Endocrinology Practice Questions

Q: Skeletal muscle primarily utilizes which glucose transporter for uptake?

GLUT-4 transporter. **Explanation:** The correct answer is **GLUT-4 transporter**. **1. Why GLUT-4 is correct:** GLUT-4 is the primary glucose transporter found in **skeletal muscle** and **adipose tissue**. It is unique because it is **insulin-dependent**. In the resting state, GLUT-4 molecules are stored in intracellular vesicles. Upon insulin stimulation (or during exercise), these vesicles translocation to the cell membrane, allowing glucose to enter the cell via facilitated diffusion. This mechanism is crucial for post-prandial glucose lowering. **2. Why other options are incorrect:** * **GLUT-1:** This is an insulin-independent transporter found in almost all tissues, but it is the primary transporter for the **Blood-Brain Barrier (BBB)** and **RBCs**. It maintains basal glucose uptake. * **GLUT-2:** A high-capacity, low-affinity transporter found in the **Liver, Pancreas (beta cells), and Kidney**. It acts as a "glucose sensor" in the pancreas and allows bidirectional transport in the liver. * **GLUT-3:** Found primarily in **Neurons** and the placenta. It has a very high affinity for glucose, ensuring the brain receives priority supply even during hypoglycemia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Exercise & GLUT-4:** Muscle contraction during exercise can trigger GLUT-4 translocation *independent* of insulin. This is why exercise is a key management strategy for Type 2 Diabetes. * **GLUT-5:** This is a specialized transporter for **Fructose**, located primarily in the small intestine and spermatozoa. * **SGLT vs. GLUT:** Remember that SGLT (Sodium-Glucose Linked Transporters) perform **active transport** (secondary), whereas all GLUT transporters perform **facilitated diffusion** (passive).

Q: Insulin-like Growth Factor II plays an important role in which of the following?

Development of the fetus. **Explanation:** **Insulin-like Growth Factor II (IGF-II)** is a polypeptide hormone structurally related to insulin. Its primary physiological role is as a **major regulator of fetal growth and development**. 1. **Why Option D is Correct:** During the prenatal period, IGF-II is highly expressed in fetal tissues. Unlike IGF-I, which is growth hormone (GH) dependent and dominates postnatal growth, **IGF-II acts independently of GH** during gestation. It promotes cell proliferation and tissue differentiation, making it the critical factor for fetal weight gain and organogenesis. 2. **Why Other Options are Incorrect:** * **Options B & C (Skeletal and Cartilage Growth):** These are primarily the functions of **IGF-I (Somatomedin C)**. Postnatally, Growth Hormone stimulates the liver to produce IGF-I, which then acts on the epiphyseal plates to promote linear bone growth and chondrocyte proliferation. * **Option A (Control of Metabolism):** While IGFs have insulin-like effects, the primary control of glucose and lipid metabolism is mediated by **Insulin** and counter-regulatory hormones (Glucagon, Cortisol, Epinephrine). **High-Yield Clinical Pearls for NEET-PG:** * **IGF-I vs. IGF-II:** Remember: **IGF-II = Fetal growth**; **IGF-I = Postnatal growth** (GH-dependent). * **Beckwith-Wiedemann Syndrome:** A classic clinical condition caused by the over-expression of the *IGF2* gene (genomic imprinting defect), leading to fetal overgrowth, macroglossia, and organomegaly. * **Receptor:** IGF-II binds primarily to the IGF-II receptor (which acts as a "sink" to clear IGF-II) but exerts its growth-promoting effects via the **IGF-I receptor**.

Q: In which physiological state are serum prolactin levels highest?

24 hours postpartum. **Explanation:** **1. Why Option A is Correct:** Prolactin levels undergo a dramatic surge during pregnancy due to high estrogen levels stimulating the lactotrophs in the anterior pituitary. However, its milk-producing action is inhibited by high progesterone levels. Immediately after delivery, the sudden withdrawal of placental steroids (estrogen and progesterone) removes this inhibition. In the **24 hours postpartum**, prolactin levels reach their physiological peak (often >200 ng/mL) to initiate lactogenesis. While suckling maintains these levels later on, the immediate postpartum period represents the highest baseline physiological state. **2. Why the Other Options are Incorrect:** * **B. 24 hours post-ovulation:** While estrogen during the follicular phase can slightly increase prolactin, the levels are negligible compared to the massive surge seen in pregnancy and the postpartum period. * **C. During REM sleep:** Prolactin secretion is pulsatile and follows a diurnal rhythm, with levels rising 60–90 minutes after sleep onset. However, the peak occurs during **non-REM (NREM) sleep**, not REM sleep, and the magnitude is far lower than the postpartum state. * **D. After one hour of running:** Physical and emotional stress (including exercise) can cause a transient rise in prolactin via the inhibition of dopamine. However, this increase is acute and minor compared to the sustained high levels required for lactation. **High-Yield NEET-PG Pearls:** * **Inhibitory Control:** Prolactin is the only anterior pituitary hormone under **predominant inhibitory control** (by Dopamine from the hypothalamus). * **Prolactin & GnRH:** High prolactin levels inhibit GnRH secretion, leading to **lactational amenorrhea** (a natural contraceptive mechanism). * **TRH Effect:** Thyrotropin-releasing hormone (TRH) acts as a potent prolactin-releasing factor; hence, **primary hypothyroidism** is a common cause of hyperprolactinemia.

Q: Angiotensin II causes all of the following, except:

Vasodilation. **Explanation:** Angiotensin II (AT-II) is a potent effector peptide of the Renin-Angiotensin-Aldosterone System (RAAS), primarily functioning to increase blood pressure and maintain fluid volume. **Why Vasodilation is the Correct Answer:** Angiotensin II is one of the most powerful **vasoconstrictors** known. It acts directly on AT1 receptors located on vascular smooth muscle cells to cause systemic vasoconstriction, which increases Total Peripheral Resistance (TPR) and elevates blood pressure. Therefore, it causes vasoconstriction, not vasodilation. **Analysis of Other Options:** * **A. Stimulation of Thirst:** AT-II acts on the subfornical organ (SFO) in the brain to stimulate the thirst center in the hypothalamus, encouraging water intake to restore blood volume. * **B. Increased ADH secretion:** AT-II stimulates the posterior pituitary to release Antidiuretic Hormone (ADH/Vasopressin), which increases water reabsorption in the collecting ducts of the kidney. * **D. Aldosterone secretion:** AT-II acts on the Zona Glomerulosa of the adrenal cortex to stimulate the synthesis and release of aldosterone, leading to sodium and water retention. **High-Yield NEET-PG Pearls:** 1. **Receptor Specificity:** Most physiological effects (vasoconstriction, aldosterone release) are mediated via **AT1 receptors**. AT2 receptors generally mediate opposing effects (vasodilation) but are less dominant in adults. 2. **Renal Effects:** AT-II preferentially constricts the **efferent arteriole**, which helps maintain the Glomerular Filtration Rate (GFR) when renal perfusion pressure is low. 3. **Clinical Correlation:** ACE inhibitors (e.g., Enalapril) and ARBs (e.g., Losartan) are used in hypertension and heart failure to block these effects, leading to vasodilation and reduced fluid overload.

Q: Most of the testosterone secreted by the testes exists in the plasma in the form of?

Testosterone bound to sex-steroid-binding globulin. ### Explanation **Correct Answer: D. Testosterone bound to sex-steroid-binding globulin** **1. Why the Correct Answer is Right:** In the plasma, testosterone (a lipophilic steroid hormone) requires carrier proteins for transport. Approximately **98% of circulating testosterone is protein-bound**, while only about 2% exists in the "free" (biologically active) form. Of the bound fraction, the majority (**~60-70%**) is bound with high affinity to **Sex Hormone-Binding Globulin (SHBG)**, also known as sex-steroid-binding globulin. The remaining ~30-40% is loosely bound to **albumin**. **2. Why the Other Options are Wrong:** * **Options A & B (Dihydrotestosterone):** While Dihydrotestosterone (DHT) is a more potent androgen, it is primarily produced in peripheral tissues (like the prostate and skin) via the action of 5-alpha-reductase on testosterone. It is not the primary secretory product of the testes, nor is it the most abundant form of testosterone in the plasma. * **Option C (Free Testosterone):** Only a tiny fraction (**1-2%**) of testosterone exists in the free, unbound state. While this is the form that can readily diffuse into cells to exert biological effects, it does not represent the "most" common form in plasma. **3. NEET-PG High-Yield Pearls:** * **Bioavailable Testosterone:** This refers to the sum of **Free Testosterone + Albumin-bound Testosterone**. Because the binding to albumin is weak (low affinity), it dissociates easily for tissue use. * **SHBG Regulation:** SHBG levels are **increased** by estrogens and hyperthyroidism, and **decreased** by androgens, obesity, and insulin resistance. * **Site of Secretion:** Testosterone is secreted by the **Leydig cells** of the testes under the influence of **Luteinizing Hormone (LH)**.

Q: What is the primary action of insulin?

Increased glucose uptake in muscle. **Explanation:** Insulin is the body’s primary anabolic hormone, secreted by the β-cells of the pancreatic islets. Its fundamental role is to lower blood glucose levels by promoting glucose utilization and storage while inhibiting glucose production. **Why Option B is correct:** Insulin facilitates glucose entry into specific tissues—primarily **skeletal muscle** and **adipose tissue**—by triggering the translocation of **GLUT-4** (an insulin-dependent glucose transporter) from intracellular vesicles to the cell membrane. Since skeletal muscle constitutes a large percentage of body mass, its increased glucose uptake is the primary mechanism for lowering postprandial blood glucose. **Why the other options are incorrect:** * **A & C (Gluconeogenesis and Glycogenolysis):** These are catabolic processes that *increase* blood glucose. Insulin **inhibits** these processes in the liver. Glucagon and epinephrine are the hormones that stimulate them. * **D (Glucose uptake in endothelium):** Glucose uptake in the vascular endothelium (as well as the brain, liver, and RBCs) is mediated by **GLUT-1** or **GLUT-2**, which are **insulin-independent**. These tissues do not require insulin to take up glucose. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT-4** is the only insulin-dependent transporter. * **Exercise** can also trigger GLUT-4 translocation in muscles, which is why physical activity helps manage Diabetes Mellitus. * **Brain and RBCs** rely on GLUT-1/3 and do not require insulin for glucose uptake, protecting vital organs during hypoglycemia. * **SGLT-1/2** are involved in active transport (sodium-dependent) in the gut and kidneys, unlike the facilitated diffusion of GLUT transporters.

Q: Rapid infusion of insulin causes which of the following electrolyte imbalances?

Hypokalemia. **Explanation:** **Mechanism of Action (Why B is Correct):** Insulin plays a critical role in electrolyte homeostasis by stimulating the **Na⁺-K⁺ ATPase pump** located on the cell membranes of skeletal muscle and liver cells. When insulin levels rise rapidly (as in rapid infusion), it increases the activity of this pump, which pumps 3 Na⁺ ions out of the cell and **2 K⁺ ions into the cell**. This shift of potassium from the extracellular fluid (ECF) into the intracellular fluid (ICF) leads to a decrease in serum potassium levels, resulting in **Hypokalemia**. **Analysis of Incorrect Options:** * **A. Hyperkalemia:** This is the opposite of insulin’s effect. Hyperkalemia is often seen in insulin deficiency (e.g., Diabetic Ketoacidosis) because potassium shifts out of cells. * **C & D. Hypernatremia/Hyponatremia:** While insulin affects the Na⁺-K⁺ pump, its primary and most immediate clinical impact is on potassium. Insulin does not have a direct, significant effect on total body sodium levels that would typically manifest as acute hyper- or hyponatremia in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Use:** Because insulin shifts potassium into cells, a combination of **Insulin + Glucose** (to prevent hypoglycemia) is a standard emergency treatment for **Hyperkalemia**. * **DKA Management:** In Diabetic Ketoacidosis (DKA), patients may have high serum potassium initially, but total body potassium is depleted. Starting insulin will cause a rapid drop in K⁺; therefore, **potassium supplementation** is often required even if initial serum levels appear normal. * **Other drugs causing Hypokalemia:** Beta-2 agonists (Salbutamol) and Diuretics (Thiazides/Loop).

Q: Which of the following is NOT an action of glucagon?

None of the above. **Explanation:** Glucagon is a peptide hormone secreted by the **alpha cells of the pancreas**. Its primary physiological role is to prevent hypoglycemia by acting as a "hormone of starvation," increasing blood glucose and fuel availability. **Why "None of the above" is correct:** All three listed actions (Gluconeogenesis, Lipolysis, and Ketogenesis) are primary physiological effects of glucagon. Since the question asks which is NOT an action, and all are indeed actions, "None of the above" is the correct choice. * **Option A: Gluconeogenic:** Glucagon is a potent stimulator of gluconeogenesis (forming glucose from non-carbohydrate sources like amino acids and glycerol) in the liver. It also stimulates glycogenolysis (breakdown of glycogen). * **Option B: Lipolytic:** Glucagon activates hormone-sensitive lipase in adipose tissue, leading to the breakdown of triglycerides into free fatty acids and glycerol, providing alternative fuel sources. * **Option C: Ketogenic:** By increasing the delivery of fatty acids to the liver and shifting hepatic metabolism toward fatty acid oxidation (via inhibition of Malonyl-CoA), glucagon promotes the formation of ketone bodies (acetoacetate and beta-hydroxybutyrate). **High-Yield NEET-PG Pearls:** 1. **Mechanism of Action:** Glucagon acts via a **G-protein coupled receptor (Gs)**, which activates Adenylyl Cyclase to increase **cAMP** levels. 2. **The Insulin/Glucagon Ratio:** The metabolic state of the body is determined more by the ratio of these two hormones than by the absolute concentration of either. 3. **Clinical Use:** Glucagon is used as an emergency treatment for severe hypoglycemia and as an antidote for **Beta-blocker poisoning** (due to its ability to increase cAMP in cardiac myocytes bypassing the beta-receptor). 4. **Inhibitor:** Somatostatin (from delta cells) inhibits the secretion of both insulin and glucagon.

Q: Parathormone secretion is stimulated by?

Decreased serum calcium. **Explanation:** The secretion of **Parathyroid Hormone (PTH)** is primarily regulated by a negative feedback loop involving ionized serum calcium levels. **Why Option B is Correct:** The chief cells of the parathyroid gland possess **Calcium-Sensing Receptors (CaSR)** on their surface. When serum ionized calcium levels drop (**Hypocalcemia**), these receptors are less stimulated, which triggers the rapid release of pre-formed PTH and increases the synthesis of new hormone. PTH then acts to restore calcium levels by increasing bone resorption, enhancing renal calcium reabsorption, and stimulating the synthesis of Calcitriol (Vitamin D3) to increase intestinal absorption. **Why Other Options are Incorrect:** * **Option A:** Increased serum calcium (**Hypercalcemia**) activates the CaSR, which inhibits PTH secretion to prevent further calcium rise. * **Options C & D:** Serum potassium levels do not have a direct regulatory effect on PTH secretion. Potassium is primarily regulated by Aldosterone and Insulin. **High-Yield Clinical Pearls for NEET-PG:** * **Magnesium’s Role:** While hypocalcemia is the primary stimulus, **mild hypomagnesemia** also stimulates PTH. However, **severe, chronic hypomagnesemia** actually inhibits PTH release and causes PTH resistance, leading to refractory hypocalcemia. * **Phosphate:** Hyperphosphatemia indirectly stimulates PTH by lowering ionized calcium and inhibiting Vitamin D activation. * **Target Organs:** PTH acts directly on the **Bone** (RANKL pathway) and **Kidney** (distal tubule), but its effect on the **Intestine** is indirect (via Vitamin D). * **PTH and Phosphorus:** Remember the phrase: *"PTH stands for Phosphate Trashing Hormone"* because it decreases renal phosphate reabsorption (causing phosphaturia).

Q: Which of the following is characteristic of a hyperthyroid state?

Lipolysis. **Explanation:** Thyroid hormones ($T_3$ and $T_4$) are the primary regulators of the body’s Basal Metabolic Rate (BMR). In a hyperthyroid state, the body enters a **hypermetabolic phase** characterized by the rapid breakdown of energy stores. **Why Lipolysis is Correct:** Thyroid hormones stimulate **lipolysis** by increasing the activity of hormone-sensitive lipase in adipose tissue. This leads to the mobilization of free fatty acids and glycerol into the plasma. While thyroid hormones also stimulate lipogenesis, the rate of lipid catabolism (lipolysis) significantly outweighs synthesis in hyperthyroidism, leading to a decrease in fat stores and body weight. **Analysis of Incorrect Options:** * **A. Increased protein synthesis:** While physiological levels of thyroid hormone are anabolic, **excessive** levels (hyperthyroidism) are **catabolic**. This leads to increased protein breakdown (proteolysis), resulting in negative nitrogen balance and muscle wasting (thyrotoxic myopathy). * **B. Decreased glycolysis:** Hyperthyroidism **increases** all aspects of carbohydrate metabolism, including glycolysis, gluconeogenesis, and glucose absorption from the GI tract, to meet the high energy demands. * **D. Increased cholesterol:** Thyroid hormones increase the expression of **LDL receptors** in the liver. In hyperthyroidism, this leads to rapid clearance of cholesterol from the blood, resulting in **hypocholesterolemia**. **High-Yield Clinical Pearls for NEET-PG:** * **Weight Loss despite Polyphagia:** A classic hallmark of hyperthyroidism due to increased BMR. * **Cholesterol Paradox:** Hypocholesterolemia is seen in hyperthyroidism, while hypercholesterolemia is a key diagnostic marker for hypothyroidism. * **Beta-Adrenergic Sensitivity:** Thyroid hormones increase the number and sensitivity of $\beta$-adrenergic receptors, explaining the tachycardia and tremors treated with Propranolol.

Question 1

Skeletal muscle primarily utilizes which glucose transporter for uptake?

Accepted Answer

GLUT-4 transporter

Answer

GLUT-1 transporter

Answer

GLUT-2 transporter

Answer

GLUT-3 transporter

Question 2

Insulin-like Growth Factor II plays an important role in which of the following?

Accepted Answer

Development of the fetus

Answer

Control of metabolism

Answer

Skeletal growth

Answer

Cartilage growth

Question 3

In which physiological state are serum prolactin levels highest?

Accepted Answer

24 hours postpartum

Answer

24 hours post-ovulation

Answer

During REM sleep

Answer

After one hour of running

Question 4

Angiotensin II causes all of the following, except:

Accepted Answer

Vasodilation

Answer

Stimulation of thirst

Answer

Increased ADH secretion

Answer

Aldosterone secretion

Question 5

Most of the testosterone secreted by the testes exists in the plasma in the form of?

Accepted Answer

Testosterone bound to sex-steroid-binding globulin

Answer

Dihydrotestosterone bound to gonadal steroid-binding hormone

Answer

Free dihydrotestosterone

Answer

Free testosterone

Question 6

What is the primary action of insulin?

Accepted Answer

Increased glucose uptake in muscle

Answer

Gluconeogenesis

Answer

Glycogenolysis

Answer

Increased glucose uptake in endothelium

Question 7

Rapid infusion of insulin causes which of the following electrolyte imbalances?

Accepted Answer

Hypokalemia

Answer

Hyperkalemia

Answer

Hypernatremia

Answer

Hyponatremia

Question 8

Which of the following is NOT an action of glucagon?

Accepted Answer

None of the above

Answer

Gluconeogenic

Answer

Lipolytic

Answer

Ketogenic

Question 9

Parathormone secretion is stimulated by?

Accepted Answer

Decreased serum calcium

Answer

Increased serum calcium

Answer

Increased serum potassium

Answer

Decreased serum potassium

Question 10

Which of the following is characteristic of a hyperthyroid state?

Accepted Answer

Lipolysis

Answer

Increased protein synthesis

Answer

Decreased glycolysis

Answer

Increased cholesterol

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?