Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 871: Which is the screening test for acromegaly?

A. Serum IGF-2
B. Oral glucose tolerance test
C. GH levels
D. Serum IGF-1 (Correct Answer)

Explanation: **Explanation:** The diagnosis of acromegaly relies on understanding the physiological secretion of Growth Hormone (GH). **1. Why Serum IGF-1 is the Correct Answer:** Serum **Insulin-like Growth Factor-1 (IGF-1)** is the preferred **screening test** because it has a long half-life and maintains stable plasma concentrations throughout the day. Unlike GH, which is secreted in pulsatile bursts and can be influenced by stress, exercise, or sleep, IGF-1 levels reflect the integrated GH secretion over the preceding 24 hours [2]. A normal age- and sex-matched IGF-1 level effectively rules out acromegaly [1]. **2. Why the Other Options are Incorrect:** * **Serum IGF-2 (A):** This factor is primarily involved in fetal development and is not used in the diagnostic algorithm for GH disorders. * **Oral Glucose Tolerance Test (B):** The 75g OGTT is the **gold standard confirmatory test**, not the screening test [1]. In a healthy individual, hyperglycemia suppresses GH to <1 ng/mL; failure of suppression confirms acromegaly. * **GH levels (C):** Random GH measurements are unreliable for screening due to the hormone's pulsatile nature and short half-life [2]. A single low value does not rule out the disease, and a single high value does not confirm it. **Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum IGF-1. * **Best Confirmatory Test:** GH suppression test (OGTT). * **Most Common Cause:** Pituitary Adenoma (Somatotroph adenoma). * **Imaging of Choice:** MRI of the Sella Turcica (performed after biochemical confirmation). * **Treatment of Choice:** Transsphenoidal surgery (except in cases where medical management with Somatostatin analogues like Octreotide is preferred) [1].

Question 872: Complications in Diabetes Mellitus Type II typically occur around:

A. 5 years of onset
B. 10 years of onset
C. 15 years of onset
D. 20 years of onset (Correct Answer)

Explanation: **Explanation:** In Type 2 Diabetes Mellitus (T2DM), the development of chronic microvascular and macrovascular complications is a progressive process driven by chronic hyperglycemia, advanced glycation end-products (AGEs), and oxidative stress [1]. **Why Option D is Correct:** Statistically, clinically significant complications (such as proliferative retinopathy, end-stage renal disease, or symptomatic neuropathy) typically manifest approximately **20 years after the onset** of the disease. While the biochemical damage begins much earlier, the "clinical threshold" for organ failure or severe disability usually peaks at the two-decade mark [2]. It is important to note that because T2DM has an insidious onset and may remain undiagnosed for years, many patients already have complications at the time of diagnosis [3]. **Analysis of Incorrect Options:** * **A (5 years):** This is too early for most chronic complications to become clinically apparent, though subclinical changes (like microalbuminuria) may begin. * **B & C (10-15 years):** While complications often start appearing during this window (e.g., background retinopathy), the classic teaching for the peak incidence of cumulative, severe complications remains the 20-year mark [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of 20":** Diabetic Retinopathy is present in nearly 99% of Type 1 and about 60% of Type 2 patients after 20 years of disease duration. * **Screening:** Unlike Type 1 DM (where screening starts 5 years after diagnosis), screening for complications in Type 2 DM must begin **at the time of diagnosis** because the actual date of onset is usually unknown [3]. * **UKPDS Study:** This landmark trial confirmed that intensive glycemic control significantly reduces microvascular complications over long-term follow-up [1]. * **Most Common Complication:** Distal Symmetrical Polyneuropathy is the most common chronic complication of DM.

Question 873: In parathyroid crisis with sudden elevations of calcium over 16 mg/dL, what is the appropriate initial treatment?

A. Parathyroidectomy for removal of adenoma (Correct Answer)
B. Thyrocalcitonin
C. Intravenous bicarbonate
D. Intravenous fluids and loop diuretics

Explanation: ### Explanation **Correct Option: A. Parathyroidectomy for removal of adenoma** **Reasoning:** Parathyroid crisis (or hypercalcemic crisis) is a life-threatening emergency characterized by severe hypercalcemia (usually >14–16 mg/dL) and profound neuropsychiatric, gastrointestinal, and renal symptoms [1]. While medical stabilization is initiated immediately, the **definitive and curative treatment** for a crisis precipitated by primary hyperparathyroidism is **emergency parathyroidectomy**. Once the patient is rehydrated and life-threatening arrhythmias are addressed, surgical removal of the overactive parathyroid tissue is the only way to rapidly and permanently drop the serum calcium levels and prevent multi-organ failure. **Why other options are incorrect:** * **B. Thyrocalcitonin:** While calcitonin can lower calcium levels rapidly (within hours), its effect is transient due to **tachyphylaxis** (rapidly diminishing response). It is an adjunctive therapy, not a definitive cure. * **C. Intravenous bicarbonate:** This is not indicated in hypercalcemia. In fact, alkalosis can sometimes worsen the clinical picture or be associated with Milk-Alkali syndrome, but it does not treat parathyroid crisis. * **D. Intravenous fluids and loop diuretics:** This is the **initial medical management** to promote calciuresis [1]. However, the question asks for the appropriate treatment for the *crisis itself* (implying the definitive resolution). Medical management alone often fails to control the extreme elevations seen in parathyroid crisis without surgical intervention. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Step:** Aggressive rehydration with 0.9% Normal Saline (3–4 L/day). * **Loop Diuretics:** Use only *after* volume expansion is complete to avoid worsening dehydration. * **Bisphosphonates (e.g., Zoledronic acid):** Potent but take 48–72 hours to reach peak effect; hence, not ideal for immediate crisis control [1]. * **Cinacalcet:** A calcimimetic used in secondary HPT or parathyroid carcinoma, but not the first-line choice for acute surgical crisis. * **EKG Finding:** Shortened QT interval is the classic sign of hypercalcemia.

Question 874: Which of the following statements about pseudohypoparathyroidism is true?

A. Caused by 'Gain of function' inherited mutation in Gsa subunit
B. Decreased formation of cyclic GMP is observed
C. Decreased formation of Inositol triphosphate is observed
D. Decreased formation of c-AMP is observed (Correct Answer)

Explanation: **Explanation:** **Pseudohypoparathyroidism (PHP)** is a group of disorders characterized by **end-organ resistance to Parathyroid Hormone (PTH)** [1]. While PTH levels are high, the body cannot respond to them, leading to biochemical hypocalcemia and hyperphosphatemia. **Why Option D is Correct:** PTH normally binds to its receptor on target cells (kidney and bone), which is coupled to a **stimulatory G-protein (Gsα)**. This activation triggers **Adenylate Cyclase**, which converts ATP into **cyclic AMP (c-AMP)** [2]. In PHP (specifically Type 1a and 1b), there is a defect in the Gsα subunit or the signaling pathway. Consequently, even when PTH binds to the receptor, the signal is not transduced, leading to **decreased formation of c-AMP**. This is the hallmark diagnostic finding: a failure of urinary c-AMP to rise following an infusion of exogenous PTH (Ellsworth-Howard test). **Why Other Options are Incorrect:** * **Option A:** PHP is caused by a **'Loss of function'** mutation in the *GNAS1* gene (encoding the Gsα subunit), not a gain of function. A gain-of-function mutation in this gene leads to McCune-Albright syndrome. * **Options B & C:** The PTH receptor signaling pathway specifically utilizes the **Adenylate Cyclase/c-AMP** second messenger system [2]. It does not primarily rely on cyclic GMP or the Inositol triphosphate (IP3)/DAG pathway for its main metabolic actions in the kidney. **High-Yield Clinical Pearls for NEET-PG:** * **Albright Hereditary Osteodystrophy (AHO):** Phenotype seen in PHP Type 1a, characterized by short stature, round face, obesity, and **short 4th/5th metacarpals** (Archibald’s sign). * **Pseudopseudohypoparathyroidism (PPHP):** Patients have the AHO phenotype but **normal** calcium and PTH levels (paternal inheritance of the same mutation) [1]. * **Biochemical Profile:** High PTH, Low Calcium, High Phosphate (mimics Chronic Kidney Disease, but with normal renal function).

Question 875: In a patient with pheochromocytoma, all of the following are seen except?

A. Diarrhea
B. Orthostatic hypotension
C. Episodic hypertension
D. Weight gain (Correct Answer)

Explanation: **Explanation:** Pheochromocytoma is a catecholamine-secreting tumor of the adrenal medulla. The clinical presentation is primarily driven by the excessive release of epinephrine and norepinephrine. **Why Weight Gain is the correct answer:** In pheochromocytoma, patients typically experience **weight loss**, not weight gain. This occurs because catecholamines induce a high metabolic state (hypermetabolic) and stimulate lipolysis and glycogenolysis. The increased basal metabolic rate (BMR) leads to significant weight loss despite a normal or increased appetite. **Analysis of other options:** * **Diarrhea:** While constipation is more common due to catecholamine-induced inhibition of gut motility, some patients experience diarrhea due to the co-secretion of other peptides (like VIP) or rapid intestinal transit during "paroxysms." However, in the context of this question, weight gain is the most definitive "incorrect" clinical feature. * **Orthostatic Hypotension:** This is a classic paradoxical finding in pheochromocytoma. It occurs due to **low intravascular volume** (chronic vasoconstriction leads to pressure natriuresis) and impaired autonomic reflexes (downregulation of adrenergic receptors). * **Episodic Hypertension:** This is the hallmark of the disease. While some patients have sustained hypertension, the classic presentation involves "paroxysms" or "spells" of severe hypertension triggered by the sudden release of catecholamines. **NEET-PG High-Yield Pearls:** * **The Rule of 10s:** 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), 10% pediatric, 10% familial. * **Classic Triad:** Episodic headache, sweating (diaphoresis), and tachycardia. * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. * **Management:** Always start **Alpha-blockers first** (e.g., Phenoxybenzamine) before Beta-blockers to avoid an unopposed alpha-mediated hypertensive crisis.

Question 876: All of the following are true about Cushing's syndrome, except?

A. Red striae
B. Increased adrenaline (Correct Answer)
C. Proximal muscle weakness
D. Edema

Explanation: **Explanation:** Cushing’s syndrome results from chronic exposure to excessive levels of glucocorticoids (cortisol) [1]. To answer this question, one must distinguish between the hormones produced by the adrenal **cortex** versus the adrenal **medulla** [3]. **Why "Increased Adrenaline" is the correct answer (The Exception):** Adrenaline (epinephrine) is a catecholamine synthesized and secreted by the **adrenal medulla** in response to sympathetic nervous system stimulation [3]. Cushing’s syndrome specifically involves the hyperfunctioning of the **adrenal cortex** (zona fasciculata) or exogenous steroid intake [1], [4]. While cortisol can permissively enhance the action of catecholamines on blood vessels [5], Cushing’s syndrome itself does not cause an increase in adrenaline production. **Analysis of Incorrect Options:** * **Red Striae:** High cortisol levels inhibit fibroblasts and lead to loss of collagen [1]. This results in thinning of the skin and rupture of dermal capillaries, manifesting as wide (>1 cm), purple/red striae, typically on the abdomen. * **Proximal Muscle Weakness:** Cortisol is catabolic to protein [1]. Excessive levels lead to muscle wasting (atrophy), particularly in the proximal limb muscles and pelvic girdle, often making it difficult for patients to rise from a chair. * **Edema:** At high concentrations, cortisol loses its specificity and binds to **mineralocorticoid receptors** (cross-reactivity). This leads to sodium and water retention, resulting in hypertension and peripheral edema. **NEET-PG High-Yield Pearls:** * **Screening Test:** 24-hour urinary free cortisol or Overnight Dexamethasone Suppression Test (ONDST). * **Most Common Cause:** Exogenous steroid administration (Iatrogenic) [2]. * **Most Common Endogenous Cause:** Cushing’s Disease (ACTH-secreting pituitary adenoma) [1]. * **Ectopic ACTH:** Classically associated with Small Cell Carcinoma of the Lung; often presents with profound hypokalemia and hyperpigmentation [2].

Question 877: Anti-TPO antibodies are present in which of the following conditions?

A. Reidel's thyroiditis
B. Grave's disease
C. Hashimoto's thyroiditis (Correct Answer)
D. DeQuervain's thyroiditis

Explanation: Explanation: 1. Why Hashimoto’s Thyroiditis is Correct: Hashimoto’s thyroiditis (Chronic Lymphocytic Thyroiditis) is an autoimmune disorder characterized by the destruction of the thyroid gland by cell-mediated and antibody-mediated immune processes. Anti-TPO (Anti-Thyroid Peroxidase) antibodies are the hallmark of this condition, present in over 95% of patients. They are not just markers but are involved in the pathogenesis of thyroid failure. Anti-thyroglobulin (Anti-Tg) antibodies are also frequently present (60-80%). 2. Analysis of Incorrect Options: * A. Riedel’s Thyroiditis: This is a rare condition characterized by dense fibrous replacement of the thyroid tissue (IgG4-related disease). While some patients may have antibodies, it is primarily a fibrotic process, not an autoimmune destruction defined by Anti-TPO. * B. Graves’ Disease: While Anti-TPO can be present in ~70% of Graves' cases, the pathognomonic antibody is TSI (Thyroid Stimulating Immunoglobulin) or TRAb (TSH Receptor Antibody), which causes hyperthyroidism [1]. * C. DeQuervain’s Thyroiditis (Subacute Granulomatous): This is typically a post-viral inflammatory condition. It is characterized by a high ESR and painful goiter; thyroid antibodies are usually absent or only transiently present in low titers [2]. 3. NEET-PG Clinical Pearls: * Most sensitive marker for Hashimoto’s: Anti-TPO antibodies. * Best initial test for thyroid function: TSH. * Histology of Hashimoto’s: Hurthle cells (Askanazy cells) and lymphocytic infiltration with germinal centers. * Risk: Patients with Hashimoto’s have an increased risk of B-cell Non-Hodgkin Lymphoma of the thyroid. * Anti-TPO in Pregnancy: Presence of these antibodies increases the risk of post-partum thyroiditis and miscarriage.

Question 878: In which condition is an intravenous glucose tolerance test typically performed?

A. Children
B. Pregnancy
C. Gastrectomy (Correct Answer)
D. Old age

Explanation: The **Oral Glucose Tolerance Test (OGTT)** is the standard diagnostic tool for diabetes [2]. However, it relies on normal gastric emptying and intestinal absorption. In patients who have undergone a **Gastrectomy** (Option C), the "gastric brake" is lost, leading to abnormally rapid gastric emptying [1]. This causes a rapid surge in blood glucose followed by an exaggerated insulin response (Alimentary Hypoglycemia/Dumping Syndrome). Because the oral route yields unreliable, "lag-storage" type curves in these patients, the **Intravenous Glucose Tolerance Test (IVGTT)** is preferred to bypass the gastrointestinal tract and assess pancreatic beta-cell function directly. **Analysis of Incorrect Options:** * **A. Children:** OGTT is the standard for children when diabetes is suspected, though it is less frequently required than in adults. * **B. Pregnancy:** This is the most common indication for **OGTT** (specifically the 75g or 100g test) to screen for Gestational Diabetes Mellitus (GDM). The IVGTT is not used as it does not reflect the physiological challenge of a meal. * **C. Old Age:** Aging is associated with decreased glucose tolerance, but the standard OGTT remains the diagnostic method of choice. **NEET-PG High-Yield Pearls:** * **IVGTT Procedure:** 0.5 g/kg of glucose is given as a 25% solution over 2–4 minutes. * **K-value:** The result of an IVGTT is expressed as the "glucose disappearance rate" (K-value). A K-value < 1.0 is suggestive of diabetes. * **Indications for IVGTT:** Malabsorption syndromes, chronic diarrhea, and post-gastric surgery (Gastrectomy/Gastrojejunostomy) [1]. * **Diagnostic Choice:** While IVGTT exists, the **HbA1c** and **Fasting Plasma Glucose** are now the primary clinical tools, with OGTT reserved for pregnancy.

Question 879: Diabetic amyotrophy characteristically presents with which of the following?

A. Pain in the anterior thigh (Correct Answer)
B. Third nerve palsy with pupillary sparing
C. Distal areflexia
D. Asymmetric motor weakness

Explanation: **Explanation:** **Diabetic Amyotrophy** (also known as Bruns-Garland syndrome or Diabetic Lumbosacral Radiculoplexus Neuropathy) is a distinct form of diabetic neuropathy typically seen in older patients with Type 2 Diabetes Mellitus [1]. **Why Option A is Correct:** The hallmark presentation is the **acute or subacute onset of severe, asymmetric pain** followed by weakness and atrophy of the proximal muscles of the lower limb. The pain is most characteristically located in the **anterior thigh, hip, or buttock**. This is due to an inflammatory, immune-mediated microvasculitis causing ischemic nerve damage to the lumbosacral plexus and femoral/obturator nerves. **Analysis of Incorrect Options:** * **B. Third nerve palsy with pupillary sparing:** This is the classic presentation of **Diabetic Mononeuropathy (CN III)**. It occurs due to microvascular ischemia of the core of the nerve, sparing the peripherally located parasympathetic pupillary fibers. * **C. Distal areflexia:** This is characteristic of **Distal Symmetric Polyneuropathy (DSPN)**, the most common form of diabetic neuropathy, which presents with a "stocking-and-glove" sensory loss [1]. * **D. Asymmetric motor weakness:** While diabetic amyotrophy *does* involve asymmetric weakness, the question asks for the **characteristic** presenting feature. Severe **pain** is almost always the initial and most distressing symptom that precedes the profound muscle wasting. **High-Yield Clinical Pearls for NEET-PG:** * **Key Muscles Involved:** Quadriceps (leading to difficulty standing from a chair), iliopsoas, and adductors. * **Reflexes:** The **knee jerk (patellar reflex)** is typically diminished or absent, while the ankle jerk is often preserved. * **Weight Loss:** Significant unintentional weight loss occurs in more than 50% of cases. * **Prognosis:** Unlike many other neuropathies, it is often self-limiting, with gradual recovery over 12–24 months, though some residual weakness may persist.

Question 880: Osteoporosis is caused by all of the following except?

A. Methotrexate
B. Glucocorticoids
C. Heparin
D. Estradiol (Correct Answer)

Explanation: The correct answer is **Estradiol**. Osteoporosis is a skeletal disorder characterized by low bone mass and micro-architectural deterioration [1]. To answer this question, one must distinguish between drugs that cause bone loss (osteoporotic agents) and those that are bone-protective. **Why Estradiol is the correct answer:** Estradiol (Estrogen) is **protective** against osteoporosis [3]. It inhibits bone resorption by decreasing the activity and lifespan of osteoclasts while promoting osteoblast survival. In postmenopausal women, the decline in estradiol levels is the primary driver of accelerated bone loss [3]. Therefore, estradiol is a treatment modality (Hormone Replacement Therapy), not a cause of the disease. **Why the other options are incorrect:** * **Glucocorticoids:** These are the most common cause of drug-induced osteoporosis [1]. They decrease osteoblast function, reduce intestinal calcium absorption, and increase renal calcium excretion [1]. * **Heparin:** Long-term use of unfractionated heparin (UFH) stimulates osteoclasts and inhibits osteoblasts, leading to decreased bone density. * **Methotrexate:** Used in high doses (e.g., in oncology), it is directly toxic to osteoblasts and triggers "methotrexate osteopathy," characterized by bone pain and fractures. **High-Yield Clinical Pearls for NEET-PG:** 1. **Other Drugs causing Osteoporosis:** Proton Pump Inhibitors (PPIs), Anticonvulsants (Phenytoin/Phenobarbital), Thiazolidinediones (Pioglitazone) [2], and Aromatase Inhibitors [2]. 2. **Gold Standard Diagnosis:** DEXA Scan (Dual-energy X-ray Absorptiometry). Osteoporosis is defined as a **T-score ≤ -2.5**. 3. **First-line Treatment:** Bisphosphonates (e.g., Alendronate), which act by inhibiting osteoclast-mediated bone resorption.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

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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