of **Asymmetrical IUGR**. In response to hypoxia, blood is shunted to the brain, heart, and adrenals at the expense of the liver and limbs. In symmetrical IUGR, the brain is not spared; the head circumference is reduced proportionately with the body. * **D. More common:** Asymmetrical IUGR is more common, accounting for approximately **70-80%** of all IUGR cases. Symmetrical IUGR accounts for only 20-30%. **High-Yield Clinical Pearls for NEET-PG:** * **Ponderal Index:** Low in asymmetrical IUGR; normal in symmetrical IUGR. * **HC/AC Ratio:** Elevated in asymmetrical IUGR (Head > Abdomen); normal in symmetrical IUGR. * **Most sensitive parameter for IUGR:** Abdominal Circumference (AC), as it reflects depleted glycogen stores in the fetal liver. * **Commonest cause of Asymmetrical IUGR:** Maternal hypertension/Placental insufficiency.
Question 618: A pregnant woman in her 1st trimester is given spiramycin, but she does not complete the course. The baby is born with hydrocephalus and infection. Which organism is the most likely cause of this infection?
- A. Herpes Simplex Virus (HSV)
- B. Treponema pallidum
- C. Toxoplasma gondii (Correct Answer)
- D. Cytomegalovirus (CMV)
Explanation: ### Explanation **Correct Answer: C. Toxoplasma gondii** The clinical scenario describes a classic case of **Congenital Toxoplasmosis**. The definitive clue is the use of **Spiramycin**, which is the drug of choice for primary maternal Toxoplasma infection in the first trimester to prevent vertical transmission. **Why Toxoplasma gondii is correct:** Toxoplasmosis is caused by the parasite *Toxoplasma gondii*. If a mother acquires a primary infection during pregnancy, the parasite can cross the placenta. While the risk of transmission is lowest in the first trimester, the severity of fetal damage is highest. The "Classic Triad" of congenital toxoplasmosis includes: 1. **Hydrocephalus** (as seen in this case) 2. **Chorioretinitis** (most common finding) 3. **Intracranial calcifications** (typically diffuse/scattered) **Why other options are incorrect:** * **HSV:** Usually transmitted during delivery (birth canal). It typically presents with skin vesicles, keratoconjunctivitis, or encephalitis, rather than hydrocephalus at birth. * **Treponema pallidum (Syphilis):** Presents with features like snuffles, Hutchinson’s teeth, saddle nose, and periostitis. Treatment is Penicillin, not Spiramycin. * **CMV:** The most common congenital infection. While it causes microcephaly and **periventricular** calcifications, it is not treated with Spiramycin (Ganciclovir is used for symptomatic neonates). **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Spiramycin is used for maternal infection (to prevent transmission). If fetal infection is confirmed (via amniotic fluid PCR), the treatment switches to **Pyrimethamine, Sulfadiazine, and Folinic acid**. * **Calcification Pattern:** Toxoplasmosis = Diffuse/Scattered; CMV = Periventricular. * **Triad of Sabin:** Chorioretinitis, Hydrocephalus, and Intracranial calcifications. * **Transmission Risk:** Increases with gestational age (highest in 3rd trimester), but severity decreases.
Question 619: Risk of damage to the fetus by maternal rubella is maximum if the mother gets infected in which period of pregnancy?
- A. 6-12 weeks of pregnancy (Correct Answer)
- B. 20-24 weeks of pregnancy
- C. 24-28 weeks of pregnancy
- D. 32-36 weeks of pregnancy
Explanation: **Explanation:** The risk of congenital malformations following maternal rubella infection is inversely proportional to the gestational age at the time of infection. This is due to the concept of **organogenesis**, which occurs primarily during the first trimester. **Why Option A is Correct:** The period between **6-12 weeks** (early first trimester) is the most critical window for fetal development. During this time, the virus can cause chronic fetal infection, leading to cell death and inhibition of cell division. If infection occurs before 11 weeks, the risk of **Congenital Rubella Syndrome (CRS)** is as high as **90%**. The classic "Gregg’s Triad" (Cataracts, Sensorineural hearing loss, and Cardiac defects like PDA) is most likely to manifest when infection occurs during this specific window. **Why Options B, C, and D are Incorrect:** * **20-24 weeks (Option B):** By the second trimester, organogenesis is largely complete. The risk of major structural defects drops significantly after 16 weeks and is negligible after 20 weeks. * **24-36 weeks (Options C & D):** While the virus can still cross the placenta in the third trimester, it typically results in intrauterine growth restriction (IUGR) or a subclinical infection rather than the structural malformations characteristic of CRS. **Clinical Pearls for NEET-PG:** * **Maximum Risk:** 0-12 weeks (up to 90% risk of CRS). * **Safe Period:** Infection after **20 weeks** rarely results in congenital defects. * **Most Common Defect:** Sensorineural hearing loss (can occur up to 16 weeks). * **Most Common Cardiac Defect:** Patent Ductus Arteriosus (PDA). * **Diagnosis:** Presence of **Rubella-specific IgM** in fetal blood or neonatal cord blood is diagnostic of congenital infection. * **Prevention:** Rubella vaccine (RA 27/3) is a live attenuated vaccine and is **contraindicated in pregnancy**. Pregnancy should be avoided for 1 month after vaccination.
Question 620: Which of the following statements related to the therapy of iron deficiency anemia is incorrect?
- A. Oral iron can be given at any stage of pregnancy if iron deficiency anemia is detected. (Correct Answer)
- B. Parenteral iron therapy markedly increases the reticulocytic count within 7-14 days.
- C. Parenteral iron therapy is ideal during 30-36 weeks of gestation.
- D. Blood transfusion may be useful in severe anemia beyond 36 weeks of gestation.
Explanation: ### Explanation **Why Option A is the Correct (Incorrect Statement):** While oral iron is the first-line treatment for iron deficiency anemia (IDA), it is **not** recommended in the **first trimester** of pregnancy. During the first trimester, oral iron often exacerbates pregnancy-induced nausea and vomiting (morning sickness), leading to poor compliance. Furthermore, the fetal iron requirement is minimal during this period. Routine iron supplementation is typically initiated after the 12th–14th week (second trimester) when the physiological demand increases and gastrointestinal tolerance improves. **Analysis of Other Options:** * **Option B:** Parenteral iron bypasses the gut and provides a rapid surge in available iron. A significant rise in the **reticulocyte count** (peaking at 7–14 days) is the earliest objective sign of hematological response, followed by a rise in hemoglobin. * **Option C:** Parenteral iron is the treatment of choice for moderate anemia (Hb 7–9 g/dL) between **30 and 36 weeks**. This "window" is critical because oral iron takes too long to raise hemoglobin levels before labor, and blood transfusion should be avoided if there is still time for pharmacological correction. * **Option D:** Severe anemia (Hb <7 g/dL) diagnosed **beyond 36 weeks** of gestation is an indication for blood transfusion. At this late stage, there is insufficient time for parenteral iron to optimize hemoglobin levels before the onset of labor and potential postpartum hemorrhage. **High-Yield Clinical Pearls for NEET-PG:** * **Prophylactic Dose:** 60 mg elemental iron + 400 µg folic acid (IFA) for 180 days (as per Anemia Mukt Bharat). * **Therapeutic Dose:** 100–200 mg elemental iron daily. * **Target:** Hemoglobin should rise by approximately **0.7–1 g/dL per week** with effective therapy. * **Parenteral Iron Formula (Ganzoni):** Total Iron Deficit (mg) = [Weight (kg) × (Target Hb - Actual Hb) × 2.4] + 500 mg (for stores).
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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