Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 281: Which one of the following statements about non-insulin-dependent diabetes mellitus (NIDDM) is NOT true?

A. Circulating islet cell antibodies are usually found. (Correct Answer)
B. There is no HLA association.
C. Ketosis is rare.
D. Relative resistance to insulin is present.

Explanation: **Explanation:** Non-insulin-dependent diabetes mellitus (NIDDM), now commonly referred to as **Type 2 Diabetes Mellitus (T2DM)**, is characterized by peripheral insulin resistance and relative insulin deficiency rather than an autoimmune destruction of beta cells [2]. **Why Option A is the correct answer (The False Statement):** Circulating islet cell antibodies (ICAs), such as anti-GAD65, IA-2, or Zinc transporter 8 antibodies, are hallmarks of **Type 1 Diabetes Mellitus (T1DM)** [3]. They indicate an autoimmune process. In T2DM, these antibodies are typically **absent**. Their presence in an adult clinically diagnosed with T2DM often suggests **LADA** (Latent Autoimmune Diabetes in Adults). **Analysis of Incorrect Options:** * **Option B (No HLA association):** Unlike T1DM, which is strongly linked to HLA-DR3 and HLA-DR4, T2DM has no strong association with the HLA system [3]. It is linked to polygenic risk factors and lifestyle. * **Option C (Ketosis is rare):** In T2DM, there is usually enough endogenous insulin to suppress lipolysis and prevent the formation of ketone bodies [1]. Therefore, patients typically present with Hyperosmolar Hyperglycemic State (HHS) rather than Diabetic Ketoacidosis (DKA). * **Option D (Relative resistance to insulin):** This is the primary pathophysiology of T2DM [4]. Tissues (muscle, liver, fat) fail to respond adequately to insulin, requiring the pancreas to produce more until beta-cell exhaustion occurs [2]. **High-Yield NEET-PG Pearls:** * **Strongest Risk Factor for T2DM:** Obesity (central/visceral) [4]. * **Genetic Predisposition:** T2DM has a **stronger** genetic component (concordance in identical twins >90%) than T1DM (approx. 50%) [3]. * **Amyloid Deposition:** Histology of the pancreas in long-standing T2DM often shows **Amylin (Islet Amyloid Polypeptide)** deposits in the Islets of Langerhans.

Question 282: Hypertension with hyperkalemia is seen in which of the following conditions?

A. Conn's syndrome
B. Gordon's syndrome (Correct Answer)
C. Addison's disease
D. Renal failure

Explanation: **Explanation:** The combination of **hypertension and hyperkalemia** is a classic "high-yield" clinical scenario. Most hypertensive endocrine disorders involve excess mineralocorticoids, which typically cause hypokalemia [1]. **1. Why Gordon’s Syndrome is correct:** Also known as **Pseudohypoaldosteronism Type II**, this is a rare genetic disorder caused by mutations in WNK kinases. This leads to overactivity of the **Na-Cl cotransporter (NCC)** in the distal convoluted tubule. The increased reabsorption of sodium and chloride causes volume expansion (hypertension). Because less sodium reaches the collecting duct, there is decreased secretion of potassium and hydrogen ions, resulting in **hyperkalemia** and metabolic acidosis, despite low or normal aldosterone levels. **2. Why the other options are incorrect:** * **Conn’s Syndrome (Primary Hyperaldosteronism):** Characterized by hypertension with **hypokalemia** (due to aldosterone-mediated potassium wasting) [2]. * **Addison’s Disease:** While it features hyperkalemia (due to aldosterone deficiency), it is characterized by **hypotension**, not hypertension. * **Renal Failure:** While advanced renal failure causes hyperkalemia and hypertension, Gordon’s syndrome is the specific endocrine/genetic "spot diagnosis" tested in this context, especially when renal function (GFR) is otherwise relatively preserved. **Clinical Pearls for NEET-PG:** * **Gordon’s Syndrome** is essentially the "mirror image" of Gitelman syndrome. * **Treatment:** It responds remarkably well to **Thiazide diuretics**, which block the overactive NCC transporter. * **Liddle’s Syndrome:** Another cause of hypertension, but it causes **hypokalemia** (due to overactive ENaC channels). * **Rule of Thumb:** Hypertension + Hyperkalemia = Think Gordon’s Syndrome or Renal Artery Stenosis with Renal Failure.

Question 283: Which of the following is NOT used in the diagnosis of insulinoma?

A. 72-hour fasting blood glucose levels
B. C-peptide levels
C. Insulin/glucose ratio
D. D-xylose test (Correct Answer)

Explanation: The diagnosis of **Insulinoma** (an insulin-secreting pancreatic islet cell tumor) relies on demonstrating endogenous hyperinsulinemic hypoglycemia [1]. **Why D-xylose test is the correct answer:** The **D-xylose test** is a diagnostic tool used to evaluate the absorptive capacity of the proximal small intestine. It is primarily used to differentiate between malabsorption caused by intestinal mucosal disease (e.g., Celiac disease) and malabsorption due to pancreatic enzyme deficiency. It has no physiological or clinical relevance to glucose metabolism or insulin secretion. **Analysis of other options:** * **72-hour fasting blood glucose:** This is the **gold standard** provocative test for insulinoma. Patients are fasted until they develop symptoms of hypoglycemia (Whipple’s triad), at which point blood is drawn for glucose, insulin, and C-peptide [1]. * **C-peptide levels:** Insulinomas secrete insulin and C-peptide in equimolar amounts. High C-peptide levels during hypoglycemia help distinguish insulinoma from **factitious insulin injection** (where C-peptide would be suppressed) [1]. * **Insulin/glucose ratio:** In normal individuals, insulin levels fall as glucose falls. In insulinoma, the ratio is inappropriately high (typically **>0.3**). **Clinical Pearls for NEET-PG:** * **Whipple’s Triad:** 1. Symptoms of hypoglycemia, 2. Low plasma glucose (<55 mg/dL), 3. Relief of symptoms after glucose administration. * **Biochemical Diagnosis:** Glucose <55 mg/dL, Insulin ≥3 μU/mL, C-peptide ≥0.6 ng/mL, and Proinsulin ≥5.0 pmol/L. * **Localization:** Endoscopic Ultrasound (EUS) is the most sensitive imaging modality for localizing the tumor. * **Association:** 10% of insulinomas are associated with **MEN-1 syndrome**.

Question 284: Hypercholesterolemia is commonly associated with which of the following?

A. Diabetes mellitus
B. Hypothyroidism
C. Nephrotic syndrome
D. All of the above (Correct Answer)

Explanation: Hypercholesterolemia is a common feature of several metabolic and systemic disorders. The correct answer is **All of the above** because each condition disrupts lipid metabolism through distinct pathophysiological mechanisms. ### **Pathophysiology of Hypercholesterolemia:** 1. **Hypothyroidism:** This is one of the most common causes of secondary hyperlipidemia. Thyroid hormones normally increase the expression of **LDL receptors** on hepatocytes. In hypothyroidism, a deficiency of these receptors leads to decreased clearance of LDL from the plasma, resulting in elevated serum cholesterol levels. 2. **Diabetes Mellitus:** Insulin deficiency or resistance leads to increased lipolysis in adipose tissue, flooding the liver with free fatty acids. This results in increased production of VLDL [2]. Furthermore, insulin is required for the activity of **Lipoprotein Lipase (LPL)**; its deficiency impairs the clearance of triglyceride-rich lipoproteins, often leading to a "diabetic dyslipidemia" characterized by high triglycerides and low HDL, but frequently accompanied by elevated LDL/Total Cholesterol [1]. 3. **Nephrotic Syndrome:** The liver compensates for the massive urinary loss of albumin by increasing the synthesis of all proteins, including **apolipoproteins (Apo-B)**. This leads to an overproduction of VLDL and LDL. Additionally, there is decreased catabolism of these lipoproteins due to reduced plasma levels of LPL. ### **NEET-PG High-Yield Pearls:** * **Most common lipid abnormality in Hypothyroidism:** Hypercholesterolemia (Type IIa or IIb phenotype). * **Most common lipid abnormality in Diabetes:** Hypertriglyceridemia [4]. * **Clinical Sign:** Look for **Xanthelasma** or **Xanthomas** in patients with severe secondary hyperlipidemia [3], [4]. * **Rule of Thumb:** Always screen for TSH and urinary protein before starting a patient on long-term statin therapy to rule out these reversible secondary causes.

Question 285: Dehydration in ketoacidosis is best treated with?

A. Isolyte P
B. Isolyte M
C. Normal saline (Correct Answer)
D. Molar 1/6 lactate

Explanation: **Explanation:** In Diabetic Ketoacidosis (DKA), the primary goal of fluid resuscitation is to restore intravascular volume, improve renal perfusion to clear ketones, and correct electrolyte imbalances. [1] **Why Normal Saline (0.9% NaCl) is the correct answer:** Normal saline is an **isotonic crystalloid** and is the fluid of choice for initial volume replacement in DKA. [2] Patients in DKA typically have a fluid deficit of 3–6 liters. [1] Normal saline effectively expands the extracellular fluid (ECF) volume, stabilizes hemodynamics, and addresses the profound dehydration caused by osmotic diuresis. [4] Once blood glucose levels drop to approximately 200–250 mg/dL, the fluid is usually switched to 5% Dextrose with 0.45% NaCl to prevent hypoglycemia and cerebral edema while continuing insulin infusion to close the anion gap. [2] **Why other options are incorrect:** * **Isolyte P & Isolyte M:** These are maintenance fluids containing lower concentrations of sodium and higher concentrations of potassium or dextrose. They are **hypotonic** compared to plasma and are inappropriate for rapid volume expansion in an emergency like DKA. * **Molar 1/6 Lactate:** This is typically used to treat metabolic acidosis (like sodium bicarbonate). However, in DKA, the acidosis is corrected by insulin (which stops ketone production) and fluid resuscitation. Using lactate or bicarbonate is generally avoided unless the pH is <6.9, as it can cause rebound alkalosis and worsen hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Fluid Rate:** Usually 1 liter of 0.9% NaCl in the first hour. [2] * **The "Rule of 50":** If blood glucose falls below 250 mg/dL, add 5% Dextrose. [2] * **Potassium Management:** Always check potassium levels before starting insulin; if K+ < 3.3 mEq/L, hold insulin and replace potassium first to avoid life-threatening arrhythmias. [2] * **Most common cause of death in children with DKA:** Cerebral edema (often due to over-aggressive fluid resuscitation). [3]

Question 286: Which disorder is associated with thyrotoxicosis but not with hyperthyroidism?

A. Graves disease
B. Hyperfunctioning ("toxic") multinodular goiter
C. Iodine-induced hyperthyroidism
D. De Quervain thyroiditis (Correct Answer)

Explanation: ### Explanation The key to answering this question lies in the physiological distinction between **thyrotoxicosis** and **hyperthyroidism**: * **Thyrotoxicosis:** A clinical state resulting from inappropriate high levels of circulating thyroid hormones ($T_3$ and $T_4$), regardless of the source. * **Hyperthyroidism:** A specific subset of thyrotoxicosis caused by **excessive synthesis and secretion** of hormones by the thyroid gland itself (hyperfunction). #### Why De Quervain Thyroiditis is Correct In **De Quervain (Subacute Granulomatous) Thyroiditis**, the thyroid gland is damaged by an inflammatory process (often post-viral). This inflammation causes the **leakage** of pre-formed thyroid hormones from the follicles into the bloodstream [1]. Because the gland is not overproducing hormone—but rather leaking stored hormone—it is a form of thyrotoxicosis **without** hyperthyroidism [2]. A hallmark of this condition is a **low radioactive iodine uptake (RAIU)** scan, as the damaged follicular cells cannot trap iodine [1], [2]. #### Why the Other Options are Incorrect * **A. Graves Disease:** The most common cause of hyperthyroidism. It involves TSH-receptor antibodies that stimulate the gland to synthesize and secrete excess hormone [3]. * **B. Toxic Multinodular Goiter (TMNG):** Characterized by autonomous nodules that overproduce thyroid hormones independently of TSH. * **C. Iodine-induced Hyperthyroidism (Jod-Basedow phenomenon):** Occurs when an iodine load (e.g., contrast or amiodarone) provides the substrate for a latent autonomous gland to synthesize excess hormone. #### NEET-PG High-Yield Pearls * **Thyrotoxicosis with Low RAIU:** Think Subacute thyroiditis, Factitious thyrotoxicosis (exogenous intake), or Struma ovarii [1], [2]. * **Thyrotoxicosis with High RAIU:** Think Graves disease, TMNG, or Toxic Adenoma. * **De Quervain Clinical Triad:** Painful/tender thyroid gland, raised ESR, and a preceding viral upper respiratory infection [1]. * **Treatment of De Quervain:** NSAIDs or steroids for pain/inflammation; Beta-blockers for symptoms [1]. Anti-thyroid drugs (PTU/Methimazole) are **ineffective** because there is no excess synthesis [1].

Question 287: Sarcodiosis can be associated with which of the following?

A. Cranial diabetes insipidus (Correct Answer)
B. Psychogenic polydypsia
C. Nephrogenic diabetes insipidus
D. Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Explanation: **Explanation:** Sarcoidosis is a multisystem granulomatous disease characterized by the formation of non-caseating granulomas. When it involves the Central Nervous System (Neurosarcoidosis), it has a predilection for the **hypothalamus and the posterior pituitary gland**. **1. Why Cranial Diabetes Insipidus (CDI) is correct:** Infiltrative granulomas in the hypothalamus or the pituitary stalk interfere with the synthesis or transport of Antidiuretic Hormone (ADH/Vasopressin). This deficiency leads to the inability of the kidneys to concentrate urine, resulting in polyuria and polydipsia [1]. CDI is the most common endocrine manifestation of neurosarcoidosis. **2. Why the other options are incorrect:** * **Psychogenic Polydipsia:** This is a primary psychiatric disorder characterized by excessive water intake. While it mimics DI symptoms, it is not caused by the granulomatous infiltration seen in sarcoidosis. In primary polydipsia, plasma osmolality is typically low, and administering DDAVP carries a risk of water intoxication [1]. * **Nephrogenic Diabetes Insipidus:** This occurs when the kidneys are resistant to ADH. While hypercalcemia (common in sarcoidosis) can cause a mild form of nephrogenic DI [1], the direct involvement of the disease process in sarcoidosis is classically associated with the central/cranial mechanism. * **SIADH:** This involves excessive ADH secretion. Sarcoidosis typically causes a *deficiency* of ADH due to tissue destruction, rather than an excess. **Clinical Pearls for NEET-PG:** * **Hypercalcemia in Sarcoidosis:** Caused by increased 1-alpha-hydroxylase activity in macrophages, leading to elevated levels of 1,25-dihydroxyvitamin D. * **Lofgren’s Syndrome:** A classic triad of Erythema nodosum, bilateral hilar adenopathy, and arthralgia. * **Heerfordt’s Syndrome (Uveoparotid fever):** Parotid enlargement, facial nerve palsy, and anterior uveitis. * **Diagnosis:** Elevated Serum ACE levels and "naked" non-caseating granulomas on biopsy.

Question 288: Which of the following agents is the drug of choice for Central Diabetes Insipidus?

A. Desmopressin (Correct Answer)
B. Demeclocycline
C. Thiazide Diuretics
D. Lithium

Explanation: **Explanation:** **Central Diabetes Insipidus (CDI)** is characterized by a deficiency in the synthesis or release of Antidiuretic Hormone (ADH/Vasopressin) from the posterior pituitary. This leads to the inability to concentrate urine, resulting in polyuria and polydipsia [1]. **Why Desmopressin (dDAVP) is the Drug of Choice:** Desmopressin is a synthetic analogue of vasopressin. It is highly selective for **V2 receptors** located in the renal collecting ducts, which mediate the antidiuretic effect [2]. Unlike natural vasopressin, it has minimal activity at V1 receptors (which cause vasoconstriction), making it safer and more potent for long-term use [2]. It can be administered intranasally, orally, or parenterally [1]. **Analysis of Incorrect Options:** * **B. Demeclocycline:** This is a tetracycline derivative that induces a state of nephrogenic DI by inhibiting ADH action in the kidney. It is used to treat **SIADH**, not CDI. * **C. Thiazide Diuretics:** While used in *Nephrogenic* DI to create mild hypovolemia (leading to increased proximal water reabsorption), they are not the first-line treatment for CDI. * **D. Lithium:** This is a common **cause** of drug-induced Nephrogenic DI; it is never used as a treatment. **NEET-PG High-Yield Pearls:** * **Water Deprivation Test:** In CDI, urine osmolality increases by >50% after exogenous ADH administration. In Nephrogenic DI, there is little to no response [1]. * **Drug of Choice for Nephrogenic DI:** Amiloride (especially if lithium-induced) or Thiazides. * **Chlorpropamide & Carbamazepine:** These can be used in partial CDI as they sensitize the kidney to remaining ADH or stimulate ADH release. * **Pregnancy:** Desmopressin is the preferred agent for DI in pregnancy as it is resistant to degradation by placental vasopressinase.

Question 289: All of the following conditions cause SIADH, except?

A. Lung abscess
B. Thymoma
C. Carcinoma of pancreas
D. Interstitial nephritis (Correct Answer)

Explanation: **Explanation:** The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by the excessive release of ADH, leading to water retention and dilutional hyponatremia [2]. **Why Interstitial Nephritis is the correct answer:** Interstitial nephritis is a cause of **Nephrogenic Diabetes Insipidus (NDI)**, not SIADH [1]. In interstitial nephritis, the renal tubules become damaged and resistant to the action of ADH. This results in the inability to concentrate urine, leading to polyuria and potential hypernatremia—the physiological opposite of SIADH. **Analysis of Incorrect Options:** * **Lung Abscess:** Pulmonary infections (abscess, pneumonia, tuberculosis) are classic triggers for SIADH [2]. The exact mechanism is unclear but is thought to involve localized hypoxia or inflammation stimulating the posterior pituitary. * **Thymoma:** Certain tumors, particularly those in the chest like thymomas and lymphomas, can cause ectopic ADH production or stimulate the neurohypophysis. * **Carcinoma of Pancreas:** This is a recognized cause of ectopic ADH secretion. While Small Cell Lung Cancer (SCLC) is the most common neoplastic cause (75%), other GI and GU malignancies like pancreatic cancer can also secrete ADH. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of SIADH:** Small Cell Carcinoma of the Lung. * **Diagnostic Criteria:** Euvolemic hyponatremia [2], low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg). * **Drug-induced SIADH:** Remember the "Cs": Cyclophosphamide, Carbamazepine, and Chlorpropamide. * **Treatment:** Fluid restriction is the first-line treatment. For severe symptomatic cases, use hypertonic saline (3%) with caution to avoid **Osmotic Demyelination Syndrome**.

Question 290: A young lady presents with tremors, diarrhea, and elevated T4. TSH levels were 8.5 mIU/L. Further examination reveals bi-temporal hemianopia. What is the next step in management?

A. Start anti-thyroid drugs and do urgent MRI Brain (Correct Answer)
B. Start beta blockers
C. Conservative management
D. Start anti-thyroid drugs and wait for symptoms to resolve

Explanation: ### Explanation This clinical scenario describes a rare but classic presentation of a **TSH-secreting pituitary adenoma (Thyrotropinoma)**. **1. Why Option A is Correct:** The patient has biochemical hyperthyroidism (elevated T4, tremors, diarrhea) but an **inappropriately normal or elevated TSH** (8.5 mIU/L). Normally, high T4 should suppress TSH to near-zero levels via negative feedback. An elevated TSH in the presence of high T4 suggests either a TSH-secreting tumor or Thyroid Hormone Resistance (RTH). The presence of **bi-temporal hemianopia** (compression of the optic chiasm) confirms a pituitary mass effect [1]. Management requires controlling the thyrotoxicosis with **anti-thyroid drugs** (to achieve euthyroidism before surgery) and an **urgent MRI Brain** to visualize the adenoma and plan neurosurgical intervention [2]. Urgent treatment is required if there is evidence of pressure on visual pathways [2]. **2. Why Other Options are Incorrect:** * **Option B:** Beta-blockers provide symptomatic relief but do not address the underlying pituitary pathology or the risk of permanent vision loss. * **Option C:** Conservative management is contraindicated as the tumor is causing neurological deficits (visual field loss) [2]. * **Option D:** Waiting for symptoms to resolve is dangerous; the tumor may continue to expand, leading to irreversible optic nerve damage [2]. **3. NEET-PG High-Yield Pearls:** * **Differential for High T4 + High TSH:** TSH-oma vs. Resistance to Thyroid Hormone (RTH). * **Distinguishing Feature:** TSH-omas usually have an elevated **alpha-subunit** level and evidence of a mass on MRI [1], whereas RTH is often familial and lacks mass effect. * **Visual Deficit:** Bi-temporal hemianopia is the hallmark of a pituitary macroadenoma (>10mm) compressing the optic chiasm [1]. * **Treatment of Choice:** Transsphenoidal surgery (TSS) is the definitive treatment for TSH-omas. Somatostatin analogues (Octreotide) can also be used to shrink the tumor and normalize TSH.

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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