Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 291: A child presents with accelerated linear growth and advanced skeletal maturity (bone age). Which underlying condition should be considered?

A. Congenital hypothyroidism
B. Hyperthyroidism (Correct Answer)
C. Rickets
D. Growth hormone deficiency

Explanation: ***Hyperthyroidism*** - **Hyperthyroidism** is associated with accelerated metabolism, leading to **advanced skeletal maturation** (bone age ahead of chronological age) due to enhanced bone turnover and increased osteoblastic activity. - Excess thyroid hormone accelerates linear growth velocity and epiphyseal maturation, though this may paradoxically lead to reduced final adult height due to premature growth plate fusion. - Other clinical features include tachycardia, weight loss despite increased appetite, tremors, and behavioral changes. *Congenital hypothyroidism* - **Congenital hypothyroidism** causes the opposite picture: delayed skeletal maturation with bone age significantly behind chronological age. - Reduced thyroid hormone levels lead to generalized slowing of metabolic processes, delayed tooth eruption, and growth retardation. - Classic features include prolonged jaundice, large fontanelles, umbilical hernia, and developmental delay. *Rickets* - **Rickets** results from vitamin D, calcium, or phosphate deficiency, causing defective bone mineralization and softened bones. - It manifests with bone deformities (bowing, rachitic rosary), delayed skeletal maturation, and growth retardation—not advanced bone age. - Biochemical findings include elevated alkaline phosphatase and low serum calcium/phosphate levels. *Growth hormone deficiency* - **Growth hormone deficiency** causes reduced growth velocity and significantly delayed skeletal maturation. - Children present with short stature, delayed bone age, and proportionate body habitus. - It does not cause advanced skeletal maturity; rather, bone age is typically delayed by 2 or more years.

Question 292: A 6-year-old girl presents with weight loss, excessive hunger, and irritability. A blood test reveals elevated blood glucose levels. What is the most likely diagnosis?

A. Type 1 Diabetes Mellitus (Correct Answer)
B. Type 2 Diabetes Mellitus
C. Hyperthyroidism
D. Cushing Syndrome

Explanation: ***Type 1 Diabetes Mellitus*** - The classic triad of **polyphagia** (excessive hunger), **weight loss**, and elevated blood glucose in a child is highly characteristic of **Type 1 Diabetes Mellitus**. - **Irritability** is a common non-specific symptom associated with uncontrolled hyperglycemia in children. *Type 2 Diabetes Mellitus* - While it involves elevated blood glucose, **Type 2 Diabetes Mellitus** typically occurs in older individuals, often associated with **obesity** and **insulin resistance**. - It usually presents with a more gradual onset and is less commonly associated with significant **weight loss** in children. *Hyperthyroidism* - **Hyperthyroidism** can cause weight loss and increased appetite, but it also presents with other symptoms like **tachycardia**, **tremors**, and **goiter**, which are not mentioned here. - The primary metabolic derangement in hyperthyroidism is **increased metabolism**, not elevated blood glucose due to insulin deficiency. *Cushing Syndrome* - **Cushing Syndrome** is characterized by elevated cortisol levels, leading to **weight gain** (especially truncal obesity), **moon facies**, and **striae**. - While it can cause **hyperglycemia**, the overall clinical picture, particularly the prominent **weight loss**, is inconsistent with Cushing Syndrome.

Question 293: In a patient with Turner syndrome (45, XO), what is the recommended hormone replacement therapy (HRT)?

A. Growth hormone + E+P (Correct Answer)
B. No HRT Needed
C. HRT only after 45 years
D. Estrogen

Explanation: ***Growth hormone + E+P*** - **Growth hormone** is essential to improve final adult height in girls with Turner syndrome, as they commonly experience **short stature**. - **Estrogen (E)** and **progesterone (P)** replacement is crucial for the development of **secondary sexual characteristics** and to prevent long-term complications of estrogen deficiency, such as osteoporosis. *Estrogen* - While **estrogen** is a component of HRT for Turner syndrome, it is insufficient on its own for comprehensive management. - **Progesterone** is also necessary to induce cyclic bleeding and protect the uterine lining from unchecked estrogenic stimulation. *No HRT Needed* - This is incorrect as **HRT is medically necessary** for almost all individuals with Turner syndrome due to **gonadal dysgenesis** and resultant estrogen deficiency. - Without HRT, patients would not develop secondary sexual characteristics, would be at high risk for osteoporosis, and experience other long-term health issues. *HRT only after 45 years* - This is incorrect as HRT should be initiated much earlier, typically in **early adolescence** (around 12-14 years old), to mimic natural puberty. - Delaying HRT would prevent the development of secondary sexual characteristics and lead to significant **bone mineral density loss** during critical developmental years.

Question 294: Which of the following conditions is most commonly associated with hypocalcemia in a child?

A. DiGeorge syndrome with normal parathyroid function
B. Vitamin D deficiency (Correct Answer)
C. Magnesium deficiency
D. Hypoparathyroidism

Explanation: ***Vitamin D deficiency*** - **Vitamin D deficiency** is the **most common cause** of hypocalcemia in the pediatric population worldwide, particularly in developing countries and at-risk populations (limited sun exposure, dark skin, exclusive breastfeeding without supplementation). - **Vitamin D** is crucial for **intestinal calcium absorption** and bone mineralization. - Severe deficiency leads to **rickets** and **hypocalcemia** due to impaired calcium uptake, with compensatory secondary hyperparathyroidism. *DiGeorge syndrome with normal parathyroid function* - **DiGeorge syndrome** (22q11.2 deletion) classically causes **hypocalcemia** due to **parathyroid hypoplasia or aplasia**, resulting in hypoparathyroidism. - However, **if parathyroid function is explicitly stated as normal**, the syndrome would NOT cause hypocalcemia, making this option incorrect as written. - The qualifier "with normal parathyroid function" is key—it eliminates the mechanism by which DiGeorge causes hypocalcemia. *Magnesium deficiency* - Severe **magnesium deficiency** can cause **hypocalcemia** by impairing **PTH secretion** and inducing **skeletal resistance to PTH**. - However, it is **uncommon** as a primary cause of hypocalcemia in the general pediatric population compared to vitamin D deficiency. *Hypoparathyroidism* - **Hypoparathyroidism** results in reduced **PTH levels**, leading to decreased renal calcium reabsorption and reduced vitamin D activation, causing **hypocalcemia**. - While it **directly** causes hypocalcemia, it is a **less common** condition than vitamin D deficiency in the general pediatric population, making vitamin D deficiency the most frequent cause overall.

Question 295: Which of the following is the MOST characteristic cause of precocious puberty?

A. Hypothyroidism
B. CNS irradiation
C. McCune-Albright syndrome (Correct Answer)
D. None of the options

Explanation: ***McCune-Albright syndrome*** - This syndrome is characterized by the **classic triad** of **fibrous dysplasia of bone**, **café-au-lait spots**, and **precocious puberty**. - It causes **peripheral (gonadotropin-independent) precocious puberty** due to **activating mutation in the GNAS gene**, leading to autonomous hormone production. - This is one of the **most characteristic and well-defined causes** of peripheral precocious puberty in pediatric endocrinology. *Hypothyroidism* - **Severe, long-standing primary hypothyroidism** can paradoxically cause precocious puberty (Van Wyk-Grumbach syndrome). - This occurs due to **receptor overlap** between TSH and gonadotropin receptors, but it is a **much rarer cause**. - Typically presents with **delayed bone age** (unlike typical precocious puberty which has advanced bone age). *CNS irradiation* - Cranial irradiation can cause **central precocious puberty** by damaging hypothalamic-pituitary axis. - However, it is an **acquired iatrogenic cause** rather than a primary disease entity classically associated with precocious puberty. - More commonly causes **growth hormone deficiency** and other endocrine deficits. *None of the options* - Incorrect, as McCune-Albright syndrome is a well-established, characteristic cause of precocious puberty.

Question 296: Which of the following is true regarding precocious puberty:

A. Sexual maturity is attained early (Correct Answer)
B. Mental function is increased
C. Reproductive function is absent
D. Body proportions remain unchanged

Explanation: ***Sexual maturity is attained early*** - **Precocious puberty** is defined by the development of secondary sexual characteristics significantly earlier than the average age. - This early onset of puberty means that affected individuals reach **sexual maturity** at a younger chronological age. *Mental function is increased* - Precocious puberty does not inherently lead to an increase in **mental function** or cognitive abilities. - While hormonal changes can influence mood and behavior, they do not enhance intelligence. *Reproductive function is absent* - Precocious puberty implies the premature activation of the **hypothalamic-pituitary-gonadal axis**, leading to the appearance of secondary sexual characteristics and, in many cases, the potential for **reproductive function**. - Girls, for example, can experience early menarche and boys can produce sperm, meaning fertility is not absent but rather accelerated. *Body proportions remain unchanged* - Precocious puberty often results in changes in **body proportions**, particularly due to the early closure of epiphyseal plates. - Although there is an initial growth spurt, the premature fusion of growth plates can lead to a shorter-than-average adult height.

Question 297: Which of the following is not a feature of hypothyroidism in infancy?

A. Umbilical hernia
B. Constipation
C. Coarse facies
D. Premature closure of posterior fontanelle (Correct Answer)

Explanation: ***Premature closure of posterior fontanelle*** - Delayed closure of fontanelles, particularly the **posterior fontanelle**, is a characteristic feature of **congenital hypothyroidism** due to impaired bone maturation. - Therefore, **premature closure** would be inconsistent with a diagnosis of hypothyroidism in infancy. *Coarse facies* - **Coarse facial features** such as a broad nasal bridge, puffy eyelids, and a protuberant tongue are common manifestations of **congenital hypothyroidism** due to the accumulation of glycosaminoglycans. - This is a direct consequence of the metabolic derangements caused by insufficient thyroid hormone. *Umbilical hernia* - An **umbilical hernia** is frequently observed in infants with hypothyroidism, resulting from generalized **hypotonia** and incomplete closure of the umbilical ring. - The reduced muscle tone characteristic of the condition contributes to this physical finding. *Constipation* - **Constipation** is a common gastrointestinal symptom in infants with hypothyroidism, caused by **decreased gut motility** secondary to reduced thyroid hormone levels. - This is a clinical indicator of the systemic metabolic slowing associated with the condition.

Question 298: What is the target HbA1c level for a 2-5 year old child with diabetes mellitus (DM)?

A. < 8 % (Correct Answer)
B. < 7 %
C. < 9 %
D. < 6 %

Explanation: ***< 8 %*** - For children aged 2-5 years with diabetes, the current **ADA (American Diabetes Association) 2024 Standards of Care** recommend a target HbA1c of **< 8%** to balance optimal glycemic control with safety. - This target acknowledges the challenges of managing glucose levels in very young children, including their **inconsistent eating patterns**, difficulty communicating hypoglycemic symptoms, and **increased risk of severe hypoglycemia** which can impair neurodevelopment. - The target prioritizes **safety** while still promoting good metabolic control to prevent long-term diabetic complications. *< 7 %* - A target HbA1c of **< 7%** is typically recommended for **older adolescents and adults** with diabetes who can recognize and manage hypoglycemic symptoms more effectively. - This stringent target is often challenging and potentially dangerous for young children aged 2-5 years, significantly increasing the risk of **frequent and severe hypoglycemic episodes** which can have long-term neurocognitive consequences. *< 9 %* - While a target of < 9% may have been recommended in **older guidelines**, it is now considered **too lenient** for children aged 2-5 years according to current evidence-based recommendations. - Current guidelines advocate for **< 8%** as it provides better long-term glycemic control without substantially increasing hypoglycemia risk when diabetes is managed appropriately with modern insulin regimens and monitoring technologies. *< 6 %* - A target HbA1c of **< 6%** is considered very aggressive and is rarely recommended for any pediatric age group, especially not for young children with diabetes. - Achieving such a low target would require intensive insulin regimens, leading to an unacceptably high risk of **severe hypoglycemia**, impaired quality of life, and potential neurodevelopmental harm in this vulnerable age group.

Question 299: In Precocious puberty, the age limit for girls is?

A. 8 years (Correct Answer)
B. 10 years
C. 9 years
D. 11 years

Explanation: ***8 years*** - Precocious puberty is defined clinically by the development of secondary sexual characteristics in girls before the age of **8 years old**. - This age cut-off is based on population studies and clinical consensus to identify children needing further evaluation for underlying causes. *10 years* - This age is generally considered within the **normal range** for the onset of puberty, not precocious. - Pubertal development typically begins between ages 8 and 13 in girls. *9 years* - While close to the precocious threshold, **9 years** is still considered within the typical window for the onset of puberty. - The established clinical definition for precocious puberty in girls is explicitly _before_ the age of 8. *11 years* - This age is well within the **normal range** for pubertal onset and progression in girls. - Development of secondary sexual characteristics at this age would not be considered precocious.

Question 300: An XX baby presenting with male genitalia (penis and scrotum) is likely due to which of the following conditions?

A. Turner syndrome
B. None of the options
C. Klinefelter syndrome
D. High level of testosterone in maternal blood (Correct Answer)

Explanation: ***High level of testosterone in maternal blood*** - An **XX baby** (genetically female) presenting with **fully masculinized external genitalia** (penis and scrotum) indicates significant **androgen exposure** during the critical period of sexual differentiation (8-12 weeks of gestation). - While the most common cause is **congenital adrenal hyperplasia (CAH)** due to fetal androgen excess, **maternal sources of androgens** can also cause complete masculinization. - Maternal causes include **virilizing tumors** (e.g., luteoma of pregnancy, Krukenberg tumor, arrhenoblastoma), **exogenous androgen administration**, or **maternal CAH**. - High sustained maternal testosterone crosses the placenta and causes **virilization of female fetus**, which can range from clitoromegaly to complete male phenotype. - This is the **only medically correct option** among the choices given, though CAH (not listed) would be the most common cause overall. *Klinefelter syndrome* - **47, XXY karyotype** - genetically male due to presence of Y chromosome with SRY gene. - Presents as phenotypic male, not relevant to an **XX individual**. - Features include hypogonadism, infertility, tall stature, and gynecomastia. *Turner syndrome* - **45, X karyotype** - monosomy X, genetically and phenotypically female. - Presents with **female external genitalia**, streak gonads, short stature, webbed neck. - Cannot explain masculinized genitalia in any scenario. *None of the options* - This is incorrect because **high level of testosterone in maternal blood** is a documented cause of XX virilization with male phenotype, though less common than fetal CAH.

Practice by Chapter

Disorders of Growth

Practice Questions

Thyroid Disorders

Practice Questions

Disorders of Puberty

Practice Questions

Adrenal Disorders

Practice Questions

Diabetes Mellitus in Children

Practice Questions

Disorders of Calcium and Phosphate Metabolism

Practice Questions

Disorders of Sexual Development

Practice Questions

Hypoglycemia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Pituitary Disorders

Practice Questions

Multiple Endocrine Neoplasia Syndromes

Practice Questions

Endocrine Emergencies

Practice Questions

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