Endocrinology of Pregnancy — MCQs

Endocrinology of Pregnancy Indian Medical PG Practice Questions and MCQs

Question 11: Which of the following is true about Turner's syndrome?

A. Normal breast development
B. Normal gonadal development
C. Normal intelligence (Correct Answer)
D. Tall stature

Explanation: **Explanation:** Turner’s Syndrome (45,XO) is the most common sex chromosomal abnormality in females. The correct answer is **Normal intelligence**, as the majority of individuals with Turner’s syndrome have a normal intelligence quotient (IQ), although they may occasionally exhibit specific learning disabilities related to visuospatial processing or mathematics. **Analysis of Options:** * **Normal breast development (Incorrect):** Due to **gonadal dysgenesis**, there is a lack of estrogen production. This leads to a failure of secondary sexual characteristics, resulting in poor breast development (Tanner Stage 1-2) and primary amenorrhea. * **Normal gonadal development (Incorrect):** The characteristic finding is **streak ovaries** (fibrous tissue devoid of follicles). Accelerated atresia of germ cells occurs in utero, leading to premature ovarian failure. * **Tall stature (Incorrect):** Short stature is the most consistent clinical feature of Turner’s syndrome, primarily due to the loss of the **SHOX gene** located on the distal short arm of the X chromosome. **High-Yield Clinical Pearls for NEET-PG:** * **Karyotype:** 45,XO is the most common (50%), followed by mosaicism (45,X/46,XX). * **Cardiovascular:** Bicuspid aortic valve (most common) and Coarctation of the aorta. * **Renal:** Horseshoe kidney. * **Physical Signs:** Webbed neck (pterygium colli), increased carrying angle (cubitus valgus), and shield chest with widely spaced nipples. * **Hormonal Profile:** Hypergonadotropic hypogonadism (High FSH/LH, Low Estrogen). * **Management:** Growth hormone therapy for height; Estrogen/Progesterone for secondary sexual characteristics and bone health.

Question 12: Which of the following statements regarding migraine in pregnancy is true?

A. Ketorolac is the preferred treatment.
B. NSAIDs are considered first-line drugs. (Correct Answer)
C. Migraine symptoms typically improve during pregnancy.
D. Sumatriptan is preferred over chlorpromazine.

Explanation: **Explanation:** **1. Why NSAIDs are the correct answer:** In the management of acute migraine during pregnancy, **NSAIDs (like Ibuprofen or Naproxen)** are considered first-line pharmacological agents, particularly during the first and second trimesters. They are effective for moderate to severe attacks when Acetaminophen (the initial drug of choice) fails. However, they must be avoided after **30-32 weeks of gestation** due to the risk of premature closure of the ductus arteriosus and oligohydramnios. **2. Analysis of Incorrect Options:** * **Option A (Ketorolac):** While an NSAID, Ketorolac is generally avoided in pregnancy due to its high potency and potential for increased fetal risks compared to Ibuprofen. * **Option C (Improvement of symptoms):** This is a common distractor. While many women experience relief due to stable estrogen levels, approximately **25% of women** see no change or even a worsening of symptoms. In the context of NEET-PG, the pharmacological "first-line" status of NSAIDs is a more definitive clinical fact than the variable clinical course of the disease. * **Option D (Sumatriptan vs. Chlorpromazine):** For severe refractory migraine (status migrainosus) in pregnancy, parenteral **metoclopramide or chlorpromazine** is often preferred over Triptans. Triptans are generally reserved as second-line therapy when other treatments fail. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Initial):** Acetaminophen (Paracetamol). * **First-line (Moderate/Severe):** NSAIDs (up to 30 weeks). * **Prophylaxis:** If required, **Propranolol** is the drug of choice. * **Contraindicated:** Ergotamine and Dihydroergotamine (due to uterine contractions and fetal vasoconstriction). * **Red Flag:** New-onset headache in the second half of pregnancy must always be evaluated to rule out **Preeclampsia**.

Question 13: What is an increased risk in pregnant women with thyroid peroxidase antibodies?

A. Pre-term delivery
B. Abruptio placenta (Correct Answer)
C. Preterm rupture of membranes
D. Placenta previa

Explanation: **Explanation:** The presence of **Thyroid Peroxidase (TPO) antibodies** in euthyroid pregnant women is a significant marker for adverse obstetric outcomes. While these antibodies are primarily associated with the development of postpartum thyroiditis, they also indicate a state of localized or systemic immune dysregulation that affects the maternal-fetal interface. **Why Abruptio Placenta is correct:** Current evidence and clinical guidelines (including ACOG and various meta-analyses) have established a strong association between TPO antibody positivity and an increased risk of **placental abruption**. The underlying mechanism is thought to involve an abnormal immune response or inflammatory process at the decidual level, leading to impaired placentation and subsequent premature separation of the placenta. **Analysis of Incorrect Options:** * **A & C (Pre-term delivery and PROM):** While some studies suggest a weak correlation between thyroid autoimmunity and preterm birth, the association is not as strongly or consistently linked in standard PG-level textbooks as the specific risk of placental abruption. * **D (Placenta previa):** This is a structural/positional anomaly of the placenta related to uterine scarring or multiparity; it has no known immunological or autoimmune pathophysiology related to thyroid antibodies. **NEET-PG High-Yield Pearls:** * **Most common cause** of hypothyroidism in pregnancy (in iodine-sufficient areas): Hashimoto’s thyroiditis (TPO antibody positive). * **Postpartum Thyroiditis:** 50% of women with TPO antibodies during early pregnancy will develop postpartum thyroiditis. * **Miscarriage Risk:** TPO antibodies are significantly associated with a **two-fold increase** in the risk of first-trimester spontaneous abortion, even if the woman is euthyroid. * **Management:** Selenium supplementation is sometimes discussed, but the primary focus is monitoring TSH levels every 4 weeks during the first half of pregnancy.

Question 14: What is the typical level of fibrinogen in a full-term pregnancy at term?

A. 200-400 mg/dL
B. 300-600 mg/dL (Correct Answer)
C. 150-200 mg/dL
D. None of these

Explanation: ### Explanation **Correct Answer: B. 300-600 mg/dL** **1. Why Option B is Correct:** Pregnancy is a **hypercoagulable state** characterized by an increase in most clotting factors and a decrease in natural anticoagulants. Fibrinogen (Factor I) undergoes a significant increase due to estrogen-mediated hepatic synthesis. While the non-pregnant level of fibrinogen is typically **200–400 mg/dL**, it rises by approximately 50% during pregnancy, reaching levels of **300–600 mg/dL** at term. This physiological adaptation serves as a protective mechanism to minimize blood loss during the placental separation phase of delivery. **2. Why Other Options are Incorrect:** * **Option A (200-400 mg/dL):** This represents the **normal range for a non-pregnant adult**. In the context of pregnancy, a fibrinogen level of 200 mg/dL is considered abnormally low and may indicate a state of consumptive coagulopathy (e.g., DIC). * **Option C (150-200 mg/dL):** These levels are subnormal even for non-pregnant individuals. In an obstetric emergency like Abruptio Placentae, a level below 150 mg/dL is a critical warning sign of severe depletion. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hypercoagulability:** Pregnancy increases Factors VII, VIII, IX, X, and Fibrinogen. Factors **XI and XIII actually decrease**. * **ESR:** Due to the rise in fibrinogen (which increases RBC sedimentation), the **ESR is physiologically elevated** in pregnancy and cannot be used as a reliable marker for infection. * **Critical Value:** In cases of Postpartum Hemorrhage (PPH) or Abruption, a fibrinogen level **<200 mg/dL** is highly predictive of severe hemorrhage and the need for blood products (Cryoprecipitate). * **Protein S:** Levels of free and total Protein S **decrease**, further contributing to the prothrombotic state.

Question 15: What is the drug of choice for the treatment of thyrotoxicosis during pregnancy?

A. Carbimazole
B. Iodine therapy
C. Propylthiouracil (Correct Answer)
D. Metimazole

Explanation: **Explanation:** The management of hyperthyroidism (thyrotoxicosis) in pregnancy requires a careful balance between maternal health and fetal safety. **Propylthiouracil (PTU)** is the drug of choice during the **first trimester** of pregnancy. **Why Propylthiouracil (PTU) is correct:** PTU is preferred in early pregnancy because it is more highly protein-bound than Methimazole, resulting in less placental transfer. More importantly, it is not associated with the specific congenital malformations (embryopathy) linked to other antithyroid drugs. **Why other options are incorrect:** * **Methimazole (D) & Carbimazole (A):** These are generally avoided in the first trimester because they are associated with **Methimazole Embryopathy**, which includes **Aplasia Cutis** (congenital skin defects on the scalp), choanal atresia, and esophageal atresia. However, they are often preferred in the second and third trimesters to avoid PTU-induced maternal hepatotoxicity. * **Iodine therapy (B):** Radioactive iodine ($I^{131}$) is strictly **contraindicated** in pregnancy as it crosses the placenta and can destroy the fetal thyroid gland, leading to permanent congenital hypothyroidism. **High-Yield NEET-PG Pearls:** 1. **Trimester-specific switch:** Use PTU in the 1st trimester; switch to Methimazole in the 2nd and 3rd trimesters to minimize the risk of PTU-related liver failure. 2. **Mechanism:** PTU has a dual action—it inhibits thyroid peroxidase and also inhibits the peripheral conversion of $T_4$ to $T_3$. 3. **Goal of therapy:** Aim to keep maternal Free $T_4$ levels at the **upper limit of the normal range** using the lowest possible dose to avoid fetal goiter/hypothyroidism. 4. **hCG effect:** Remember that high levels of hCG in early pregnancy can weakly stimulate the TSH receptor, leading to "Gestational Transient Thyrotoxicosis," which usually does not require antithyroid drugs.

Question 16: Which of the following statements regarding calcium homeostasis in pregnancy is FALSE?

A. Serum non-ionized calcium levels fall
B. Serum ionized calcium levels fall (Correct Answer)
C. Intestinal absorption of calcium is increased
D. Levels of 1,25-dihydroxyvitamin D are increased

Explanation: In pregnancy, the body undergoes significant physiological adaptations to meet the fetal demand for calcium (approximately 30g), primarily through enhanced intestinal absorption rather than maternal bone resorption. **Explanation of the Correct Answer (B):** The hallmark of calcium homeostasis in pregnancy is that **serum ionized calcium levels remain constant (unchanged).** Ionized calcium is the physiologically active fraction regulated tightly by the parathyroid hormone (PTH). While total serum calcium levels fall due to hemodilution and decreased albumin, the free, ionized portion does not change. Therefore, the statement that ionized calcium levels "fall" is **false**. **Analysis of Incorrect Options:** * **Option A (True statement):** Serum **non-ionized (bound) calcium** levels fall. This occurs because total serum albumin levels decrease due to plasma volume expansion (hemodilution). Since a large portion of calcium is bound to albumin, the total (non-ionized) calcium concentration decreases. * **Option C (True statement):** Intestinal absorption of calcium **doubles** starting from the first trimester. This is the primary mechanism to meet fetal needs and protect maternal bone mineral density. * **Option D (True statement):** Levels of **1,25-dihydroxyvitamin D (Calcitriol)** increase significantly. This is driven by increased PTHrP (from the placenta/breasts) and direct stimulation of 1-alpha-hydroxylase in the maternal kidneys and placenta. **High-Yield NEET-PG Pearls:** * **Total Calcium:** Decreases (due to low albumin). * **Ionized Calcium:** Remains **Unchanged**. * **24-hour Urinary Calcium:** Increases (absorptive hypercalciuria); hence, pregnancy is a pro-lithogenic state for kidney stones. * **PTH:** May slightly decrease in the first trimester but generally remains in the normal range or increases slightly later in pregnancy.

Question 17: What is the primary drug used in the treatment of hirsutism in Polycystic Ovarian Disease (PCOD)?

A. Menopausal Gonadotropin
B. Gonadotropin-Releasing Hormone (GnRH)
C. Spironolactone (Correct Answer)
D. Human Chorionic Gonadotropin (hCG)

Explanation: **Explanation:** **Polycystic Ovarian Disease (PCOD/PCOS)** is characterized by hyperandrogenism, which clinically manifests as hirsutism. The management of hirsutism focuses on blocking androgen action at the hair follicle. **Why Spironolactone is correct:** Spironolactone is a potassium-sparing diuretic that acts as a potent **androgen receptor antagonist**. It also inhibits **5-alpha reductase** (the enzyme converting testosterone to the more potent dihydrotestosterone) and interferes with ovarian steroidogenesis. Due to this dual mechanism, it is the most commonly used anti-androgen for treating hirsutism in PCOS when Combined Oral Contraceptives (COCs) alone are insufficient. **Why other options are incorrect:** * **Menopausal Gonadotropin (hMG) & hCG:** These are used for **ovulation induction** in infertile patients with PCOS. They stimulate the ovaries and can actually increase androgen production, potentially worsening hirsutism. * **GnRH:** While GnRH analogs can suppress the pituitary-ovarian axis to reduce androgens, they are not the "primary" treatment due to side effects (bone loss, vasomotor symptoms) and high cost. **High-Yield Clinical Pearls for NEET-PG:** * **First-line treatment:** Lifestyle modification and **COCs** are usually the first-line medical therapy for PCOS. Spironolactone is added if there is no improvement after 6 months. * **Teratogenicity:** Spironolactone can cause feminization of a male fetus; therefore, it **must** be used with effective contraception. * **Other Anti-androgens:** Cyproterone acetate, Finasteride, and Flutamide are also used, but Spironolactone remains a classic exam favorite. * **Eflornithine:** A topical cream used specifically for facial hirsutism.

Question 18: What are the common clinical features of Turner syndrome?

A. Secondary amenorrhea
B. Edema of hands and feet (Correct Answer)
C. XY genotype
D. Mental retardation is common

Explanation: **Explanation:** Turner Syndrome (45,XO) is the most common cause of primary amenorrhea and results from complete or partial monosomy of the X chromosome. **Why Option B is Correct:** **Lymphedema of the hands and feet** is a classic clinical feature, especially in neonates. It occurs due to congenital hypoplasia or malformation of the lymphatic system. In addition to peripheral edema, this lymphatic dysfunction often manifests as a **cystic hygroma** or a **webbed neck** (pterygium colli) in older children. **Why the other options are incorrect:** * **Option A:** Turner syndrome typically presents with **Primary Amenorrhea** due to "streak ovaries" (accelerated oocyte atresia). While secondary amenorrhea can occur in mosaic forms (e.g., 45,X/46,XX), primary amenorrhea is the hallmark. * **Option C:** The genotype is **45,XO** (monosomy). An XY genotype is seen in Swyer syndrome or Androgen Insensitivity Syndrome. * **Option D:** **Intelligence is usually normal** in Turner syndrome. While there may be specific learning disabilities (e.g., visuospatial tasks), generalized mental retardation is not a characteristic feature, unlike in autosomal trisomies (e.g., Down syndrome). **High-Yield Clinical Pearls for NEET-PG:** * **Short Stature:** The most consistent clinical finding (due to loss of the *SHOX* gene). * **Cardiac Anomalies:** Bicuspid aortic valve (most common) and Coarctation of the aorta. * **Renal Anomalies:** Horseshoe kidney. * **Hormonal Profile:** Hypergonadotropic hypogonadism (High FSH/LH, Low Estrogen). * **Ultrasound:** Increased Nuchal Translucency (NT) in the first trimester.

Question 19: Schwangerschafts protein 1 (SP1) is a biochemical marker of?

A. Gestational trophoblastic disease
B. Ectopic pregnancy (Correct Answer)
C. Placenta accreta
D. Severe pregnancy-induced hypertension

Explanation: **Explanation:** **Schwangerschafts protein 1 (SP1)**, also known as Pregnancy-Specific Beta-1 Glycoprotein, is a protein produced by the syncytiotrophoblast of the placenta. It appears in maternal serum shortly after implantation and increases steadily throughout a normal pregnancy. **Why Ectopic Pregnancy is correct:** In a healthy intrauterine pregnancy, SP1 levels rise predictably. However, in an **ectopic pregnancy**, there is suboptimal trophoblastic growth and function. This leads to abnormally low or slowly rising levels of SP1 compared to a normal pregnancy of the same gestational age. While hCG is the primary marker used, SP1 serves as a complementary biochemical marker to help differentiate an ectopic pregnancy from a viable intrauterine one. **Analysis of Incorrect Options:** * **A. Gestational Trophoblastic Disease (GTD):** While SP1 is produced by trophoblasts, it is not the primary marker for GTD. Beta-hCG remains the gold standard for diagnosis and monitoring of molar pregnancies. * **C. Placenta Accreta:** This is a structural/adhesion abnormality of the placenta. Diagnosis is primarily radiological (Ultrasound/MRI), not biochemical. * **D. Severe PIH:** Pregnancy-induced hypertension is monitored via blood pressure, proteinuria, and markers of end-organ damage (liver enzymes, platelets), not trophoblastic proteins like SP1. **High-Yield Facts for NEET-PG:** * **SP1** is one of the earliest markers of trophoblastic activity, detectable as early as 7–10 days after ovulation. * **PAPP-A (Pregnancy-associated plasma protein A):** Low levels in the first trimester are associated with Down Syndrome and future risk of FGR/Pre-eclampsia. * **hPL (Human Placental Lactogen):** Reflects placental mass; low levels are seen in placental insufficiency. * **Progesterone:** A single serum progesterone level <5 ng/mL is highly suggestive of a non-viable pregnancy (either ectopic or missed abortion).

Question 20: By what percentage does the glomerular filtration rate increase during pregnancy?

A. 15%
B. 25%
C. 40%
D. 50% (Correct Answer)

Explanation: **Explanation:** The correct answer is **50%**. During pregnancy, profound physiological changes occur in the renal system to accommodate the metabolic demands of the fetus and the increase in maternal blood volume. **Why 50% is correct:** The Glomerular Filtration Rate (GFR) begins to increase as early as the 6th week of gestation, reaching a peak increase of approximately **50%** by the end of the first trimester. This rise is primarily driven by: 1. **Increased Renal Plasma Flow (RPF):** RPF increases by 60–80% due to systemic vasodilation and increased cardiac output. 2. **Hormonal Influence:** Relaxin and progesterone decrease renal vascular resistance, allowing for higher filtration. **Analysis of Incorrect Options:** * **A (15%) & B (25%):** These values are too low. While cardiac output increases by about 30–40%, the renal system undergoes a disproportionately higher increase in filtration capacity. * **C (40%):** While closer, 40% represents the increase in blood volume. The GFR specifically exceeds this, consistently hitting the 50% mark in clinical literature (e.g., Williams Obstetrics). **High-Yield Clinical Pearls for NEET-PG:** * **Creatinine/BUN:** Because GFR increases by 50%, serum creatinine and BUN levels **decrease** during pregnancy. A "normal" non-pregnant creatinine (e.g., 1.0 mg/dL) may actually indicate renal impairment in a pregnant patient. * **Glucosuria:** The increased GFR often exceeds the renal threshold for glucose reabsorption, making mild glucosuria (trace to 1+) physiological and not necessarily indicative of diabetes. * **Peak:** The GFR remains elevated until delivery, returning to pre-pregnancy levels approximately 3 months postpartum.

Practice by Chapter

Endocrine Changes in Normal Pregnancy

Practice Questions

Thyroid Disorders in Pregnancy

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Diabetes in Pregnancy

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Adrenal Disorders in Pregnancy

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Pituitary Disorders in Pregnancy

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Hyperemesis Gravidarum

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Hormonal Regulation of Labor

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Pharmacokinetics of Hormones in Pregnancy

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Fetal Endocrine Development

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Placental Hormones

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