Endocrinology — MCQs
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Tertiary hyperparathyroidism is defined as:
A female patient presents with anorexia, weight loss, hyperpigmentation, bowel changes, and lightheadedness on standing. The cosyntropin stimulation test shows a random serum cortisol of 11 mcg/dL (normal is greater than or equal to 20 mcg/dL). Serum cortisol 1 hour after 0.25 mg cosyntropin IM is 14 mcg/dL (the rise in cortisol is expected to be > 7 mcg/dL). Aldosterone level is 10 ng/dL. Which of the following is an appropriate treatment for this patient?
Which of the following is NOT true about Hashimoto's thyroiditis?
A false positive oral glucose tolerance test (OGTT) is seen in all of the following conditions EXCEPT?
A patient presents with raised serum alkaline phosphatase and raised parathormone levels, along with low calcium and low phosphate levels. What is the most likely diagnosis?
Increased blood levels of cholesterol seen in hypothyroidism are most likely due to which of the following mechanisms?
A vasopressin analogue does not produce a therapeutic effect through the vasopressin V-2 receptor in which of the following conditions?
A high carbohydrate diet can precipitate which of the following conditions?
What is the most common presentation of endemic goiter?
All are causes of Gynaecomastia, except?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 781: Tertiary hyperparathyroidism is defined as:
- A. An autonomous state due to monoclonal outgrowth of previously hyperplastic parathyroid glands (Correct Answer)
- B. Increased sensitivity to serum calcium
- C. A condition seen in patients with parathyroid adenoma
- D. A state dependent on hypothalamic stimulus
Explanation: **Explanation:** **Tertiary Hyperparathyroidism (tHPT)** occurs when long-standing secondary hyperparathyroidism (usually due to Chronic Kidney Disease) leads to irreversible changes in the parathyroid glands [2]. 1. **Why Option A is correct:** In secondary hyperparathyroidism, the glands undergo diffuse hyperplasia to compensate for low calcium/high phosphate [1]. Over time, specific cells undergo a genetic transformation, leading to **monoclonal outgrowth**. These cells become **autonomous**, meaning they continue to secrete high levels of Parathyroid Hormone (PTH) even after the underlying cause (e.g., renal failure) is corrected (such as via renal transplant) [2]. This results in hypercalcemia. 2. **Why the other options are wrong:** * **Option B:** In tHPT, there is actually a **decreased sensitivity** to serum calcium (an upward shift in the set-point of the calcium-sensing receptor), allowing PTH secretion despite high calcium levels [1]. * **Option C:** Parathyroid adenoma is the hallmark of **Primary** Hyperparathyroidism, not Tertiary [4]. Tertiary involves four-gland hyperplasia that has turned autonomous. * **Option D:** Parathyroid function is regulated by serum ionized calcium levels and the Calcium-Sensing Receptor (CaSR); it is **not** under the control of the hypothalamus or pituitary gland [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence:** Primary (Adenoma) → Secondary (Hypocalcemia/CKD) → Tertiary (Post-CKD/Transplant with Hypercalcemia). * **Biochemical Profile of tHPT:** Very high PTH + Hypercalcemia + Hyperphosphatemia. * **Treatment of Choice:** Subtotal parathyroidectomy (3.5 glands) or total parathyroidectomy with autotransplantation. * **Key Trigger:** Often diagnosed after a successful renal transplant when PTH remains high despite normalized renal function [2].
Question 782: A female patient presents with anorexia, weight loss, hyperpigmentation, bowel changes, and lightheadedness on standing. The cosyntropin stimulation test shows a random serum cortisol of 11 mcg/dL (normal is greater than or equal to 20 mcg/dL). Serum cortisol 1 hour after 0.25 mg cosyntropin IM is 14 mcg/dL (the rise in cortisol is expected to be > 7 mcg/dL). Aldosterone level is 10 ng/dL. Which of the following is an appropriate treatment for this patient?
- A. Hydrocortisone 15 mg daily for life
- B. Prednisone 5 mg daily for life
- C. Hydrocortisone 15 mg and fludrocortisone 0.1 mg daily for life (Correct Answer)
- D. Prednisone 60 mg daily tapering to 10 mg a day and fludrocortisone 0.1 mg daily for life
Explanation: ### Explanation **1. Why Option C is Correct:** The patient presents with classic features of **Primary Adrenocortical Insufficiency (Addison’s Disease)**: weight loss, hyperpigmentation (due to increased ACTH/POMC), and orthostatic hypotension [1], [2]. The diagnosis is confirmed by the **Cosyntropin (ACTH) stimulation test**, where the peak cortisol level is <18–20 mcg/dL and the rise is inadequate (<7 mcg/dL) [1]. In Primary Adrenal Insufficiency, there is a deficiency of **both glucocorticoids and mineralocorticoids** because the entire adrenal cortex is affected [1]. Therefore, treatment requires: * **Glucocorticoid replacement:** Hydrocortisone (15–25 mg/day) is preferred due to its short half-life and mineralocorticoid activity [1]. * **Mineralocorticoid replacement:** Fludrocortisone (0.05–0.2 mg/day) is essential to maintain electrolyte balance and blood pressure [1]. **2. Why Other Options are Incorrect:** * **Options A & B:** These provide only glucocorticoid replacement. While this might suffice for *Secondary* Adrenal Insufficiency (where the renin-angiotensin-aldosterone axis is intact), it is insufficient for *Primary* disease, leaving the patient at risk for hyponatremia, hyperkalemia, and hypotension [3]. * **Option D:** This represents a pharmacological "stress dose" or a regimen for inflammatory conditions. Maintenance therapy for Addison’s aims for physiological replacement, not supraphysiological suppression. **3. NEET-PG High-Yield Pearls:** * **Hyperpigmentation:** Only seen in Primary Adrenal Insufficiency (due to ACTH cross-reactivity with MSR-1 receptors). It is absent in Secondary (Pituitary) disease [3]. * **Electrolytes:** Look for **Hyponatremia, Hyperkalemia, and Metabolic Acidosis** in Addison’s [1]. * **Crisis Management:** In an acute adrenal crisis, the drug of choice is **IV Hydrocortisone (100mg bolus)** and aggressive saline resuscitation [1]. * **Monitoring:** Fludrocortisone dosage is adjusted based on blood pressure and plasma renin activity, not serum electrolytes alone.
Question 783: Which of the following is NOT true about Hashimoto's thyroiditis?
- A. Presence of antithyroid microsomal antibodies
- B. Presence of antithyroid nuclear antibodies (Correct Answer)
- C. Presence of anti-TSH receptor antibodies
- D. Increased levels of thyroid hormones
Explanation: Hashimoto’s Thyroiditis (Chronic Lymphocytic Thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient regions. It is an autoimmune disorder characterized by the destruction of thyroid follicles by T-cells and autoantibodies. **Why Option B is the correct answer:** **Antithyroid nuclear antibodies** are not a feature of Hashimoto’s thyroiditis. While Antinuclear Antibodies (ANA) are markers for systemic autoimmune diseases like SLE, they are not specific to or diagnostic of Hashimoto’s. The primary antibodies involved in Hashimoto's target thyroid-specific antigens, not nuclear components. **Analysis of other options:** * **Option A (Antithyroid microsomal antibodies):** These are now commonly known as **Anti-TPO (Thyroid Peroxidase) antibodies**. They are present in >95% of patients and are the hallmark of the disease. * **Option C (Anti-TSH receptor antibodies):** While typically associated with Graves’ disease (stimulating type), **TSH-receptor blocking antibodies** can occur in Hashimoto’s, contributing to thyroid atrophy and hypothyroidism [1]. * **Option D (Increased levels of thyroid hormones):** Although Hashimoto’s typically causes hypothyroidism, patients can experience a transient thyrotoxic phase called **"Hashitoxicosis"** due to the leakage of preformed hormones from damaged follicles [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for **Hurthle cells** (Askanazy cells)—large eosinophilic follicular cells—and dense lymphocytic infiltrates with **germinal centers**. * **Risk Factor:** Strongly associated with **HLA-DR3 and HLA-DR5**. * **Complication:** Patients have an increased risk of developing **Primary Thyroid B-cell Lymphoma** (MALToma). * **Physical Exam:** Typically presents as a firm, painless, diffuse goiter.
Question 784: A false positive oral glucose tolerance test (OGTT) is seen in all of the following conditions EXCEPT?
- A. Malnutrition
- B. Infection
- C. Severe emotional stress
- D. Exercise (Correct Answer)
Explanation: **Explanation:** The Oral Glucose Tolerance Test (OGTT) is a dynamic test used to diagnose Diabetes Mellitus and Impaired Glucose Tolerance. A **false positive** result occurs when a patient’s glucose levels appear abnormally high (diabetic range) due to factors other than true diabetes [2]. **Why Exercise is the Correct Answer:** Exercise increases insulin sensitivity and promotes glucose uptake by skeletal muscles via the translocation of GLUT-4 receptors [3]. This leads to **lower** blood glucose levels. Therefore, exercise would more likely cause a false negative or a lower-than-expected reading, rather than a false positive. For an accurate OGTT, patients are advised to remain seated and avoid strenuous activity during the test. **Analysis of Incorrect Options (Causes of False Positives):** * **Malnutrition:** Prolonged starvation or a low-carbohydrate diet leads to "starvation diabetes." The body shifts to fat metabolism, and the pancreas becomes "sluggish" in releasing insulin when suddenly challenged with a glucose load. * **Infection and Severe Emotional Stress:** These are states of high physiological stress. They trigger the release of **counter-regulatory hormones** (Cortisol, Adrenaline, Glucagon, and Growth Hormone). These hormones antagonize insulin and promote gluconeogenesis, leading to transient hyperglycemia [1]. **NEET-PG Clinical Pearls:** * **Preparation for OGTT:** The patient must consume at least **150g of carbohydrates per day** for 3 days prior to the test to ensure the pancreas is adequately "primed." * **WHO Criteria:** For a 75g OGTT, a 2-hour post-load plasma glucose of **≥200 mg/dL** is diagnostic of Diabetes, while **140–199 mg/dL** indicates Impaired Glucose Tolerance (IGT) [2]. * **Drugs causing False Positives:** Thiazide diuretics, Glucocorticoids, and Oral Contraceptive Pills [1].
Question 785: A patient presents with raised serum alkaline phosphatase and raised parathormone levels, along with low calcium and low phosphate levels. What is the most likely diagnosis?
- A. Primary hyperparathyroidism
- B. Paget's disease
- C. Osteoporosis
- D. Vitamin D deficiency (Correct Answer)
Explanation: ### Explanation The biochemical profile described—**low calcium, low phosphate, raised PTH, and raised Alkaline Phosphatase (ALP)**—is the classic presentation of **Vitamin D deficiency** (leading to Osteomalacia in adults or Rickets in children) [1]. **1. Why Vitamin D Deficiency is Correct:** Vitamin D is essential for the intestinal absorption of calcium and phosphate [2]. Its deficiency leads to: * **Low Calcium & Phosphate:** Reduced intestinal absorption [1]. * **Secondary Hyperparathyroidism:** Low serum calcium triggers the parathyroid glands to secrete more **PTH** to mobilize calcium from bones [2]. * **Raised ALP:** Increased osteoblastic activity occurs as the bone attempts to remineralize the unmineralized osteoid matrix [1]. **2. Why Other Options are Incorrect:** * **Primary Hyperparathyroidism:** Characterized by **high calcium** and low phosphate (due to PTH-induced phosphaturia). * **Paget’s Disease:** Typically presents with isolated **markedly elevated ALP**. Calcium, phosphate, and PTH levels are usually **normal**. * **Osteoporosis:** A quantitative rather than qualitative bone defect. All biochemical markers (Calcium, Phosphate, ALP, and PTH) are typically **normal**. **3. NEET-PG High-Yield Pearls:** * **PTH Effects:** PTH increases calcium but decreases phosphate (phosphaturic effect) in the kidneys [2]. * **Vitamin D vs. PTH:** Both Vitamin D deficiency and Hypoparathyroidism present with low calcium. However, PTH will be **high** in Vitamin D deficiency (Secondary) and **low** in Hypoparathyroidism [1]. * **Renal Osteodystrophy:** Similar to Vitamin D deficiency but will have **high phosphate** (due to decreased renal excretion) [1]. * **ALP:** Always think of increased bone turnover or osteoblastic activity when ALP is raised in a non-hepatic context [1].
Question 786: Increased blood levels of cholesterol seen in hypothyroidism are most likely due to which of the following mechanisms?
- A. Decreased calorigenesis
- B. Decreased production of LDL receptors in the liver, leading to decreased hepatic clearance
- C. Decreased production of LDL receptors in adipose tissue and increased release of cholesterol from adipose tissue (Correct Answer)
- D. Increased breakdown of lipoproteins releasing cholesterol into circulation
Explanation: **Explanation** In hypothyroidism, the characteristic elevation of serum cholesterol (specifically LDL) is primarily driven by a **reduction in the clearance of lipoproteins** rather than an increase in their synthesis [1]. **1. Why the Correct Answer is Right:** Thyroid hormones (T3/T4) play a critical role in lipid metabolism by upregulating the expression of **LDL receptors** on the surface of hepatocytes and peripheral tissues, including adipose tissue [1]. In a hypothyroid state, there is a **decreased production of LDL receptors**, which impairs the hepatic and peripheral uptake of LDL-cholesterol from the blood [1]. Additionally, while lipolysis is generally slowed, the overall metabolic shift leads to an altered lipid profile where the lack of receptor-mediated clearance is the dominant factor causing hypercholesterolemia. **2. Analysis of Incorrect Options:** * **Option A (Decreased calorigenesis):** While decreased calorigenesis (low BMR) is a hallmark of hypothyroidism, it explains symptoms like cold intolerance and weight gain, but it is not the direct molecular mechanism for elevated cholesterol [1]. * **Option B (Decreased production of LDL receptors in the liver only):** While hepatic clearance is vital, the physiological impact involves a systemic reduction in LDL receptors across tissues. However, in many standard textbooks, the reduction of LDL receptors is the primary mechanism; the specific mention of adipose tissue in the correct option reflects the systemic nature of the receptor deficit [1]. * **Option D (Increased breakdown of lipoproteins):** This is incorrect because hypothyroidism actually leads to **decreased** activity of enzymes like Lipoprotein Lipase (LPL) and Hepatic Lipase, resulting in slower breakdown and prolonged circulation of lipoproteins. **3. High-Yield Clinical Pearls for NEET-PG:** * **Lipid Profile in Hypothyroidism:** Characterized by increased Total Cholesterol, increased LDL, and often increased Triglycerides (due to decreased LPL activity). * **Secondary Hyperlipidemia:** Hypothyroidism is a leading cause of secondary hyperlipidemia. Always check TSH levels in patients with newly diagnosed high cholesterol before starting statins. * **Statin Risk:** Hypothyroid patients have an increased risk of **statin-induced myopathy**; hence, achieving a euthyroid state is a priority.
Question 787: A vasopressin analogue does not produce a therapeutic effect through the vasopressin V-2 receptor in which of the following conditions?
- A. Central diabetes insipidus
- B. Bleeding esophageal varices (Correct Answer)
- C. Type 1 von Willebrand's disease
- D. Primary nocturnal enuresis
Explanation: **Explanation:** The therapeutic effect of vasopressin analogues depends on which receptor subtype is targeted: **V1 receptors** (located on vascular smooth muscle, causing vasoconstriction) or **V2 receptors** (located in the renal collecting ducts for water reabsorption and on vascular endothelium to trigger factor release) [1]. **Why Option B is correct:** In **Bleeding Esophageal Varices**, the goal is to reduce portal venous pressure. Vasopressin analogues (specifically **Terlipressin**) act via **V1 receptors** to cause splanchnic vasoconstriction, thereby reducing blood flow into the portal system. This effect is independent of the V2 receptor. **Why the other options are incorrect:** * **Central Diabetes Insipidus (A):** Desmopressin (a selective V2 agonist) is the drug of choice. it acts on **V2 receptors** in the renal collecting ducts to increase water permeability via aquaporin-2 channels [1]. * **Type 1 von Willebrand’s Disease (C):** Desmopressin acts on **V2 receptors** on vascular endothelial cells to stimulate the release of stored von Willebrand factor (vWF) and Factor VIII. * **Primary Nocturnal Enuresis (D):** Desmopressin is used to decrease urine production overnight by activating renal **V2 receptors**, helping children who have a nocturnal deficiency of ADH. **High-Yield NEET-PG Pearls:** * **Desmopressin (dDAVP):** Highly selective for **V2**; preferred for DI and bleeding disorders because it lacks the pressor (V1) side effects. * **Terlipressin:** Selective for **V1**; drug of choice for Hepatorenal Syndrome and Variceal bleeding. * **V3 Receptors:** Located in the anterior pituitary; they mediate the release of ACTH [1]. * **Side Effect:** Hyponatremia is a critical risk when using V2 agonists like Desmopressin.
Question 788: A high carbohydrate diet can precipitate which of the following conditions?
- A. Hypokalemic periodic paralysis (Correct Answer)
- B. Hyperkalemic periodic paralysis
- C. Hysterical paralysis
- D. Myasthenia gravis
Explanation: **Explanation:** **Hypokalemic Periodic Paralysis (HPP)** is the correct answer because of the physiological relationship between glucose, insulin, and potassium. 1. **Mechanism of the Correct Answer:** A high carbohydrate diet triggers a significant release of **insulin**. Insulin acts on the Na+/K+-ATPase pump, shifting potassium from the extracellular fluid into the intracellular compartment (skeletal muscle) [2]. In individuals with genetic mutations in calcium or sodium channels (e.g., CACNA1S or SCN4A), this shift leads to acute hypokalemia and muscle membrane inexcitability, resulting in flaccid paralysis. Common triggers include high-carb meals, strenuous exercise followed by rest, and emotional stress [1]. 2. **Analysis of Incorrect Options:** * **Hyperkalemic Periodic Paralysis:** This condition is typically precipitated by fasting, rest after exercise, or potassium intake—not high carbohydrates [1]. In fact, glucose/insulin can be used to *treat* an acute attack by lowering potassium levels. * **Hysterical Paralysis (Conversion Disorder):** This is a psychiatric manifestation of neurological symptoms without a physiological cause. It is triggered by psychological stress, not dietary intake. * **Myasthenia Gravis:** This is an autoimmune disorder involving antibodies against acetylcholine receptors. It presents with fatigable weakness (ptosis, diplopia) and is unrelated to carbohydrate metabolism or potassium shifts. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most cases are Autosomal Dominant [1]. * **Thyrotoxic Periodic Paralysis (TPP):** A common secondary cause of HPP, especially in Asian males; it presents identically but is triggered by hyperthyroidism. * **Management:** Acute attacks are treated with oral potassium (preferred over IV to avoid rebound hyperkalemia). Prophylaxis includes **Acetazolamide** (a carbonic anhydrase inhibitor) and avoiding high-carb meals.
Question 789: What is the most common presentation of endemic goiter?
- A. Diffuse goiter (Correct Answer)
- B. Solitary nodule
- C. Hypothyroid
- D. Hyperthyroid
Explanation: **Explanation:** **Endemic goiter** is primarily caused by **iodine deficiency**, which remains the most common cause of goiter worldwide. 1. **Why "Diffuse Goiter" is correct:** When iodine intake is insufficient, the thyroid gland cannot produce adequate amounts of T3 and T4. This leads to a compensatory rise in **Thyroid Stimulating Hormone (TSH)** from the anterior pituitary. TSH exerts a trophic effect on the thyroid follicular cells, causing generalized hyperplasia and hypertrophy. In the early stages of endemic iodine deficiency, this results in a **symmetrical, smooth, and diffuse enlargement** of the gland (Diffuse Goiter) [1]. 2. **Why other options are incorrect:** * **Solitary Nodule:** While long-standing endemic goiters can eventually become "Multinodular Goiters" (MNG) due to alternating cycles of hyperplasia and involution, a solitary nodule is not the primary or most common initial presentation. * **Hypothyroid/Hyperthyroid:** Most patients with endemic goiter are clinically **euthyroid**. The compensatory enlargement of the gland is usually successful in maintaining normal circulating thyroid hormone levels. Overt hypothyroidism (Cretinism in children or Myxedema in adults) only occurs in cases of severe, prolonged deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** A goiter is considered "endemic" if it affects >5% of the population (or >10% of children). * **Evolution:** The natural history of endemic goiter follows the sequence: **Diffuse Goiter → Multinodular Goiter (MNG) → Toxic MNG (Plummer Disease).** [1] * **Jod-Basedow Phenomenon:** This refers to iodine-induced hyperthyroidism, which can occur when iodine is suddenly supplemented in a patient with a long-standing endemic goiter. * **Treatment:** The most cost-effective prevention is **iodization of salt** (minimum requirement: 150 μg/day for adults).
Question 790: All are causes of Gynaecomastia, except?
- A. Cimetidine therapy
- B. Androgen therapy (Correct Answer)
- C. Leprosy
- D. Small cell carcinoma of the lung
Explanation: Gynecomastia is the benign proliferation of glandular breast tissue in males, primarily caused by an **altered ratio of active estrogen to androgen**. [1] **Why Androgen Therapy is the correct answer:** While exogenous androgens can sometimes be converted to estrogen (aromatization), **pure Androgen therapy** (like Dihydrotestosterone or Testosterone replacement in hypogonadal men) typically suppresses breast tissue growth. In the context of this question, androgens are used to *treat* certain types of gynecomastia or represent the hormonal balance that prevents it. Therefore, it is the least likely cause compared to the other options. **Analysis of Incorrect Options:** * **Cimetidine:** A classic H2-receptor antagonist that causes gynecomastia by acting as a competitive inhibitor of the androgen receptor and increasing prolactin levels. * **Leprosy:** Specifically Lepromatous Leprosy causes testicular atrophy and orchitis, leading to primary hypogonadism and a subsequent rise in estrogen-androgen ratio. * **Small Cell Carcinoma of the Lung:** While more commonly associated with ectopic ACTH or SIADH, various lung malignancies can secrete **hCG (human Chorionic Gonadotropin)**. [1] hCG stimulates Leydig cells to produce estrogen, leading to paraneoplastic gynecomastia. **NEET-PG High-Yield Pearls:** * **Drugs causing Gynecomastia (Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common), **C**imetidine, **O**estrogens/Ketoconazole. * **Physiological causes:** Neonatal, Pubertal, and Senile (old age) are normal. [1] * **Klinefelter Syndrome (47, XXY):** The most common genetic cause of gynecomastia and carries a significantly higher risk of male breast cancer. * **Spironolactone** causes gynecomastia by displacing dihydrotestosterone (DHT) from its receptors. Eplerenone is the alternative that does not cause this.
Practice by Chapter
Diabetes Mellitus
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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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