Endocrinology of Pregnancy — MCQs

Endocrinology of Pregnancy Indian Medical PG Practice Questions and MCQs

Question 151: Basal metabolic rate (BMR) changes by what percentage during pregnancy?

A. Increases by 25% (Correct Answer)
B. Decreases by 25%
C. Increases by 50%
D. Decreases by 50%

Explanation: **Explanation:** The Basal Metabolic Rate (BMR) increases significantly during pregnancy, primarily to meet the increased oxygen demands of the growing fetus, the placenta, and the expansion of maternal tissues (such as the uterus and breasts). **Why Option A is Correct:** During a normal singleton pregnancy, the BMR increases by approximately **20% to 25%**. This rise is most pronounced during the third trimester. The physiological drivers include: * **Increased Cardiac Work:** The maternal heart works harder to maintain increased cardiac output. * **Respiratory Effort:** Increased work of breathing to sustain higher oxygen consumption. * **Fetal-Placental Unit:** The metabolic activity of the fetus and placenta accounts for a significant portion of the total energy expenditure. **Why Other Options are Incorrect:** * **Option B & D:** Pregnancy is a hypermetabolic state; therefore, any decrease in BMR is physiologically incorrect. * **Option C:** An increase of 50% is excessive for a singleton pregnancy. While BMR can rise further in multifetal gestations (e.g., twins), the standard physiological benchmark for medical exams is 25%. **NEET-PG High-Yield Pearls:** 1. **Total Weight Gain:** The average weight gain in a healthy pregnancy (BMI 18.5–24.9) is **11 kg to 16 kg**. 2. **Caloric Requirement:** To support the increased BMR, an additional **300–350 kcal/day** is required during the second and third trimesters. 3. **Thyroid Function:** Although BMR increases, a healthy pregnant woman remains **euthyroid**. Total T3 and T4 levels rise due to increased Thyroid Binding Globulin (TBG), but Free T3 and T4 remain within normal limits. 4. **Insulin Resistance:** Pregnancy is a "diabetogenic state" due to Human Placental Lactogen (hPL), which ensures a steady glucose supply to the fetus.

Question 152: What are the changes in the respiratory system during pregnancy?

A. Vital capacity is increased
B. Subcostal angle remains unchanged
C. Tidal volume remains unaltered
D. Residual volume is decreased (Correct Answer)

Explanation: **Explanation:** Respiratory changes in pregnancy are primarily driven by the mechanical effects of the enlarging uterus and the stimulatory effects of progesterone. **Why the correct answer (D) is right:** As the uterus enlarges, it elevates the diaphragm by approximately 4 cm. This upward displacement reduces the space available in the lungs at the end of expiration. Consequently, the **Residual Volume (RV)** and the **Functional Residual Capacity (FC)** decrease by approximately 20%. Despite the elevation, diaphragmatic excursion actually increases to maintain ventilation. **Analysis of incorrect options:** * **A. Vital capacity is increased:** Vital capacity (VC) remains **unchanged** or may show a very slight increase. While the diaphragm rises, there is a compensatory increase in the transverse and anteroposterior diameters of the chest wall. * **B. Subcostal angle remains unchanged:** The subcostal angle **increases** significantly (from about 68° to 103°) due to the hormonal relaxation of rib ligaments and the mechanical pressure of the uterus, widening the thoracic cage. * **C. Tidal volume remains unaltered:** Tidal volume (TV) **increases** by approximately 40%. Progesterone acts as a direct respiratory stimulant, increasing the sensitivity of the respiratory center to CO2, leading to deeper breaths (hyperventilation of pregnancy). **High-Yield NEET-PG Pearls:** * **Most common change:** Increase in Tidal Volume. * **Parameters that Decrease:** Residual Volume (RV), Functional Residual Capacity (FRC), Total Lung Capacity (TLC), and Expiratory Reserve Volume (ERV). * **Parameters that Increase:** Tidal Volume (TV), Minute Ventilation, and Inspiratory Capacity. * **Acid-Base Status:** Pregnancy is a state of **compensated respiratory alkalosis** (decreased $PCO_2$ to facilitate CO2 transfer from the fetus).

Question 153: Delayed puberty is seen in which of the following conditions?

A. Hypothyroidism
B. Turner's syndrome
C. Malabsorption syndrome
D. Chronic disease (Correct Answer)

Explanation: **Explanation:** Delayed puberty is defined as the absence of secondary sexual characteristics by age 13 in girls or age 14 in boys. The underlying mechanism involves the suppression of the **Hypothalamic-Pituitary-Gonadal (HPG) axis**. **Why Chronic Disease is the Correct Answer:** Chronic systemic illnesses (e.g., Chronic Kidney Disease, Cystic Fibrosis, or Inflammatory Bowel Disease) act as metabolic stressors. They lead to a state of negative energy balance and chronic inflammation, which increases cortisol and suppresses the pulsatile release of **GnRH** from the hypothalamus. This results in **functional hypogonadotropic hypogonadism**, delaying the onset of puberty until the underlying health status improves. **Analysis of Other Options:** * **Hypothyroidism:** While severe untreated hypothyroidism can cause growth retardation, it is classically associated with **Precocious Puberty** (Van Wyk-Grumbach Syndrome) due to high TSH levels cross-reacting with FSH receptors. * **Turner’s Syndrome (45, XO):** This is the most common cause of **Primary Amenorrhea** and hypergonadotropic hypogonadism. While it causes a failure to progress through puberty, it is a genetic/chromosomal dysgenesis rather than a functional delay caused by systemic illness. * **Malabsorption Syndrome:** While it can cause delayed puberty due to malnutrition, it is generally categorized under the broader umbrella of "Chronic Disease" or "Constitutional Delay" in many clinical classifications. However, in the context of this specific question, generalized **Chronic Disease** is the most comprehensive clinical category for functional HPG suppression. **NEET-PG High-Yield Pearls:** * **Most common cause of delayed puberty:** Constitutional Delay of Growth and Puberty (CDGP). * **Van Wyk-Grumbach Syndrome:** Combination of juvenile hypothyroidism, precocious puberty, and multicystic ovaries. * **Kallmann Syndrome:** Hypogonadotropic hypogonadism associated with anosmia (failure of GnRH neurons to migrate).

Question 154: The corpus luteum supports the endometrium in pregnancy until which gestational period?

A. 6-10 weeks (Correct Answer)
B. 12-24 weeks
C. 36 weeks
D. 42 weeks

Explanation: **Explanation:** The maintenance of early pregnancy depends on the secretion of progesterone by the **corpus luteum of pregnancy**. This process is driven by Human Chorionic Gonadotropin (hCG), which rescues the corpus luteum from regression. 1. **Why Option A is Correct:** The transition of progesterone production from the corpus luteum to the placenta is known as the **Luteal-Placental Shift**. This shift begins around the 6th-7th week and is typically complete by the **10th week** of gestation. While the corpus luteum persists throughout pregnancy, its functional necessity for endometrial support ends once the trophoblastic cells (placenta) produce sufficient progesterone to maintain the pregnancy independently. 2. **Why Other Options are Incorrect:** * **Option B (12-24 weeks):** By 12 weeks, the placenta is the primary source of progesterone. Surgical removal of the corpus luteum after 10 weeks usually does not result in miscarriage. * **Options C & D (36-42 weeks):** These represent late third trimester and post-term periods. The corpus luteum is functionally redundant for hormonal support long before this stage. **NEET-PG High-Yield Pearls:** * **Luteectomy:** If the corpus luteum is surgically removed before **8 weeks**, exogenous progesterone supplementation is mandatory to prevent abortion. Between 8–10 weeks, it is controversial but often supplemented. After 10 weeks, it is generally unnecessary. * **hCG Peak:** hCG levels peak at approximately **8–10 weeks**, coinciding with the maximum stimulation of the corpus luteum before the placental shift is finalized. * **Source of Progesterone:** 0–6 weeks (Corpus Luteum); 7–10 weeks (Transition); >10 weeks (Placenta).

Question 155: A 16-year-old female presents with primary amenorrhea. Examination shows a short, blind vagina and an absent uterus. What is the next investigation of choice?

A. Karyotyping (Correct Answer)
B. Intravenous pyelogram (IVP)
C. Gonadotrophin levels
D. Serum prolactin

Explanation: **Explanation:** The clinical presentation of primary amenorrhea with a **short, blind vagina and an absent uterus** points toward two primary differential diagnoses: **Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome** and **Androgen Insensitivity Syndrome (AIS)**. 1. **Why Karyotyping is the Correct Answer:** Karyotyping is the definitive next step to differentiate between these two conditions. * **MRKH syndrome:** The karyotype is **46,XX** (female). It is a Mullerian agenesis where ovaries are functional, but the uterus and upper vagina fail to develop. * **AIS:** The karyotype is **46,XY** (male). It is a defect in androgen receptors; the testes produce Anti-Mullerian Hormone (AMH), leading to an absent uterus, but the peripheral conversion of testosterone to estrogen results in a female phenotype. Distinguishing between the two is critical for management (e.g., gonadectomy is required in AIS to prevent malignancy). 2. **Why Other Options are Incorrect:** * **Intravenous pyelogram (IVP):** While renal anomalies are common in MRKH (up to 40%), an IVP or renal ultrasound is performed *after* the diagnosis is established, not as the initial investigation to determine the cause of amenorrhea. * **Gonadotrophin levels (FSH/LH):** These are typically normal in both MRKH and AIS because the hypothalamic-pituitary-ovarian/testicular axis is intact. They do not help differentiate between the two. * **Serum prolactin:** This is used to rule out hyperprolactinemia, which presents with secondary (or rarely primary) amenorrhea but would not be associated with an absent uterus. **High-Yield Clinical Pearls for NEET-PG:** * **MRKH:** 46,XX; Normal female testosterone levels; Ovaries present; Associated with renal and skeletal (VACTERL) anomalies. * **AIS:** 46,XY; Elevated/Male testosterone levels; Testes present (usually inguinal/intra-abdominal); Scant pubic/axillary hair. * **Initial Investigation for Primary Amenorrhea:** Always start with a physical exam and Ultrasound (to check for the presence of a uterus). If the uterus is absent, the next step is **Karyotyping**.

Question 156: A female patient presents with normal breast development but scanty pubic hair. What condition is she likely suffering from?

A. Turner syndrome
B. Testicular feminization syndrome (Correct Answer)
C. Mullerian agenesis
D. Gonadal dysgenesis

Explanation: **Explanation:** The clinical presentation of **normal breast development** combined with **scanty or absent pubic/axillary hair** is the classic hallmark of **Testicular Feminization Syndrome** (now more commonly known as **Complete Androgen Insensitivity Syndrome - CAIS**). **1. Why the correct answer is right:** In CAIS, the individual has a **46, XY** karyotype. Due to a mutation in the androgen receptor, the body is unresponsive to testosterone. * **Breast development:** Occurs because the high levels of testosterone (produced by undescended testes) are peripherally converted to estrogen (aromatization). * **Scanty pubic hair:** Pubic and axillary hair growth is dependent on androgens. Since the receptors are non-functional, hair growth is minimal to absent. **2. Why the other options are incorrect:** * **Turner Syndrome (45, XO):** Characterized by "streak ovaries," resulting in estrogen deficiency. This leads to **absent breast development** (primary amenorrhea) and short stature. * **Mullerian Agenesis (MRKH Syndrome):** These patients are **46, XX** with normal ovaries. They have **normal breast development AND normal pubic hair**, as their androgen receptors and estrogen production are entirely normal. The primary issue is the absence of the uterus and upper vagina. * **Gonadal Dysgenesis:** Similar to Turner syndrome, the lack of functional gonads leads to a lack of estrogen, resulting in a failure of secondary sexual characteristics (no breast development). **Clinical Pearls for NEET-PG:** * **Karyotype:** CAIS is 46, XY; MRKH is 46, XX. * **Gonads:** In CAIS, testes are present (often intra-abdominal/inguinal) and must be removed after puberty to prevent gonadoblastoma. * **Vagina:** Both CAIS and MRKH present with a blind-ending vaginal pouch and primary amenorrhea. * **Key Differentiator:** The presence or absence of **axillary/pubic hair** is the most important clinical sign to distinguish CAIS from MRKH.

Question 157: What is the recommended treatment for gestational diabetes mellitus?

A. Glibenclamide
B. Chlorpropamide
C. Glipizide
D. Insulin (Correct Answer)

Explanation: **Explanation:** **1. Why Insulin is the Correct Choice:** Insulin is the **gold standard** and first-line pharmacological treatment for Gestational Diabetes Mellitus (GDM) when Medical Nutrition Therapy (MNT) fails to achieve glycemic targets. The primary medical reason is that insulin **does not cross the placenta** (due to its large molecular weight), ensuring no risk of fetal hypoglycemia. It allows for precise titration to manage the progressive insulin resistance seen in the second and third trimesters. **2. Why the Other Options are Incorrect:** * **Glibenclamide (Glyburide):** While sometimes used in international guidelines, it is generally avoided as a first-line agent because it crosses the placenta and has been associated with higher rates of neonatal hypoglycemia and macrosomia compared to insulin. * **Chlorpropamide:** This is a first-generation sulfonylurea. It is contraindicated in pregnancy due to its long half-life and significant risk of crossing the placenta, which can cause prolonged fetal hyperinsulinemia and neonatal hypoglycemia. * **Glipizide:** Like other sulfonylureas, it is not recommended as a primary treatment in GDM due to concerns regarding placental transfer and the lack of long-term safety data compared to insulin. **3. High-Yield Clinical Pearls for NEET-PG:** * **First-line Management:** The initial management for GDM is always **Medical Nutrition Therapy (MNT)** for 1–2 weeks. * **DIPSI Criteria:** In India, GDM is often diagnosed using the DIPSI (Diabetes in Pregnancy Study Group India) method: 75g oral glucose load regardless of last meal; a 2-hour plasma glucose **≥140 mg/dL** is diagnostic. * **Target Blood Sugars:** Fasting <95 mg/dL, 1-hour postprandial <140 mg/dL, and 2-hour postprandial <120 mg/dL. * **Metformin:** Though it crosses the placenta, it is increasingly used as an alternative to insulin in some protocols, but insulin remains the definitive answer for exams unless "initial lifestyle modification" is an option.

Question 158: A 32-year-old female with diabetes presents at 6 weeks of amenorrhea. She is not on any treatment. What is the first step in her management?

A. Start insulin therapy
B. Initiate dietary modifications
C. Perform HbA1c test (Correct Answer)
D. Perform postprandial blood glucose tests

Explanation: **Explanation:** The correct answer is **C. Perform HbA1c test.** **1. Why HbA1c is the first step:** In a patient with pre-existing diabetes (or suspected overt diabetes) presenting in the first trimester, the primary concern is the risk of **congenital malformations**. HbA1c reflects glycemic control over the preceding 8–12 weeks, covering the critical period of organogenesis. A high HbA1c level (>7%) is strongly associated with an increased risk of anomalies (e.g., Sacral agenesis, VSD). It serves as a baseline to assess the risk of teratogenicity and guides the intensity of management. **2. Why other options are incorrect:** * **A & B (Insulin/Diet):** While glycemic control is essential, management cannot be initiated without first assessing the severity of the baseline glycemic status and the risk to the fetus. HbA1c provides the necessary prognostic information before deciding on the therapeutic regimen. * **D (Postprandial glucose):** While daily monitoring is vital for ongoing management, a single point-in-time glucose test does not provide information about the glycemic control during the early weeks of pregnancy (organogenesis), which is the priority at 6 weeks gestation. **3. NEET-PG High-Yield Pearls:** * **Most common malformation** in infants of diabetic mothers: **VSD** (Ventricular Septal Defect). * **Most specific malformation:** **Caudal Regression Syndrome** (Sacral Agenesis). * **Target HbA1c:** Ideally, HbA1c should be **<6.5%** (or <6% if achievable without hypoglycemia) to minimize the risk of malformations. * **Overt Diabetes vs. GDM:** If fasting plasma glucose is ≥126 mg/dL or HbA1c is ≥6.5% at the first prenatal visit, it is classified as **Overt Diabetes**, not Gestational Diabetes Mellitus (GDM).

Question 159: Which of the following is a feature of diabetes mellitus in pregnancy?

A. Postdatism
B. Hydramnios (Correct Answer)
C. Neonatal hyperglycemia
D. All of the above

Explanation: **Explanation:** **1. Why Hydramnios is Correct:** Polyhydramnios (Hydramnios) is a classic complication of maternal diabetes. The underlying mechanism is **fetal osmotic diuresis**. High maternal blood glucose levels cross the placenta, leading to **fetal hyperglycemia**. This stimulates the fetal kidneys to produce excessive urine (polyuria) to clear the glucose load. Since fetal urine is the primary source of amniotic fluid in the second and third trimesters, this results in an increased amniotic fluid index (AFI). **2. Why the Other Options are Incorrect:** * **Postdatism (Option A):** Diabetes is actually associated with an increased risk of **preterm labor** (due to polyhydramnios or preeclampsia) and is an indication for **planned induction of labor** (usually by 39 weeks). Post-term pregnancy is avoided to prevent sudden intrauterine fetal death (IUFD) and macrosomia-related complications. * **Neonatal Hyperglycemia (Option C):** This is a common distractor. While the fetus is hyperglycemic *in utero*, the neonate suffers from **Neonatal Hypoglycemia**. After birth, the maternal glucose supply is cut off, but the neonate’s pancreas remains in a state of hyperinsulinemia (due to chronic stimulation in utero), causing a rapid drop in blood sugar levels. **3. NEET-PG High-Yield Clinical Pearls:** * **Most common fetal anomaly in DM:** Cardiac anomalies (specifically **Ventricular Septal Defect**). * **Most specific fetal anomaly in DM:** **Caudal Regression Syndrome** (Sacral agenesis). * **Macrosomia:** Defined as birth weight >4000g or 4500g; characterized by increased shoulder-to-head circumference ratio, increasing the risk of **shoulder dystocia**. * **Target HbA1c:** Ideally <6% preconception to minimize the risk of congenital malformations.

Question 160: Which of the following hormones is NOT secreted by the placenta?

A. hCG
B. TRH
C. ACTH
D. Insulin (Correct Answer)

Explanation: **Explanation:** The placenta acts as a sophisticated transient endocrine organ, producing a wide array of protein and steroid hormones to maintain pregnancy. **Why Insulin is the Correct Answer:** Insulin is a peptide hormone produced exclusively by the **beta cells of the Islets of Langerhans in the pancreas**. While the placenta produces hormones that significantly influence maternal glucose metabolism (like Human Placental Lactogen/hPL), it does **not** synthesize insulin. Furthermore, maternal insulin does not cross the placental barrier; the fetus relies entirely on its own pancreatic production for glycemic control. **Analysis of Incorrect Options:** * **hCG (Human Chorionic Gonadotropin):** This is the first hormone secreted by the syncytiotrophoblast. It is essential for maintaining the corpus luteum in early pregnancy. * **TRH (Thyrotropin-Releasing Hormone):** The placenta produces various hypothalamic-like releasing hormones, including TRH, GnRH, and CRH. These function locally to regulate placental hormone secretion. * **ACTH (Adrenocorticotropic Hormone):** The placenta synthesizes POMC-derived peptides, including ACTH. Unlike pituitary ACTH, placental ACTH is relatively resistant to feedback suppression by glucocorticoids. **High-Yield Clinical Pearls for NEET-PG:** * **hPL (Human Placental Lactogen):** Also known as Human Chorionic Somatomammotropin (hCS), it is the primary hormone responsible for the **diabetogenic state** of pregnancy (insulin resistance). * **Progesterone:** Often called the "hormone of pregnancy," the placenta takes over its production from the corpus luteum at approximately **7–9 weeks** (Luteo-placental shift). * **Estriol (E3):** The dominant estrogen in pregnancy; its synthesis requires the **fetal adrenal gland** (DHEAS) and **fetal liver** (16-alpha-hydroxylation), making it a marker of feto-placental well-being.

Practice by Chapter

Endocrine Changes in Normal Pregnancy

Practice Questions

Thyroid Disorders in Pregnancy

Practice Questions

Diabetes in Pregnancy

Practice Questions

Adrenal Disorders in Pregnancy

Practice Questions

Pituitary Disorders in Pregnancy

Practice Questions

Hyperemesis Gravidarum

Practice Questions

Hormonal Regulation of Labor

Practice Questions

Pharmacokinetics of Hormones in Pregnancy

Practice Questions

Fetal Endocrine Development

Practice Questions

Placental Hormones

Practice Questions

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