Endocrinology — MCQs

A 35 year old male presents with increased urine output. On evaluation, his urinary output was around 4L/day; urinary osmolality was 200 mosmol/L. Which of the following are various differential diagnosis? I. Psychogenic polydipsia II. Solute diuresis III. Central diabetes insipidus IV. Nephrogenic diabetes insipidus Select the correct answer using the code given below :

Q1324

Which one of the following conditions can cause euvolaemic hyponatraemia?

Q1325

Consider the following statements: Statement I: Waist circumference and waist to hip ratio are more powerful predictors of subsequent risk of type 2 diabetes than Body Mass Index (BMI). Statement II: Central obesity is an important determinant of insulin resistance, the underlying abnormality in most cases of type 2 diabetes. Which one of the following is correct in respect of the above statements?

Q1326

Which of the following are the clinical features of hyperprolactinemia? 1. Hypergonadotropic hypogonadism 2. Hypogonadotropic hypergonadism 3. Oligomenorrhea 4. Heavy menstruation

Q1327

What is the best and most sensitive investigation for hypothyroidism ?

Q1328

Primary hyper-aldosteronism presents with all of the following except :

Q1329

The commonest cause of primary hyper-parathyroidism is

Q1330

Which of the following most strongly suggests the diagnosis of primary hyper-parathyroidism ?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1321: Which of the following are causes of hypocalcemia in a child? I. Hypomagnesemia II. Hypophosphatemia III. Metabolic acidosis IV. Pseudohypoparathyroidism Select the correct answer using the code given below :

A. II and III
B. I and II
C. I and IV (Correct Answer)
D. III and IV

Explanation: ***I and IV*** - **Hypomagnesemia** impairs parathyroid hormone (PTH) secretion and causes target organ resistance to PTH, leading to hypocalcemia. - **Pseudohypoparathyroidism** is a genetic disorder where target organs are resistant to PTH, resulting in hypocalcemia and hyperphosphatemia despite normal or elevated PTH levels [1]. *II and III* - **Hypophosphatemia** is typically associated with **hypercalcemia** rather than hypocalcemia, as phosphate binds to calcium [3]. - **Metabolic acidosis** often causes an increase in **ionized calcium** (the physiologically active form) due to reduced protein binding, rather than overall hypocalcemia. *I and II* - While **hypomagnesemia** causes hypocalcemia, **hypophosphatemia** is generally associated with hypercalcemia, making this option incorrect [2]. - Hypophosphatemia reduces the formation of calcium-phosphate complexes, thus increasing free calcium levels. *III and IV* - **Pseudohypoparathyroidism** does cause hypocalcemia, but **metabolic acidosis** typically leads to higher ionized calcium levels, not hypocalcemia. - The compensatory mechanisms for acidosis tend to mobilize calcium from bone, further counteracting hypocalcemia.

Question 1322: A 28 year female presented to emergency with fever, agitation and delirium. She was on regular medication of Carbimazole 40 mg daily, but missed her doses for the last 2 days. Which of the following scoring systems would you like to do to assess severity of disease?

A. Sequential Organ Failure Assessment Score
B. DAS 28 score
C. Burch-Wartofsky score (Correct Answer)
D. Expanded Disability Status Scale

Explanation: ***Burch-Wartofsky score*** - The patient's symptoms of **fever, agitation, and delirium** following missed carbimazole doses are highly suggestive of **thyroid storm** [1]. - The **Burch-Wartofsky score** is specifically designed to assess the **likelihood and severity of thyroid storm**, evaluating symptoms related to thermoregulation, central nervous system, gastrointestinal/hepatic dysfunction, cardiovascular dysfunction, and precipitating factors. *Sequential Organ Failure Assessment Score* - The **SOFA score** is used to track the progression of organ dysfunction and predict mortality in critically ill patients, often in the context of **sepsis or general critical illness**. - While thyroid storm can lead to multi-organ dysfunction, the SOFA score does not specifically diagnose or assess the severity of **thyroid storm** itself. *DAS 28 score* - The **DAS28 (Disease Activity Score 28)** is a validated tool for measuring disease activity in patients with **rheumatoid arthritis**. - It assesses joint count, patient global assessment, and inflammatory markers, which are irrelevant to the clinical picture of **fever and delirium**. *Expanded Disability Status Scale* - The **Expanded Disability Status Scale (EDSS)** is a method of quantifying disability in **multiple sclerosis**. - It evaluates neurological function in various systems and is not applicable to an acute presentation of **fever, agitation, and delirium** [2].

Question 1323: A 35 year old male presents with increased urine output. On evaluation, his urinary output was around 4L/day; urinary osmolality was 200 mosmol/L. Which of the following are various differential diagnosis? I. Psychogenic polydipsia II. Solute diuresis III. Central diabetes insipidus IV. Nephrogenic diabetes insipidus Select the correct answer using the code given below :

A. I and IV only
B. II and IV
C. I, III and IV (Correct Answer)
D. I and III only

Explanation: ***I, III and IV*** - **Polyuria** with a **low urine osmolality** (200 mosmol/L, which is less than plasma osmolality) indicates the excretion of a large volume of dilute urine [1]. - This pattern is characteristic of conditions involving water diuresis, specifically **psychogenic polydipsia**, **central diabetes insipidus**, and **nephrogenic diabetes insipidus**, where the body fails to concentrate urine appropriately [2]. *I and IV only* - While **psychogenic polydipsia** and **nephrogenic diabetes insipidus** can cause polyuria with dilute urine, this option incorrectly excludes **central diabetes insipidus**, which presents with very similar urinary findings [2]. - **Central diabetes insipidus** is a primary disorder of ADH secretion, leading to an inability to concentrate urine [1]. *II and IV* - **Solute diuresis** typically results in urine with a relatively normal or slightly elevated osmolality as it's due to the excretion of osmotically active substances, not pure water. The urine osmolality of 200 mosmol/L points away from significant solute diuresis. - This option also omits **central diabetes insipidus** and **psychogenic polydipsia**, which are strong differentials for dilute polyuria. *I and III only* - This option includes **psychogenic polydipsia** and **central diabetes insipidus** but incorrectly excludes **nephrogenic diabetes insipidus**. - **Nephrogenic diabetes insipidus** also results in the inability to respond to ADH, leading to the excretion of dilute urine and polyuria [2].

Question 1324: Which one of the following conditions can cause euvolaemic hyponatraemia?

A. Adrenocortical failure
B. Nephrotic syndrome
C. Burns
D. Hypothyroidism (Correct Answer)

Explanation: ***Hypothyroidism*** - Severe hypothyroidism can lead to **euvolaemic hyponatraemia** through impaired water excretion [1]. - This occurs due to increased **antidiuretic hormone (ADH)** secretion and decreased renal free water clearance [1]. *Adrenocortical failure* - **Adrenocortical failure** (e.g., Addison's disease) typically causes **hypovolaemic hyponatraemia** due to reduced mineralocorticoid activity, leading to sodium and water loss [1]. - It's also associated with hyperkalemia, which is not characteristic of euvolaemic hyponatremia. *Nephrotic syndrome* - **Nephrotic syndrome** causes **hypervolaemic hyponatraemia** due to significant protein loss, leading to reduced plasma oncotic pressure, fluid shifts to the interstitial space, and secondary hyperaldosteronism [1]. - The primary fluid imbalance is fluid overload with edema [1]. *Burns* - Severe **burns** primarily lead to **hypovolaemic hyponatraemia** or **hypernatraemia** depending on fluid resuscitation and evaporative losses [1]. - The massive fluid shifts and plasma loss usually result in fluid and electrolyte imbalances that are not euvolaemic [1].

Question 1325: Consider the following statements: Statement I: Waist circumference and waist to hip ratio are more powerful predictors of subsequent risk of type 2 diabetes than Body Mass Index (BMI). Statement II: Central obesity is an important determinant of insulin resistance, the underlying abnormality in most cases of type 2 diabetes. Which one of the following is correct in respect of the above statements?

A. Both Statement I and Statement II are correct and Statement II is the correct explanation of Statement I (Correct Answer)
B. Statement I is incorrect but Statement II is correct
C. Statement I is correct but Statement II is incorrect
D. Both Statement I and Statement II are correct but Statement II is not the correct explanation of Statement I

Explanation: **Both Statement I and Statement II are correct and Statement II is the correct explanation of Statement I** * **Central obesity**, measured by **waist circumference** and **waist-to-hip ratio**, is a stronger predictor of type 2 diabetes risk because it reflects **visceral fat**, which is metabolically active and directly linked to insulin resistance [1]. * **Visceral adipose tissue** releases inflammatory cytokines and free fatty acids, directly impairing insulin signaling and leading to **insulin resistance**, which is the primary pathophysiological defect in the development of type 2 diabetes [1]. *Statement I is incorrect but Statement II is correct* * Statement I is actually correct; **waist circumference** and **waist-to-hip ratio** are indeed superior to BMI in predicting type 2 diabetes risk because they specifically quantify central obesity, which is more metabolically harmful [1], [2]. * Therefore, the premise that Statement I is incorrect is flawed, and this option is not suitable. *Statement I is correct but Statement II is incorrect* * Statement II is fundamentally correct as **central obesity** is a well-established driver of **insulin resistance**, a key mechanism in type 2 diabetes development [1], [3]. * The argument that Statement II is incorrect directly contradicts established medical understanding of diabetes pathogenesis. *Both Statement I and Statement II are correct but Statement II is not the correct explanation of Statement I* * Statement II provides the causal link between **central obesity** and **insulin resistance**, which explains *why* **waist circumference** and **waist-to-hip ratio** (measures of central obesity) are better predictors of type 2 diabetes risk than BMI [1]. * Therefore, Statement II *does* correctly explain Statement I by detailing the underlying pathological mechanism.

Question 1326: Which of the following are the clinical features of hyperprolactinemia? 1. Hypergonadotropic hypogonadism 2. Hypogonadotropic hypergonadism 3. Oligomenorrhea 4. Heavy menstruation

A. 2. Hypogonadotropic hypergonadism
B. 1. Hypergonadotropic hypogonadism
C. 4. Heavy menstruation
D. 3. Oligomenorrhea (Correct Answer)

Explanation: ***Oligomenorrhea*** - **Oligomenorrhea** (infrequent or light menstruation) is a common symptom of **hyperprolactinemia** due to prolactin's inhibitory effect on **GnRH** and, consequently, **gonadotropin** release [1], [2]. - The resulting **estrogen deficiency** can lead to menstrual irregularities, including anovulation and delayed periods [3]. *Hypogonadotropic hypergonadism* - This condition involves **low gonadotropins** (LH, FSH) despite **high sex hormones**, which is not characteristic of **hyperprolactinemia**. - **Hyperprolactinemia** typically causes **hypogonadotropic hypogonadism** by suppressing pituitary gonadotropin release [2]. *Hypergonadotropic hypogonadism* - This is characterized by **high gonadotropins** (LH, FSH) and **low sex hormones**, indicating primary gonadal failure. - **Hyperprolactinemia** causes **low gonadotropins** by inhibiting **GnRH** pulsatility, leading to secondary gonadal dysfunction [1]. *Heavy menstruation* - **Heavy menstruation (menorrhagia)** is generally not associated with **hyperprolactinemia**; rather, **oligomenorrhea** or **amenorrhea** are typical due to **estrogen deficiency** [3]. - **Estrogen deficiency** results in an underdeveloped uterine lining, which is less likely to cause heavy bleeding.

Question 1327: What is the best and most sensitive investigation for hypothyroidism ?

A. T3, T4 levels
B. TRH levels
C. Radioactive I2 uptake
D. TSH levels (Correct Answer)

Explanation: TSH levels - **Thyroid-Stimulating Hormone (TSH)** is the most sensitive and specific test for diagnosing **primary hypothyroidism** because even slight decreases in thyroid hormone levels cause significant increases in TSH [1]. - TSH is released from the **pituitary gland** and acts as a direct feedback mechanism to regulate thyroid hormone production [1]. A high TSH level indicates that the thyroid gland is not producing enough hormones. *T3, T4 levels* - While **T3 (triiodothyronine)** and **T4 (thyroxine)** levels are direct measures of thyroid hormones, their values may remain within the normal range in early or subclinical hypothyroidism [1]. - They are less sensitive than TSH for initial screening and often become abnormal only after hypothyroidism is well-established [1]. *TRH levels* - **Thyrotropin-Releasing Hormone (TRH)** is produced by the hypothalamus and stimulates TSH release from the pituitary [1]. - Measuring TRH levels is generally not used as a primary diagnostic test for hypothyroidism due to its complexity and lack of direct clinical utility in routine screening. *Radioactive I2 uptake* - **Radioactive iodine uptake (RAIU)** measures the thyroid gland's ability to take up iodine, which is used to produce thyroid hormones. - It is primarily used to differentiate causes of hyperthyroidism (e.g., Graves' disease vs. thyroiditis), not as a diagnostic test for hypothyroidism [1].

Question 1328: Primary hyper-aldosteronism presents with all of the following except :

A. Hyperkalemia (Correct Answer)
B. Hypertension
C. Frontal headache
D. Periodic paralysis

Explanation: ***Hyperkalemia*** - Primary hyperaldosteronism is characterized by **excessive aldosterone secretion**, which promotes sodium reabsorption and potassium excretion in the renal tubules [1]. - Therefore, patients typically present with **hypokalemia**, not hyperkalemia, due to increased urinary potassium loss [1]. *Hypertension* - **Elevated aldosterone** leads to increased **sodium reabsorption** and water retention, resulting in expanded extracellular fluid volume and **hypertension** [2]. - This is a hallmark clinical feature of primary hyperaldosteronism, often severe and resistant to conventional therapy. *Frontal headache* - **Hypertension**, a common manifestation of primary hyperaldosteronism, can cause various symptoms, including **headaches**, which can be frontal. - While not specific to hyperaldosteronism, it is a frequent symptom secondary to the elevated blood pressure. *Periodic paralysis* - **Severe hypokalemia**, a characteristic feature of primary hyperaldosteronism, can lead to muscle weakness and **periodic paralysis** [3]. - This occurs because potassium is essential for normal muscle function, and its depletion impairs nerve and muscle excitability [3].

Question 1329: The commonest cause of primary hyper-parathyroidism is

A. Idiopathic parathyroid hyperplasia
B. Familial hyperparathyroidism
C. Primary parathyroid carcinoma
D. Parathyroid adenoma (Correct Answer)

Explanation: ***Parathyroid adenoma*** - **Parathyroid adenomas** account for approximately **85% of all cases** of primary hyperparathyroidism. [1] - This condition involves a **benign tumor** of one or more parathyroid glands that secretes excessive parathyroid hormone (PTH), leading to hypercalcemia. [1] *Idiopathic parathyroid hyperplasia* - **Idiopathic parathyroid hyperplasia** is responsible for about **10-15% of cases** of primary hyperparathyroidism, making it less common than adenomas. - In hyperplasia, **all four parathyroid glands** are typically enlarged and overactive, unlike the localized growth in an adenoma. *Familial hyperparathyroidism* - **Familial hyperparathyroidism** is a rare cause, accounting for **less than 1% of cases**, and is often associated with genetic syndromes like **MEN1** or **MEN2A**. - It involves inherited genetic mutations that predispose individuals to parathyroid gland overactivity, which distinguishes it from sporadic causes. *Primary parathyroid carcinoma* - **Primary parathyroid carcinoma** is an **extremely rare malignancy**, accounting for **less than 1%** of all primary hyperparathyroidism cases. - While it causes severe hypercalcemia, its rarity means it is not the commonest cause.

Question 1330: Which of the following most strongly suggests the diagnosis of primary hyper-parathyroidism ?

A. Serum calcium above 11 mg/dL (Correct Answer)
B. Serum acid phosphatase above 120 IU/L
C. Urinary calcium below 100 mg/day
D. Serum alkaline phosphatase above 120 IU/L

Explanation: ***Serum calcium above 11 mg/dL*** - **Hypercalcemia** is the hallmark of primary hyperparathyroidism, as excessive parathyroid hormone (PTH) leads to increased calcium reabsorption from bones and kidneys [1, 3]. - A serum calcium level significantly above the normal range (typically 8.5-10.2 mg/dL) strongly suggests a parathyroid-related issue; specifically, levels exceeding 11.4 mg/dL (2.85 mmol/L) often warrant surgical consideration [1]. *Serum acid phosphatase above 120 IU/L* - **Elevated acid phosphatase** is more commonly associated with conditions like **prostatic carcinoma** with bone metastases or certain hematologic malignancies. - It is not a primary diagnostic marker for hyperparathyroidism. *Urinary calcium below 100 mg/day* - **Low urinary calcium** (hypocalciuria) is characteristic of **familial hypocalciuric hypercalcemia (FHH)**, a genetic condition that can mimic primary hyperparathyroidism [1]. - In primary hyperparathyroidism, **urinary calcium excretion is typically normal or high** due to the PTH-mediated increase in filtered calcium load. *Serum alkaline phosphatase above 120 IU/L* - **Elevated alkaline phosphatase** can indicate increased **bone turnover**, which can be seen in severe, prolonged primary hyperparathyroidism as an indicator of bone resorption [1, 2]. - However, it is a non-specific marker and can also be elevated in various liver diseases or other bone disorders; it is not as specific as hypercalcemia for diagnosing primary hyperparathyroidism [2].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free