Endocrinology Practice Questions

Q: Which of the following is the most likely metabolic effect of insulin on adipose tissue?

Decrease in lipolysis. Insulin is the body’s primary anabolic hormone, functioning to store energy and prevent the breakdown of stored fuels. Its effect on adipose tissue is centered on promoting lipid storage and inhibiting lipid mobilization [2]. **Why "Decrease in lipolysis" is correct:** Insulin is a potent inhibitor of **Hormone-Sensitive Lipase (HSL)**. HSL is the enzyme responsible for breaking down stored triglycerides into free fatty acids and glycerol. By inhibiting HSL, insulin effectively **decreases lipolysis** [1], [4]. Simultaneously, insulin promotes the storage of fat by stimulating **Lipoprotein Lipase (LPL)**, which clears chylomicrons and VLDL from the blood to provide fatty acids for esterification within the adipocyte. **Analysis of Incorrect Options:** * **A & B: Decrease in glucose transport/phosphorylation:** These are incorrect because insulin **increases** glucose uptake in adipose tissue by recruiting **GLUT-4** transporters to the cell membrane [2], [4]. Once inside, insulin increases glucose phosphorylation (via hexokinase) to trap glucose for glycerol-3-phosphate production, which is essential for triglyceride synthesis [1], [4]. * **D: Decrease in lipoprotein lipase:** As mentioned, insulin **increases** LPL activity in adipose tissue to facilitate the uptake of exogenous fatty acids for storage. (Note: Insulin *decreases* LPL in muscle, diverting lipids toward storage rather than oxidation). **NEET-PG Clinical Pearls:** * **GLUT-4** is the only insulin-dependent glucose transporter (found in adipose tissue and skeletal muscle) [2]. * **Hormone-Sensitive Lipase (HSL)** is activated by glucagon, epinephrine, and ACTH (via cAMP), and inhibited by insulin [3], [4]. * **Lipodystrophy:** Repeated insulin injections at the same site can cause localized hypertrophy or atrophy of adipose tissue due to insulin’s potent lipogenic effects.

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

70 mg%. 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].

Q: All of the following are features of thyrotoxicosis, except?

Diastolic murmur. **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."

Q: Tertiary hyperparathyroidism is:

Secondary hyperparathyroidism with chief cell hyperplasia. 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.

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

Obesity is a common feature.. **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].

Q: Gynaecomastia is seen in all except?

Hypothyroidism. **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].

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

Klinefelter's syndrome. **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 1

Which of the following is the most likely metabolic effect of insulin on adipose tissue?

Accepted Answer

Decrease in lipolysis

Answer

Decrease in glucose transport

Answer

Decrease in glucose phosphorylation

Answer

Decrease in lipoprotein lipase

Question 2

Gynecomastia is seen in all of the following conditions except?

Accepted Answer

Kidney failure

Answer

Klinefelter's syndrome

Answer

Liver failure

Answer

Leprosy

Question 3

What is the treatment of choice for secondary hyperaldosteronism?

Accepted Answer

Drug management

Answer

Unilateral adrenalectomy

Answer

Both

Answer

None

Question 4

Insulin synthesis is stimulated by glucose levels above what threshold?

Accepted Answer

70 mg%

Answer

30 mg%

Answer

40 mg%

Answer

50 mg%

Question 5

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?

Accepted Answer

Syndrome of inappropriate antidiuretic hormone (SIADH) production

Answer

Nephrotic syndrome

Answer

Renal metastases from lung cancer

Answer

Lung metastases from hypernephroma

Question 6

All of the following are features of thyrotoxicosis, except?

Accepted Answer

Diastolic murmur

Answer

Soft non-ejection systolic murmur

Answer

Irregularly irregular pulse

Answer

Scratching sound in systole

Question 7

Tertiary hyperparathyroidism is:

Accepted Answer

Secondary hyperparathyroidism with chief cell hyperplasia

Answer

High PO4 level with metastasis

Answer

Secondary hyperparathyroidism with chronic renal failure

Answer

Primary hyperparathyroidism with low Ca++ levels

Question 8

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

Accepted Answer

Obesity is a common feature.

Answer

Patients are prone to Diabetic Ketoacidosis (DKA).

Answer

There is reduced serum insulin level.

Answer

Susceptibility genes are located on Chromosome 6.

Question 9

Gynaecomastia is seen in all except?

Accepted Answer

Hypothyroidism

Answer

Spironolactone

Answer

Klinefelters syndrome

Answer

Cirrhotic liver diseases

Question 10

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

Accepted Answer

Klinefelter's syndrome

Answer

Viral Orchitis

Answer

Kallman's Syndrome

Answer

Noonan Syndrome

Endocrinology — MCQs

Endocrinology — MCQs

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