Endocrinology Practice Questions

Q: A 45-year old woman is admitted to the hospital following a head injury. She has severe polyuria (producing 1 L of urine every 2 hours) and polydipsia (drinking 3 to 4 glasses of water every hour). During a 24-hour period in the hospital, the woman produces 10 L of urine, containing no glucose. She is placed on overnight water restriction for further evaluation. The following morning, she is weak and confused. Her serum osmolarity is 330 mOsm/L, her serum sodium is 164 mEq/L, and her urine osmolarity is 70 mOsm/L. She is treated with dDAVP by nasal spray. Within 24 hours of initiating the treatment, her serum osmolarity is 295 mOsm/L and her urine osmolarity is 620 mOsm/L. What is the most likely diagnosis?

Central Diabetes Insipidus. ### Explanation **1. Why Central Diabetes Insipidus (CDI) is the Correct Answer:** The patient presents with the classic triad of **polyuria, polydipsia, and hypernatremic dehydration** following a head injury (a common cause of damage to the hypothalamus or posterior pituitary). * **Water Deprivation Test:** The patient’s urine remains dilute (70 mOsm/L) despite high serum osmolarity (330 mOsm/L), indicating a failure to concentrate urine. This confirms Diabetes Insipidus (DI). * **Response to dDAVP (Desmopressin):** This is the "gold standard" for differentiation. In this case, administering dDAVP (an ADH analogue) caused a dramatic increase in urine osmolarity (from 70 to 620 mOsm/L). This significant response (>50% increase) proves that the kidneys are sensitive to ADH, but the body is not producing it. Thus, the diagnosis is **Central Diabetes Insipidus**. **2. Why Other Options are Incorrect:** * **Options A & B (Diabetes Mellitus):** While DM causes polyuria and polydipsia, it is characterized by **glycosuria** and osmotic diuresis. The question explicitly states there is "no glucose" in the urine. * **Option D (Juvenile Diabetes Insipidus):** This is not a standard clinical classification for this presentation. CDI can occur at any age, and in this case, it is clearly secondary to trauma. **3. NEET-PG High-Yield Pearls:** * **Etiology:** Head trauma, pituitary surgery (Sheehan syndrome), or idiopathic are common causes of CDI. * **Nephrogenic DI:** If the urine osmolarity had remained low after dDAVP, the diagnosis would be Nephrogenic DI (ADH resistance), often caused by Lithium or mutations in V2 receptors. * **Diagnostic Cut-off:** A urine osmolarity increase of **>50%** after desmopressin indicates Central DI; an increase of **<10%** indicates Nephrogenic DI. * **Normal Serum Osmolarity:** 275–295 mOsm/L. This patient’s 330 mOsm/L indicates severe dehydration.

Q: Which of the following hormones is an example of a peptide hormone?

Parathormone. **Explanation:** Hormones are classified based on their chemical structure into three main categories: peptides/proteins, steroids, and amino acid derivatives. **1. Why Parathormone is Correct:** **Parathormone (PTH)** is a classic **peptide hormone** consisting of a single chain of 84 amino acids. It is synthesized as a pre-prohormone in the ribosomes of the parathyroid glands, processed in the Golgi apparatus, and stored in secretory vesicles. Other examples of peptide/protein hormones include Insulin, Glucagon, GH, and ADH. **2. Why the Other Options are Incorrect:** * **Adrenaline (Option B):** This is an **amino acid derivative** (specifically a catecholamine) derived from the amino acid **Tyrosine**. * **Cortisol (Option C):** This is a **steroid hormone** derived from **cholesterol**. Steroid hormones are lipid-soluble and act via intracellular receptors. * **Thyroxine (Option D):** Although derived from the amino acid **Tyrosine**, T4 (and T3) are unique because they are lipid-soluble and behave more like steroid hormones in their mechanism of action. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Most peptide hormones (like PTH) are water-soluble and cannot cross the lipid bilayer; therefore, they bind to **cell surface receptors** and utilize **second messengers** (e.g., cAMP). * **PTH Function:** It increases serum calcium by acting on bone (resorption), kidneys (reabsorption), and intestines (via Vitamin D activation). * **Memory Aid:** If a hormone comes from the **P**ituitary, **P**ancreas, or **P**arathyroid, it is likely a **P**eptide/Protein hormone.

Q: Glucagon is secreted by which cells?

Alpha cells of pancreas. **Explanation:** The pancreas is a dual-function organ containing endocrine units known as the **Islets of Langerhans**. These islets consist of several distinct cell types, each secreting specific hormones directly into the bloodstream to regulate metabolism. **1. Why Alpha Cells are Correct:** Glucagon is synthesized and secreted by the **Alpha (α) cells**, which constitute approximately 20% of the islet cells. Glucagon is a catabolic hormone; its primary role is to increase blood glucose levels during fasting states by stimulating **glycogenolysis** (breakdown of glycogen) and **gluconeogenesis** (synthesis of glucose) in the liver. **2. Analysis of Incorrect Options:** * **Beta (β) cells:** These are the most abundant cells (approx. 65-75%) in the islets. They secrete **Insulin**, which lowers blood glucose, and **Amylin**. * **Gamma (γ) cells (also known as F or PP cells):** These cells secrete **Pancreatic Polypeptide**, which helps regulate pancreatic exocrine secretions and gallbladder contraction. * **Delta (δ) cells (not listed but high-yield):** These secrete **Somatostatin**, which acts paratrinely to inhibit the secretion of both insulin and glucagon. **High-Yield NEET-PG Clinical Pearls:** * **Glucagonoma:** A rare tumor of alpha cells characterized by the "4 Ds": Diabetes mellitus, Dermatitis (Necrolytic Migratory Erythema), Deep vein thrombosis, and Depression. * **Glucagon as an Antidote:** It is the drug of choice for **Beta-blocker overdose** because it increases intracellular cAMP in the myocardium via non-adrenergic pathways, exerting a positive inotropic effect. * **Inhibitor:** Glucagon secretion is inhibited by high blood glucose levels and insulin (via paracrine action).

Q: Aldosterone is secreted by which layer of the adrenal cortex?

Zona glomerulosa. **Explanation:** The adrenal cortex is histologically divided into three distinct layers, each responsible for secreting specific steroid hormones. A common mnemonic to remember these layers from superficial to deep is **GFR** (Glomerulosa, Fasciculata, Reticularis). 1. **Zona Glomerulosa (Correct Answer):** This is the outermost layer. It contains the enzyme *aldosterone synthase*, making it the exclusive site for the synthesis of **Mineralocorticoids**, primarily **Aldosterone**. Aldosterone plays a critical role in blood pressure regulation by promoting sodium reabsorption and potassium excretion in the distal nephron. 2. **Zona Fasciculata (Incorrect):** This is the middle and widest layer. It primarily secretes **Glucocorticoids** (mainly Cortisol) in response to ACTH. 3. **Adrenal Medulla (Incorrect):** This is the innermost core of the adrenal gland, not part of the cortex. It is derived from neural crest cells and secretes **Catecholamines** (Epinephrine and Norepinephrine). 4. **Pituitary Gland (Incorrect):** This is a master endocrine gland located at the base of the brain. While it regulates the adrenal cortex via ACTH, it does not secrete aldosterone. **High-Yield NEET-PG Pearls:** * **Regulation:** Unlike the other layers, the Zona Glomerulosa is primarily regulated by **Angiotensin II** and **extracellular Potassium levels**, and only minimally by ACTH. * **Conn’s Syndrome:** Primary hyperaldosteronism, usually caused by an adrenal adenoma, leading to hypertension and hypokalemia. * **Mnemonic for Hormones:** **"Salt, Sugar, Sex"** (Glomerulosa = Salt/Mineraloids; Fasciculata = Sugar/Glucocorticoids; Reticularis = Sex/Androgens).

Q: Growth hormone is also known as:

Somatotropin. **Explanation:** **Growth Hormone (GH)** is a peptide hormone synthesized and secreted by the **somatotrophs** of the anterior pituitary gland. It is also known as **Somatotropin** because it exerts a "tropic" (stimulating) effect on body growth and cellular regeneration. **Analysis of Options:** * **Somatotropin (Correct):** This is the synonymous term for Growth Hormone. It promotes protein synthesis, lipolysis, and gluconeogenesis, while indirectly stimulating skeletal growth via IGF-1. * **Somatostatin (Incorrect):** Also known as Growth Hormone Inhibiting Hormone (GHIH), it is secreted by the hypothalamus (and delta cells of the pancreas) to **inhibit** the release of GH and TSH. * **Somatocrinin (Incorrect):** This is another name for Growth Hormone Releasing Hormone (GHRH), produced by the hypothalamus to **stimulate** GH secretion. * **Somatomedin (Incorrect):** These are insulin-like growth factors (primarily **IGF-1**) produced mainly in the liver in response to GH. They mediate the growth-promoting effects of GH on bone and cartilage. **High-Yield NEET-PG Pearls:** 1. **Pulsatile Secretion:** GH is secreted in pulses, with the largest burst occurring during **deep sleep (Stage N3/SWS)**. 2. **Metabolic Effects:** GH is **diabetogenic** (increases blood glucose) and **lipolytic** (increases free fatty acids). 3. **Clinical Correlation:** Excess GH leads to **Gigantism** (pre-puberty) or **Acromegaly** (post-puberty). Deficiency in children leads to **Dwarfism** (e.g., Laron dwarfism, which is due to GH receptor insensitivity). 4. **Stimuli:** Hypoglycemia, fasting, and exercise are potent stimulators of GH release.

Q: Refeeding edema is due to increased release of-

Insulin. **Explanation:** **Refeeding edema** occurs when a patient who has been in a prolonged state of starvation or malnutrition (such as in Anorexia Nervosa or Marasmus) begins to consume carbohydrates again. **Why Insulin is the Correct Answer:** During starvation, insulin levels are low, and the body relies on ketone bodies and fatty acids. Upon refeeding, the sudden intake of carbohydrates triggers a **massive release of insulin**. Insulin has a potent **antinatriuretic effect** on the kidneys; it acts directly on the proximal convoluted tubule and the distal nephron to increase the reabsorption of sodium and water. This sudden expansion of extracellular fluid (ECF) volume leads to dependent edema and, in severe cases, heart failure. **Why Other Options are Incorrect:** * **Growth Hormone (GH):** While GH can cause some fluid retention, it is not the primary mediator of the acute fluid shifts seen in refeeding syndrome. * **Glucocorticoids (Cortisol):** Cortisol levels are typically elevated during the stress of starvation. Refeeding actually tends to normalize (decrease) cortisol levels rather than increase them. * **Thyroxine (T4):** Starvation often leads to "Euthyroid Sick Syndrome" (low T3). Refeeding helps restore thyroid function, but thyroxine does not cause acute sodium retention or edema. **Clinical Pearls for NEET-PG:** * **Refeeding Syndrome:** Characterized by the "Hallmark Triad" of **Hypophosphatemia, Hypokalemia, and Hypomagnesemia**. * **Mechanism of Hypophosphatemia:** Insulin drives phosphorus into cells for glycolysis and ATP production, leading to a dangerous drop in serum phosphorus levels. * **Management:** "Start low and go slow" with caloric intake and aggressively supplement electrolytes (especially Phosphorus and Thiamine).

Q: In a fetus, when does insulin secretion begin?

3rd month. **Explanation:** The development of the endocrine pancreas is a critical milestone in fetal physiology. The correct answer is **3rd month (Option A)** because the differentiation of the pancreas into endocrine and exocrine components occurs early in gestation. * **Why 3rd month is correct:** The pancreatic buds appear around the 5th week of gestation. By the **10th to 12th week (end of the 1st trimester/early 3rd month)**, the Islets of Langerhans develop, and beta cells begin secreting insulin. While insulin is present in the fetal circulation by this time, it is important to note that fetal insulin secretion is primarily regulated by amino acids and glucose, though the fetal beta cells are less sensitive to glucose than adult cells. * **Why Options B, C, and D are incorrect:** These options represent the 2nd and 3rd trimesters. By the **5th month (20 weeks)**, insulin levels are already well-established and play a major role in fetal accretion and growth. Waiting until the **7th or 9th month** would be too late for the metabolic demands of the developing fetus, as insulin is the primary anabolic hormone for fetal tissue growth. **High-Yield Clinical Pearls for NEET-PG:** 1. **Growth Hormone of the Fetus:** Insulin is considered the primary "growth hormone" of the fetus. Unlike maternal insulin, maternal glucose crosses the placenta. 2. **Maternal Diabetes:** In gestational diabetes, maternal hyperglycemia leads to fetal hyperglycemia, which causes **fetal hyperinsulinemia**. This results in **macrosomia** (large baby) and potential neonatal hypoglycemia after birth. 3. **Placental Barrier:** Insulin **does not** cross the placenta. All insulin found in the fetal circulation is produced by the fetal pancreas. 4. **Glucagon:** Alpha cells differentiate even earlier than beta cells, with glucagon detectable by the 8th week of gestation.

Q: Which hormone is primarily responsible for prostatic hypertrophy?

DHT. **Explanation:** The correct answer is **Dihydrotestosterone (DHT)**. **1. Why DHT is correct:** While testosterone is the primary circulating androgen, it acts as a pro-hormone in the prostate gland. Within the prostatic stromal and epithelial cells, the enzyme **5-alpha reductase (Type 2)** converts testosterone into DHT. DHT is significantly more potent than testosterone because it has a higher affinity for the androgen receptor and forms a more stable receptor-ligand complex. DHT stimulates the production of growth factors (like FGF and TGF-β), leading to the proliferation of prostatic tissue, which is the hallmark of **Benign Prostatic Hyperplasia (BPH)**. **2. Why the other options are incorrect:** * **Testosterone (A):** Although it is the precursor, testosterone itself has a minimal direct effect on prostatic growth. Men with a genetic deficiency of 5-alpha reductase do not develop BPH, despite having normal or high testosterone levels. * **FSH (B) & LH (C):** These are gonadotropins secreted by the anterior pituitary. LH stimulates Leydig cells to produce testosterone, and FSH stimulates Sertoli cells for spermatogenesis. While they regulate the androgen pathway, they do not directly cause prostatic hypertrophy. **Clinical Pearls for NEET-PG:** * **Pharmacology Link:** **Finasteride** and **Dutasteride** are 5-alpha reductase inhibitors used to treat BPH by lowering intraprostatic DHT levels. * **Anatomy Link:** BPH primarily involves the **Transitional Zone** of the prostate, whereas Prostate Cancer typically arises in the **Peripheral Zone**. * **Estrogen Role:** In aging men, the estrogen/androgen ratio increases, which may sensitize the prostate to the effects of DHT.

Q: What is the effect of steroids on calcium?

Increased excretion of calcium from the kidney. **Explanation:** Glucocorticoids (steroids) exert a significant **antagonistic effect on calcium metabolism**, primarily leading to a reduction in total body calcium. 1. **Why Option C is Correct:** Steroids directly inhibit calcium reabsorption in the renal tubules. By decreasing tubular reabsorption, they promote **hypercalciuria** (increased excretion of calcium in the urine). This is a key mechanism used clinically to treat hypercalcemia (e.g., in sarcoidosis or Vitamin D toxicity). 2. **Why Option B is Incorrect:** Steroids actually **decrease** the intestinal absorption of calcium. They antagonize the actions of Vitamin D in the gut and inhibit the expression of calbindin (the calcium-binding protein), leading to reduced calcium uptake. 3. **Why Option A is Incorrect:** Because steroids decrease gut absorption and increase renal excretion, the net effect is a **decrease in plasma calcium levels** (hypocalcemia). This drop in plasma calcium triggers a secondary rise in Parathyroid Hormone (PTH), which then mobilizes calcium from the bones. **Clinical Pearls for NEET-PG:** * **Steroid-Induced Osteoporosis:** The combination of decreased gut absorption, increased renal loss, and secondary hyperparathyroidism leads to increased osteoclast activity and bone resorption. * **Vitamin D Antagonism:** Steroids are the treatment of choice for **Vitamin D toxicity** because they counteract Vitamin D’s effect on the gut and kidneys. * **Growth:** In children, the chronic use of steroids can lead to growth retardation partly due to these alterations in calcium and bone metabolism.

Question 1

A 45-year old woman is admitted to the hospital following a head injury. She has severe polyuria (producing 1 L of urine every 2 hours) and polydipsia (drinking 3 to 4 glasses of water every hour). During a 24-hour period in the hospital, the woman produces 10 L of urine, containing no glucose. She is placed on overnight water restriction for further evaluation. The following morning, she is weak and confused. Her serum osmolarity is 330 mOsm/L, her serum sodium is 164 mEq/L, and her urine osmolarity is 70 mOsm/L. She is treated with dDAVP by nasal spray. Within 24 hours of initiating the treatment, her serum osmolarity is 295 mOsm/L and her urine osmolarity is 620 mOsm/L. What is the most likely diagnosis?

Accepted Answer

Central Diabetes Insipidus

Answer

Diabetes Mellitus Type I

Answer

Diabetes Mellitus Type II

Answer

Juvenile Diabetes Insipidus

Question 2

Which of the following hormones is an example of a peptide hormone?

Accepted Answer

Parathormone

Answer

Adrenaline

Answer

Cortisol

Answer

Thyroxine

Question 3

Glucagon is secreted by which cells?

Accepted Answer

Alpha cells of pancreas

Answer

Beta cells of pancreas

Answer

Gamma cells of pancreas

Answer

None of the above

Question 4

Aldosterone is secreted by which layer of the adrenal cortex?

Accepted Answer

Zona glomerulosa

Answer

Pituitary gland

Answer

Zona fasciculata

Answer

Adrenal medulla

Question 5

All of the following statements regarding calcium are true except:

Accepted Answer

Intestinal calcium absorption efficiency is inversely related to calcium intake.

Answer

It serves as a second messenger for the actions of many hormones.

Answer

Tubular reabsorption of calcium is regulated by parathyroid hormone.

Answer

Ionized calcium in the plasma exerts physiological effects.

Question 6

Growth hormone is also known as:

Accepted Answer

Somatotropin

Answer

Somatostatin

Answer

Somatocrinin

Answer

Somatomedin

Question 7

Refeeding edema is due to increased release of-

Accepted Answer

Insulin

Answer

Growth hormone

Answer

Glucocorticoids

Answer

Thyroxine

Question 8

In a fetus, when does insulin secretion begin?

Accepted Answer

3rd month

Answer

5th month

Answer

7th month

Answer

9th month

Question 9

Which hormone is primarily responsible for prostatic hypertrophy?

Accepted Answer

DHT

Answer

Testosterone

Answer

FSH

Answer

LH

Question 10

What is the effect of steroids on calcium?

Accepted Answer

Increased excretion of calcium from the kidney

Answer

Increased plasma calcium level

Answer

Increased absorption of calcium from the gut

Answer

None of the above

Endocrinology — MCQs

Endocrinology — MCQs

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