Endocrinology — MCQs

A 20-year-old woman with Hirschsprung disease presents with acute leg pain. An X-ray film of the leg reveals a fracture of the left tibia. Laboratory studies show elevated serum levels of calcium and parathyroid hormone. A CT scan of the patient's neck demonstrates a solitary parathyroid mass. Two years later, the patient presents with hypertension, and a CT scan of the abdomen displays a 4-cm mass in the right adrenal. Genetic studies conducted on this patient would likely reveal germline mutations in which of the following protooncogenes?

Q819Easy

Hirsutism may be found in any of these disorders, except?

Q820Easy

Type I Diabetes Mellitus is initially managed by?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 811: What is the leading cause of ACTH-independent Cushing syndrome?

A. Adrenocortical carcinoma
B. Macronodular adrenal hyperplasia
C. Micronodular adrenal hyperplasia
D. Adrenocortical adenoma (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Adrenocortical adenoma** Cushing syndrome is classified into two categories based on the source of cortisol excess: **ACTH-dependent** (usually a pituitary adenoma or ectopic source) and **ACTH-independent** (primary adrenal pathology). [1] In **ACTH-independent Cushing syndrome**, the adrenal cortex autonomously overproduces cortisol, which subsequently suppresses pituitary ACTH via negative feedback. **Adrenocortical adenoma** is the most common cause of this subtype, accounting for approximately 60% of ACTH-independent cases. These are typically unilateral, benign tumors that function independently of hypothalamic-pituitary control. **Why the other options are incorrect:** * **A. Adrenocortical carcinoma:** While these also cause ACTH-independent Cushing syndrome, they are much rarer than adenomas. They often present with rapid onset of symptoms and signs of androgen excess (virilization). * **B & C. Macronodular and Micronodular adrenal hyperplasia:** These are rare genetic or sporadic conditions. Macronodular hyperplasia (AIMAH) involves bilateral large nodules, while micronodular disease (e.g., Carney Complex) involves small, pigmented nodules. Neither is as common as a solitary adenoma. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Cushing Syndrome overall:** Iatrogenic (Exogenous steroid use). [1] * **Most common endogenous cause:** Cushing Disease (Pituitary ACTH-secreting adenoma) ~70%. [1] * **Biochemical Hallmark:** In ACTH-independent Cushing, serum **ACTH levels will be low (<5 pg/mL)** due to negative feedback. * **Imaging:** Contrast-enhanced CT of the adrenals is the investigation of choice to differentiate between a unilateral adenoma and bilateral hyperplasia.

Question 812: Which of the following drugs is NOT used in the treatment of idiopathic hypercalcemia?

A. Allopurinol
B. Furosemide
C. Acetazolamide
D. Thiazide (Correct Answer)

Explanation: The core principle in managing hypercalcemia is to promote urinary calcium excretion and inhibit bone resorption. **Why Thiazides are the Correct Answer:** Thiazide diuretics (e.g., Hydrochlorothiazide) are **contraindicated** in hypercalcemia. They act on the distal convoluted tubule to inhibit the Na+/Cl- symporter, which indirectly **increases renal calcium reabsorption**. By reducing urinary calcium excretion and causing mild volume depletion, thiazides can exacerbate or even induce hypercalcemia. They are, however, the drug of choice for *hypercalciuria* (to prevent stones). **Analysis of Other Options:** * **Furosemide (Loop Diuretic):** This is a mainstay of treatment. It inhibits the Na+/K+/2Cl- cotransporter in the thick ascending limb of Henle, which abolishes the positive luminal potential, thereby **promoting calcium excretion** (calciuresis). It must be administered with aggressive normal saline hydration. * **Acetazolamide:** As a carbonic anhydrase inhibitor, it can increase the excretion of various electrolytes, including calcium, and is sometimes used as an adjunct in specific hypercalcemic states. [1] * **Allopurinol:** While not a primary treatment for calcium levels, it is used in conditions like **Sarcoidosis** (a common cause of idiopathic hypercalcemia/Williams syndrome) to manage associated hyperuricemia and prevent uric acid stones. **NEET-PG High-Yield Pearls:** * **Mnemonic:** "Loop Loses calcium (Furosemide), Thiazide Takes it back." * **First-line emergency treatment:** Aggressive IV hydration with 0.9% Normal Saline. [2] * **Drug of choice for malignancy-induced hypercalcemia:** IV Bisphosphonates (e.g., Zoledronic acid). [2] * **Williams Syndrome:** Characterized by "elfin" facies, supravalvular aortic stenosis, and idiopathic infantile hypercalcemia.

Question 813: A patient presents with hypercalcemia and a suppressed parathyroid hormone level. What is the most likely diagnosis?

A. Hodgkin's lymphoma (Correct Answer)
B. Hyperthyroidism
C. Parathyroid carcinoma
D. Small-cell lung cancer

Explanation: **Explanation:** The clinical presentation of **hypercalcemia with suppressed Parathyroid Hormone (PTH)** indicates **PTH-independent hypercalcemia** [1]. This occurs when calcium levels rise due to factors other than the parathyroid gland, leading to negative feedback that shuts down endogenous PTH production. **Why Hodgkin’s Lymphoma is correct:** In Hodgkin’s lymphoma (and other granulomatous diseases like sarcoidosis), the primary mechanism of hypercalcemia is the **extra-renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (Calcitriol)** [1]. This is mediated by the enzyme **1-alpha-hydroxylase** expressed by activated macrophages/lymphoma cells [2]. Increased calcitriol leads to enhanced intestinal calcium absorption, which suppresses PTH. **Analysis of Incorrect Options:** * **B. Hyperthyroidism:** While it can cause mild hypercalcemia due to increased bone turnover (thyrotoxicosis), it is a less common cause compared to malignancy-associated mechanisms in exam scenarios [1]. * **C. Parathyroid Carcinoma:** This would present with **markedly elevated PTH levels** (often >5–10 times the upper limit), as the tumor autonomously secretes PTH [3]. * **D. Small-cell Lung Cancer:** This is classically associated with **SIADH** or **Ectopic ACTH**. Hypercalcemia of malignancy via PTHrP (PTH-related protein) is typically associated with **Squamous Cell Lung Cancer**, not small-cell. **NEET-PG High-Yield Pearls:** * **Most common cause of hypercalcemia (Outpatient):** Primary Hyperparathyroidism (↑ PTH). * **Most common cause of hypercalcemia (Inpatient):** Malignancy (↓ PTH) [1]. * **Mechanism in Squamous Cell CA:** Secretion of **PTHrP** (mimics PTH but is not detected by standard PTH assays). * **Mechanism in Multiple Myeloma:** Local osteolytic bone destruction via cytokines (IL-6, RANKL) [1]. * **Mechanism in Lymphoma/Sarcoid:** Increased **1,25-dihydroxyvitamin D** [1].

Question 814: All are features of Cushing's disease except?

A. Central obesity
B. Episodic hypertension (Correct Answer)
C. Easy bruising
D. Glucose intolerance

Explanation: **Explanation:** **Cushing’s disease** refers specifically to hypercortisolism caused by a pituitary adenoma secreting excess ACTH [1]. The hallmark of this condition is chronic, sustained elevation of glucocorticoids. [1] **Why "Episodic Hypertension" is the correct answer:** Hypertension in Cushing’s disease is typically **sustained**, not episodic. It occurs due to cortisol’s mineralocorticoid effects (sodium retention), increased sensitivity to catecholamines, and activation of the renin-angiotensin system. **Episodic (paroxysmal) hypertension** is the classic clinical triad of **Pheochromocytoma**, along with palpitations and diaphoresis. **Analysis of Incorrect Options:** * **Central Obesity:** This is the most common feature. Cortisol causes redistribution of fat to the trunk, face (moon facies), and interscapular area (buffalo hump) while causing peripheral muscle wasting. * **Easy Bruising:** Excess cortisol leads to the breakdown of dermal collagen and connective tissue [1]. This results in thin, friable skin and capillary fragility, manifesting as easy bruising and purple striae [1]. * **Glucose Intolerance:** Cortisol is a potent counter-regulatory hormone that stimulates gluconeogenesis and causes peripheral insulin resistance, often leading to secondary diabetes mellitus. **NEET-PG High-Yield Pearls:** * **Screening Test:** Overnight Dexamethasone Suppression Test (ONDST) or 24-hour urinary free cortisol [2]. * **Gold Standard for Localization:** Inferior Petrosal Sinus Sampling (IPSS) is used to differentiate a pituitary source (Cushing’s disease) from ectopic ACTH production [3]. * **Hypokalemia:** While common in ectopic ACTH syndrome (e.g., Small Cell Lung Cancer), it is less common in pituitary Cushing’s disease.

Question 815: Which is the screening test for evaluation of mineralocorticoid excess?

A. Saline infusion test
B. Salt loading test
C. Cosyntropin test
D. Aldosterone renin ratio (Correct Answer)

Explanation: The evaluation of mineralocorticoid excess (Primary Aldosteronism/Conn’s Syndrome) follows a specific diagnostic hierarchy: **Screening → Confirmation → Localization.** **1. Why Aldosterone Renin Ratio (ARR) is correct:** The ARR is the preferred **initial screening test**. In primary aldosteronism, the adrenal gland autonomously produces high levels of aldosterone, which suppresses renin via negative feedback. Therefore, a high plasma aldosterone concentration (PAC) combined with a low plasma renin activity (PRA) results in an elevated ratio (typically >20-30). It is highly sensitive and can be performed while the patient is ambulatory. **2. Why other options are incorrect:** * **A & B (Saline infusion/Salt loading tests):** These are **confirmatory tests**, not screening tests. They work on the principle that in a normal individual, a high salt load should suppress aldosterone. Failure to suppress aldosterone levels after salt loading confirms the diagnosis of autonomous production. * **C (Cosyntropin test):** This is the gold standard for diagnosing **Adrenal Insufficiency** (Addison’s disease), not mineralocorticoid excess [1]. It measures the cortisol response to synthetic ACTH [1]. **Clinical Pearls for NEET-PG:** * **Classic Triad:** Hypertension, hypokalemia, and metabolic alkalosis (though many patients are normokalemic). * **Drug Interference:** Spironolactone (aldosterone antagonist) must be stopped for at least 4–6 weeks before testing ARR as it can cause false positives [2]. * **Localization:** Once confirmed, the next step is a **CT scan** of the adrenals [2]. If imaging is inconclusive, **Adrenal Venous Sampling (AVS)** is the gold standard to differentiate between a unilateral adenoma (surgery) and bilateral hyperplasia (medical management) [2].

Question 816: A 26-year-old man was admitted with electrolyte disturbances. Which of the following is typically NOT seen in primary hyperaldosteronism?

A. Diastolic hypertension
B. Pedal edema (Correct Answer)
C. Polyuria
D. Hypokalemia

Explanation: The hallmark of primary hyperaldosteronism (Conn’s Syndrome) is the autonomous overproduction of aldosterone, leading to sodium retention and potassium excretion [1]. ### **Why Pedal Edema is NOT seen (The "Aldosterone Escape" Phenomenon)** In primary hyperaldosteronism, excess aldosterone causes initial sodium and water retention, which increases extracellular fluid (ECF) volume [1]. However, this volume expansion triggers compensatory mechanisms: 1. **Atrial Natriuretic Peptide (ANP) release:** Increased atrial stretch leads to ANP secretion. 2. **Pressure Natriuresis:** Elevated blood pressure promotes sodium excretion by the kidneys [1]. These mechanisms result in a "spontaneous diuresis" of sodium and water, preventing significant fluid overload. Consequently, patients remain **euvolemic** and do **not** develop clinical edema. ### **Analysis of Other Options** * **Diastolic Hypertension:** Increased sodium reabsorption and peripheral vascular resistance lead to hypertension, often characterized by a significant rise in diastolic pressure. * **Hypokalemia:** Aldosterone acts on the principal cells of the collecting duct to secrete potassium into the urine [2]. This can lead to muscle weakness or cardiac arrhythmias. * **Polyuria:** Chronic hypokalemia causes **nephrogenic diabetes insipidus** (impaired urinary concentrating ability), leading to polyuria and polydipsia. ### **High-Yield Clinical Pearls for NEET-PG** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20–30** is highly suggestive. * **Metabolic State:** Patients typically show **Hypokalemic Metabolic Alkalosis** (due to H+ ion secretion in the distal tubule) [1]. * **Triad of Conn’s:** Hypertension, Hypokalemia, and Metabolic Alkalosis [1]. * **Most Common Cause:** Adrenal Adenoma (Conn's Syndrome), followed by Bilateral Adrenal Hyperplasia.

Question 817: Low serum calcium and high serum phosphate are typically seen in which condition?

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

Explanation: **Explanation:** The biochemical hallmark of **Hypoparathyroidism** is the combination of **hypocalcemia** and **hyperphosphatemia** [1]. This occurs due to a deficiency of Parathyroid Hormone (PTH). **1. Why Hypoparathyroidism is correct:** PTH is the primary regulator of calcium and phosphate homeostasis. Under normal conditions, PTH increases serum calcium (by mobilizing it from bone and increasing renal reabsorption) and decreases serum phosphate (by inhibiting reabsorption in the proximal convoluted tubule, causing phosphaturia) [2]. In hypoparathyroidism, the absence of PTH leads to: * **Decreased renal calcium reabsorption** and decreased bone resorption (leading to low serum calcium). * **Increased renal phosphate reabsorption** (leading to high serum phosphate) [1]. **2. Why other options are incorrect:** * **Hyperparathyroidism:** Characterized by high PTH levels, resulting in **hypercalcemia** and **hypophosphatemia** (due to excessive renal phosphate wasting) [3]. * **Hyperthyroidism & Hypothyroidism:** Thyroid hormone disorders primarily affect metabolic rate. While severe hyperthyroidism can occasionally cause mild hypercalcemia due to increased bone turnover, they do not typically present with the classic reciprocal calcium-phosphate pattern seen in PTH disorders [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Pseudohypoparathyroidism:** Presents with the same biochemical profile (Low Ca²⁺, High PO₄³⁻) but with **high PTH** levels due to end-organ resistance [1]. * **Clinical Signs:** Look for **Chvostek’s sign** (facial twitching) and **Trousseau’s sign** (carpedal spasm) as indicators of hypocalcemia. * **ECG Finding:** The most characteristic finding in hypocalcemia is **QT interval prolongation** [1]. * **Basal Ganglia Calcification:** A classic radiological association with chronic hypoparathyroidism due to high phosphate levels.

Question 818: A 20-year-old woman with Hirschsprung disease presents with acute leg pain. An X-ray film of the leg reveals a fracture of the left tibia. Laboratory studies show elevated serum levels of calcium and parathyroid hormone. A CT scan of the patient's neck demonstrates a solitary parathyroid mass. Two years later, the patient presents with hypertension, and a CT scan of the abdomen displays a 4-cm mass in the right adrenal. Genetic studies conducted on this patient would likely reveal germline mutations in which of the following protooncogenes?

A. BRCA1
B. Rb
C. RET (Correct Answer)
D. VHL

Explanation: **Explanation:** The clinical presentation describes a classic case of **Multiple Endocrine Neoplasia Type 2A (MEN 2A)**. The patient exhibits primary hyperparathyroidism (elevated calcium/PTH, parathyroid mass) and a pheochromocytoma (hypertension, adrenal mass). The crucial diagnostic clue is the history of **Hirschsprung disease**, which is strongly associated with germline mutations in the **RET proto-oncogene**. 1. **Why RET is correct:** The *RET* gene (located on chromosome 10) encodes a receptor tyrosine kinase. Gain-of-function mutations lead to MEN 2A (Medullary Thyroid Carcinoma, Pheochromocytoma, and Parathyroid hyperplasia) and MEN 2B. Interestingly, loss-of-function mutations in the same *RET* gene are the most common genetic cause of Hirschsprung disease. 2. **Why other options are incorrect:** * **BRCA1:** Associated with hereditary breast and ovarian cancer syndromes. * **Rb:** A tumor suppressor gene associated with Retinoblastoma and Osteosarcoma. * **VHL:** Associated with Von Hippel-Lindau syndrome (Hemangioblastomas, Renal Cell Carcinoma, and Pheochromocytoma), but it does not involve parathyroid tumors or Hirschsprung disease. **High-Yield Clinical Pearls for NEET-PG:** * **MEN 2A (Sipple Syndrome):** MPH — **M**edullary Thyroid CA (100%), **P**heochromocytoma, **H**yperparathyroidism. * **MEN 2B (Williams-Pollock Syndrome):** MMP — **M**edullary Thyroid CA, **M**arfanoid habitus/Mucosal neuromas, **P**heochromocytoma. * **Prophylactic Thyroidectomy:** Recommended for *RET* mutation carriers because Medullary Thyroid Carcinoma is nearly 100% penetrant. * **Screening:** Always rule out Pheochromocytoma (via urinary/plasma metanephrines) before any surgery to prevent a hypertensive crisis.

Question 819: Hirsutism may be found in any of these disorders, except?

A. Cushing's syndrome
B. Hypothyroidism (Correct Answer)
C. Congenital adrenal hyperplasia
D. Polycystic ovarian syndrome

Explanation: ### Explanation **Hirsutism** is defined as the presence of terminal hair in females in a male-pattern distribution (e.g., face, chest, back). It is primarily driven by an excess of androgens or increased sensitivity of hair follicles to androgens [1]. #### Why Hypothyroidism is the Correct Answer: **Hypothyroidism** is typically associated with **hair loss (alopecia)** or thinning of the hair, particularly the loss of the outer third of the eyebrows (Queen Anne’s sign) [3]. It does not cause hirsutism. In fact, hypothyroidism increases Sex Hormone-Binding Globulin (SHBG) less effectively than hyperthyroidism, but its primary clinical manifestation regarding hair is brittle, coarse hair and telogen effluvium, not androgenic hair growth [3]. #### Analysis of Other Options: * **Cushing’s Syndrome:** Excess cortisol is often accompanied by excess adrenal androgens (especially in ACTH-dependent Cushing's), leading to hirsutism and acne. * **Congenital Adrenal Hyperplasia (CAH):** Specifically the non-classic form or 21-hydroxylase deficiency leads to a "shunting" of precursors toward the androgen pathway, causing significant hirsutism and virilization. * **Polycystic Ovarian Syndrome (PCOS):** This is the **most common cause** of hirsutism [2]. It involves hyperandrogenism due to increased LH stimulation of ovarian theca cells [1]. #### NEET-PG High-Yield Pearls: * **Ferriman-Gallwey Score:** Used to quantify hirsutism; a score $\geq$ 8 is generally considered diagnostic. * **Drug-Induced Hirsutism/Hypertrichosis:** Common culprits include Minoxidil, Cyclosporine, and Phenytoin. * **Rapid Onset Hirsutism:** If hirsutism develops rapidly along with virilization (clitoromegaly, voice deepening), always suspect an **Androgen-secreting tumor** (Adrenal or Ovarian) [2]. * **First-line treatment for PCOS-related hirsutism:** Combined Oral Contraceptive Pills (COCPs).

Question 820: Type I Diabetes Mellitus is initially managed by?

A. Metformin
B. Sulfonylureas
C. Meglitinides
D. Insulin (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Insulin** **Mechanism and Rationale:** Type 1 Diabetes Mellitus (T1DM) is characterized by an **absolute deficiency of insulin** due to the autoimmune destruction of pancreatic beta cells in the Islets of Langerhans. Since the body cannot produce endogenous insulin, exogenous insulin replacement is the **only** definitive and life-saving treatment [3]. It is required from the time of diagnosis to prevent metabolic derangements, most notably Diabetic Ketoacidosis (DKA) [2]. **Why Incorrect Options are Wrong:** * **A. Metformin:** This is a Biguanide that works primarily by decreasing hepatic glucose production and improving insulin sensitivity. It requires the presence of endogenous insulin to be effective and is the first-line treatment for Type 2 DM, not Type 1. * **B. Sulfonylureas (e.g., Glipizide):** These are "insulin secretagogues" that act by stimulating the pancreas to release more insulin [1]. In T1DM, the beta cells are destroyed; therefore, there is no insulin to secrete, making these drugs ineffective. * **C. Meglitinides (e.g., Repaglinide):** Similar to sulfonylureas, these stimulate postprandial insulin secretion. They are useless in T1DM due to the lack of functional beta-cell mass. **High-Yield NEET-PG Pearls:** * **Pathogenesis:** T1DM is associated with HLA-DR3 and HLA-DR4 [5]. * **Antibodies:** The most common markers are Anti-GAD65 (Glutamic Acid Decarboxylase), Anti-IA2, and Zinc Transporter 8 (ZnT8) antibodies. * **C-Peptide:** In T1DM, C-peptide levels are low or undetectable (a key marker to differentiate from T2DM). * **Honeymoon Phase:** A transient period shortly after starting insulin where the remaining beta cells temporarily recover, leading to reduced exogenous insulin requirements. * **Standard Regimen:** The preferred management is a **Basal-Bolus regimen** (long-acting insulin for basal needs and rapid-acting insulin for meals) [4].

Practice by Chapter

Diabetes Mellitus

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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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