Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 771: All of the following are seen in Addison's disease EXCEPT?

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

Explanation: **Explanation:** Addison’s disease (Primary Adrenocortical Insufficiency) is characterized by the destruction of the adrenal cortex, leading to a deficiency of both **cortisol** and **aldosterone** [1]. **Why Metabolic Alkalosis is the Correct Answer:** Aldosterone normally acts on the distal convoluted tubules and collecting ducts to reabsorb sodium and water in exchange for secreting potassium ($K^+$) and hydrogen ions ($H^+$) [2]. In Addison’s disease, the **absence of aldosterone** leads to the retention of $H^+$ ions. This results in **Hyperchloremic Metabolic Acidosis**, not alkalosis [3]. Metabolic alkalosis is instead a hallmark of mineralocorticoid excess, such as in Conn’s syndrome or Cushing’s syndrome [3]. **Analysis of Incorrect Options:** * **Hyponatremia (A):** Lack of aldosterone causes "salt wasting" (loss of $Na^+$ in urine). Additionally, cortisol deficiency leads to increased ADH secretion, causing water retention and dilutional hyponatremia [4]. * **Hyperkalemia (B):** Without aldosterone, the kidney cannot effectively excrete potassium, leading to its accumulation in the serum [2]. * **Hypotension (C):** Chronic volume depletion (due to $Na^+$ loss) and the loss of cortisol’s permissive effect on catecholamines (which maintain vascular tone) result in orthostatic or persistent hypotension [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperpigmentation:** Seen only in *Primary* insufficiency due to increased ACTH/POMC levels (stimulating melanocytes). It is absent in secondary (pituitary) insufficiency [1]. * **The "Addisonian Triad":** Hyponatremia, Hyperkalemia, and Azotemia. * **Gold Standard Test:** ACTH Stimulation Test (Cosyntropin test) [4]. * **ECG Changes:** Look for tall peaked T-waves due to hyperkalemia.

Question 772: What is the immediate effect of rapid intravenous insulin administration in a patient with diabetic ketoacidosis?

A. Hypokalemia (Correct Answer)
B. Hypernatremia
C. Hyperkalemia
D. Hypocalcemia

Explanation: The correct answer is **Hypokalemia (Option A)**. **Mechanism:** Insulin acts as a potent stimulator of the **Na+/K+-ATPase pump** located on cell membranes. When rapid intravenous insulin is administered, it drives potassium from the extracellular fluid (ECF) into the intracellular fluid (ICF) compartment [2]. In Diabetic Ketoacidosis (DKA), patients often have a total body potassium deficit due to osmotic diuresis, despite having normal or high serum potassium levels initially (due to acidosis-induced shift) [1][2]. Rapid insulin administration causes a swift drop in serum potassium, which can lead to life-threatening arrhythmias [4]. **Analysis of Incorrect Options:** * **B. Hypernatremia:** Insulin does not directly cause hypernatremia. In DKA, sodium levels are often low (pseudohyponatremia) due to hyperglycemia; as glucose falls, sodium levels typically normalize or rise slightly, but this is not the "immediate" effect of insulin itself [2]. * **C. Hyperkalemia:** This is the opposite of the physiological effect. While acidosis causes hyperkalemia, insulin therapy is a standard treatment to *lower* potassium [2]. * **D. Hypocalcemia:** Insulin does not have a significant immediate effect on serum calcium levels. **High-Yield Clinical Pearls for NEET-PG:** * **The "Potassium Rule" in DKA:** Never start insulin if the serum potassium is **<3.3 mEq/L**. Always replace potassium first to prevent cardiac arrest [3]. * **The Shift:** For every 0.1 unit decrease in arterial pH, serum potassium increases by approximately 0.6 mEq/L. * **Management Goal:** In DKA, the goal of insulin is to close the anion gap and stop ketogenesis, but monitoring electrolytes (especially K+) is the priority during the first few hours of replacement [3].

Question 773: Which of the following is NOT a feature of MEN2B syndrome?

A. Mucosal neuroma
B. Marfanoid habitus
C. Medullated corneal nerve fibers
D. Meningioma (Correct Answer)

Explanation: **Explanation:** Multiple Endocrine Neoplasia type 2B (MEN2B) is an autosomal dominant syndrome caused by a specific germline mutation in the **RET proto-oncogene** (typically codon 918). It is characterized by a distinct constellation of endocrine and physical findings. **Why Meningioma is the correct answer:** Meningiomas are not associated with MEN2B. They are classically seen in **Neurofibromatosis Type 2 (NF2)**, which is characterized by the mnemonic "MISME" (Multiple Inherited Schwannomas, Meningiomas, and Ependymomas). [1] **Analysis of Incorrect Options:** * **Mucosal Neuromas:** These are the most specific clinical sign of MEN2B, typically appearing as painless, fleshy bumps on the tongue, lips, and eyelids. * **Marfanoid Habitus:** Patients often exhibit a tall, slender build with long extremities and joint laxity, mimicking Marfan syndrome, though they lack the ectopia lentis and aortic root dilation seen in true Marfan syndrome. * **Medullated Corneal Nerve Fibers:** Thickened, visible corneal nerves are a highly characteristic ophthalmologic finding in MEN2B, detectable via slit-lamp examination. **High-Yield Clinical Pearls for NEET-PG:** 1. **Components of MEN2B:** Medullary Thyroid Carcinoma (MTC) - 100%, Pheochromocytoma - 50%, Mucosal Neuromas, and Marfanoid habitus. 2. **MEN2A vs. MEN2B:** MEN2A includes Parathyroid hyperplasia; MEN2B does **not** have parathyroid involvement but includes neuromas and marfanoid features. 3. **MTC Prophylaxis:** In MEN2B, MTC is highly aggressive and occurs early; prophylactic thyroidectomy is recommended in **infancy (before age 1)**. 4. **GI Involvement:** Intestinal ganglioneuromatosis is common, often presenting as chronic constipation or megacolon.

Question 774: All of the following are components of Whipple's triad except?

A. Symptoms of hypoglycemia
B. Increased insulin levels (Correct Answer)
C. Symptoms improve after glucose administration
D. Low blood glucose

Explanation: Explanation: Whipple’s triad is the clinical gold standard used to diagnose true hypoglycemia and initiate investigations for conditions like insulinoma [1]. The triad consists of clinical and biochemical findings, but it **does not** include specific hormone levels like insulin. **Why "Increased insulin levels" is the correct answer:** While hyperinsulinism is a common *cause* of hypoglycemia (as seen in insulinomas), it is not a *component* of Whipple’s triad. The triad is designed to confirm the state of hypoglycemia regardless of the underlying etiology. Insulin, C-peptide, and pro-insulin levels are measured only *after* the triad is established to differentiate between causes (e.g., exogenous insulin vs. insulinoma) [1]. **Analysis of other options:** * **Low blood glucose (Option D):** A biochemical documentation of low plasma glucose (typically <55 mg/dL) is a mandatory component [1]. * **Symptoms of hypoglycemia (Option A):** The patient must present with neuroglycopenic symptoms (confusion, lethargy, seizures) or autonomic symptoms (tremors, palpitations, sweating) [1], [2]. * **Symptoms improve after glucose administration (Option C):** The prompt resolution of symptoms following the elevation of plasma glucose confirms that the symptoms were indeed due to hypoglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Insulinoma:** The most common cause of fasting hypoglycemia in healthy adults. It is characterized by the "72-hour fast test" where Whipple’s triad is demonstrated. * **Biochemical markers in Insulinoma:** Low glucose + High Insulin (>3 μU/mL) + High C-peptide (>0.6 ng/mL) + High Pro-insulin. * **Factitious Hypoglycemia:** If a patient self-injects insulin, they will have high insulin but **low/suppressed C-peptide** (since exogenous insulin lacks the C-peptide chain) [1].

Question 775: Fasting hyperglycemia is almost always seen in which of the following conditions?

A. Gastric carcinoma
B. Pheochromocytoma (Correct Answer)
C. Adrenal tumor
D. Carcinoid tumor

Explanation: **Explanation:** **Pheochromocytoma** is a catecholamine-secreting tumor (usually of the adrenal medulla) that leads to fasting hyperglycemia through several synergistic mechanisms [1]. High levels of circulating epinephrine and norepinephrine stimulate **alpha-2 adrenergic receptors** on pancreatic beta cells, which directly inhibits insulin secretion. Simultaneously, catecholamines promote **glycogenolysis** and **gluconeogenesis** in the liver and induce peripheral insulin resistance [1], [2]. This combination of "insulin deficiency" and "glucose overproduction" makes hyperglycemia a classic feature of the condition. **Analysis of Incorrect Options:** * **Gastric Carcinoma:** This is more commonly associated with **hypoglycemia** (if it causes paraneoplastic syndromes or malnutrition) or "dumping syndrome" post-surgery, rather than fasting hyperglycemia. * **Adrenal Tumor:** While a cortisol-secreting adrenal adenoma (Cushing’s Syndrome) can cause hyperglycemia, the term "Adrenal tumor" is non-specific. Pheochromocytoma is the more "classic" and potent driver of acute fasting glucose elevation in this context. * **Carcinoid Tumor:** These tumors primarily secrete serotonin and kallikrein. They are associated with flushing and diarrhea (Carcinoid syndrome) but do not typically present with fasting hyperglycemia. **NEET-PG High-Yield Pearls:** * **Rule of 10s:** Pheochromocytoma is 10% bilateral, 10% malignant, 10% extra-adrenal, and 10% familial. * **Clinical Triad:** Episodic headache, sweating, and tachycardia. * **Diagnosis:** Best initial screening test is **urinary or plasma metanephrines**. * **Management:** Always give **Alpha-blockers (e.g., Phenoxybenzamine) BEFORE Beta-blockers** to avoid a hypertensive crisis from unopposed alpha-stimulation.

Question 776: All of the following are causes of hypertension with hypokalemia except?

A. Bilateral renal artery stenosis
B. End-stage renal disease (Correct Answer)
C. Primary hyperaldosteronism
D. Cushing's disease

Explanation: ### Explanation The combination of **hypertension and hypokalemia** is a classic clinical triad suggesting an overactive mineralocorticoid effect, either due to primary excess or secondary activation of the Renin-Angiotensin-Aldosterone System (RAAS) [1]. **Why End-Stage Renal Disease (ESRD) is the correct answer:** In ESRD, the kidneys lose their ability to excrete potassium effectively. As the Glomerular Filtration Rate (GFR) falls below 15-20 mL/min, patients typically develop **hyperkalemia**, not hypokalemia. While hypertension is common in ESRD (due to fluid overload and RAAS activation), the electrolyte profile is characterized by potassium retention. **Analysis of Incorrect Options:** * **Bilateral Renal Artery Stenosis:** This causes decreased renal perfusion, triggering the RAAS. High levels of Renin lead to high Aldosterone (Secondary Hyperaldosteronism), which causes sodium retention (hypertension) and potassium wasting (hypokalemia). * **Primary Hyperaldosteronism (Conn’s Syndrome):** An adrenal adenoma or hyperplasia secretes aldosterone autonomously [2]. This leads to suppressed renin but high aldosterone, causing classic hypertension with hypokalemia. * **Cushing’s Disease:** Excess cortisol can saturate the 11β-HSD2 enzyme in the kidneys. Once saturated, cortisol acts on mineralocorticoid receptors, mimicking aldosterone action and leading to hypertension and hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** 1. **Liddle’s Syndrome:** A rare genetic cause of hypertension + hypokalemia that mimics hyperaldosteronism but presents with **low renin and low aldosterone**. 2. **Screening:** The best initial test for primary hyperaldosteronism is the **Aldosterone-to-Renin Ratio (ARR)**. 3. **Diuretics:** Always rule out diuretic use (Thiazides/Loop) as the most common "extrinsic" cause of hypertension with hypokalemia before pursuing endocrine workups.

Question 777: A patient presents with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Which of the following medications is the most appropriate treatment?

A. Antidiuretic hormone antagonists (Correct Answer)
B. Thiazide diuretics
C. Loop diuretics
D. Insulin

Explanation: **Explanation:** **SIADH (Syndrome of Inappropriate Antidiuretic Hormone)** is characterized by the excessive release of ADH (Vasopressin) from the posterior pituitary or ectopic sources [1]. This leads to water retention, dilutional hyponatremia [2], and concentrated urine, despite normal intravascular volume (euvolemic hyponatremia) [2]. 1. **Why Option A is Correct:** **Antidiuretic hormone antagonists** (Vaptans, such as **Tolvaptan** and **Conivaptan**) are the most appropriate pharmacological treatment. They work by selectively blocking V2 receptors in the renal collecting ducts [1], promoting "aquaresis" (excretion of free water without loss of electrolytes). This directly addresses the underlying pathophysiology of ADH excess. 2. **Why Other Options are Incorrect:** * **B. Thiazide Diuretics:** These are contraindicated in SIADH as they inhibit sodium reabsorption in the distal convoluted tubule, which can worsen hyponatremia [2]. * **C. Loop Diuretics:** While sometimes used with saline in severe cases to induce water loss, they are not the primary "most appropriate" medication compared to specific ADH antagonists. * **D. Insulin:** Insulin has no role in the management of SIADH; it is used for glycemic control or hyperkalemia. **NEET-PG High-Yield Pearls:** * **First-line management:** Fluid restriction (<800ml/day) is the initial step for mild-to-moderate SIADH. * **Demeclocycline:** An antibiotic (Tetracycline) used in chronic SIADH because it induces a reversible state of nephrogenic diabetes insipidus. * **Correction Rate:** Avoid rapid correction of hyponatremia to prevent **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)**. Aim for <8-10 mEq/L in 24 hours. * **Common Causes:** Small cell carcinoma of the lung (ectopic ADH), CNS disorders, and drugs (SSRIs, Carbamazepine, Cyclophosphamide).

Question 778: Hypomagnesemia is seen in all of the following conditions except?

A. Gitelman syndrome
B. Hungry bone disease
C. Paget disease (Correct Answer)
D. Prolonged thiazide therapy

Explanation: ### Explanation The correct answer is **Paget disease**. **1. Why Paget disease is the correct answer:** Paget disease of the bone is characterized by excessive, disorganized bone remodeling (increased resorption followed by increased formation) [1]. In most cases, serum levels of **Calcium, Phosphate, and Magnesium remain normal**. The hallmark biochemical finding is a significantly elevated **Alkaline Phosphatase (ALP)**. Hypomagnesemia is not a feature of this condition. **2. Analysis of Incorrect Options:** * **Gitelman Syndrome:** This is a salt-losing tubulopathy affecting the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule. It typically presents with **hypomagnesemia** (due to renal magnesium wasting), hypokalemia, and hypocalciuric hypercalcemia. * **Hungry Bone Disease:** Occurs post-parathyroidectomy for hyperparathyroidism. The sudden drop in PTH leads to a rapid influx of Calcium, Phosphate, and **Magnesium** into the bone, resulting in profound serum deficiencies. * **Prolonged Thiazide Therapy:** While thiazides are "calcium-sparing," they promote the renal excretion of magnesium. Long-term use often leads to mild-to-moderate **hypomagnesemia** due to inhibition of magnesium reabsorption in the distal tubule. **3. High-Yield Clinical Pearls for NEET-PG:** * **Magnesium & Potassium:** Refractory hypokalemia cannot be corrected until the underlying hypomagnesemia is treated (Magnesium is a cofactor for the ROMK channels). * **Magnesium & PTH:** Severe hypomagnesemia causes **functional hypoparathyroidism** by inhibiting PTH release and inducing end-organ resistance to PTH. * **Bartter vs. Gitelman:** Hypomagnesemia is much more prominent and characteristic in **Gitelman syndrome** than in Bartter syndrome. * **Paget’s Marker:** The most sensitive marker for disease activity in Paget disease is **Serum ALP**; the most sensitive marker for bone resorption is **Urinary N-telopeptide**.

Question 779: Hypothyroidism may be caused by which of the following conditions?

A. Lithium
B. Hematochromatosis
C. Scleroderma
D. All of the above (Correct Answer)

Explanation: Hypothyroidism can result from primary thyroid gland failure or secondary causes affecting the pituitary-hypothalamic axis [1]. This question highlights how systemic drugs and infiltrative diseases can impair thyroid function. * **Lithium (Option A):** Lithium is a well-known goitrogen. It inhibits the release of thyroid hormones (T4 and T3) from the thyroid gland and can interfere with iodine organification. Approximately 5–15% of patients on long-term lithium therapy develop overt hypothyroidism. * **Hemochromatosis (Option B):** This is an infiltrative/storage disorder where iron deposition occurs in various organs. In the context of the thyroid, iron can deposit directly in the thyroid parenchyma (causing primary hypothyroidism) or, more commonly, in the anterior pituitary (causing secondary hypothyroidism due to TSH deficiency) [2]. * **Scleroderma (Option C):** Systemic sclerosis (Scleroderma) can lead to fibrosis of the thyroid gland. Chronic inflammatory changes and replacement of thyroid tissue with fibrous tissue result in decreased hormone production. **Conclusion:** Since all three conditions are recognized etiologies of thyroid dysfunction, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Amiodarone:** A high-yield drug that can cause both hypothyroidism (Wolff-Chaikoff effect) and hyperthyroidism (Jod-Basedow phenomenon). * **Riedel’s Thyroiditis:** A rare cause of hypothyroidism characterized by "rock-hard" thyroid due to dense fibrosis, often associated with IgG4-related systemic disease. * **Most Common Cause:** Worldwide, iodine deficiency is the most common cause; in iodine-sufficient areas (like many urban parts of India), Hashimoto’s thyroiditis is the leading cause [1].

Question 780: Tertiary hyperparathyroidism is defined as:

A. An autonomous state due to monoclonal outgrowth of previously hyperplastic parathyroid glands (Correct Answer)
B. Increased sensitivity to serum calcium
C. A condition seen in patients with parathyroid adenoma
D. A state dependent on hypothalamic stimulus

Explanation: **Explanation:** **Tertiary Hyperparathyroidism (tHPT)** occurs when long-standing secondary hyperparathyroidism (usually due to Chronic Kidney Disease) leads to irreversible changes in the parathyroid glands [2]. 1. **Why Option A is correct:** In secondary hyperparathyroidism, the glands undergo diffuse hyperplasia to compensate for low calcium/high phosphate [1]. Over time, specific cells undergo a genetic transformation, leading to **monoclonal outgrowth**. These cells become **autonomous**, meaning they continue to secrete high levels of Parathyroid Hormone (PTH) even after the underlying cause (e.g., renal failure) is corrected (such as via renal transplant) [2]. This results in hypercalcemia. 2. **Why the other options are wrong:** * **Option B:** In tHPT, there is actually a **decreased sensitivity** to serum calcium (an upward shift in the set-point of the calcium-sensing receptor), allowing PTH secretion despite high calcium levels [1]. * **Option C:** Parathyroid adenoma is the hallmark of **Primary** Hyperparathyroidism, not Tertiary [4]. Tertiary involves four-gland hyperplasia that has turned autonomous. * **Option D:** Parathyroid function is regulated by serum ionized calcium levels and the Calcium-Sensing Receptor (CaSR); it is **not** under the control of the hypothalamus or pituitary gland [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence:** Primary (Adenoma) → Secondary (Hypocalcemia/CKD) → Tertiary (Post-CKD/Transplant with Hypercalcemia). * **Biochemical Profile of tHPT:** Very high PTH + Hypercalcemia + Hyperphosphatemia. * **Treatment of Choice:** Subtotal parathyroidectomy (3.5 glands) or total parathyroidectomy with autotransplantation. * **Key Trigger:** Often diagnosed after a successful renal transplant when PTH remains high despite normalized renal function [2].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

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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