Endocrinology — MCQs

A 64-year-old man presents with severe polyuria and polydipsia, consuming 3 to 4 glasses of water and producing over 0.5 liters of urine each hour. After overnight water restriction, the following test results were obtained: Plasma sodium concentration: 155 mEq/L; Urine osmolarity: 90 mOsmol/L; Urine glucose concentration: 0 mg/dL. Which of the following is the most likely diagnosis?

Q377Medium

Which of the following conditions is a common cause of hypercalcemia?

Q378Medium

All of the following are true about Hypercalcemia, except:

Q379Easy

Which of the following is seen in Addison's disease?

Q380Medium

All of the following are true about Diabetes mellitus EXCEPT:

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 371: All of the following are true about acromegaly except:

A. Increased IGF-1 levels
B. Excessive growth occurs before fusion of the epiphyses of the long bones (Correct Answer)
C. Somatostatin analogues can be used
D. Growth hormone levels are increased

Explanation: ### Explanation **1. Why Option B is the Correct Answer (The "Except"):** The distinction between **Acromegaly** and **Gigantism** depends entirely on the timing of growth hormone (GH) excess relative to epiphyseal closure. * **Gigantism:** Occurs when GH excess occurs **before** the fusion of the epiphyses. This results in increased linear bone growth and tall stature [2]. * **Acromegaly:** Occurs **after** the fusion of the epiphyses. Since the long bones can no longer grow in length, the excess GH causes thickening of bones (membranous bone growth) and soft tissue enlargement (acral enlargement) [2]. Therefore, Option B is a description of Gigantism, not Acromegaly. **2. Analysis of Other Options:** * **Option A (Increased IGF-1):** GH stimulates the liver to produce Insulin-like Growth Factor-1 (IGF-1). IGF-1 mediates most of the growth-promoting effects and is the **best screening test** for acromegaly because its levels remain stable throughout the day [1]. * **Option D (Increased GH levels):** Acromegaly is caused by a GH-secreting pituitary adenoma in >95% of cases, leading to pathologically elevated GH levels. * **Option C (Somatostatin analogues):** Drugs like **Octreotide and Lanreotide** are somatostatin analogues that inhibit GH secretion and are a mainstay in the medical management of acromegaly. **3. NEET-PG High-Yield Clinical Pearls:** * **Best Screening Test:** Serum IGF-1 levels. * **Gold Standard Diagnostic Test:** Oral Glucose Tolerance Test (OGTT). Failure of GH to suppress below **1 ng/mL** after 75g of glucose is diagnostic [3]. * **Treatment of Choice:** Transsphenoidal surgery (except in cases where medical therapy is preferred first) [3]. * **Common Comorbidities:** Hypertension, Diabetes Mellitus (GH is diabetogenic), and **Colonic Polyps/Carcinoma** (increased risk requires screening colonoscopy) [3]. * **Most common cause of death:** Cardiovascular disease (Cardiomyopathy).

Question 372: Casal's necklace is a feature of which condition?

A. Addison disease
B. Pellagra (Correct Answer)
C. Dermatomyositis
D. Systemic lupus erythematosus (SLE)

Explanation: **Explanation:** **Casal’s necklace** is a pathognomonic dermatological sign of **Pellagra**, a systemic disease caused by a deficiency of **Niacin (Vitamin B3)** or its precursor, the amino acid **Tryptophan** [1]. The condition is classically characterized by the "4 Ds": Dermatitis, Diarrhea, Dementia, and, if untreated, Death [1], [2]. The dermatitis in Pellagra is typically photosensitive [3]. Casal’s necklace refers to a well-demarcated, erythematous, scaly rash that forms a ring-like distribution around the lower neck and upper chest (the C3-C4 dermatome area exposed to sunlight) [2]. **Analysis of Incorrect Options:** * **Addison Disease:** Characterized by hyperpigmentation due to increased ACTH levels, but it typically involves skin creases, pressure points, and mucous membranes (buccal mucosa) rather than a specific necklace-like photosensitive rash. * **Dermatomyositis:** Features a **"V-sign"** (rash on the chest) and **"Shawl sign"** (rash on the back/shoulders), along with Gottron papules and Heliotrope rash, but these are distinct from the specific hyperkeratotic, pigmented necklace of Pellagra. * **Systemic Lupus Erythematosus (SLE):** Classically presents with a **Malar (butterfly) rash** sparing the nasolabial folds [3]. While photosensitive, it does not present as Casal’s necklace. **High-Yield Clinical Pearls for NEET-PG:** * **Hartnup Disease:** A genetic disorder of tryptophan transport that can present with Pellagra-like symptoms. * **Carcinoid Syndrome:** Can lead to Pellagra because dietary tryptophan is diverted to produce massive amounts of Serotonin instead of Niacin. * **Dietary Link:** Pellagra is common in populations where **maize (corn)** is the staple food, as the niacin in maize is bound (niacytin) and unavailable for absorption unless treated with alkali.

Question 373: Which of the following malignancies most frequently causes hypercalcemia, except?

A. Breast
B. Kidney
C. Lung
D. Head and Neck (Correct Answer)

Explanation: **Explanation:** Hypercalcemia of malignancy (HCM) is the most common cause of hypercalcemia in hospitalized patients [1]. It occurs via three main mechanisms: secretion of **PTH-related peptide (PTHrP)** [2], local osteolytic bone destruction, or 1,25-dihydroxyvitamin D production. The correct answer is **Head and Neck** because, while squamous cell carcinomas of the head and neck frequently cause hypercalcemia via PTHrP, they are statistically less common causes compared to the other options listed. In clinical practice and standard textbooks (like Harrison’s), the most frequent malignancies associated with hypercalcemia are **Lung (specifically Squamous Cell), Breast, and Multiple Myeloma.** [1] **Analysis of Options:** * **Lung (Option C):** Squamous cell carcinoma of the lung is the most common cause of Humoral Hypercalcemia of Malignancy (HHM) due to PTHrP secretion [2]. * **Breast (Option A):** Breast cancer is a very frequent cause, often through a combination of local osteolytic bone metastases and PTHrP production [1], [2]. * **Kidney (Option B):** Renal cell carcinoma is a classic producer of PTHrP and is a frequent cause of HHM [1], [2]. * **Head and Neck (Option D):** While these cancers do cause hypercalcemia, they are ranked lower in overall frequency compared to the high prevalence of Lung and Breast cancers. **NEET-PG High-Yield Pearls:** 1. **Most common cause of hypercalcemia overall:** Primary Hyperparathyroidism (outpatient) [1]. 2. **Most common cause of hypercalcemia in hospitalized patients:** Malignancy [1]. 3. **Most common mechanism of HCM:** PTHrP secretion (80% of cases) [2]. 4. **Multiple Myeloma:** Causes hypercalcemia via local osteolysis (RANKL-mediated) rather than PTHrP [1]. 5. **Treatment of choice for acute severe HCM:** Aggressive IV hydration with normal saline, followed by IV Bisphosphonates (Zoledronic acid).

Question 374: Obesity is not a feature of which of the following conditions?

A. Hypothyroidism
B. Adrenal insufficiency (Correct Answer)
C. Hypogonadism
D. Cushing's syndrome

Explanation: ### Explanation The correct answer is **Adrenal insufficiency**. **1. Why Adrenal Insufficiency is the correct answer:** Adrenal insufficiency (Addison’s disease) is characterized by a deficiency of cortisol and, in primary cases, aldosterone [1]. Cortisol is a glucocorticoid essential for metabolic homeostasis. Its absence leads to decreased gluconeogenesis and increased insulin sensitivity, often resulting in **weight loss** and anorexia rather than obesity. Weight loss is a hallmark clinical feature of chronic adrenal insufficiency, often accompanied by hyperpigmentation (in primary cases) and hypotension. **2. Why the other options are incorrect:** * **Hypothyroidism:** Low levels of thyroid hormones (T3/T4) lead to a decreased Basal Metabolic Rate (BMR) and accumulation of glycosaminoglycans (myxedema), which causes fluid retention and weight gain. * **Hypogonadism:** Testosterone and estrogen play roles in body fat distribution and muscle mass. Deficiency in these hormones (especially testosterone in males) leads to increased adiposity and decreased lean body mass. * **Cushing’s Syndrome:** This is characterized by chronic glucocorticoid excess [3]. It causes "centripetal obesity" (trunk, buffalo hump, and moon facies) due to the redistribution of fat and stimulation of adipogenesis [3]. **3. NEET-PG High-Yield Pearls:** * **Weight Loss Triad in Endocrinology:** Adrenal insufficiency, Hyperthyroidism, and Type 1 Diabetes Mellitus. * **Secondary Adrenal Insufficiency:** Unlike primary Addison’s, there is **no hyperpigmentation** (due to low ACTH) and **no mineralocorticoid deficiency** (regulated by the RAAS, not ACTH) [2]. * **Cushing’s vs. Simple Obesity:** In Cushing’s, the obesity is typically "central" with thin extremities (due to muscle wasting), whereas simple obesity is usually generalized [3].

Question 375: Which of the following is NOT true of de Quervain's thyroiditis?

A. Pain
B. Increased ESR
C. Increased radioactive iodine uptake (Correct Answer)
D. Fever

Explanation: De Quervain’s thyroiditis (also known as **Subacute Granulomatous Thyroiditis**) is a self-limiting inflammatory condition of the thyroid, typically following a viral upper respiratory tract infection. **Why Option C is the correct answer:** In de Quervain's thyroiditis, the inflammation causes the **destruction of thyroid follicles**, leading to the leakage of preformed thyroid hormones into the bloodstream (thyrotoxic phase). Because the follicular cells are damaged and inflamed, they are unable to actively trap iodine [1]. Therefore, the **Radioactive Iodine Uptake (RAIU) is characteristically low (<5%)**, despite the patient appearing clinically hyperthyroid [1][2]. This "diagnostic dissociation" (high T3/T4 with low RAIU) is a hallmark of the disease. **Why the other options are incorrect:** * **A. Pain:** This is the most characteristic clinical feature. Patients present with severe pain in the anterior neck that may radiate to the jaw or ears [1]. * **B. Increased ESR:** As an inflammatory condition, the Erythrocyte Sedimentation Rate (ESR) is typically markedly elevated (often >50–100 mm/hr), serving as a key diagnostic marker [1]. * **D. Fever:** Systemic symptoms including fever, malaise, and myalgia are common during the acute phase of the illness [1]. **NEET-PG High-Yield Pearls:** * **Etiology:** Post-viral (Coxsackie, Mumps, Adenovirus). * **Pathology:** Giant cells and granulomatous inflammation on biopsy. * **Treatment:** NSAIDs for mild cases; Glucocorticoids (Prednisone) for severe pain [1]. * **Key Distinction:** Unlike Graves' disease (High RAIU), de Quervain's has **Low RAIU**. Unlike painless thyroiditis, de Quervain's is **exquisitely tender**.

Question 376: A 64-year-old man presents with severe polyuria and polydipsia, consuming 3 to 4 glasses of water and producing over 0.5 liters of urine each hour. After overnight water restriction, the following test results were obtained: Plasma sodium concentration: 155 mEq/L; Urine osmolarity: 90 mOsmol/L; Urine glucose concentration: 0 mg/dL. Which of the following is the most likely diagnosis?

A. Addison's disease
B. Fanconi syndrome
C. Diabetes insipidus (Correct Answer)
D. Diabetes mellitus

Explanation: ### Explanation **1. Why Diabetes Insipidus (DI) is the Correct Answer:** The clinical hallmark of DI is the inability to concentrate urine despite rising plasma osmolality. This patient presents with the classic triad: **polyuria** (>3L/day), **polydipsia**, and **hypernatremia** (155 mEq/L). [4] * **Water Restriction Test:** In a normal individual, water restriction triggers ADH release, leading to concentrated urine. Here, the urine remains significantly dilute (**90 mOsmol/L**), which is far below the normal response (>600 mOsmol/L) and even below the plasma osmolality. [1] * The absence of glycosuria rules out osmotic diuresis from glucose, confirming that the polyuria is due to a lack of ADH effect (either Central or Nephrogenic DI). **2. Why the Other Options are Incorrect:** * **Addison’s Disease:** Typically presents with **hyponatremia** (due to aldosterone deficiency) and hyperkalemia, not hypernatremia and dilute polyuria. [3] * **Fanconi Syndrome:** While it can cause polyuria due to proximal tubule dysfunction, it is characterized by **glycosuria** (at normal blood glucose levels), phosphaturia, and aminoaciduria. This patient has 0 mg/dL urine glucose. * **Diabetes Mellitus:** Causes osmotic diuresis due to hyperglycemia. The urine would show a **high glucose concentration** and a higher osmolarity than 90 mOsmol/L. **3. NEET-PG High-Yield Clinical Pearls:** * **Diagnostic Cut-off:** DI is suspected when urine osmolarity is **<300 mOsmol/L** in the presence of high plasma osmolarity (>295 mOsmol/L). [2] * **Differentiation:** To distinguish Central from Nephrogenic DI, administer **Desmopressin (dDAVP)**. A >50% increase in urine osmolarity indicates Central DI; little to no response indicates Nephrogenic DI. [2] * **Common Causes:** Central DI is often post-neurosurgery or idiopathic; Nephrogenic DI is commonly caused by **Lithium** or hypercalcemia. [2]

Question 377: Which of the following conditions is a common cause of hypercalcemia?

A. Adrenocortical insufficiency
B. Amyloidosis
C. Hyperthyroidism (Correct Answer)
D. Vitamin C intoxication

Explanation: **Explanation:** Hypercalcemia is a common clinical finding in endocrinology, primarily driven by increased bone resorption or decreased renal excretion [1]. **Why Hyperthyroidism is Correct:** Thyroid hormones (T3 and T4) have a direct stimulatory effect on osteoclasts, leading to increased bone turnover and resorption. In approximately 15-20% of patients with thyrotoxicosis, this accelerated bone breakdown exceeds the rate of bone formation, resulting in mild hypercalcemia [1]. Additionally, the increased calcium load suppresses Parathyroid Hormone (PTH), leading to hypercalciuria. **Analysis of Incorrect Options:** * **A. Adrenocortical insufficiency:** While Addison’s disease can cause hypercalcemia (due to decreased renal calcium clearance and increased bone resorption), it is considered an **uncommon** cause compared to the metabolic impact of hyperthyroidism [1]. * **B. Amyloidosis:** This is a restrictive/infiltrative disease. While it can lead to renal failure (which causes *hypocalcemia* due to phosphate retention and low Vitamin D) [2], it is not a recognized cause of hypercalcemia. * **D. Vitamin C intoxication:** Vitamin C (Ascorbic acid) is not involved in calcium metabolism. It is **Vitamin D** intoxication (increased intestinal absorption) [1] or **Vitamin A** intoxication (increased bone resorption) that causes hypercalcemia. **High-Yield NEET-PG Pearls:** * **Most common cause overall:** Primary Hyperparathyroidism (outpatient) and Malignancy (inpatient) [1]. * **Mnemonic for Hypercalcemia (CHIMPANZEES):** **C**alcium supplements, **H**yperparathyroidism, **I**atrogenic/Immobilization, **M**ilk-alkali syndrome, **P**aget’s disease, **A**ddison’s/Acromegaly, **N**eoplasia, **Z**ollinger-Ellison (MEN1), **E**xcess Vitamin D, **E**xcess Vitamin A, **S**arcoidosis [1]. * **ECG Finding:** Shortened QT interval is the classic sign of hypercalcemia.

Question 378: All of the following are true about Hypercalcemia, except:

A. Management of primary cause
B. Management of primary cause
C. IV fluid with furosemide is given
D. Pamidronate is not effective (Correct Answer)

Explanation: ### Explanation **Hypercalcemia** is a common clinical emergency in endocrinology, most frequently caused by primary hyperparathyroidism or malignancy [1]. **Why Option D is the Correct Answer (The False Statement):** **Pamidronate** is a potent intravenous **bisphosphonate** and is highly effective in treating hypercalcemia, especially when associated with malignancy. It works by inhibiting osteoclast-mediated bone resorption [2]. While it takes 48–72 hours to reach its peak effect, it is a cornerstone of long-term calcium stabilization. Therefore, stating it is "not effective" is medically incorrect. **Analysis of Other Options:** * **Options A & B (Management of primary cause):** These are true. Definitive treatment of hypercalcemia always requires addressing the underlying etiology (e.g., parathyroidectomy for adenoma or treating the underlying cancer) [1]. * **Option C (IV fluid with furosemide):** This is a standard initial treatment. **Aggressive hydration with Normal Saline (0.9% NaCl)** is the first step to restore volume and promote urinary calcium excretion [1]. **Furosemide** (a loop diuretic) is added *after* volume resuscitation to further enhance calciuresis and prevent fluid overload. **Clinical Pearls for NEET-PG:** 1. **First-line treatment:** Isotonic saline (Normal Saline) is the most important initial step. 2. **Bisphosphonates:** Zoledronic acid is generally preferred over Pamidronate due to higher potency and shorter infusion time. 3. **Calcitonin:** Used for rapid, short-term reduction of calcium (works within hours) but is limited by **tachyphylaxis** (effect wears off after 48 hours). 4. **Avoid Thiazides:** Thiazide diuretics are contraindicated in hypercalcemia as they increase renal calcium reabsorption. 5. **ECG Finding:** Look for a **shortened QT interval**, a classic sign of hypercalcemia.

Question 379: Which of the following is seen in Addison's disease?

A. Hypernatremia
B. Hypokalemia
C. Hyperglycemia
D. Hypercalcemia (Correct Answer)

Explanation: Addison’s disease (Primary Adrenocortical Insufficiency) results from the destruction of the adrenal cortex, leading to a deficiency of cortisol, aldosterone, and adrenal androgens [1]. **Why Hypercalcemia is correct:** Hypercalcemia is seen in approximately 10–20% of patients with Addison’s disease. The underlying mechanisms include: 1. **Decreased Renal Excretion:** Cortisol normally inhibits renal tubular reabsorption of calcium; its absence leads to increased calcium retention. 2. **Increased Bone Resorption:** Glucocorticoids normally antagonize the effects of Vitamin D; their deficiency leads to increased calcium mobilization from bones. 3. **Hemoconcentration:** Dehydration (due to mineralocorticoid deficiency) leads to a relative increase in serum calcium levels [3]. **Analysis of Incorrect Options:** * **A. Hypernatremia:** Incorrect. Aldosterone deficiency leads to "salt wasting" (loss of sodium in urine), resulting in **Hyponatremia** [1]. * **B. Hypokalemia:** Incorrect. Aldosterone normally promotes potassium excretion. Its absence leads to potassium retention, resulting in **Hyperkalemia** [1]. * **C. Hyperglycemia:** Incorrect. Cortisol is a counter-regulatory hormone that promotes gluconeogenesis. Its deficiency leads to **Hypoglycemia**. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis (Non-gap). * **Hyperpigmentation:** Seen only in *Primary* Adrenal Insufficiency due to increased ACTH (which shares a precursor with Melanocyte Stimulating Hormone - POMC) [2]. * **Diagnosis:** The screening test of choice is the **ACTH Stimulation Test** (Cosyntropin test) [2]. * **Hematology:** Patients often show eosinophilia and lymphocytosis.

Question 380: All of the following are true about Diabetes mellitus EXCEPT:

A. Diabetic ketoacidosis is commoner in type I diabetes mellitus. (Correct Answer)
B. Hyperosmolar hyperglycemic state is primarily seen in individuals with type II diabetes mellitus.
C. Serum sodium in diabetic ketoacidosis is typically in the range of 125-135 mEq/L.
D. Serum bicarbonate in diabetic ketoacidosis is less than 15 mEq/L.

Explanation: This question requires an understanding of the metabolic complications of Diabetes Mellitus (DM). **Explanation of the Correct Answer:** The question asks for the **EXCEPT** statement. Option A is actually a **true** statement: Diabetic Ketoacidosis (DKA) is indeed more common in Type 1 DM due to absolute insulin deficiency, which leads to unrestrained lipolysis and ketone body formation [1]. However, in the context of this specific question's formatting (where A is marked as the "correct" answer to an "Except" question), it implies that the statement is considered false or there is a technical error in the question's premise. In standard clinical medicine, A, B, and D are true. **Option C** is often the intended "Except" in similar exams because serum sodium in DKA is highly variable; while it is often low (pseudohyponatremia due to osmotic shifts), it can be normal or even high depending on the degree of water loss [3]. **Analysis of Options:** * **Option B (True):** HHS occurs primarily in Type 2 DM. These patients have enough residual insulin to prevent lipolysis/ketogenesis but not enough to prevent extreme hyperglycemia and osmotic diuresis. * **Option C (Variable):** In DKA, hyperglycemia draws water out of cells, diluting serum sodium. For every 100 mg/dL increase in glucose above 100 mg/dL, sodium decreases by approximately 1.6 mEq/L [3]. * **Option D (True):** According to ADA criteria, mild DKA is defined by a bicarbonate of 15-18 mEq/L, while moderate to severe DKA involves levels **<15 mEq/L**. **NEET-PG High-Yield Pearls:** 1. **DKA Triad:** Hyperglycemia (>250 mg/dL), Ketosis (ketonemia/ketonuria), and Metabolic Acidosis (pH <7.3, HCO3 <18). 2. **HHS Characteristics:** Glucose >600 mg/dL, Serum Osmolality >320 mOsm/kg, and absence of significant ketosis. 3. **Management Priority:** The first step in managing both DKA and HHS is **aggressive fluid resuscitation** (Normal Saline), followed by potassium correction and insulin infusion [2]. 4. **Potassium Paradox:** In DKA, total body potassium is depleted, but serum potassium may appear normal or high due to the extracellular shift caused by acidosis [3]. Always check K+ before starting insulin.

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