Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 151: Gynecomastia is seen in all of the following conditions except?

A. Klinefelter's syndrome
B. Liver failure
C. Kidney failure (Correct Answer)
D. Leprosy

Explanation: **Explanation:** Gynecomastia is the benign proliferation of glandular breast tissue in males, primarily caused by an imbalance between estrogen and androgen action [1]. **Why Kidney Failure is the correct answer:** While chronic kidney disease (CKD) can cause transient gynecomastia during the "refeeding" phase of dialysis, it is **not** a classic or primary feature of kidney failure itself. In fact, uremia in kidney failure typically leads to hypogonadism and decreased libido, but the high levels of prolactin and metabolic disturbances usually do not manifest as overt gynecomastia unless associated with specific drug therapies (like Spironolactone for fluid overload). **Analysis of Incorrect Options:** * **Klinefelter’s Syndrome (47, XXY):** This is a classic cause [2]. The primary testicular failure leads to low testosterone and high LH/FSH. The increased LH stimulates aromatase activity in Leydig cells, converting precursors to estrogen, leading to a high Estrogen:Androgen ratio [3]. * **Liver Failure:** Cirrhosis leads to gynecomastia via two mechanisms: 1) Decreased hepatic clearance of androstenedione (which is peripherally converted to estrone) and 2) Increased production of Sex Hormone Binding Globulin (SHBG), which binds testosterone more tightly than estrogen, increasing free estrogen levels. * **Leprosy:** Specifically **Lepromatous Leprosy** causes gynecomastia due to direct testicular invasion by *Mycobacterium leprae* (orchitis), leading to primary testicular failure and subsequent androgen deficiency [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common physiological cause:** Puberty (usually resolves within 1–2 years) [1]. * **Drug-induced gynecomastia (Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone, **C**imetidine, **O**estrogens/Ketoconazole. * **Spironolactone** is the most common drug cause (blocks androgen receptors and inhibits testosterone synthesis). * **Distinction:** True gynecomastia (glandular tissue) must be differentiated from **pseudogynecomastia** (fat deposition seen in obese males) [1].

Question 152: What is the treatment of choice for secondary hyperaldosteronism?

A. Drug management (Correct Answer)
B. Unilateral adrenalectomy
C. Both
D. None

Explanation: In secondary hyperaldosteronism, the overproduction of aldosterone is driven by an external stimulus—most commonly the activation of the **Renin-Angiotensin-Aldosterone System (RAAS)** due to decreased renal perfusion (e.g., renal artery stenosis, heart failure, or cirrhosis) [1], [2]. ### **Explanation of Options** * **A. Drug Management (Correct):** Since the pathology is extrinsic to the adrenal gland, the treatment focuses on managing the underlying cause and blocking the effects of aldosterone [1]. **Mineralocorticoid Receptor Antagonists (MRAs)** like **Spironolactone** or **Eplerenone** are the mainstays. They counteract the salt and water retention caused by excess aldosterone. In cases like renal artery stenosis, ACE inhibitors or ARBs may also be used to block the RAAS cascade [1]. * **B. Unilateral Adrenalectomy (Incorrect):** This is the treatment of choice for **Primary Hyperaldosteronism (Conn’s Syndrome)** caused by a unilateral aldosterone-producing adenoma. In secondary hyperaldosteronism, the adrenal glands are usually structurally normal or show bilateral hyperplasia; removing one gland will not address the underlying systemic stimulus (high renin). * **C & D (Incorrect):** Based on the physiological mechanism, surgical intervention is not the standard of care for secondary causes. ### **High-Yield Clinical Pearls for NEET-PG** 1. **The Renin Key:** The hallmark differentiator is **Renin levels** [2]. * *Primary Hyperaldosteronism:* Low Renin (due to feedback inhibition). * *Secondary Hyperaldosteronism:* High Renin (the driver of the condition). 2. **Bartter and Gitelman Syndromes:** These are important genetic causes of secondary hyperaldosteronism characterized by hypokalemic metabolic alkalosis with normal to low blood pressure. 3. **Spironolactone Side Effects:** Be mindful of gynecomastia and decreased libido in males (due to non-specific binding to androgen receptors); Eplerenone is a more selective alternative.

Question 153: Insulin synthesis is stimulated by glucose levels above what threshold?

A. 30 mg%
B. 40 mg%
C. 50 mg%
D. 70 mg% (Correct Answer)

Explanation: The synthesis and secretion of insulin by the pancreatic beta cells are tightly regulated by blood glucose concentrations. The correct answer is **70 mg% (70 mg/dL)** because this represents the physiological "set-point" or threshold at which the beta cells initiate the insulin response to prevent hyperglycemia [1]. Glucose enters the beta cell via **GLUT-2** transporters [3]. Once inside, it is phosphorylated by **Glucokinase** (the glucose sensor) [3]. When blood glucose levels rise above **70 mg/dL**, the rate of glycolysis increases, leading to an rise in the ATP/ADP ratio. This closes ATP-sensitive K+ channels, causing cell depolarization, calcium influx, and subsequent insulin release and synthesis [1, 3]. Below this threshold, insulin secretion is basal or suppressed to prevent hypoglycemia [1]. **Analysis of Options:** * **A, B, and C (30, 40, and 50 mg%):** These levels are considered hypoglycemic. At these concentrations, insulin synthesis is inhibited, and counter-regulatory hormones (like glucagon and epinephrine) are triggered to increase blood glucose [1]. Specifically, symptoms of hypoglycemia typically begin around 50–55 mg/dL [1]. * **D (70 mg%):** This is the recognized threshold where the metabolic machinery of the beta cell activates insulin production to maintain euglycemia. **High-Yield Clinical Pearls for NEET-PG:** * **Glucokinase:** Acts as the "glucose sensor." Mutations in this enzyme lead to **MODY-2** (Maturity-Onset Diabetes of the Young). * **Biphasic Release:** Insulin release is biphasic; the first phase is the release of stored insulin, while the second phase involves the synthesis of new insulin [2]. * **GLUT-2 vs. GLUT-4:** Remember that GLUT-2 (pancreas/liver) is insulin-independent, whereas GLUT-4 (muscle/adipose) is insulin-dependent [3].

Question 154: A 77-year-old man with a mass in the lung develops asymptomatic hyponatremia. His JVP is 4 cm, heart sounds are normal, and the lungs are clear. The urine sodium is 64 mEq/L and osmolality 550 mOsm/kg. Which of the following is the most likely diagnosis?

A. Nephrotic syndrome
B. Syndrome of inappropriate antidiuretic hormone (SIADH) production (Correct Answer)
C. Renal metastases from lung cancer
D. Lung metastases from hypernephroma

Explanation: The clinical presentation is a classic case of **SIADH (Syndrome of Inappropriate Antidiuretic Hormone)**, likely secondary to a paraneoplastic syndrome from lung cancer (most commonly Small Cell Lung Carcinoma) [1]. **1. Why SIADH is correct:** The patient exhibits the three hallmarks of SIADH: * **Euvolemic Hyponatremia:** A JVP of 4 cm (normal <8 cm) and clear lungs indicate a clinically normal extracellular fluid volume (euvolemia) [2]. * **Inappropriate Urine Concentration:** A urine osmolality of 550 mOsm/kg (in the presence of serum hyponatremia) signifies that ADH is actively preventing water excretion despite low serum tonicity [3]. * **Natriuresis:** Urine sodium >40 mEq/L (here 64 mEq/L) is characteristic of SIADH as the body attempts to maintain euvolemia by excreting sodium [2]. **2. Why other options are incorrect:** * **Nephrotic Syndrome:** This causes **hypervolemic** hyponatremia. Patients typically present with edema, high JVP, and low urine sodium (<20 mEq/L) due to secondary hyperaldosteronism [2]. * **Renal Metastases/Hypernephroma:** While these involve the kidneys, they do not typically present with this specific pattern of euvolemic hyponatremia and concentrated urine unless they trigger a specific paraneoplastic syndrome, which is far less common than SIADH in lung mass cases [1]. **Clinical Pearls for NEET-PG:** * **Most common cause of SIADH:** Small Cell Lung Cancer (SCLC) [1]. * **Diagnostic Criteria:** Hyponatremia + Low plasma osmolality + High urine osmolality (>100 mOsm/kg) + Urine Na >40 mEq/L + Euvolemia. * **Treatment:** Fluid restriction is the first-line treatment for asymptomatic SIADH. For severe symptoms, use 3% hypertonic saline. * **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).**

Question 155: All of the following are features of thyrotoxicosis, except?

A. Diastolic murmur (Correct Answer)
B. Soft non-ejection systolic murmur
C. Irregularly irregular pulse
D. Scratching sound in systole

Explanation: **Explanation:** Thyrotoxicosis induces a hyperdynamic circulatory state due to increased metabolic demand and the direct effect of thyroid hormones on the myocardium and peripheral vasculature. **1. Why Diastolic Murmur is the Correct Answer:** Diastolic murmurs [2] are almost always pathological (e.g., mitral stenosis or aortic regurgitation) and are **not** a feature of thyrotoxicosis. Hyperdynamic states primarily increase the velocity of blood flow during ventricular contraction, leading to systolic, rather than diastolic, findings. **2. Analysis of Incorrect Options:** * **Soft non-ejection systolic murmur:** This is a common finding in thyrotoxicosis. It is a "flow murmur" caused by increased cardiac output and rapid ejection of blood into the great vessels. * **Irregularly irregular pulse:** Thyrotoxicosis is a classic cause of **Atrial Fibrillation (AF)** [1], especially in elderly patients. The increased adrenergic tone and direct electrophysiological effects on the atria lead to this characteristic pulse. * **Scratching sound in systole (Means-Lerman Scratch):** This is a high-yield clinical sign. It is a systolic scratching sound heard over the upper left sternal border during expiration. It is thought to be caused by the rubbing of the hyperdynamic heart against the pleura or pericardium, mimicking a friction rub. **Clinical Pearls for NEET-PG:** * **Most common arrhythmia** in thyrotoxicosis: Sinus tachycardia [1]. * **Most common chronic arrhythmia**: Atrial Fibrillation (occurs in 10-15% of patients). * **Pulse Pressure:** Thyrotoxicosis causes a **wide pulse pressure** [3] (increased systolic BP due to stroke volume and decreased diastolic BP due to peripheral vasodilation). * **Heart Failure:** It can cause "High-output heart failure."

Question 156: Tertiary hyperparathyroidism is:

A. High PO4 level with metastasis
B. Secondary hyperparathyroidism with chronic renal failure
C. Primary hyperparathyroidism with low Ca++ levels
D. Secondary hyperparathyroidism with chief cell hyperplasia (Correct Answer)

Explanation: Explanation: Tertiary hyperparathyroidism occurs when prolonged Secondary Hyperparathyroidism (usually due to Chronic Kidney Disease) leads to the parathyroid glands becoming autonomous [2]. 1. Why Option D is Correct: In chronic renal failure, persistent hypocalcemia and hyperphosphatemia cause continuous stimulation of the parathyroid glands [1]. Over time, this leads to diffuse chief cell hyperplasia. Eventually, these hyperplastic cells lose their sensitivity to calcium levels and begin secreting Parathyroid Hormone (PTH) autonomously, regardless of serum calcium [2]. This transition from reactive (secondary) to autonomous (tertiary) secretion results in hypercalcemia in a patient who previously had secondary hyperparathyroidism [2]. 2. Why Other Options are Incorrect: * Option A: High phosphate with metastasis (calciphylaxis or metastatic calcification) is a complication of high calcium-phosphate products but does not define the endocrine state of tertiary hyperparathyroidism. * Option B: This describes Secondary Hyperparathyroidism itself, where the gland is still responding physiologically to low calcium/high phosphate [1], [3]. * Option C: Primary hyperparathyroidism is characterized by high calcium levels due to an adenoma or hyperplasia, not low levels [1]. Clinical Pearls for NEET-PG: * Primary: High PTH, High Ca++, Low PO4 (Usually a single Adenoma). * Secondary: High PTH, Low/Normal Ca++, High PO4 (Chronic Renal Failure) [3]. * Tertiary: Very High PTH, High Ca++, High PO4 (Autonomous hyperplasia after long-standing CRF) [2]. * Treatment: Tertiary hyperparathyroidism often requires surgical intervention (subtotal parathyroidectomy) because the glands no longer respond to medical management.

Question 157: Which of the following statements is FALSE about Type I Diabetes Mellitus?

A. Patients are prone to Diabetic Ketoacidosis (DKA).
B. Obesity is a common feature. (Correct Answer)
C. There is reduced serum insulin level.
D. Susceptibility genes are located on Chromosome 6.

Explanation: **Explanation:** Type 1 Diabetes Mellitus (T1DM) is characterized by an absolute deficiency of insulin due to the autoimmune destruction of pancreatic beta cells. **Why Option B is the correct answer (False statement):** Unlike Type 2 Diabetes Mellitus (T2DM), where insulin resistance is strongly linked to adiposity, **obesity is not a common feature of T1DM** [1]. In fact, patients with T1DM typically present with **weight loss** at the time of diagnosis [2]. This occurs because the lack of insulin leads to a catabolic state, causing the breakdown of fat and muscle stores to provide energy [2]. **Analysis of other options:** * **Option A (True):** Due to the absolute lack of insulin, patients are highly prone to **Diabetic Ketoacidosis (DKA)** [1]. Without insulin, lipolysis is unchecked, leading to the production of ketone bodies [2]. * **Option C (True):** The hallmark of T1DM is **reduced or absent serum insulin** and C-peptide levels, resulting from the destruction of >90% of beta-cell mass. * **Option D (True):** Genetic susceptibility is strongly linked to the **HLA region on Chromosome 6p21** [1]. Specifically, **HLA-DR3 and HLA-DR4** alleles are found in approximately 95% of T1DM patients. **High-Yield NEET-PG Pearls:** * **Most common age of onset:** Bimodal peaks at 4–6 years and 10–14 years. * **Autoantibodies:** Anti-GAD65 (most persistent), Anti-IA2, and Zinc Transporter 8 (ZnT8) antibodies are key diagnostic markers [1]. * **Honeymoon Phase:** A temporary period after starting insulin where remaining beta cells function briefly, reducing exogenous insulin requirements. * **Association:** T1DM is often associated with other autoimmune conditions like Hashimoto’s thyroiditis and Celiac disease [3].

Question 158: Gynaecomastia is seen in all except?

A. Spironolactone
B. Hypothyroidism (Correct Answer)
C. Klinefelters syndrome
D. Cirrhotic liver diseases

Explanation: **Explanation:** Gynecomastia is the benign proliferation of glandular breast tissue in males, primarily caused by an imbalance between estrogen and androgen action. **Why Hypothyroidism is the Correct Answer:** **Hyperthyroidism**, not hypothyroidism, is a classic cause of gynecomastia. In hyperthyroidism, increased thyroid hormones stimulate the production of **Sex Hormone-Binding Globulin (SHBG)**. SHBG has a higher affinity for testosterone than estrogen; thus, it binds free testosterone, decreasing the testosterone-to-estrogen ratio. Conversely, hypothyroidism is generally not associated with gynecomastia. **Analysis of Other Options:** * **Spironolactone:** This is the most common drug-induced cause [1]. It acts as a competitive antagonist at the androgen receptor and inhibits testosterone synthesis. * **Klinefelter Syndrome (47, XXY):** This is the most common congenital cause. It presents with primary testicular failure (low testosterone) and elevated gonadotropins. The increased LH stimulates aromatase activity in Leydig cells, leading to increased conversion of testosterone to estradiol. * **Cirrhotic Liver Disease:** Liver failure leads to gynecomastia via two mechanisms: decreased degradation of androstenedione (which is peripherally converted to estrogen) and increased SHBG production by the liver, which lowers free testosterone levels. **High-Yield Clinical Pearls for NEET-PG:** * **Physiological Gynecomastia:** Seen in neonates, during puberty (most common), and in the elderly [1]. * **Drug Mnemonic (DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone, **C**imetidine, **O**estrogens/Ketoconazole [1]. * **Refeeding Syndrome:** Can cause "refeeding gynecomastia" due to a rebound in pituitary gonadotropin production after malnutrition. * **Testicular Tumors:** Leydig cell tumors and hCG-secreting germ cell tumors are important pathological differentials [1].

Question 159: Which of the following is the most common cause of hypergonadotropic hypogonadism in males?

A. Viral Orchitis
B. Klinefelter's syndrome (Correct Answer)
C. Kallman's Syndrome
D. Noonan Syndrome

Explanation: **Explanation:** **Hypergonadotropic hypogonadism** (Primary Hypogonadism) is characterized by low testosterone levels due to testicular failure, resulting in a compensatory rise in gonadotropins (FSH and LH) from the pituitary gland [1]. **Why Klinefelter’s Syndrome is correct:** **Klinefelter’s syndrome (47, XXY)** is the **most common congenital cause** and the overall most common cause of primary hypogonadism in males [1]. It involves progressive hyalinization and fibrosis of the seminiferous tubules and dysfunction of Leydig cells [2]. This leads to azoospermia and low testosterone, triggering high levels of FSH and LH [2]. **Analysis of Incorrect Options:** * **Viral Orchitis (e.g., Mumps):** While a common *acquired* cause of testicular failure, it is less frequent than Klinefelter’s syndrome in the general population [1]. * **Kallmann’s Syndrome:** This is a cause of **hypogonadotropic hypogonadism** (Secondary Hypogonadism). It involves a deficiency of GnRH associated with anosmia; therefore, both testosterone and gonadotropins (FSH/LH) are low [3]. * **Noonan Syndrome:** Often called the "Male Turner Syndrome" (though it affects both sexes), it can cause cryptorchidism and primary hypogonadism, but it is significantly rarer than Klinefelter’s [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad of Klinefelter’s:** Small firm testes (<2 cm), gynecomastia, and azoospermia/infertility [2]. * **Biochemical Profile:** ↓ Testosterone, ↑ FSH, ↑ LH, ↑ Estradiol [2]. * **Increased Risks:** Patients have a higher risk of **Breast Cancer** (20x higher than normal males) and Germ Cell Tumors (specifically mediastinal) [1]. * **Barr Body:** Positive on buccal smear (due to the extra X chromosome).

Question 160: Which of the following is true about hypercalcemia?

A. Treatment of the primary cause (Correct Answer)
B. Malignancy does not produce hypercalcemia
C. Intravenous fluids with furosemide are given
D. Amidarone is not effective

Explanation: Hypercalcemia is a common clinical scenario in internal medicine, most frequently caused by **Primary Hyperparathyroidism (PHPT)** in the outpatient setting and **Malignancy** in hospitalized patients [1]. **1. Why Option A is Correct:** The definitive management of hypercalcemia always focuses on **treating the underlying cause**. For instance, if the cause is PHPT, surgical parathyroidectomy is the cure [1]. If it is due to sarcoidosis, steroids are used. While acute stabilization is necessary for severe cases, the hypercalcemia will recur unless the primary pathology is addressed. **2. Analysis of Incorrect Options:** * **Option B:** This is incorrect. Malignancy is the **second most common cause** of hypercalcemia. It occurs via three mechanisms: secretion of PTHrP (Squamous cell CA), local osteolytic bone destruction (Breast CA, Multiple Myeloma), or 1,25-dihydroxyvitamin D production (Lymphomas) [1]. * **Option C:** While IV fluids (Normal Saline) are the first-line treatment to restore volume, the routine use of **Furosemide is no longer recommended** unless the patient is in fluid overload (heart failure/renal failure). It can worsen dehydration and electrolyte imbalances if used prematurely. * **Option D:** This is a distractor. **Amiodarone** is associated with thyroid dysfunction (hypo/hyperthyroidism) but is not a standard treatment modality for hypercalcemia. **Clinical Pearls for NEET-PG:** * **First-line treatment:** Aggressive hydration with 0.9% Normal Saline [1]. * **Drug of choice for Malignancy-associated hypercalcemia:** Intravenous Bisphosphonates (e.g., Zoledronic acid) [1]. * **ECG finding:** Shortened QT interval (mnemonic: "Short cow" - Short QT in Hypercalcemia). * **Milk-Alkali Syndrome:** Characterized by the triad of hypercalcemia, metabolic alkalosis, and renal insufficiency [1].

Practice by Chapter

Diabetes Mellitus

Practice Questions

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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