Endocrinology of Pregnancy Practice Questions

Q: What change occurs in the resistance of the uteroplacental vasculature during pregnancy?

High resistance to low resistance.. ### Explanation The correct answer is **B. High resistance to low resistance.** **1. Why it is correct:** In a non-pregnant state, the uterine arteries are high-resistance vessels. During pregnancy, the demand for blood flow to the fetus increases significantly (from ~50 mL/min to ~600–700 mL/min). To accommodate this, a process called **trophoblastic invasion** occurs. Cytotrophoblasts invade the maternal **spiral arteries**, replacing the muscular and elastic layers with fibrinoid material. This transforms narrow, high-resistance vessels into dilated, tortuous, **low-resistance channels**. This physiological adaptation ensures a continuous, high-volume blood supply to the intervillous space, independent of maternal vasoconstrictive stimuli. **2. Why the other options are wrong:** * **Option A:** Low to high resistance would cause fetal growth restriction and ischemia. This is the pathological state seen in preeclampsia, not normal pregnancy. * **Option C:** If resistance did not change, the uterine blood flow could not increase 10–15 fold, leading to placental insufficiency. * **Option D:** The change is highly predictable and essential for a viable pregnancy; it is a hallmark of normal placentation. **3. High-Yield Clinical Pearls for NEET-PG:** * **Waveform Change:** On Doppler ultrasound, this transition is marked by the **disappearance of the diastolic notch** in the uterine artery by 20–24 weeks. * **Preeclampsia Connection:** Failure of the second wave of trophoblastic invasion (which involves the intramyometrial portion of spiral arteries) leads to persistent high resistance, resulting in **Preeclampsia** and **IUGR**. * **Refractoriness:** During pregnancy, the uteroplacental vasculature becomes refractory to the pressor effects of **Angiotensin II**, further maintaining the low-resistance state.

Q: Which hormone is essential for the salvage of the corpus luteum?

hCG. **Explanation:** The correct answer is **hCG (human Chorionic Gonadotropin)**. **1. Why hCG is correct:** In a normal menstrual cycle, the corpus luteum (CL) has a finite lifespan of about 14 days, after which it degenerates (luteolysis), leading to a drop in progesterone and the onset of menstruation. However, if fertilization occurs, the syncytiotrophoblast of the developing blastocyst begins secreting **hCG**. This hormone is structurally similar to LH (Luteinizing Hormone) and binds to LH receptors on the corpus luteum. This "rescues" or salvages the CL, preventing its regression and stimulating it to continue producing **progesterone**, which is vital for maintaining the decidua and the early pregnancy until the placenta takes over (luteal-placental shift) at around 7–10 weeks. **2. Why the other options are incorrect:** * **FSH (Follicle Stimulating Hormone):** Its primary role is the recruitment and growth of ovarian follicles during the follicular phase; it does not maintain the corpus luteum. * **AFP (Alpha-Fetoprotein):** This is a glycoprotein produced by the fetal yolk sac and liver. It serves as a marker for neural tube defects and chromosomal anomalies but has no endocrine role in maintaining the CL. * **Estrogen:** While produced by the CL and the placenta, estrogen does not "salvage" the CL; rather, its rising levels are a result of a functional CL or placenta. **Clinical Pearls for NEET-PG:** * **Doubling Time:** In early pregnancy, hCG levels double every 48 hours. * **Luteal-Placental Shift:** Occurs between **7–10 weeks**. If the corpus luteum is removed before 7 weeks without progesterone supplementation, miscarriage will occur. * **Structure:** hCG is a glycoprotein with an $\alpha$ and $\beta$ subunit. The **$\beta$ subunit** is unique and used for pregnancy testing.

Q: What is the drug of choice for imminent eclampsia?

Magnesium sulfate. **Explanation:** **Magnesium Sulfate (MgSO₄)** is the drug of choice for both the **prevention** of seizures in imminent eclampsia and the **treatment** of seizures in established eclampsia. The underlying medical concept relies on its role as a potent neuromuscular blocker and CNS depressant. It acts by inhibiting NMDA receptors, blocking calcium influx into neurons, and decreasing acetylcholine release at the motor endplate, thereby raising the seizure threshold. Large-scale trials (like the Magpie Trial) have proven its superiority over diazepam and phenytoin in preventing the progression of pre-eclampsia to eclampsia. **Analysis of Incorrect Options:** * **Hydralazine (A) & Labetalol (B):** These are antihypertensive agents. While they are used to manage hypertensive emergencies in pregnancy (BP ≥160/110 mmHg), they do not possess anti-convulsant properties and cannot prevent seizures. Labetalol is often the first-line IV antihypertensive, but it is not the drug of choice for "imminent eclampsia." * **Methyldopa (D):** This is a centrally acting alpha-2 agonist. It is the drug of choice for **chronic hypertension** in pregnancy due to its long-term safety profile, but it is too slow-acting for acute management or seizure prophylaxis. **High-Yield Clinical Pearls for NEET-PG:** * **Pritchard Regimen:** 4g IV (loading) + 10g IM (5g in each buttock), followed by 5g IM every 4 hours. * **Therapeutic Range:** 4–7 mEq/L. * **Monitoring:** Always check for **Patellar reflex** (earliest sign of toxicity), **Respiratory rate** (>12/min), and **Urine output** (>30ml/hr). * **Antidote:** 10 ml of 10% **Calcium Gluconate** IV (given over 10 minutes).

Q: What is the main source of prolactin in amniotic fluid?

Decidua. **Explanation:** The correct answer is **Decidua**. **1. Why Decidua is the correct answer:** While prolactin is primarily secreted by the anterior pituitary gland in non-pregnant states, during pregnancy, the **decidua** (the modified endometrium) becomes a major extra-pituitary source. Decidual cells synthesize and secrete prolactin into the amniotic fluid via a process regulated by local factors (like IGF-1 and cytokines) rather than dopamine. Prolactin levels in amniotic fluid are significantly higher (up to 10–100 times) than in maternal or fetal plasma, peaking at 15–20 weeks of gestation. Its primary role in the amniotic fluid is **osmoregulation**, preventing fetal dehydration by regulating the transport of water and electrolytes across the chorioamnion. **2. Why the other options are incorrect:** * **Syncytiotrophoblast:** This layer is the primary source of **hCG** (human Chorionic Gonadotropin) and **hPL** (human Placental Lactogen), not prolactin. * **Cytotrophoblast:** These are the stem cells of the placenta that primarily secrete **GnRH** and other releasing hormones. * **Yolk sac of fetus:** The yolk sac is responsible for early hematopoiesis and the production of **Alpha-fetoprotein (AFP)**, but it does not contribute to amniotic prolactin levels. **Clinical Pearls for NEET-PG:** * **Source of Amniotic Prolactin:** Decidua (specifically the decidua capsularis and parietalis). * **Source of Maternal Serum Prolactin:** Maternal Anterior Pituitary. * **Source of Fetal Serum Prolactin:** Fetal Anterior Pituitary. * **Function:** Amniotic prolactin is crucial for maintaining **amniotic fluid volume** and electrolyte balance. * **Bromocriptine Fact:** Dopamine agonists like Bromocriptine inhibit pituitary prolactin but **do not** inhibit decidual prolactin production.

Q: Which of the following is NOT correct regarding respiratory function during the late trimester of normal pregnancy?

Lung compliance is decreased.. In normal pregnancy, significant physiological adaptations occur in the respiratory system to meet the increased oxygen demands of the fetus and the mother. **Explanation of the Correct Answer (C):** **Lung compliance does NOT change** during pregnancy. While the enlarging uterus causes the diaphragm to rise by approximately 4 cm, the chest wall diameter increases and the ribs flare out (mediated by the hormone relaxin). This maintains the overall compliance of the respiratory system. Therefore, the statement that lung compliance is decreased is incorrect. **Analysis of Incorrect Options:** * **Option A:** Progesterone acts as a direct respiratory stimulant. It increases the sensitivity of the respiratory center to $CO_2$, leading to an increase in **Tidal Volume (by ~40%)** and **Resting Minute Ventilation (by ~40-50%)**. * **Option B:** Due to the elevation of the diaphragm, the **Functional Residual Capacity (FRC)** and **Residual Volume (RV)** are decreased by approximately 20%. This is a high-yield fact often tested in exams. * **Option D:** Progesterone causes relaxation of the smooth muscles in the tracheobronchial tree, which leads to a **reduction in total pulmonary resistance**. **High-Yield NEET-PG Pearls:** 1. **Vital Capacity (VC)** and **Inspiratory Capacity (IC)** remain unchanged or may slightly increase. 2. **Respiratory Rate** remains largely **unchanged**; the increase in minute ventilation is primarily due to increased tidal volume. 3. Pregnancy is a state of **compensated respiratory alkalosis** (pH 7.40–7.45) due to hyperventilation, which facilitates $CO_2$ transfer from the fetus to the mother. 4. **Dyspnea of pregnancy** is common and physiological, often starting in the first or second trimester.

Q: When is termination of pregnancy indicated in hyperemesis gravidarum?

Decrease in renal output. **Explanation:** Hyperemesis Gravidarum (HG) is a severe form of nausea and vomiting in pregnancy that leads to dehydration, electrolyte imbalance, and weight loss. While modern supportive care makes termination of pregnancy (TOP) rare, it remains a life-saving indication when conservative management fails and multi-organ dysfunction begins. **Why "Decrease in renal output" is the correct answer:** A decrease in renal output (oliguria) signifies severe, decompensated dehydration and the onset of **acute kidney injury (AKI)**. In the context of HG, this indicates that the body’s compensatory mechanisms have failed. Along with other "danger signs" like jaundice (liver failure), retinal hemorrhage, or Wernicke’s encephalopathy (neurological damage), persistent oliguria is a definitive indication for termination to save the mother’s life. **Why the other options are incorrect:** * **A. Presence of acetone in urine:** Ketonuria is a common finding in HG due to starvation and fat metabolism. It is a marker for hospitalization and IV fluid resuscitation, not an indication for termination. * **C. Vomiting persists beyond three months:** While HG typically resolves by 16–20 weeks, persistence alone is not life-threatening. Many women continue to have mild symptoms throughout pregnancy without requiring termination. **NEET-PG High-Yield Pearls:** * **Wernicke’s Encephalopathy:** Caused by Vitamin B1 (Thiamine) deficiency due to prolonged vomiting. Always replenish Thiamine *before* giving Glucose to avoid precipitating this condition. * **Electrolyte Imbalance:** The most common pattern is **Hypokalemic Hypochloremic Metabolic Alkalosis**. * **Mallory-Weiss Tear:** Hematemesis in HG is often due to esophageal mucosal tears from forceful vomiting. * **Drug of Choice:** Pyridoxine (Vitamin B6) + Doxylamine is the first-line pharmacological treatment.

Q: What is true about diabetes in pregnancy?

All of the above. Diabetes in pregnancy encompasses both **Pre-gestational (Type 1 or 2)** and **Gestational Diabetes Mellitus (GDM)**. The fetal outcomes depend significantly on the timing and severity of hyperglycemia. ### **Explanation of Options:** * **A. Macrosomia:** This is the most common complication. According to the **Pedersen Hypothesis**, maternal hyperglycemia leads to fetal hyperglycemia. This stimulates the fetal pancreas to secrete excess insulin (hyperinsulinemia). Since insulin is a potent growth hormone, it causes excessive deposition of fat and glycogen, leading to a large-for-gestational-age fetus (>4kg). * **B. Intrauterine Growth Restriction (IUGR):** While GDM typically causes macrosomia, **Pre-gestational diabetes** (especially with long-standing vascular complications like White’s Class R or F) can lead to placental insufficiency. This results in restricted nutrient delivery, causing IUGR. * **C. Congenital Anomalies:** These occur due to **teratogenicity** from hyperglycemia during organogenesis (first trimester). Therefore, they are seen in **Pre-gestational diabetes** but *not* in GDM (which develops after the first trimester). The most specific anomaly is **Caudal Regression Syndrome**, though Cardiac defects (VSD) are the most common. ### **High-Yield Clinical Pearls for NEET-PG:** * **Most common malformation:** Ventricular Septal Defect (VSD). * **Most specific malformation:** Caudal Regression Syndrome (Sacral agenesis). * **HbA1c Goal:** Ideally <6.0% pre-conception to minimize anomaly risks. * **Neonatal Complications:** Hypoglycemia (due to persistent fetal hyperinsulinemia), Hypocalcemia, Hyperbilirubinemia, and Polycythemia. * **Respiratory Distress Syndrome (RDS):** Hyperinsulinemia inhibits cortisol-induced surfactant production by Type II pneumocytes.

Question 1

What change occurs in the resistance of the uteroplacental vasculature during pregnancy?

Accepted Answer

High resistance to low resistance.

Answer

Low resistance to high resistance.

Answer

No change in resistance.

Answer

Resistance varies unpredictably.

Question 2

Which hormone is essential for the salvage of the corpus luteum?

Accepted Answer

hCG

Answer

FSH

Answer

AFP

Answer

Estrogen

Question 3

What is the drug of choice for imminent eclampsia?

Accepted Answer

Magnesium sulfate

Answer

Hydralazine

Answer

Labetalol

Answer

Methyldopa

Question 4

What is the main source of prolactin in amniotic fluid?

Accepted Answer

Decidua

Answer

Syncytiotrophoblast

Answer

Cytotrophoblast

Answer

Yolk sac of fetus

Question 5

All of the following are true about gestational diabetes except:

Accepted Answer

Approximately one-third of cases progress to permanent diabetes.

Answer

Increased chances of recurrence in subsequent pregnancies.

Answer

Congenital malformations are common complications.

Answer

Insulin is the treatment of choice.

Question 6

Which of the following is NOT correct regarding respiratory function during the late trimester of normal pregnancy?

Accepted Answer

Lung compliance is decreased.

Answer

Tidal volume and resting minute ventilation increase.

Answer

Functional residual capacity and residual volume are decreased.

Answer

Total pulmonary resistance is reduced.

Question 7

When is termination of pregnancy indicated in hyperemesis gravidarum?

Accepted Answer

Decrease in renal output

Answer

Presence of acetone in urine

Answer

Vomiting persists beyond three months

Answer

All of the above

Question 8

Which of the following is true of thyroid nodules during pregnancy?

Accepted Answer

Can be safely removed before 24 weeks gestation.

Answer

Are poorly assessed by fine-needle aspiration.

Answer

When smaller than 0.5 cm, can be reliably detected sonographically.

Answer

If cancerous, confer worse prognosis than if found in non-pregnant controls.

Question 9

Related to calcium metabolism, which of the following does not occur during pregnancy?

Accepted Answer

Serum ionized calcium levels fall.

Answer

Total serum calcium levels fall.

Answer

80% of fetal calcium deposition occurs in the third trimester.

Answer

Fetal skeleton excretes approximately 30g of calcium by term.

Question 10

What is true about diabetes in pregnancy?

Accepted Answer

All of the above

Answer

Macrosomia

Answer

Intrauterine growth restriction (IUGR)

Answer

Congenital anomalies

Endocrinology of Pregnancy — MCQs

Endocrinology of Pregnancy — MCQs

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