Endocrinology Practice Questions

Q: Prolactin secretion is inhibited by which of the following?

Dopamine excess. **Explanation:** The regulation of prolactin (PRL) is unique among anterior pituitary hormones because it is under **tonic inhibitory control** by the hypothalamus. **1. Why Option A is Correct:** The primary Prolactin Inhibiting Factor (PIF) is **Dopamine**. Dopamine is secreted by the tuberoinfundibular neurons into the hypophyseal portal system. It binds to **D2 receptors** on the lactotrophs in the anterior pituitary, leading to the inhibition of prolactin synthesis and release. Therefore, an excess of dopamine directly suppresses prolactin levels. **2. Why the Other Options are Incorrect:** * **B. Metoclopramide:** This is a dopamine (D2) receptor antagonist. By blocking the inhibitory effect of dopamine, it causes a rise in prolactin levels (hyperprolactinemia). * **C. Hypothyroidism:** In primary hypothyroidism, low levels of thyroid hormones lead to a compensatory increase in **Thyrotropin-Releasing Hormone (TRH)**. TRH acts as a potent prolactin-releasing factor; thus, hypothyroidism is a common cause of hyperprolactinemia. * **D. Emotional Stress:** Prolactin is a stress-responsive hormone. Physical or emotional stress stimulates the release of prolactin via various neuroendocrine pathways. **High-Yield Clinical Pearls for NEET-PG:** * **Prolactinoma:** The most common secretory tumor of the pituitary. Treatment of choice is medical (Dopamine agonists like **Cabergoline** or Bromocriptine), not surgery. * **Stalk Effect:** Any lesion compressing the pituitary stalk prevents dopamine from reaching the pituitary, leading to elevated prolactin (the only pituitary hormone that increases when the stalk is cut). * **Hook Effect:** In cases of extremely high prolactin (giant prolactinomas), lab assays may show falsely low levels; serial dilution is required for accurate diagnosis.

Q: Primary Adrenal Insufficiency causes all of the following, except?

Increased protein breakdown. **Explanation:** Primary Adrenal Insufficiency (Addison’s Disease) is characterized by the destruction of the adrenal cortex, leading to a deficiency of both **Mineralocorticoids (Aldosterone)** and **Glucocorticoids (Cortisol)**. **Why "Increased protein breakdown" is the correct answer:** Cortisol is a catabolic hormone. Its primary role in protein metabolism is to stimulate the breakdown of proteins in peripheral tissues (like muscle) to provide amino acids for gluconeogenesis. In adrenal insufficiency, there is a **deficiency of cortisol**, which leads to **decreased protein breakdown** and impaired gluconeogenesis. Therefore, increased protein breakdown does not occur. **Analysis of incorrect options:** * **Low Blood Pressure:** Aldosterone deficiency leads to "pressure natriuresis" (loss of sodium and water), resulting in hypovolemia. Additionally, cortisol is required to maintain the sensitivity of blood vessels to catecholamines. Lack of both leads to hypotension. * **Decrease in ECF:** The loss of sodium (and consequently water) due to lack of aldosterone directly reduces the extracellular fluid volume. * **Decreased sodium-potassium ratio:** Aldosterone normally causes Na+ reabsorption and K+ excretion. Its absence leads to **Hyponatremia** and **Hyperkalemia**, which mathematically decreases the Na+:K+ ratio (a classic diagnostic marker). **High-Yield Clinical Pearls for NEET-PG:** * **Hyperpigmentation:** Seen only in *Primary* Adrenal Insufficiency due to compensatory increase in ACTH (which shares a precursor with MSH, POMC). * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Gold Standard Test:** ACTH Stimulation Test (Cosyntropin test). * **Crisis Management:** Immediate IV Hydrocortisone and aggressive fluid resuscitation with Normal Saline.

Q: Laron dwarfism is caused by which of the following?

GH receptor defect. **Explanation:** **Laron Dwarfism (Laron Syndrome)** is an autosomal recessive condition characterized by a mutation in the **Growth Hormone Receptor (GHR)** gene. In this condition, the body produces normal or even elevated levels of Growth Hormone (GH), but the receptors are non-functional. Consequently, the liver cannot produce **Insulin-like Growth Factor-1 (IGF-1)** in response to GH. Since IGF-1 is the primary mediator of GH’s growth-promoting effects on bone and cartilage, its absence leads to severe short stature. **Analysis of Options:** * **Option B (Correct):** The primary pathology is a **GH receptor defect** (insensitivity to GH). Laboratory findings typically show **High GH** and **Low IGF-1**. * **Option A:** Deficiency of GH causes **Pituitary Dwarfism**. Unlike Laron syndrome, these patients respond to exogenous GH therapy. * **Option C:** Deficiency of thyroxin in childhood leads to **Cretinism**, characterized by stunted growth and significant mental retardation. * **Option D:** Thyroxin receptor defects lead to **Thyroid Hormone Resistance Syndrome (Refetoff Syndrome)**, which presents with features of hypothyroidism or goiter, but is not the cause of Laron dwarfism. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Lab Profile:** ↑ GH, ↓ IGF-1, and ↓ GH-Binding Protein (GHBP). * **Clinical Feature:** Patients often have a characteristic "doll-like" face (prominent forehead, depressed nasal bridge) and a high-pitched voice. * **Metabolic Paradox:** Interestingly, individuals with Laron syndrome have a significantly **reduced risk of developing cancer and Type 2 Diabetes Mellitus**, despite their growth deficits. * **Treatment:** Since the defect is at the receptor level, exogenous GH is ineffective. Treatment requires **recombinant IGF-1 (Mecasermin)**.

Q: Growth hormone increases all of the following except?

Metabolism of carbohydrates. **Explanation:** Growth Hormone (GH) is primarily an anabolic hormone regarding proteins, but it acts as a **"Diabetogenic"** and **"Glucose-sparing"** hormone regarding fuel metabolism. **Why "Metabolism of carbohydrates" is the correct answer:** GH actually **decreases** the peripheral utilization (metabolism) of carbohydrates. It induces insulin resistance by inhibiting the uptake of glucose by skeletal muscle and adipose tissue. By sparing glucose, the body shifts its energy source from carbohydrates to fats. Therefore, saying GH "increases" carbohydrate metabolism is physiologically incorrect. **Analysis of Incorrect Options:** * **A. Blood glucose concentration:** GH increases blood glucose by stimulating gluconeogenesis in the liver and reducing glucose uptake in peripheral tissues (Anti-insulin effect). * **B. Blood free fatty acid concentration:** GH is highly **lipolytic**. It activates hormone-sensitive lipase, breaking down triglycerides into free fatty acids (FFAs) to be used as the primary energy source. * **C. Protein synthesis:** GH is a potent anabolic agent. It increases amino acid transport into cells, enhances DNA transcription/translation, and decreases protein catabolism, leading to a positive nitrogen balance. **NEET-PG High-Yield Pearls:** * **Ketogenic Effect:** Due to excessive mobilization of FFAs, GH is considered ketogenic. * **IGF-1 (Somatomedin C):** Most growth-promoting effects of GH (bone and cartilage growth) are mediated via IGF-1, produced mainly in the liver. * **Pulsatile Secretion:** GH is secreted in pulses, with the largest spike occurring during **Deep Sleep (Stage N3)**. * **Stimuli:** Hypoglycemia, fasting, and exercise are potent stimulators of GH release.

Q: Insulin-like growth factor-II (IGF-II) is synthesized in all of the following tissues EXCEPT:

Cartilage. **Explanation:** The synthesis of Insulin-like Growth Factors (IGFs) is a critical component of the growth hormone (GH) axis. While **IGF-I** is primarily GH-dependent and synthesized in the liver and peripheral tissues like **cartilage** (where it acts locally via autocrine/paracrine mechanisms to promote bone growth), **IGF-II** follows a different physiological pattern. **Why Cartilage is the Correct Answer:** IGF-II is primarily a **fetal growth factor**. While it is synthesized in various adult tissues, it is notably **not synthesized in cartilage**. In contrast, cartilage is a major site for IGF-I synthesis, which mediates the longitudinal growth effects of Growth Hormone. **Analysis of Incorrect Options:** * **Liver (B):** The liver is the primary site of synthesis for both IGF-I and IGF-II in adults. IGF-II levels in the blood remain relatively high throughout adulthood, though its metabolic role is less dominant than IGF-I. * **Brain (A) and Pancreas (D):** IGF-II is widely expressed in several extrahepatic tissues. It is synthesized in the **brain** (where it plays a role in cognitive function and neurogenesis) and the **pancreas** (involved in beta-cell mass regulation). **High-Yield NEET-PG Pearls:** * **IGF-I (Somatomedin C):** Major mediator of postnatal growth; synthesis is GH-dependent. * **IGF-II:** Major mediator of fetal growth; synthesis is largely GH-independent. * **Receptors:** IGF-I acts via a tyrosine kinase receptor (similar to insulin). The IGF-II receptor is identical to the **Mannose-6-Phosphate receptor**, which is involved in lysosomal enzyme targeting. * **Clinical Correlation:** Excessive IGF-II production by non-islet cell tumors can lead to **hypoglycemia** (Doege-Potter Syndrome).

Q: Which of the following acts on nuclear receptors?

Thyroxine. **Explanation:** The mechanism of hormone action is determined by the chemical nature of the hormone. Receptors are generally classified into cell surface receptors (for water-soluble hormones) and intracellular receptors (for lipid-soluble hormones). **1. Why Thyroxine (B) is the Correct Answer:** Thyroid hormones (T3 and T4) are unique. Although they are derived from the amino acid tyrosine, they are lipophilic. They enter the cell via carrier-mediated transport and bind directly to **nuclear receptors** (specifically the Thyroid Hormone Receptor, TR). Once bound, they act as hormone-activated transcription factors, altering gene expression. **2. Analysis of Incorrect Options:** * **Glucocorticoids (A) and Progesterone (C):** These are steroid hormones. While they act on intracellular receptors, their primary receptors are located in the **cytoplasm**. Upon binding, the hormone-receptor complex translocates into the nucleus. Therefore, while they have nuclear effects, "Thyroxine" is the classic textbook answer for a receptor that is constitutively located *inside* the nucleus. * **Insulin (D):** This is a peptide hormone. It is water-soluble and cannot cross the lipid bilayer. It binds to a **transmembrane receptor** with intrinsic **Tyrosine Kinase** activity (Enzyme-linked receptor). **High-Yield NEET-PG Pearls:** * **Pure Nuclear Receptors:** Thyroid hormones (T3/T4), Retinoic acid (Vitamin A), and Vitamin D. * **Cytoplasmic Receptors:** Steroid hormones (Glucocorticoids, Mineralocorticoids, Progesterone, Estrogen, Testosterone). * **Mnemonic for Tyrosine Kinase:** "PIG" (Prolactin, Insulin, Growth Hormone). * **Note:** In many recent physiological classifications, both steroids and thyroid hormones are grouped as "Intracellular Receptors," but if "Thyroxine" is an option, it is the most specific answer for a receptor located permanently on the chromatin.

Q: Which of the following is secreted by the pineal gland?

Melatonin. **Explanation:** The **pineal gland** (epiphysis cerebri) is a small, pine-cone-shaped endocrine gland located in the midline of the brain, behind the third ventricle. Its primary function is the synthesis and secretion of **Melatonin**, a hormone derived from the amino acid **Tryptophan**. **1. Why Melatonin is correct:** Melatonin is synthesized via a pathway involving Serotonin. Its secretion is strictly regulated by the light-dark cycle (circadian rhythm). Light signals from the retina travel via the suprachiasmatic nucleus (SCN) to the pineal gland; darkness stimulates melatonin release, while light inhibits it. It plays a crucial role in regulating the sleep-wake cycle and has antioxidant properties. **2. Why the other options are incorrect:** * **Melanin (A):** This is a pigment produced by **melanocytes** in the skin and hair. It is not a hormone secreted by the pineal gland. (Note: MSH—Melanocyte Stimulating Hormone—is secreted by the anterior pituitary). * **ANP (C):** Atrial Natriuretic Peptide is a hormone secreted by the **atria of the heart** in response to high blood pressure/stretch. * **GH (D):** Growth Hormone is secreted by the somatotrophs of the **Anterior Pituitary gland**. **High-Yield Facts for NEET-PG:** * **Precursor:** Tryptophan → 5-Hydroxytryptophan → Serotonin → Melatonin. * **Rate-limiting enzyme:** N-acetyltransferase (NAT). * **Biological Clock:** The Suprachiasmatic Nucleus (SCN) of the hypothalamus is the master pacemaker that controls the pineal gland. * **Clinical Correlation:** Melatonin is used therapeutically for **jet lag** and delayed sleep phase syndrome. * **Brain Sand:** Calcification of the pineal gland (corpora arenacea) is a common radiological finding in adults, used as a midline marker on X-rays/CT scans.

Question 1

Which of the following statements about calcitonin is incorrect?

Accepted Answer

It plays a major role in the regulation of calcium levels in humans.

Answer

It inhibits osteoclast-mediated bone resorption.

Answer

It increases phosphate excretion in the kidneys.

Answer

It is useful in treating acute hypercalcemic crisis.

Question 2

Prolactin secretion is inhibited by which of the following?

Accepted Answer

Dopamine excess

Answer

Metoclopramide

Answer

Hypothyroidism

Answer

Emotional stress

Question 3

Which one of the following statements regarding Growth Hormone (GH) secretion is true?

Accepted Answer

GH secretion increases after exercise, stress, and hypoglycemia.

Answer

GH secretion is maximum during the evening.

Answer

GH is produced equally in all age groups.

Answer

GH decreases circulating IGF and somatostatin.

Question 4

Aldosterone secretion is controlled by all of the following except:

Accepted Answer

Increase in ECF volume

Answer

ACTH

Answer

Increase in potassium ion concentration in ECF

Answer

Decrease in the sodium ion concentration in ECF

Question 5

Primary Adrenal Insufficiency causes all of the following, except?

Accepted Answer

Increased protein breakdown

Answer

Low Blood Pressure

Answer

Decrease in Extracellular Fluid (ECF)

Answer

Decreased sodium-potassium ratio

Question 6

Laron dwarfism is caused by which of the following?

Accepted Answer

GH receptor defect

Answer

Deficiency of Growth Hormone (GH)

Answer

Deficiency of thyroxin

Answer

Thyroxin receptor defect

Question 7

Growth hormone increases all of the following except?

Accepted Answer

Metabolism of carbohydrates

Answer

Blood glucose concentration

Answer

Blood free fatty acid concentration

Answer

Protein synthesis

Question 8

Insulin-like growth factor-II (IGF-II) is synthesized in all of the following tissues EXCEPT:

Accepted Answer

Cartilage

Answer

Brain

Answer

Liver

Answer

Pancreas

Question 9

Which of the following acts on nuclear receptors?

Accepted Answer

Thyroxine

Answer

Glucocorticoids

Answer

Progesterone

Answer

Insulin

Question 10

Which of the following is secreted by the pineal gland?

Accepted Answer

Melatonin

Answer

Melanin

Answer

ANP

Answer

GH

Endocrinology — MCQs

Endocrinology — MCQs

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