Endocrinology Practice Questions

Q: Which of the following is NOT true about Hashimoto's thyroiditis?

Presence of antithyroid nuclear antibodies. 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.

Q: A false positive oral glucose tolerance test (OGTT) is seen in all of the following conditions EXCEPT?

Exercise. **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].

Q: 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?

Vitamin D deficiency. ### 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].

Q: A vasopressin analogue does not produce a therapeutic effect through the vasopressin V-2 receptor in which of the following conditions?

Bleeding esophageal varices. **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.

Q: A high carbohydrate diet can precipitate which of the following conditions?

Hypokalemic periodic paralysis. **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.

Q: What is the most common presentation of endemic goiter?

Diffuse goiter. **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).

Q: All are causes of Gynaecomastia, except?

Androgen therapy. 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.

Question 1

Tertiary hyperparathyroidism is defined as:

Accepted Answer

An autonomous state due to monoclonal outgrowth of previously hyperplastic parathyroid glands

Answer

Increased sensitivity to serum calcium

Answer

A condition seen in patients with parathyroid adenoma

Answer

A state dependent on hypothalamic stimulus

Question 2

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?

Accepted Answer

Hydrocortisone 15 mg and fludrocortisone 0.1 mg daily for life

Answer

Hydrocortisone 15 mg daily for life

Answer

Prednisone 5 mg daily for life

Answer

Prednisone 60 mg daily tapering to 10 mg a day and fludrocortisone 0.1 mg daily for life

Question 3

Which of the following is NOT true about Hashimoto's thyroiditis?

Accepted Answer

Presence of antithyroid nuclear antibodies

Answer

Presence of antithyroid microsomal antibodies

Answer

Presence of anti-TSH receptor antibodies

Answer

Increased levels of thyroid hormones

Question 4

A false positive oral glucose tolerance test (OGTT) is seen in all of the following conditions EXCEPT?

Accepted Answer

Exercise

Answer

Malnutrition

Answer

Infection

Answer

Severe emotional stress

Question 5

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?

Accepted Answer

Vitamin D deficiency

Answer

Primary hyperparathyroidism

Answer

Paget's disease

Answer

Osteoporosis

Question 6

Increased blood levels of cholesterol seen in hypothyroidism are most likely due to which of the following mechanisms?

Accepted Answer

Decreased production of LDL receptors in adipose tissue and increased release of cholesterol from adipose tissue

Answer

Decreased calorigenesis

Answer

Decreased production of LDL receptors in the liver, leading to decreased hepatic clearance

Answer

Increased breakdown of lipoproteins releasing cholesterol into circulation

Question 7

A vasopressin analogue does not produce a therapeutic effect through the vasopressin V-2 receptor in which of the following conditions?

Accepted Answer

Bleeding esophageal varices

Answer

Central diabetes insipidus

Answer

Type 1 von Willebrand's disease

Answer

Primary nocturnal enuresis

Question 8

A high carbohydrate diet can precipitate which of the following conditions?

Accepted Answer

Hypokalemic periodic paralysis

Answer

Hyperkalemic periodic paralysis

Answer

Hysterical paralysis

Answer

Myasthenia gravis

Question 9

What is the most common presentation of endemic goiter?

Accepted Answer

Diffuse goiter

Answer

Solitary nodule

Answer

Hypothyroid

Answer

Hyperthyroid

Question 10

All are causes of Gynaecomastia, except?

Accepted Answer

Androgen therapy

Answer

Cimetidine therapy

Answer

Leprosy

Answer

Small cell carcinoma of the lung

Endocrinology — MCQs

Endocrinology — MCQs

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