Maternal-Fetal Medicine Practice Questions

Q: 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?

Multiple infarcts. ### 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.

Q: What is the approximate percentage of water in amniotic fluid?

99%. **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.

Q: Which of the following is NOT true regarding the management of suspected myocardial infarction in pregnancy?

Immediate delivery is indicated.. **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.

Q: What is a true statement about symmetrical IUGR compared to asymmetrical IUGR?

Worse prognosis. **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.

Q: 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?

Toxoplasma gondii. ### 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.

Q: Risk of damage to the fetus by maternal rubella is maximum if the mother gets infected in which period of pregnancy?

6-12 weeks of pregnancy. **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 1

In pregnancy, what is the drug of choice for initial treatment of immune thrombocytopenic purpura?

Accepted Answer

Systemic corticosteroids

Answer

Azathioprine

Answer

Intravenous immunoglobulins

Answer

Laparoscopic splenectomy

Question 2

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?

Accepted Answer

Multiple infarcts

Answer

Chorioamnionitis

Answer

Chronic villitis

Answer

Hydropic villi

Question 3

What is the approximate percentage of water in amniotic fluid?

Accepted Answer

99%

Answer

42%

Answer

64%

Answer

76%

Question 4

Which of the following is NOT true regarding the management of suspected myocardial infarction in pregnancy?

Accepted Answer

Immediate delivery is indicated.

Answer

The patient should be started on a beta-blocker.

Answer

Daily low-dose aspirin should be given to the patient.

Answer

Troponin levels are helpful in the diagnosis of MI in pregnancy.

Question 5

Placenta previa is associated with all of the following conditions except?

Accepted Answer

Primigravida

Answer

Large placenta

Answer

Previous Cesarean section scar

Answer

Previous placenta previa

Question 6

Which of the following statements about acute fatty liver of pregnancy is true?

Accepted Answer

It is the most common cause of acute liver failure during pregnancy.

Answer

It typically manifests in the early weeks of pregnancy.

Answer

Hepatic dysfunction persists postpartum.

Answer

Some patients develop transient diabetes mellitus in the postpartum period.

Question 7

What is a true statement about symmetrical IUGR compared to asymmetrical IUGR?

Accepted Answer

Worse prognosis

Answer

Late onset

Answer

Brain sparing effect

Answer

More common

Question 8

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?

Accepted Answer

Toxoplasma gondii

Answer

Herpes Simplex Virus (HSV)

Answer

Treponema pallidum

Answer

Cytomegalovirus (CMV)

Question 9

Risk of damage to the fetus by maternal rubella is maximum if the mother gets infected in which period of pregnancy?

Accepted Answer

6-12 weeks of pregnancy

Answer

20-24 weeks of pregnancy

Answer

24-28 weeks of pregnancy

Answer

32-36 weeks of pregnancy

Question 10

Which of the following statements related to the therapy of iron deficiency anemia is incorrect?

Accepted Answer

Oral iron can be given at any stage of pregnancy if iron deficiency anemia is detected.

Answer

Parenteral iron therapy markedly increases the reticulocytic count within 7-14 days.

Answer

Parenteral iron therapy is ideal during 30-36 weeks of gestation.

Answer

Blood transfusion may be useful in severe anemia beyond 36 weeks of gestation.

Maternal-Fetal Medicine — MCQs

Maternal-Fetal Medicine — MCQs

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