Endocrinology — MCQs

A 19-year-old man presents with early fatigue and muscle cramps during sports. He is asymptomatic during walking or less intense activities. Physical examination and vital signs are normal. Muscle bulk, tone, and strength in proximal muscles are normal, with no fatigue during repetitive arm grip exercises. Following an exercise stress test, his serum creatine kinase (CK) is elevated, and lactate level is normal. Which of the following is the most likely diagnosis?

Q1253Medium

A 52-year-old alcoholic presents with a skin rash on his chest, diarrhea, and abdominal pain. Examination reveals a scaly and pigmented rash on sun-exposed areas, a soft abdomen, and impaired short-term memory. The patient exhibits dermatitis, diarrhea, and dementia syndrome. What is the most likely diagnosis for this patient's vitamin deficiency or excess?

Q1254Medium

All of the following drugs alter calcium hemostasis except-

Q1255Medium

Hypoglycemia is a recognized feature of all of the following conditions, except?

Q1256Medium

Tumor-induced hypoglycemia is seen in all of the following EXCEPT:

Q1257Medium

Syndrome of apparent mineralocorticoid excess is due to?

Q1258Easy

In thyrotoxicosis, which of the following is NOT controlled by beta-blockers?

Q1259Easy

Which of the following is true about primary aldosteronism?

Q1260Easy

A patient with pheochromocytoma would secrete which of the following in a higher concentration?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1251: Thyrotoxic periodic paralysis leads to extreme muscle weakness due to?

A. Hypokalemia (Correct Answer)
B. Hypocalcemia
C. Hypomagnesemia
D. Hyponatremia

Explanation: **Thyrotoxic Periodic Paralysis (TPP)** is a rare but life-threatening complication of hyperthyroidism characterized by sudden episodes of extreme muscle weakness and **hypokalemia**. **Why Hypokalemia is the correct answer:** The pathophysiology involves an intracellular shift of potassium rather than a total body deficit. Excess thyroid hormones increase the activity of the **Na+/K+-ATPase pump**, which drives potassium from the extracellular fluid into the muscle cells. This leads to hyperpolarization of the muscle membrane, making it non-excitable and resulting in acute flaccid paralysis. This shift is often triggered by high carbohydrate meals (insulin also stimulates the Na+/K+ pump) or strenuous exercise. **Why other options are incorrect:** * **Hypocalcemia:** Typically presents with tetany, carpopedal spasm, and Chvostek/Trousseau signs, rather than periodic flaccid paralysis. * **Hypomagnesemia:** Often co-exists with hypokalemia but is not the primary driver of the paralytic episodes in thyrotoxicosis. * **Hyponatremia:** Usually presents with neurological symptoms like confusion, seizures, or coma due to cerebral edema, not focal or global muscle paralysis. **High-Yield Clinical Pearls for NEET-PG:** * **Demographics:** Most common in **Asian males**, despite hyperthyroidism being more common in females. * **Triggers:** High-carb meals, alcohol, and rest after heavy exercise. * **Management:** Propranolol (non-selective beta-blocker) is the treatment of choice as it reverses the overactivity of the Na+/K+ pump [1]. * **Caution:** Be careful with aggressive K+ replacement; as the episode resolves, potassium shifts back out of cells, leading to a risk of **rebound hyperkalemia**.

Question 1252: A 19-year-old man presents with early fatigue and muscle cramps during sports. He is asymptomatic during walking or less intense activities. Physical examination and vital signs are normal. Muscle bulk, tone, and strength in proximal muscles are normal, with no fatigue during repetitive arm grip exercises. Following an exercise stress test, his serum creatine kinase (CK) is elevated, and lactate level is normal. Which of the following is the most likely diagnosis?

A. Gaucher disease
B. Tay-Sachs disease
C. McArdle disease (glycogen storage disease) (Correct Answer)
D. Hemochromatosis

Explanation: The clinical presentation of exercise-induced fatigue, muscle cramps, and elevated creatine kinase (CK) with a **normal lactate response** is classic for **McArdle disease (Glycogen Storage Disease Type V)** [1]. **1. Why McArdle Disease is Correct:** McArdle disease is caused by a deficiency of **myophosphorylase**, the enzyme responsible for breaking down glycogen into glucose-1-phosphate in muscles. During high-intensity exercise, muscles rely on glycogenolysis for energy [2]. In its absence, patients experience "exercise intolerance" and cramps. A hallmark diagnostic finding is the **failure of blood lactate to rise** during an ischemic exercise test because the metabolic block prevents the conversion of glycogen to glucose, and subsequently to lactate [1]. The "second wind" phenomenon (improvement in symptoms after 10–15 minutes of exercise due to increased fatty acid delivery) is also characteristic. **2. Why Other Options are Incorrect:** * **Gaucher Disease:** A lysosomal storage disease (glucocerebrosidase deficiency) characterized by hepatosplenomegaly, bone pain (Erlenmeyer flask deformity), and cytopenias, not exercise-induced muscle cramps. * **Tay-Sachs Disease:** A neurodegenerative condition (hexosaminidase A deficiency) presenting in infancy with developmental regression, cherry-red spots on the macula, and seizures. * **Hemochromatosis:** An iron overload disorder leading to "bronze diabetes," cirrhosis, and cardiomyopathy. It does not typically present with acute exercise-induced muscle breakdown. **Clinical Pearls for NEET-PG:** * **Enzyme Defect:** Myophosphorylase (Muscle Phosphorylase) [1]. * **Biochemical Marker:** Flat lactate curve with a significant rise in ammonia during exercise. * **Key Symptom:** "Second Wind" phenomenon. * **Complication:** Risk of rhabdomyolysis and myoglobinuria (red-brown urine) after intense exertion.

Question 1253: A 52-year-old alcoholic presents with a skin rash on his chest, diarrhea, and abdominal pain. Examination reveals a scaly and pigmented rash on sun-exposed areas, a soft abdomen, and impaired short-term memory. The patient exhibits dermatitis, diarrhea, and dementia syndrome. What is the most likely diagnosis for this patient's vitamin deficiency or excess?

A. niacin (Correct Answer)
B. thiamine
C. pyridoxine
D. vitamin C

Explanation: ### Explanation The patient presents with the classic clinical triad of **Pellagra**: **Dermatitis, Diarrhea, and Dementia** (the "3 Ds") [1], [2]. This condition is caused by a deficiency of **Niacin (Vitamin B3)** [1]. **1. Why Niacin is Correct:** Niacin is a precursor to NAD and NADP, essential for redox reactions. Deficiency leads to impaired cellular repair in high-turnover tissues (skin and GI tract) and the brain. * **Dermatitis:** Characteristically occurs in sun-exposed areas (photosensitivity) [2]. A specific finding is **Casal’s necklace** (rash around the lower neck) [1]. * **Diarrhea:** Due to atrophy of the gastrointestinal columnar epithelium [1]. * **Dementia:** Presents as memory loss, disorientation, or encephalopathy [1]. * **Risk Factors:** Chronic alcoholism (due to poor diet and impaired absorption) and diets dependent on corn/maize (which lacks bioavailable niacin and tryptophan). **2. Why the Other Options are Incorrect:** * **Thiamine (B1):** Deficiency causes **Beriberi** (wet/dry) or **Wernicke-Korsakoff syndrome** [3]. While common in alcoholics, it presents with ophthalmoplegia, ataxia, and high-output heart failure, not a photosensitive rash. * **Pyridoxine (B6):** Deficiency causes peripheral neuropathy, sideroblastic anemia, and seborrheic dermatitis, but not the classic triad of pellagra. (Note: B6 is required to convert Tryptophan to Niacin) [2]. * **Vitamin C:** Deficiency causes **Scurvy**, characterized by perifollicular hemorrhages, bleeding gums, and "corkscrew" hairs. **NEET-PG High-Yield Pearls:** * **The 4th D:** If untreated, Pellagra leads to **Death** [2]. * **Tryptophan Connection:** Niacin is synthesized from the amino acid Tryptophan. Conditions like **Hartnup disease** (impaired tryptophan absorption) or **Carcinoid syndrome** (diverts tryptophan to serotonin) can cause secondary Pellagra. * **Isoniazid (INH) Therapy:** This TB drug inhibits B6, which in turn prevents Niacin synthesis, potentially leading to Pellagra.

Question 1254: All of the following drugs alter calcium hemostasis except-

A. Fluoride
B. Indomethacin (Correct Answer)
C. Mithramycin
D. Thiazides

Explanation: Calcium homeostasis is a tightly regulated process involving bone resorption, renal excretion, and intestinal absorption [1]. The correct answer is **Indomethacin**, as it does not have a primary or clinically significant effect on systemic calcium levels. **1. Why Indomethacin is the Correct Answer:** Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) that acts by inhibiting cyclooxygenase (COX) enzymes. **2. Analysis of Incorrect Options:** * **Fluoride:** It is a potent stimulator of osteoblasts. Chronic exposure (fluorosis) leads to increased bone density and can cause **hypocalcemia** as calcium is rapidly deposited into the newly formed bone matrix. * **Mithramycin (Plicamycin):** This is a cytotoxic antibiotic that inhibits osteoclast activity. It was historically used as a potent agent to lower serum calcium in cases of **hypercalcemia of malignancy**. * **Thiazides:** These diuretics increase distal renal tubular calcium reabsorption [1]. They are a well-known cause of **mild hypercalcemia** and are therapeutically used to reduce hypercalciuria in patients with recurrent calcium stones. **Clinical Pearls for NEET-PG:** * **Thiazides** cause **Hyper**calcemia, whereas **Loop diuretics** (Furosemide) cause **Hypo**calcemia ("Loops lose calcium"). * **Mithramycin** is rarely used today due to hepatotoxicity and thrombocytopenia, replaced by Bisphosphonates and Denosumab. * **Vitamin D toxicity, Sarcoidosis, and Lithium** are other high-yield causes of drug/disease-induced hypercalcemia.

Question 1255: Hypoglycemia is a recognized feature of all of the following conditions, except?

A. Uremia
B. Acromegaly (Correct Answer)
C. Addison's disease
D. Hepatocellular failure

Explanation: The correct answer is **Acromegaly**. **1. Why Acromegaly is the correct answer:** Acromegaly is characterized by an excess of **Growth Hormone (GH)**. GH is a potent **counter-regulatory hormone** that antagonizes the action of insulin [1]. It stimulates gluconeogenesis and reduces peripheral glucose uptake, leading to **hyperglycemia** and glucose intolerance (Diabetes Mellitus occurs in ~25% of patients). Therefore, it causes high blood sugar, not hypoglycemia. **2. Why the other options are incorrect:** * **Addison’s Disease (Primary Adrenal Insufficiency):** Glucocorticoids (cortisol) are essential for gluconeogenesis [1]. A deficiency in cortisol leads to impaired glucose production and increased insulin sensitivity, frequently resulting in **fasting hypoglycemia**. * **Hepatocellular Failure:** The liver is the primary site for glycogen storage (glycogenolysis) and de novo glucose synthesis (gluconeogenesis) [1]. In severe liver failure, these processes are compromised, and the liver cannot maintain blood glucose levels, leading to profound hypoglycemia. * **Uremia (Chronic Kidney Disease):** Hypoglycemia in uremia is multifactorial. It occurs due to reduced renal clearance of insulin, impaired renal gluconeogenesis (the kidney contributes ~20% of glucose production), and often associated malnutrition or "dialysis-induced" factors [2]. **Clinical Pearls for NEET-PG:** * **Growth Hormone vs. Insulin:** GH is "diabetogenic." Conversely, GH deficiency (e.g., in Sheehan’s syndrome or Panhypopituitarism) is a classic cause of hypoglycemia. * **Critical Organs for Glucose:** Always consider the **Liver** (production), **Kidney** (gluconeogenesis/insulin clearance), and **Adrenals** (cortisol/epinephrine) when evaluating a patient with unexplained hypoglycemia. * **IGF-1 Note:** While IGF-1 has insulin-like structural properties, in Acromegaly, the hyperglycemic effect of GH dominates. Non-islet cell tumor hypoglycemia (NICTH) is caused by "Big-IGF-2," not GH [2].

Question 1256: Tumor-induced hypoglycemia is seen in all of the following EXCEPT:

A. Mesenchymal tumors
B. Hepatocellular carcinoma
C. Adrenal carcinoma
D. Lymphoma (Correct Answer)

Explanation: Tumor-induced hypoglycemia (TIH) primarily occurs through the production of **"Big" IGF-II** (Insulin-like Growth Factor II). This is a high-molecular-weight precursor that, unlike normal IGF-II, does not bind well to carrier proteins. It freely binds to insulin receptors, leading to increased glucose utilization and suppressed gluconeogenesis, a phenomenon known as **Non-Islet Cell Tumor Hypoglycemia (NICTH).** **Why Lymphoma is the Correct Answer:** While lymphomas can occasionally cause hypoglycemia through massive glucose consumption or cytokine release, they are **not** classically associated with the "Big" IGF-II mechanism that defines typical tumor-induced hypoglycemia. In the context of standard medical examinations, lymphoma is the outlier compared to the classic solid tumors listed. **Analysis of Incorrect Options:** * **Mesenchymal Tumors:** These are the most common cause of NICTH (e.g., Solitary Fibrous Tumors, Hemangiopericytomas, and Fibrosarcomas) [1]. They characteristically secrete "Big" IGF-II. * **Hepatocellular Carcinoma (HCC):** HCC is a well-known cause of paraneoplastic hypoglycemia, occurring via IGF-II secretion or, in end-stage disease, due to massive destruction of liver parenchyma (impaired gluconeogenesis) [1]. * **Adrenal Carcinoma:** Large adrenocortical carcinomas are documented secretors of IGF-II precursors, leading to significant clinical hypoglycemia. **NEET-PG High-Yield Pearls:** * **Mechanism:** The "Big" IGF-II suppresses both Insulin and Growth Hormone (GH) levels. The principal circulating somatomedins are IGF-I and IGF-II, which are closely related to insulin [3]. * **Diagnosis:** Low blood glucose + Low Insulin + Low C-peptide + **Low IGF-I** + **High IGF-II:IGF-I ratio** (>10:1). Measurement of insulin and C-peptide concentrations during an episode is helpful in determining the underlying cause [2]. * **Treatment:** The definitive treatment is surgical resection of the tumor. Glucocorticoids or GH can be used for symptomatic management to increase hepatic glucose output [4].

Question 1257: Syndrome of apparent mineralocorticoid excess is due to?

A. Increased aldosterone production
B. Lack of inactivation of aldosterone
C. Increased cortisol production
D. Lack of inactivation of cortisol to cortisone (Correct Answer)

Explanation: Syndrome of Apparent Mineralocorticoid Excess (SAME) is a genetic or acquired condition characterized by hypertension, hypokalemia, and metabolic alkalosis, despite having low plasma renin and low aldosterone levels. 1. Why the correct answer is right: The mineralocorticoid receptor (MR) in the distal tubule has an equal affinity for both aldosterone and cortisol. Under normal physiological conditions, the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) converts active cortisol into inactive cortisone [1]. This ensures that only aldosterone can activate the MR. In SAME, there is a deficiency or inhibition of 11β-HSD2. Consequently, cortisol is not inactivated; it floods the MR, mimicking the effects of aldosterone (mineralocorticoid excess) despite aldosterone levels being suppressed. 2. Why other options are wrong: * A & B: In SAME, aldosterone levels are actually suppressed (low) due to the negative feedback loop caused by the cortisol-induced volume expansion and hypertension. * C: Increased cortisol production is characteristic of Cushing’s Syndrome. While severe Cushing’s can overwhelm the 11β-HSD2 enzyme, SAME specifically refers to the failure of the inactivation process rather than primary overproduction. 3. NEET-PG High-Yield Pearls: * Etiology: Autosomal recessive mutation in the HSD11B2 gene or acquired via Licorice ingestion (Glycyrrhetinic acid inhibits 11β-HSD2). * Biochemical Marker: An increased ratio of Urinary Cortisol to Urinary Cortisone (THF+αTHF/THE). * Treatment: Potassium-sparing diuretics (Spironolactone or Eplerenone) or low-dose glucocorticoids (to suppress ACTH and endogenous cortisol production). * Differential: Liddle’s Syndrome also presents with low renin/aldosterone but is due to a gain-of-function mutation in the ENaC channel.

Question 1258: In thyrotoxicosis, which of the following is NOT controlled by beta-blockers?

A. Anxiety
B. Tremors
C. Tachycardia
D. Oxygen consumption (Correct Answer)

Explanation: Explanation: In thyrotoxicosis, the clinical manifestations arise from two distinct mechanisms: **increased sympathetic (adrenergic) activity** and a **hypermetabolic state** caused by direct action of thyroid hormones ($T_3$ and $T_4$) on tissues. **1. Why Oxygen Consumption is the Correct Answer:** Beta-blockers (like Propranolol) act by antagonizing $\beta$-adrenergic receptors. While they effectively mitigate the symptoms of sympathetic overactivity, they have **no effect on the basal metabolic rate (BMR)** or the direct calorigenic effects of thyroid hormones [2,3]. Increased oxygen consumption is a result of thyroid hormone-induced stimulation of $Na^+/K^+$ ATPase activity and mitochondrial respiration [4]. Since this is a direct metabolic effect and not mediated by catecholamines, beta-blockers cannot control it. **2. Why the other options are incorrect:** * **Anxiety and Tremors:** These are neurological manifestations of increased $\beta$-adrenergic sensitivity [3]. Beta-blockers cross the blood-brain barrier (especially Propranolol) and block peripheral receptors to effectively reduce these symptoms [1]. * **Tachycardia:** This is driven by increased $\beta_1$ receptor expression in the myocardium [4]. Beta-blockers are the first-line treatment to rapidly control heart rate in thyrotoxic patients [1]. **Clinical Pearls for NEET-PG:** * **Drug of Choice:** Propranolol is preferred in thyrotoxic crisis (thyroid storm) because, in high doses, it also inhibits the **peripheral conversion of $T_4$ to $T_3$** (by inhibiting 5'-deiodinase). * **Contraindication:** Avoid beta-blockers in patients with thyrotoxicosis who have co-existing **asthma**; use cardioselective agents (e.g., Atenolol) or Calcium Channel Blockers (Diltiazem) instead. * **Key Concept:** Beta-blockers provide **symptomatic relief** but do not treat the underlying hyperthyroidism [1].

Question 1259: Which of the following is true about primary aldosteronism?

A. Pedal edema
B. Increased renin
C. Increased sodium reabsorption (Correct Answer)
D. All of the above

Explanation: Primary Aldosteronism (Conn’s Syndrome) is characterized by the autonomous overproduction of aldosterone from the adrenal cortex, independent of the renin-angiotensin system. ### Explanation of Options * Correct Answer: C (Increased sodium reabsorption) Aldosterone acts on the principal cells of the distal convoluted tubule and collecting duct. It increases the expression of apical epithelial sodium channels (ENaC) and the basolateral Na+/K+ ATPase pump [1]. This leads to increased sodium reabsorption and water retention, resulting in hypertension. * Incorrect: A (Pedal edema) Despite significant sodium and water retention, patients with primary aldosteronism rarely present with edema. This is due to the "Aldosterone Escape" phenomenon: the initial volume expansion triggers the release of Atrial Natriuretic Peptide (ANP), which promotes pressure natriuresis, preventing overt fluid overload and edema [1, 2]. * Incorrect: B (Increased renin) In primary aldosteronism, the high levels of aldosterone cause volume expansion and hypertension, which provide negative feedback to the juxtaglomerular apparatus [2]. This results in suppressed (low) plasma renin activity. A high Aldosterone-to-Renin Ratio (ARR) is the classic screening tool. ### High-Yield Clinical Pearls for NEET-PG * Classic Triad: Hypertension, Hypokalemia, and Metabolic Alkalosis [1]. * Screening Test: Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio > 20-30. * Confirmatory Test: Saline infusion test (failure to suppress aldosterone) or Oral salt loading test. * Most Common Cause: Adrenal Adenoma (Conn’s Syndrome), followed by Bilateral Adrenal Hyperplasia. * Treatment: Surgical resection for unilateral adenoma; Spironolactone (Aldosterone antagonist) for bilateral hyperplasia.

Question 1260: A patient with pheochromocytoma would secrete which of the following in a higher concentration?

A. Norepinephrine (Correct Answer)
B. Epinephrine
C. Dopamine
D. VMA

Explanation: Explanation: Pheochromocytoma is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla. Understanding the biosynthetic pathway of catecholamines is key to identifying the primary secretion. **1. Why Norepinephrine is Correct:** In the normal adrenal medulla, approximately 80% of secretion is Epinephrine and 20% is Norepinephrine [1]. However, in **Pheochromocytoma**, this ratio is reversed. Most pheochromocytomas predominantly secrete **Norepinephrine**. This occurs because these tumors often lack the enzyme **Phenylethanolamine N-methyltransferase (PNMT)**, which is required to convert norepinephrine into epinephrine [2]. PNMT induction requires high local concentrations of cortisol (from the adrenal cortex); since tumor cells may lose this paracrine regulation, they primarily release norepinephrine [2]. **2. Analysis of Incorrect Options:** * **B. Epinephrine:** While some tumors secrete epinephrine (especially those associated with MEN 2 syndrome), it is less common than norepinephrine secretion. Pure epinephrine secretion suggests a tumor localized strictly to the adrenal medulla. * **C. Dopamine:** Rare; dopamine-secreting tumors are more frequently associated with extra-adrenal paragangliomas or malignant pheochromocytomas. * **D. VMA (Vanillylmandelic Acid):** VMA is a metabolic end-product of catecholamines excreted in the urine. While VMA levels are elevated, the question asks for what the tumor *secretes*. The tumor secretes catecholamines, which are then metabolized into VMA by the liver and kidneys. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paraganglioma). * **Diagnosis:** Best initial screening test is **Plasma free metanephrines**; most sensitive confirmatory test is **24-hour urinary metanephrines**. * **Management:** Always give **Alpha-blockers (Phenoxybenzamine)** before Beta-blockers to avoid a hypertensive crisis (unopposed alpha-stimulation).

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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