Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 541: A 25-year-old young lady presented with a complaint of acute hirsutism and hoarseness of voice. Which of the following is the best investigation for diagnosis?

A. Blood pregnenolone levels
B. Blood DHEA levels (Correct Answer)
C. 17-ketosteroids level
D. LH and FSH levels

Explanation: ### Explanation The clinical presentation of **acute-onset hirsutism** accompanied by **virilization** (hoarseness of voice, clitoromegaly, or male-pattern baldness) in a young female is a red flag. It strongly suggests a **virilizing tumor** rather than a functional disorder like PCOS, which typically has a slow, peripubertal onset. **1. Why Blood DHEA levels is the correct answer:** In cases of rapid virilization, the primary goal is to differentiate between an ovarian and an adrenal source of excess androgens. **DHEA-S (Dehydroepiandrosterone sulfate)** is a specific marker for the adrenal glands (95% originates from the adrenals). Markedly elevated levels (typically >700 µg/dL) are highly suggestive of an **Adrenal Carcinoma** or an androgen-secreting adrenal adenoma. While the option says "DHEA," in clinical practice, DHEA-S is preferred due to its longer half-life and stable serum levels. **2. Why other options are incorrect:** * **Blood Pregnenolone:** This is a precursor hormone. While elevated in certain rare congenital adrenal hyperplasias (CAH), it is not a standard diagnostic marker for acute virilization or adrenal tumors. * **17-ketosteroids:** This is a 24-hour urine test that measures metabolites of androgens. It is largely obsolete in modern practice because serum assays (DHEA-S and Testosterone) are more accurate, convenient, and specific. * **LH and FSH levels:** These are used to diagnose PCOS (where LH:FSH ratio may be >2:1) or primary ovarian failure. They do not help in identifying the source of a virilizing tumor. **Clinical Pearls for NEET-PG:** * **Rule of Thumb:** If Testosterone is >200 ng/dL, suspect an **Ovarian tumor** (e.g., Sertoli-Leydig cell tumor). If DHEA-S is >700 µg/dL, suspect an **Adrenal tumor**. * **PCOS** is the most common cause of hirsutism, but it **never** causes rapid virilization or voice deepening. * **Initial Step:** Always measure Total Testosterone and DHEA-S to localize the pathology.

Question 542: SIADH secretion is seen in all except:

A. Lung abscess
B. Interstitial Nephritis (Correct Answer)
C. Vinka alkaloids
D. Bronchial adenoma

Explanation: **Explanation:** The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by the excessive release of ADH, leading to water retention and dilutional hyponatremia [1], [2]. **Why Interstitial Nephritis is the correct answer:** Interstitial nephritis is a cause of **Nephrogenic Diabetes Insipidus (NDI)**, not SIADH [3]. In NDI, the renal tubules become resistant to the action of ADH [3]. This results in the inability to concentrate urine, leading to polyuria and hypernatremia—the physiological opposite of SIADH. **Analysis of Incorrect Options:** * **Lung Abscess:** Pulmonary pathologies (pneumonia, abscess, tuberculosis) are classic triggers for SIADH. * **Vinca Alkaloids:** Drugs like Vincristine and Vinblastine are well-known causes of SIADH. They exert a direct neurotoxic effect on the hypothalamus and neurohypophyseal tract, leading to unregulated ADH release. * **Bronchial Adenoma:** Ectopic ADH production is a hallmark of certain tumors. While Small Cell Lung Cancer (SCLC) is the most common, bronchial adenomas (carcinoid tumors) can also secrete ADH autonomously. **NEET-PG High-Yield Pearls:** 1. **Diagnosis:** SIADH is a diagnosis of exclusion. Key features: Euvolemic hyponatremia, low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg) [1]. 2. **Drug Causes (Mnemonic: "S-C-V"):** **S**SRIs, **C**arbamazepine/Cyclophosphamide, and **V**inca alkaloids. 3. **Treatment:** Fluid restriction is the first-line treatment. For severe symptoms, use hypertonic saline (3%). **Vaptans** (Tolvaptan) are vasopressin receptor antagonists used in chronic cases. 4. **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome** (Central Pontine Myelinolysis). Keep correction <8–10 mmol/L in 24 hours.

Question 543: 11-hydroxylase deficiency leads to which of the following?

A. Hypertension (Correct Answer)
B. Hypotension
C. Hypoglycemia
D. Normal puberty

Explanation: **Explanation:** Congenital Adrenal Hyperplasia (CAH) due to **11β-hydroxylase deficiency** is the second most common cause of CAH. Understanding the steroid biosynthesis pathway is key to solving this [1]: 1. **Why Hypertension is Correct:** 11β-hydroxylase is responsible for converting **11-deoxycorticosterone (DOC)** to corticosterone and **11-deoxycortisol** to cortisol. When this enzyme is deficient, there is a buildup of 11-deoxycorticosterone (DOC) [1]. DOC is a potent mineralocorticoid [2]. Its accumulation leads to sodium and water retention and potassium excretion, resulting in **hypertension** and hypokalemia. This distinguishes it from 21-hydroxylase deficiency, which presents with hypotension (salt-wasting). 2. **Why other options are incorrect:** * **Hypotension:** This occurs in 21-hydroxylase deficiency due to the lack of mineralocorticoids (aldosterone). In 11β-hydroxylase deficiency, the excess DOC prevents hypotension. * **Hypoglycemia:** While cortisol (a glucocorticoid) is low, the clinical hallmark of 11β-hydroxylase deficiency is the mineralocorticoid excess effect (hypertension) and androgen excess. * **Normal Puberty:** This is incorrect because the "shunting" of precursors leads to **excess adrenal androgens**. This causes virilization in females (ambiguous genitalia) and precocious pseudopoterty in males. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 1s":** If the enzyme starts with **1** (11β-hydroxylase, 17α-hydroxylase), it causes **Hypertension**. * **Virilization:** Both 21 and 11β-hydroxylase deficiencies cause virilization (increased androgens), whereas 17α-hydroxylase deficiency causes delayed puberty/sexual infantilism. * **Biochemical Marker:** Elevated levels of **11-deoxycortisol** and **S-androstenedione** are diagnostic for 11β-hydroxylase deficiency.

Question 544: Which of the following conditions is associated with pituitary adenoma?

A. Multiple Endocrine Neoplasia type 2A (MEN2A)
B. Multiple Endocrine Neoplasia type 2B (MEN2B)
C. Multiple Endocrine Neoplasia type 3 (MEN3)
D. Multiple Endocrine Neoplasia type 4 (MEN4) (Correct Answer)

Explanation: **Explanation:** The correct answer is **Multiple Endocrine Neoplasia type 4 (MEN4)**. **1. Why MEN4 is correct:** MEN4 is a rare autosomal dominant syndrome caused by a germline mutation in the **CDKN1B gene** (encoding the p27 protein), which acts as a cyclin-dependent kinase inhibitor. Clinically, MEN4 presents very similarly to MEN1. It is characterized by a "3P" pattern, though with lower penetrance: **Pituitary adenomas**, **Parathyroid adenomas**, and **Pancreatic neuroendocrine tumors**. Therefore, pituitary adenoma is a hallmark feature of this condition. **2. Why the other options are incorrect:** * **MEN2A:** Caused by **RET proto-oncogene** mutations. It is characterized by the "MPH" triad: Medullary thyroid carcinoma (MTC), Pheochromocytoma, and Hyperparathyroidism. It does **not** involve the pituitary gland. * **MEN2B (formerly MEN3):** Also caused by RET mutations. It presents with MTC, Pheochromocytoma, and mucosal neuromas/Marfanoid habitus. Pituitary adenomas are not part of this syndrome. * **MEN3:** This is an older nomenclature for MEN2B and is no longer used as a separate category in modern classification. **3. NEET-PG High-Yield Pearls:** * **MEN1 (Wermer Syndrome):** The classic "3Ps" (Pituitary, Parathyroid, Pancreas). Caused by the *MEN1* gene (Menin). * **MEN4:** Think of it as "MEN1-like" but caused by *CDKN1B*. * **Pituitary involvement:** Only seen in **MEN1** and **MEN4**. * **Medullary Thyroid Carcinoma:** Present in 100% of MEN2A and 2B cases; prophylactic thyroidectomy is often indicated. * **Most common pituitary tumor in MEN1/4:** Prolactinoma.

Question 545: Which of the following could develop with a mucosal neuroma on the lower lip, a family history of medullary thyroid carcinoma, and recent introduction of severe headaches, perspiration, palpitations, and hypertension?

A. Gastrinoma
B. Insulinoma
C. Parathyroid adenoma
D. Pheochromocytoma (Correct Answer)

Explanation: ### Explanation The clinical presentation described is classic for **Multiple Endocrine Neoplasia Type 2B (MEN 2B)**. This autosomal dominant syndrome, caused by a mutation in the **RET proto-oncogene**, is characterized by a triad of: 1. **Medullary Thyroid Carcinoma (MTC):** Often aggressive and occurs early in life (explaining the family history). 2. **Pheochromocytoma:** Occurs in approximately 50% of cases. 3. **Mucosal Neuromas:** Typically found on the tongue, lips (as seen here), and eyelids, often accompanied by a **Marfanoid habitus**. The patient’s "recent introduction" of severe headaches, perspiration, palpitations, and hypertension forms the classic **"PHE" triad** (Palpitations, Headache, Episodic sweating), which is pathognomonic for a **Pheochromocytoma** (Option D). #### Analysis of Incorrect Options: * **A & B (Gastrinoma/Insulinoma):** These are Pancreatic Neuroendocrine Tumors (NETs) [1], which are components of **MEN 1** (the "3 Ps": Pituitary, Parathyroid, Pancreas), not MEN 2B. Insulinomas are confirmed as a pancreatic NET associated with hormone excess syndromes [3]. * **C (Parathyroid Adenoma):** While parathyroid hyperplasia/adenoma is a key feature of **MEN 1** and **MEN 2A**, it is characteristically **characteristically absent** in MEN 2B. #### NEET-PG High-Yield Pearls: * **MEN 2A (Sipple Syndrome):** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B (Wagenmann–Froboese Syndrome):** MTC + Pheochromocytoma + Mucosal Neuromas/Marfanoid habitus. * **Rule of 10s for Pheochromocytoma:** 10% bilateral, 10% malignant, 10% extra-adrenal, 10% pediatric, and 10% familial [2]. * **Clinical Priority:** In any MEN 2 patient, always screen for and surgically remove a Pheochromocytoma **before** addressing the thyroid to prevent a lethal hypertensive crisis during anesthesia [2].

Question 546: Which of the following is NOT associated with adrenal insufficiency?

A. Hyponatremia
B. Hyperkalemia
C. Hypoglycemia
D. Metabolic alkalosis (Correct Answer)

Explanation: **Explanation:** Adrenal insufficiency (specifically primary adrenal insufficiency or Addison’s disease) results from the deficiency of adrenal cortical hormones: **Aldosterone, Cortisol, and Androgens.** [1] **Why Metabolic Alkalosis is the Correct Answer:** Adrenal insufficiency is characterized by **Metabolic Acidosis** (specifically Normal Anion Gap Metabolic Acidosis), not alkalosis. Aldosterone normally acts on the distal convoluted tubules to reabsorb sodium and excrete potassium and hydrogen ions ($H^+$). [1] In its absence, $H^+$ ions are retained in the blood, leading to acidosis. Metabolic alkalosis is instead associated with conditions of mineralocorticoid excess like Conn's syndrome. [2] **Analysis of Incorrect Options:** * **A. Hyponatremia:** Aldosterone deficiency leads to "salt wasting" (loss of $Na^+$ in urine). Additionally, cortisol deficiency increases ADH secretion, causing water retention and dilutional hyponatremia. * **B. Hyperkalemia:** Without aldosterone, the kidneys cannot effectively secrete potassium into the urine, leading to elevated serum potassium levels. [1] * **C. Hypoglycemia:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis and antagonizes insulin. Its absence leads to impaired glucose production and increased insulin sensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** Hyponatremia occurs in both, but **Hyperkalemia** is seen *only* in Primary Adrenal Insufficiency (because aldosterone is regulated by the RAAS, which remains intact in secondary/pituitary causes). * **Hyperpigmentation:** Seen only in Primary Adrenal Insufficiency due to increased ACTH and POMC levels (stimulating melanocytes). * **Cosyntropin Stimulation Test:** The gold standard for diagnosis. * **Acute Crisis Management:** Immediate IV fluids (Normal Saline) and IV Hydrocortisone. Do not wait for lab confirmation if a crisis is suspected.

Question 547: Brown tumors, compression syndromes, and erythropoietin resistance are seen in which condition?

A. Hypothyroidism
B. Hyperthyroidism
C. Hyperparathyroidism (Correct Answer)
D. Osteoporosis

Explanation: ### Explanation **Correct Answer: C. Hyperparathyroidism** The clinical triad of brown tumors, compression syndromes, and erythropoietin (EPO) resistance is characteristic of **Hyperparathyroidism (HPT)**, particularly in the context of chronic kidney disease (Secondary/Tertiary HPT) or severe Primary HPT [1]. * **Brown Tumors (Osteitis Fibrosa Cystica):** Excess Parathyroid Hormone (PTH) stimulates intense osteoclastic activity [1]. This leads to bone resorption and the formation of cystic lesions filled with fibrous tissue and vascularized hemorrhage. The breakdown of hemoglobin into hemosiderin gives these lesions a "brown" appearance. * **Compression Syndromes:** Extensive bone remodeling and brown tumors (especially in the vertebrae or skull) can lead to nerve root or spinal cord compression. * **Erythropoietin Resistance:** High levels of PTH have a direct toxic effect on erythropoiesis and promote bone marrow fibrosis (myelofibrosis). This reduces the marrow's responsiveness to EPO, leading to refractory anemia. **Why Incorrect Options are Wrong:** * **Hypothyroidism:** Characterized by systemic slowing (bradycardia, constipation, weight gain) and myxedema, but does not cause focal lytic bone lesions or EPO resistance. * **Hyperthyroidism:** While it can cause increased bone turnover and osteoporosis, it does not typically result in brown tumors or marrow fibrosis leading to EPO resistance. * **Osteoporosis:** This is a quantitative decrease in bone density. While it increases fracture risk, it is not associated with the fibro-cystic changes or the hematologic complications seen in HPT. **NEET-PG High-Yield Pearls:** * **Radiology:** Look for "Salt and pepper" skull and subperiosteal resorption (most common on the radial aspect of the middle phalanx). * **Biochemistry:** Primary HPT shows ↑Ca²⁺, ↓PO₄³⁻, and ↑PTH [1]. Secondary HPT (CKD) shows ↓Ca²⁺, ↑PO₄³⁻, and ↑PTH [1]. * **Rugger-Jersey Spine:** A classic radiological sign of the vertebral changes in secondary hyperparathyroidism.

Question 548: Which of the following is NOT a cause of Gynaecomastia?

A. Hypothyroidism (Correct Answer)
B. Kallmann syndrome
C. Obesity
D. Klinefelter syndrome

Explanation: Gynaecomastia is the benign proliferation of glandular breast tissue in males, primarily caused by an imbalance between estrogen and androgen action. **Why Hypothyroidism is the correct answer:** While **Hyperthyroidism** is a well-known cause of gynaecomastia (due to increased Sex Hormone Binding Globulin (SHBG) levels which lower free testosterone and increase peripheral aromatization), **Hypothyroidism** is generally not associated with it. In fact, primary hypothyroidism in prepubertal boys may cause precocious puberty, but it does not typically cause gynaecomastia in adults. **Analysis of Incorrect Options:** * **Kallmann Syndrome:** This is a form of hypogonadotropic hypogonadism (GnRH deficiency). Low levels of testosterone lead to an increased estrogen-to-androgen ratio, resulting in gynaecomastia. * **Obesity:** Adipose tissue contains the enzyme **aromatase**, which converts androgens (androstenedione and testosterone) into estrogens (estrone and estradiol) [1]. Increased fat mass leads to higher systemic estrogen levels. * **Klinefelter Syndrome (47, XXY):** This is the most common genetic cause of male hypogonadism [2]. It features primary testicular failure (low testosterone) and elevated gonadotropins (LH/FSH). The high LH stimulates Leydig cell aromatase, significantly increasing estrogen production. **NEET-PG High-Yield Pearls:** * **Physiological Gynaecomastia:** Occurs in three peaks: Neonatal (maternal estrogens), Pubertal (transient imbalance), and Senile (declining testosterone) [1]. * **Drug-induced Gynaecomastia (Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common), **C**imetidine, **O**estrogens/Ketoconazole. * **Clinical Distinction:** True gynaecomastia (glandular tissue) must be differentiated from **pseudogynaecomastia** (fat deposition seen in obesity) by palpation [1].

Question 549: A 20-year-old male presents with chronic constipation, headache, and palpitations. On examination, he has Marfanoid habitus, neuromas of the tongue, medullated corneal nerve fibers, and a 2 x 2 cm nodule in the right lobe of the thyroid. This patient is a case of -

A. Sporadic medullary carcinoma of the thyroid
B. Familial medullary carcinoma of the thyroid
C. Multiple Endocrine Neoplasia (MEN) IIA
D. Multiple Endocrine Neoplasia (MEN) IIB (Correct Answer)

Explanation: ### Explanation The patient presents with a classic constellation of symptoms diagnostic of **Multiple Endocrine Neoplasia Type 2B (MEN 2B)**. **Why Option D is Correct:** MEN 2B is characterized by the triad of **Medullary Thyroid Carcinoma (MTC)**, **Pheochromocytoma**, and **Mucosal Neuromas**. * **Marfanoid Habitus:** Unlike MEN 2A, patients with MEN 2B often exhibit a thin body habitus with long limbs and joint laxity. * **Mucosal Neuromas:** The "neuromas of the tongue" and "medullated corneal nerve fibers" are pathognomonic features of MEN 2B. * **Pheochromocytoma:** The symptoms of headache and palpitations suggest an underlying catecholamine-secreting tumor. * **MTC:** The thyroid nodule represents MTC, which is more aggressive and occurs earlier in MEN 2B than in other forms. **Why Other Options are Incorrect:** * **Option A & B:** While MTC is present, these options do not account for the extra-thyroidal manifestations like mucosal neuromas and Marfanoid habitus. * **Option C (MEN 2A):** While MEN 2A also features MTC and Pheochromocytoma, it is associated with **Primary Hyperparathyroidism** rather than mucosal neuromas or Marfanoid habitus. **High-Yield Clinical Pearls for NEET-PG:** 1. **Genetics:** Both MEN 2A and 2B are caused by germline mutations in the **RET proto-oncogene** (Chromosome 10). 2. **MTC Screening:** In MEN 2B, MTC is highly aggressive; prophylactic thyroidectomy is often recommended within the **first year of life**. 3. **Gastrointestinal Involvement:** Chronic constipation in these patients can be due to **intestinal ganglioneuromatosis**, a common feature of MEN 2B. 4. **Rule of Thumb:** If you see "Mucosal Neuromas" or "Marfanoid Habitus" in a thyroid case, think **MEN 2B**.

Question 550: What are the causes of primary hyperparathyroidism?

A. Parathyroid carcinoma (Correct Answer)
B. Renal failure
C. Rickets
D. Malabsorption

Explanation: **Explanation:** Primary Hyperparathyroidism (PHPT) is characterized by the autonomous overproduction of parathyroid hormone (PTH), leading to hypercalcemia [2]. **Why Option A is Correct:** The most common cause of PHPT is a solitary **parathyroid adenoma** (~85%) [4], followed by four-gland hyperplasia (~15%). **Parathyroid carcinoma** is a rare but recognized cause (<1%). In all these conditions, the pathology lies within the parathyroid gland itself, resulting in elevated PTH despite high serum calcium levels [3]. **Why Other Options are Incorrect:** * **Renal Failure (B):** Chronic Kidney Disease (CKD) leads to **Secondary Hyperparathyroidism**. In CKD, there is phosphate retention and decreased Vitamin D activation, leading to hypocalcemia [1]. The parathyroid glands hyperfunction as a *compensatory* response to low calcium [2]. * **Rickets (C) and Malabsorption (D):** These conditions cause Vitamin D deficiency, leading to poor intestinal calcium absorption [1]. The resulting hypocalcemia triggers a secondary increase in PTH to maintain calcium homeostasis [2]. These are classic causes of **Secondary Hyperparathyroidism**. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Hallmark:** Elevated Serum Calcium + Elevated (or inappropriately normal) PTH + Low Serum Phosphate [2]. * **Clinical Presentation:** Often asymptomatic but can present as "stones, bones, abdominal groans, and psychic overtones" [3]. * **Hungry Bone Syndrome:** A common post-operative complication after parathyroidectomy where rapid bone remineralization causes profound hypocalcemia. * **MEN Syndromes:** Always screen for MEN 1 and MEN 2A if PHPT is associated with multiglandular hyperplasia [3].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

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Adrenal Gland Disorders

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Pituitary Disorders

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Calcium and Bone Metabolism

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Reproductive Endocrinology

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Lipid Disorders

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Endocrine Hypertension

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Multiple Endocrine Neoplasia

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Obesity and Metabolic Syndrome

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Neuroendocrine Tumors

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Endocrine Emergencies

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