Endocrinology — MCQs

A 70-year-old male presented with severe confusion, shortness of breath, and obtundation. Lab findings revealed moderately raised serum calcium, mildly raised serum creatinine, mildly raised BUN, normal PTH, elevated PTHrP, and an abnormal chest x-ray. Which of the following drugs can be given for the treatment of hypercalcemia?

Q469Easy

A patient presents with thyrotoxicosis and exophthalmos. What would thyroid function tests reveal?

Q470Easy

Which of the following is NOT true regarding Cushing syndrome?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 461: A 60-year-old woman presents with menorrhagia. Her history is significant for lethargy, constipation, cold intolerance, and muscle stiffness. What is the most likely diagnosis?

A. Uterine carcinoma
B. Systemic lupus erythematosus
C. Hypothyroidism (Correct Answer)
D. Severe iron deficiency anemia

Explanation: **Explanation:** The patient presents with a classic constellation of symptoms—**lethargy, constipation, cold intolerance, and muscle stiffness**—which are hallmark clinical features of **Hypothyroidism** [1]. In adult women, hypothyroidism is a significant systemic cause of **menorrhagia** (heavy menstrual bleeding). **Why Hypothyroidism is correct:** Hypothyroidism leads to menstrual irregularities through two primary mechanisms: 1. **Hormonal Imbalance:** Low levels of thyroxine ($T_4$) lead to an increase in Thyrotropin-Releasing Hormone (TRH). TRH stimulates the pituitary to release not only TSH but also **Prolactin**. Hyperprolactinemia interferes with the pulsatile release of GnRH, leading to anovulatory cycles and dysfunctional uterine bleeding. 2. **Coagulation Defects:** Hypothyroidism can cause a decrease in levels of clotting factors (specifically Factor VII, VIII, and IX) and may lead to acquired von Willebrand syndrome, further exacerbating menstrual blood loss. **Why other options are incorrect:** * **Uterine Carcinoma:** While it causes postmenopausal bleeding or abnormal uterine bleeding in older women, it does not explain systemic symptoms like cold intolerance or constipation. * **Systemic Lupus Erythematosus (SLE):** SLE typically presents with malar rash, joint pain, and photosensitivity. While it can cause anemia, it is not a primary cause of menorrhagia. * **Severe Iron Deficiency Anemia:** This is a *consequence* of menorrhagia, not the cause. While it explains lethargy, it does not account for cold intolerance or constipation. **NEET-PG High-Yield Pearls:** * **Wolff-Chaikoff Effect:** Autoregulation where a large burst of iodine inhibits thyroid hormone synthesis. * **Hoffmann’s Syndrome:** Hypothyroidism presenting with muscular pseudohypertrophy and stiffness (as seen in this patient). * **Most common cause:** Hashimoto’s thyroiditis (look for anti-TPO antibodies). * **Lab finding:** Elevated TSH is the most sensitive screening test for primary hypothyroidism.

Question 462: All of the following conditions are associated with hyperthyroidism, except?

A. Hashimoto's thyroiditis (Correct Answer)
B. Graves' disease
C. Toxic multinodular goiter
D. Struma ovarii

Explanation: The correct answer is **A. Hashimoto’s thyroiditis**. **1. Why Hashimoto’s thyroiditis is the correct answer:** Hashimoto’s thyroiditis is the most common cause of **hypothyroidism** in iodine-sufficient regions. It is an autoimmune destruction of the thyroid gland mediated by T-cells and anti-thyroid peroxidase (anti-TPO) antibodies. While a transient "Hashitoxicosis" can occur early in the disease due to the leakage of preformed hormones from damaged follicles, the definitive clinical state is chronic hypothyroidism. **2. Analysis of incorrect options:** * **Graves’ Disease:** The most common cause of hyperthyroidism. It involves Type II hypersensitivity where thyroid-stimulating immunoglobulins (TSI) bind to and activate the TSH receptor, causing excessive hormone synthesis [1]. * **Toxic Multinodular Goiter (Plummer Disease):** Characterized by focal patches of thyroid autonomy. These nodules function independently of TSH stimulation, leading to hyperthyroidism (usually in older adults). * **Struma Ovarii:** A rare form of monodermal teratoma where ovarian tissue contains >50% thyroid tissue. If this ectopic tissue becomes overactive, it causes hyperthyroidism without thyroid gland enlargement (low iodine uptake in the neck, high uptake in the pelvis). **Clinical Pearls for NEET-PG:** * **Jod-Basedow Phenomenon:** Iodine-induced hyperthyroidism (often after IV contrast or Amiodarone). * **Wolff-Chaikoff Effect:** A transient reduction in thyroid hormone levels caused by the ingestion of a large amount of iodine (the basis for using Lugol’s iodine before surgery). * **Amiodarone:** Can cause both Type 1 (excess iodine) and Type 2 (destructive thyroiditis) thyrotoxicosis, as well as hypothyroidism. * **Diagnosis:** Low TSH with high Free T4/T3 confirms hyperthyroidism. Radioactive Iodine Uptake (RAIU) is **high** in Graves’/TMNG but **low** in thyroiditis and Struma ovarii.

Question 463: A patient presents with hyperphosphatemia, "sho" metacarpals, and cataracts. What is the most likely diagnosis?

A. Pseudohypoparathyroidism (Correct Answer)
B. Hypophosphatasia
C. Hyperparathyroidism
D. Osteomalacia

Explanation: ### Explanation **Correct Option: A. Pseudohypoparathyroidism (PHP)** Pseudohypoparathyroidism is a genetic disorder characterized by **end-organ resistance to Parathyroid Hormone (PTH)** [1]. Despite high levels of circulating PTH, the body cannot respond to it, leading to biochemical features of hypoparathyroidism: **hyperphosphatemia** and hypocalcemia [1]. The clinical presentation described—shortened 4th and 5th metacarpals (Archibald’s sign), cataracts (due to chronic hypocalcemia), and often a round face and short stature—is known as **Albright’s Hereditary Osteodystrophy (AHO)** [1]. This phenotype is most classically associated with **PHP Type 1a**, caused by a mutation in the *GNAS1* gene, often exhibiting genetic imprinting [1]. **Why other options are incorrect:** * **B. Hypophosphatasia:** This is a rare genetic disorder characterized by low levels of alkaline phosphatase and defective bone mineralization. It typically presents with **hypophosphatemia** (not hyper) and premature loss of deciduous teeth. * **C. Hyperparathyroidism:** This condition results in **hypophosphatemia** (due to increased renal phosphate excretion) and hypercalcemia, which is the opposite of the biochemical profile described [1]. * **D. Osteomalacia:** Usually caused by Vitamin D deficiency, it presents with **low or normal phosphate** and low calcium [1]. It does not feature the specific skeletal deformities like short metacarpals. **High-Yield Clinical Pearls for NEET-PG:** * **PTH Levels:** In Hypoparathyroidism, PTH is low. In **Pseudohypoparathyroidism**, PTH is **high** (compensatory) [1]. * **Pseudopseudohypoparathyroidism (PPHP):** Patients have the AHO phenotype (short metacarpals, round face) but have **normal** calcium and phosphate levels [1]. * **Archibald’s Sign:** Dimpling over the knuckles of the 4th and 5th metacarpals when making a fist; a classic sign of PHP. * **Basal Ganglia Calcification:** Can also be seen in PHP due to chronic hyperphosphatemia and calcium-phosphate product deposition.

Question 464: Which of the following is NOT a recommended site for insulin administration?

A. Dorsum of hands (Correct Answer)
B. Arms
C. Lateral aspect of thigh
D. Abdomen around the umbilicus

Explanation: Explanation: Insulin must be administered into the **subcutaneous fat** layer to ensure predictable absorption and minimize pain [1]. **Why Option A is correct:** The **dorsum of the hands** is an inappropriate site because it lacks sufficient subcutaneous adipose tissue. Injecting here increases the risk of **intramuscular (IM) injection**, which leads to rapid, unpredictable absorption and severe hypoglycemia [1]. Furthermore, the presence of superficial tendons, nerves, and vessels makes it clinically unsafe. Examination of a patient with diabetes should always include checking insulin injection sites [2]. **Why the other options are incorrect:** * **Abdomen (Option D):** This is the preferred site for insulin administration. It offers the most rapid and consistent absorption rate. Patients are advised to inject at least 2 inches away from the umbilicus. * **Arms (Option B):** The posterior surface (triceps area) of the upper arm is a standard site with moderate absorption speed. * **Lateral Thigh (Option C):** The upper-outer aspect of the thigh is used for slower absorption, which can be beneficial for basal insulin. **High-Yield NEET-PG Pearls:** 1. **Absorption Speed:** Abdomen > Arms > Thighs > Buttocks. 2. **Lipohypertrophy:** Repeated injections in the exact same spot cause fatty lumps that delay insulin absorption. **Site rotation** is the most important preventive measure. 3. **Exercise Effect:** Injecting into a limb that is about to be exercised (e.g., thigh before running) increases blood flow and accelerates insulin absorption, risking hypoglycemia. 4. **Angle of Injection:** Usually 90 degrees with short needles (4-6mm); a 45-degree angle or skin fold may be used in very thin individuals to avoid IM injection [1].

Question 465: A 52-year-old woman presents with palpitations, sweating, and heat intolerance. Physical examination reveals a palpable mass over the anterior aspect of the neck. Which of the following features is most associated with this condition?

A. Constipation
B. Elevated thyroid-stimulating hormone (TSH)
C. Ophthalmoplegia (Correct Answer)
D. Slow relaxing reflexes

Explanation: ### **Explanation** The clinical presentation of palpitations, sweating, heat intolerance, and a neck mass (goiter) is classic for **Hyperthyroidism**. In a middle-aged woman, the most common cause of hyperthyroidism is **Graves' Disease**, an autoimmune disorder caused by TSH-receptor antibodies (TRAb) [1, 3]. **Why Option C is Correct:** **Ophthalmoplegia** (weakness or paralysis of extraocular muscles) is a hallmark of **Graves' Ophthalmopathy**. This occurs due to the activation of orbital fibroblasts by TSH-receptor antibodies, leading to the accumulation of glycosaminoglycans (GAGs), edema, and fibrosis of the extraocular muscles [2]. This results in proptosis, diplopia, and restricted eye movements. It is specific to Graves' disease and not seen in other causes of thyrotoxicosis [1]. **Why the Other Options are Incorrect:** * **A & D (Constipation and Slow relaxing reflexes):** These are classic features of **Hypothyroidism** [3]. In hyperthyroidism, patients typically experience increased frequency of bowel movements (diarrhea) and **brisk (hyperreflexic)** deep tendon reflexes. * **B (Elevated TSH):** In primary hyperthyroidism (like Graves'), high levels of circulating T3 and T4 exert negative feedback on the pituitary, leading to **suppressed (low) TSH levels** [2]. Elevated TSH with high T4 is rare and suggests a TSH-secreting pituitary adenoma. ### **NEET-PG High-Yield Pearls** * **Graves' Triad:** Hyperthyroidism (Goiter), Ophthalmopathy (Exophthalmos), and Dermopathy (Pretibial Myxedema) [1]. * **Most common muscle involved in Graves' Ophthalmopathy:** Inferior rectus (leading to restricted upward gaze). * **Diagnosis:** Low TSH, High Free T4, and positive **TSH-receptor antibodies (TRAb)** [1, 3]. * **Radioactive Iodine Uptake (RAIU):** Shows **diffuse, increased uptake** in Graves' disease, distinguishing it from thyroiditis (low uptake) [3].

Question 466: Pheochromocytoma is a tumor of which of the following?

A. Adrenal cortex
B. Parathyroids
C. Pituitary
D. None of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **None of the above** because Pheochromocytoma is a catecholamine-secreting tumor derived from the **chromaffin cells** of the **adrenal medulla**, not the adrenal cortex or other endocrine glands listed. **1. Why the correct answer is "None of the above":** Pheochromocytoma originates from the embryonic neural crest cells. Specifically, it arises from the chromaffin cells of the adrenal medulla (85-90%) or extra-adrenal sympathetic ganglia (10-15%, where they are termed paragangliomas). These cells synthesize and secrete catecholamines (epinephrine and norepinephrine) [4]. **2. Why the other options are incorrect:** * **Adrenal cortex:** This is the outer layer of the adrenal gland derived from mesoderm. It produces steroid hormones: mineralocorticoids (Aldosterone), glucocorticoids (Cortisol), and androgens [2]. Tumors here lead to Conn’s syndrome or Cushing’s syndrome [1]. * **Parathyroids:** These glands regulate calcium homeostasis via Parathyroid Hormone (PTH). Tumors here cause hyperparathyroidism. * **Pituitary:** This gland produces trophic hormones (ACTH, TSH, GH, etc.). While pituitary adenomas are part of MEN 1 syndrome, they are not the site of pheochromocytomas. **High-Yield Clinical Pearls for NEET-PG:** * **The Rule of 10s:** 10% are bilateral, 10% are extra-adrenal, 10% are malignant, and 10% are familial. * **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia (palpitations). * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. Serum chromogranin A may also be elevated [3]. * **Genetic Association:** Associated with **MEN 2A and 2B**, von Hippel-Lindau (VHL) disease, and Neurofibromatosis type 1 (NF1) [3]. * **Management:** Always give **Alpha-blockers first** (e.g., Phenoxybenzamine) before Beta-blockers to avoid a hypertensive crisis caused by unopposed alpha-stimulation.

Question 467: Which of the following can cause osteonecrosis?

A. Sickle cell anemia
B. Corticosteroid use
C. Diabetes Mellitus
D. Systemic Lupus Erythematosus (SLE) (Correct Answer)

Explanation: **Explanation:** **Osteonecrosis (Avascular Necrosis)** is the death of bone components due to an interruption of blood supply, most commonly affecting the femoral head. **Why SLE is the Correct Answer:** Systemic Lupus Erythematosus (SLE) is a major risk factor for osteonecrosis. The pathogenesis is multifactorial, involving **vasculitis**, secondary **antiphospholipid syndrome (APLS)** leading to thrombosis, and, most significantly, the chronic use of **high-dose corticosteroids** to manage the disease. In many clinical scenarios, SLE is considered an independent risk factor even when steroid doses are controlled. **Analysis of Other Options:** * **A. Sickle Cell Anemia:** While Sickle Cell Anemia is a classic cause of osteonecrosis (due to vaso-occlusive crises), in the context of this specific question format, SLE is often highlighted as the systemic autoimmune prototype. However, it is important to note that both A and B are technically well-known causes. * **B. Corticosteroid Use:** This is the **most common** non-traumatic cause of osteonecrosis. It induces fat hypertrophy in the marrow, increasing intraosseous pressure and reducing blood flow. * **C. Diabetes Mellitus:** While DM causes various bone pathologies (like Charcot joint), it is **not** a direct or primary cause of osteonecrosis. **NEET-PG High-Yield Pearls:** * **Most common site:** Femoral head (due to retrograde blood supply via the medial circumflex femoral artery). * **Imaging of choice:** **MRI** is the most sensitive investigation for early detection (shows "double line sign"). * **X-ray finding:** "Crescent sign" (subchondral collapse) is a late finding. * **Mnemonic for Causes (PLASTIC RAGS):** **P**ancreatitis, **L**upus (SLE), **A**lcohol, **S**ickle cell, **T**rauma, **I**diopathic, **C**aisson disease, **R**adiation, **A**myloidosis, **G**aucher disease, **S**teroids.

Question 468: A 70-year-old male presented with severe confusion, shortness of breath, and obtundation. Lab findings revealed moderately raised serum calcium, mildly raised serum creatinine, mildly raised BUN, normal PTH, elevated PTHrP, and an abnormal chest x-ray. Which of the following drugs can be given for the treatment of hypercalcemia?

A. Calcitonin
B. Furosemide
C. Normal Saline
D. Prednisolone (Correct Answer)

Explanation: ### Explanation **Correct Option: D (Prednisolone)** The clinical presentation (elderly male, confusion, abnormal chest X-ray, elevated PTHrP, and normal PTH) strongly suggests **Humoral Hypercalcemia of Malignancy (HHM)**, likely due to Squamous Cell Carcinoma of the lung [1]. **Why Prednisolone?** In the context of hypercalcemia associated with malignancies (especially lymphomas, multiple myeloma, or certain solid tumors), glucocorticoids like **Prednisolone** are effective. They work by: 1. Decreasing intestinal calcium absorption. 2. Inhibiting bone resorption by decreasing cytokine release. 3. Increasing urinary calcium excretion. *Note: While IV fluids are the immediate first step, among the pharmacological options provided, Prednisolone is a specific treatment for malignancy-associated hypercalcemia.* **Analysis of Incorrect Options:** * **A. Calcitonin:** While it works rapidly to lower calcium by inhibiting osteoclasts, its effect is transient (tachyphylaxis develops within 24–48 hours). It is rarely used as monotherapy. * **B. Furosemide:** Loop diuretics are no longer recommended for routine management unless the patient is in fluid overload. They can worsen dehydration, which is the primary driver of hypercalcemic crisis. * **C. Normal Saline:** This is the **initial** step in management (volume expansion) [1]. However, it is considered "supportive fluid therapy" rather than a "drug" treatment in the context of specific pharmacological management of the underlying cause. **High-Yield Clinical Pearls for NEET-PG:** * **PTHrP (PTH-related protein):** The most common cause of hypercalcemia in non-metastatic solid tumors (e.g., Squamous cell CA of lung, esophagus, or renal cell CA). * **Treatment Hierarchy:** 1. **Immediate:** Aggressive hydration with Normal Saline [1]. 2. **Intermediate:** Calcitonin (for rapid, short-term drop). 3. **Definitve/Long-term:** Bisphosphonates [1] (Zoledronic acid is the drug of choice) or Denosumab. * **Glucocorticoids** are the first-line treatment for hypercalcemia caused by **Vitamin D toxicity**, **Sarcoidosis**, and **Lymphomas** (due to increased 1,25-dihydroxyvitamin D production) [1].

Question 469: A patient presents with thyrotoxicosis and exophthalmos. What would thyroid function tests reveal?

A. Increased T3, increased T4, normal TSH
B. Decreased T3, decreased T4, increased TSH
C. Increased T3, increased T4, decreased TSH (Correct Answer)
D. Decreased T3, normal T4, decreased TSH

Explanation: **Explanation:** The clinical presentation of **thyrotoxicosis** (excess circulating thyroid hormones) combined with **exophthalmos** (proptosis) is pathognomonic for **Graves' Disease**, the most common cause of hyperthyroidism [3], [4]. **1. Why Option C is Correct:** In Graves' Disease, the body produces Thyroid Stimulating Immunoglobulins (TSI) that bind to and activate the TSH receptors on the thyroid gland [3]. This leads to the autonomous and excessive synthesis and secretion of **T3 and T4**. Through the **negative feedback mechanism**, these high levels of circulating thyroid hormones inhibit the anterior pituitary from secreting Thyroid Stimulating Hormone (TSH) [2]. Therefore, the classic biochemical profile is **elevated T3/T4 with a suppressed (decreased) TSH** [4]. **2. Why Other Options are Incorrect:** * **Option A:** Normal TSH in the presence of high T3/T4 is physiologically inconsistent due to negative feedback, unless there is a rare TSH-secreting pituitary adenoma (Secondary Hyperthyroidism), which does not present with exophthalmos [1]. * **Option B:** This profile (Low T3/T4, High TSH) represents **Primary Hypothyroidism** (e.g., Hashimoto’s Thyroiditis) [1], [2]. * **Option C:** This profile (Low T3, Normal T4, Low TSH) is often seen in **Sick Euthyroid Syndrome**, not thyrotoxicosis. **3. NEET-PG High-Yield Pearls:** * **Exophthalmos:** Specific to Graves' Disease; caused by TSH-receptor antibodies reacting with orbital fibroblasts (not seen in other causes of thyrotoxicosis like toxic multinodular goiter) [3], [4]. * **Best Initial Test:** Serum TSH (most sensitive) [2]. * **T3 Toxicosis:** In early Graves', T3 may rise before T4. * **Wolff-Chaikoff Effect:** Reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.

Question 470: Which of the following is NOT true regarding Cushing syndrome?

A. Purplish striae
B. Plethora
C. Hypoglycemia (Correct Answer)
D. Obesity

Explanation: ### Explanation **Cushing Syndrome** is characterized by chronic exposure to excessive levels of glucocorticoids (cortisol). [1] To identify the incorrect statement, one must understand the metabolic and physical effects of cortisol. #### Why Hypoglycemia is the Correct Answer (The "NOT" True Statement) Cortisol is a **counter-regulatory hormone** that opposes the action of insulin. It promotes gluconeogenesis in the liver and decreases glucose uptake in peripheral tissues (muscle and adipose). Therefore, Cushing syndrome leads to **Hyperglycemia** (or impaired glucose tolerance/Diabetes Mellitus), not hypoglycemia. #### Why the Other Options are Incorrect (True Features of Cushing) * **Purplish Striae:** Excess cortisol inhibits fibroblasts and interferes with collagen synthesis, leading to thinning of the skin. [1] When the underlying blood vessels show through the stretched, thin skin, wide (>1 cm) violaceous or purplish striae appear, typically on the abdomen. * **Plethora:** Cortisol causes thinning of the facial skin and may increase red cell mass (polycythemia), resulting in a "facial plethora" or a chronically flushed appearance. * **Obesity:** This is the most common feature. It is specifically **centripetal (central) obesity**, characterized by fat redistribution to the abdomen, mediastinum, and neck ("buffalo hump" and "moon facies"), while the limbs remain thin due to muscle wasting. [1] --- ### NEET-PG High-Yield Clinical Pearls * **Screening Tests:** The best initial tests are the 24-hour urinary free cortisol, late-night salivary cortisol, or the Low-Dose Dexamethasone Suppression Test (LDDST). [2], [3] * **Electrolyte Abnormality:** Severe Cushing (especially ectopic ACTH) often presents with **Hypokalemic Metabolic Alkalosis** due to the mineralocorticoid effects of high cortisol. * **Proximal Myopathy:** Patients often complain of difficulty climbing stairs or rising from a chair due to protein catabolism in the proximal muscles. [1] * **Osteoporosis:** Cortisol decreases bone formation and increases bone resorption, making pathological fractures a known complication.

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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