Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 131: Diabetic ketoacidosis is best managed by?

A. Crystalline insulin given intravenously. (Correct Answer)
B. Human insulin given intramuscularly.
C. Lente insulin given subcutaneously.
D. Isophane insulin given intradermally.

Explanation: **Explanation:** The management of **Diabetic Ketoacidosis (DKA)** focuses on correcting hyperglycemia, acidosis, and dehydration [1]. The gold standard for glycemic control in DKA is the administration of **Crystalline (Regular) Insulin via the Intravenous (IV) route.** **Why Option A is Correct:** * **Pharmacokinetics:** Regular insulin given IV has an immediate onset of action and a very short half-life (approx. 5–10 minutes). This allows for rapid titration based on hourly blood glucose monitoring. * **Tissue Perfusion:** Patients in DKA are often severely dehydrated and in a state of peripheral vasoconstriction [1]. IV administration bypasses the skin and muscle, ensuring 100% bioavailability regardless of the patient's circulatory status. **Why Other Options are Incorrect:** * **Option B (Intramuscular):** While IM insulin can be used in mild cases if IV access is unavailable, it is less predictable and more painful. Absorption is delayed compared to the IV route. * **Option C (Lente/Subcutaneous):** Lente is an intermediate-acting insulin. Subcutaneous absorption is significantly impaired in DKA due to dehydration and poor skin perfusion. Furthermore, long-acting insulins cannot be quickly adjusted if hypoglycemia occurs [2]. * **Option D (Isophane/Intradermal):** Isophane (NPH) is intermediate-acting and not suitable for acute emergencies. The intradermal route is not used for insulin therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Protocol:** Start with an IV bolus (0.1 U/kg) followed by a continuous infusion (0.1 U/kg/hr). * **The Goal:** The aim is to reduce blood glucose by **50–70 mg/dL per hour**. * **Potassium Rule:** Never start insulin if serum Potassium is **<3.3 mEq/L**, as insulin shifts potassium intracellularly, potentially causing fatal arrhythmias [1]. * **Switching:** Transition to subcutaneous insulin only when the **anion gap has closed**, the patient is conscious, and they can tolerate oral intake [2].

Question 132: Increased urinary excretion of calcium is seen in which of the following conditions?

A. Sarcoidosis
B. Glucocorticoid excess
C. Wilson's disease
D. All the above (Correct Answer)

Explanation: Hypercalciuria (increased urinary calcium excretion) occurs through various pathophysiological mechanisms involving bone resorption, intestinal absorption, and renal tubular handling. **1. Sarcoidosis:** In sarcoidosis, activated macrophages within granulomas contain the enzyme **1-alpha-hydroxylase**. This enzyme converts 25-hydroxyvitamin D into **1,25-dihydroxyvitamin D (Calcitriol)** in an unregulated manner [1]. Elevated calcitriol levels lead to increased intestinal calcium absorption and bone resorption, resulting in hypercalcemia and subsequent hypercalciuria as the kidneys attempt to excrete the excess load [1]. **2. Glucocorticoid Excess (Cushing’s Syndrome/Exogenous Steroids):** Glucocorticoids induce hypercalciuria primarily by **inhibiting renal tubular reabsorption of calcium**. Additionally, they decrease intestinal calcium absorption (leading to secondary hyperparathyroidism) and increase bone resorption, both of which contribute to a higher filtered load of calcium. **3. Wilson’s Disease:** This condition can cause **Fanconi Syndrome** (Type 2 Proximal Renal Tubular Acidosis) due to copper deposition in the proximal renal tubules. The resulting tubular dysfunction leads to a "leak" of various substances, including calcium, glucose, and amino acids, into the urine. **High-Yield Clinical Pearls for NEET-PG:** * **Thiazide Diuretics:** These *decrease* urinary calcium (used in treating calcium stones). * **Loop Diuretics (Furosemide):** These *increase* urinary calcium ("Loops lose calcium"). * **Williams Syndrome:** Associated with idiopathic hypercalcemia and hypercalciuria. * **Vitamin D Toxicity:** A classic cause of hypercalciuria due to excessive intestinal absorption [1].

Question 133: A 36-year-old female presents with symptoms of hyperparathyroidism, a tumor in the pancreas, adrenal cortical hyperplasia, pituitary adenomas, an islet cell tumor, and cutaneous angiofibromas. What is the diagnosis?

A. Multiple Endocrine Neoplasia Type I (MEN I) (Correct Answer)
B. Multiple Endocrine Neoplasia Type IIA (MEN 2A)
C. Multiple Endocrine Neoplasia Type IIB (MEN 2B)
D. Multiple Endocrine Neoplasia Type IIC (MEN 2C)

Explanation: The patient presents with the classic triad of **Multiple Endocrine Neoplasia Type I (MEN 1)**, also known as **Wermer’s Syndrome**. This autosomal dominant condition is caused by a mutation in the *MEN1* gene (encoding the protein Menin). The diagnosis is confirmed by the presence of the **"3 Ps"**: 1. **Parathyroid:** Hyperparathyroidism (most common initial manifestation, usually due to multiglandular hyperplasia). 2. **Pancreas:** Enteropancreatic tumors (e.g., Gastrinomas, Insulinomas, or non-functional islet cell tumors). 3. **Pituitary:** Adenomas (most commonly Prolactinomas). Additionally, MEN 1 is associated with non-endocrine manifestations such as **cutaneous angiofibromas**, collagenomas, lipomas, and **adrenal cortical tumors** (usually non-functional hyperplasia), all of which are present in this clinical vignette. [1] **Why other options are incorrect:** * **MEN 2A (Sipple Syndrome):** Characterized by Medullary Thyroid Carcinoma (MTC), Pheochromocytoma, and Parathyroid hyperplasia. It does not involve the pituitary or pancreas. [1] * **MEN 2B:** Characterized by MTC, Pheochromocytoma, Mucosal neuromas, and Marfanoid habitus. It lacks parathyroid involvement. * **MEN 2C:** This is not a standard clinical classification in current medical literature; MEN 2 is strictly divided into 2A, 2B, and Familial MTC. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant; Gene: *MEN1* (Chromosome 11q13). * **Most common feature:** Primary Hyperparathyroidism (>95% of patients). * **Most common pancreatic tumor:** Gastrinoma (Zollinger-Ellison Syndrome). * **Screening:** Annual biochemical screening (Calcium, PTH, Gastrin, Prolactin) is recommended for first-degree relatives. [1]

Question 134: Which of the following is a parenteral agent used in the management of diabetes mellitus?

A. Rosiglitazone
B. Exenatide (Correct Answer)
C. Repaglinide
D. Canagliflozin

Explanation: **Explanation:** The correct answer is **Exenatide**. **Why Exenatide is correct:** Exenatide is a **GLP-1 Receptor Agonist** (Incretin mimetic). These agents work by stimulating glucose-dependent insulin secretion, suppressing glucagon release, and slowing gastric emptying [1]. Because GLP-1 agonists are peptide-based molecules, they are susceptible to degradation by gastrointestinal enzymes if taken orally. Therefore, they must be administered via **subcutaneous injection** (parenteral route) [1]. **Why the other options are incorrect:** * **Rosiglitazone (Option A):** A Thiazolidinedione (TZD) that acts as a PPAR-gamma agonist to improve insulin sensitivity [1]. It is administered **orally**. * **Repaglinide (Option B):** A Meglitinide (Glinide) that acts as a short-acting insulin secretagogue by closing ATP-sensitive potassium channels. It is administered **orally** before meals. * **Canagliflozin (Option D):** An SGLT-2 inhibitor that prevents glucose reabsorption in the proximal convoluted tubule of the kidney. It is administered **orally**. **High-Yield Clinical Pearls for NEET-PG:** * **Parenteral Antidiabetic Agents:** Include all **Insulins**, **GLP-1 Agonists** (e.g., Liraglutide, Dulaglutide), and **Pramlintide** (an Amylin analogue). * **Exception:** *Semaglutide* is the only GLP-1 agonist currently available in both oral and injectable forms. * **Key Side Effects:** GLP-1 agonists are associated with weight loss (beneficial in obese diabetics) but carry a risk of pancreatitis and are contraindicated in patients with a history of Medullary Thyroid Carcinoma (MTC). * **Weight Neutrality:** Metformin and DPP-4 inhibitors are weight neutral; GLP-1 agonists and SGLT-2 inhibitors promote weight loss; Sulfonylureas, TZDs, and Insulin cause weight gain.

Question 135: All are true about pheochromocytoma except?

A. 90% are malignant (Correct Answer)
B. 95% occur in the abdomen
C. They secrete catecholamines
D. They arise from sympathetic ganglia

Explanation: Explanation: Pheochromocytoma is a catecholamine-secreting tumor derived from chromaffin cells. Understanding the "Rule of 10s" is crucial for solving this question. 1. Why Option A is the Correct Answer (The False Statement): Historically, pheochromocytoma follows the "Rule of 10s," which states that only 10% of cases are malignant, while 90% are benign. Therefore, the statement that "90% are malignant" is factually incorrect. Malignancy is defined not by histology, but by the presence of tumor cells in non-chromaffin sites (e.g., bone, liver, or lymph nodes). 2. Analysis of Other Options: * Option B: Approximately 95% occur in the abdomen. While 85-90% arise from the adrenal medulla, the remainder occur in extra-adrenal sites (Paragangliomas), most commonly at the organ of Zuckerkandl (near the aortic bifurcation). * Option C: These tumors secrete catecholamines (primarily norepinephrine and epinephrine), leading to the classic triad of episodic headache, sweating, and tachycardia. * Option D: Extra-adrenal pheochromocytomas (paragangliomas) arise from sympathetic ganglia (along the sympathetic chain) or parasympathetic ganglia (e.g., carotid body). Clinical Pearls for NEET-PG: * The Rule of 10s: 10% Bilateral, 10% Extra-adrenal, 10% Malignant, 10% Pediatric, and 10% Familial (though genetic links are now known to be closer to 30-40%). * Diagnosis: Best initial screening test is 24-hour urinary fractionated metanephrines or plasma free metanephrines. * Pre-op Management: Always give Alpha-blockers first (e.g., Phenoxybenzamine) followed by Beta-blockers to avoid a hypertensive crisis. * Associated Syndromes: MEN 2A, MEN 2B, von Hippel-Lindau (VHL), and Neurofibromatosis type 1 (NF1).

Question 136: A patient with an endocrine abnormality shows a 'hung up' reflex. Which of the following conditions causes a 'hung up' reflex?

A. Myxedema
B. Hyperthyroidism
C. Hypothyroidism (Correct Answer)
D. Pheochromocytoma

Explanation: ### Explanation **Correct Answer: C. Hypothyroidism** The **'hung up' reflex** (also known as Woltman’s sign) refers to a delayed relaxation phase of the deep tendon reflexes, most commonly observed in the Achilles tendon (ankle jerk). **Underlying Pathophysiology:** In hypothyroidism, the slowed relaxation is not due to a defect in nerve conduction, but rather a **mechanical delay in the muscle fibers**. Low levels of thyroid hormone lead to: 1. Decreased activity of the **calcium-ATPase pump** (SERCA) in the sarcoplasmic reticulum, which slows the reuptake of calcium required for muscle relaxation. 2. Changes in myosin isoform expression and slowed ATP turnover. **Analysis of Incorrect Options:** * **A. Myxedema:** While myxedema is a severe form of hypothyroidism, the term "Hypothyroidism" (Option C) is the broader, standard clinical diagnosis associated with this sign [1]. In many exams, if both are present, the primary disease state is preferred. * **B. Hyperthyroidism:** This condition typically presents with **brisk or hyperreflexic** deep tendon reflexes due to increased neuromuscular excitability. * **D. Pheochromocytoma:** This catecholamine-secreting tumor causes hypertension and tachycardia; it does not typically affect the relaxation phase of reflexes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Woltman’s Sign:** Specifically refers to the delayed relaxation in hypothyroidism. * **Differential Diagnosis for Delayed Relaxation:** Besides hypothyroidism, it can be seen in anorexia nervosa, hypothermia, diabetes mellitus (rarely), and with certain drugs like beta-blockers. * **Pendular Knee Jerk:** Contrast this with the "hung up" reflex; pendular jerks are characteristic of **cerebellar lesions**. * **Pseudomyotonia:** Another term sometimes used to describe the slow relaxation phase in hypothyroid patients.

Question 137: Increased anion gap is a characteristic feature of which condition?

A. Hyperosmolar non-ketotic diabetic coma
B. Hypoglycaemic coma
C. Phenformin toxicity with coma (Correct Answer)
D. Renal tubular acidosis

Explanation: **Explanation:** The **Anion Gap (AG)** is calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. An increased anion gap indicates the presence of unmeasured metabolic acids in the blood [1]. **Why Option C is Correct:** **Phenformin** (a biguanide similar to metformin, but with a much higher risk profile) causes **Lactic Acidosis**. It interferes with mitochondrial oxidative phosphorylation and inhibits gluconeogenesis, leading to the accumulation of lactate [1]. Since lactate is an unmeasured anion, it replaces bicarbonate, resulting in a **High Anion Gap Metabolic Acidosis (HAGMA)**. **Analysis of Incorrect Options:** * **A. Hyperosmolar Non-Ketotic Coma (HONK/HHS):** Characterized by extreme hyperglycemia and hyperosmolarity without significant ketone production. Because there is enough insulin to prevent lipolysis, ketoacids do not accumulate; thus, the anion gap is typically normal or only minimally elevated. * **B. Hypoglycaemic Coma:** This is a metabolic emergency due to low fuel substrate for the brain. It does not inherently involve the accumulation of organic acids, so the anion gap remains normal. * **D. Renal Tubular Acidosis (RTA):** This is a classic cause of **Normal Anion Gap Metabolic Acidosis (NAGMA)** or hyperchloremic acidosis [1]. The drop in bicarbonate is compensated for by a proportional increase in chloride. **NEET-PG High-Yield Pearls:** * **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, **Lactic acidosis**, Ethylene glycol, Salicylates). * **Mnemonic for NAGMA:** **HARDUP** (Hyperalimentation, Acetazolamide, **RTA**, Diarrhea, Uretero-sigmoidostomy, Pancreatic fistula). * **Clinical Note:** Phenformin was withdrawn in many countries due to this specific risk of fatal lactic acidosis; Metformin carries a much lower risk but is still contraindicated in severe renal failure [1].

Question 138: What is the most common presentation of Multiple Endocrine Neoplasia type 1 (MEN I)?

A. Primary hyperparathyroidism (Correct Answer)
B. Hyperprolactinemia
C. Hypergastrinemia
D. Acromegaly

Explanation: **Explanation:** **Multiple Endocrine Neoplasia type 1 (MEN 1)**, also known as Wermer’s syndrome, is an autosomal dominant disorder caused by a mutation in the *MEN1* gene (encoding the protein Menin). It is classically characterized by the **"3 Ps"**: **P**arathyroid, **P**ancreas, and **P**ituitary tumors. 1. **Why Primary Hyperparathyroidism is correct:** Primary hyperparathyroidism (PHPT) is the **most common** (occurring in >95% of patients) and usually the **earliest** clinical manifestation of MEN 1. Unlike sporadic cases, PHPT in MEN 1 typically involves multiglandular hyperplasia rather than a single adenoma, often presenting between the ages of 20 and 25. 2. **Why the other options are incorrect:** * **B. Hyperprolactinemia:** Pituitary adenomas occur in about 30–40% of MEN 1 patients. While a prolactinoma is the most common pituitary tumor in this syndrome, it occurs less frequently than hyperparathyroidism. * **C. Hypergastrinemia:** Pancreatic neuroendocrine tumors (NETs) occur in 30–70% of patients. Gastrinomas (causing Zollinger-Ellison Syndrome) are the most common symptomatic pancreatic NETs, but they are still less prevalent than parathyroid involvement. * **D. Acromegaly:** This results from growth hormone-secreting pituitary tumors, which occur in less than 10% of MEN 1 cases. **High-Yield Clinical Pearls for NEET-PG:** * **Screening:** The first biochemical sign of MEN 1 is often an elevated serum calcium or PTH level. * **Order of frequency:** Parathyroid (>95%) > Pancreatic NETs (30-70%) > Pituitary (30-40%). * **Gastrinoma location:** In MEN 1, gastrinomas are more commonly found in the **duodenum** than the pancreas. * **Associated tumors:** Adrenal cortical tumors, facial angiofibromas, collagenomas, and lipomas are also seen in MEN 1.

Question 139: Which of the following conditions causes hypercalcemia with a normal or low parathyroid hormone (PTH) level?

A. Parathyroid adenoma
B. Familial hypocalciuric hypercalcemia
C. Parathyroid hyperplasia
D. Sarcoidosis (Correct Answer)

Explanation: ### Explanation The key to solving this question lies in understanding the **feedback loop** between serum calcium and Parathyroid Hormone (PTH). In a normal physiological state, hypercalcemia should suppress PTH secretion [2]. **1. Why Sarcoidosis is Correct:** Sarcoidosis is a granulomatous disease. Macrophages within the granulomas contain the enzyme **1-alpha-hydroxylase**, which independently converts 25-hydroxyvitamin D into its active form, **1,25-dihydroxyvitamin D (Calcitriol)**. This leads to increased intestinal calcium absorption [2]. The resulting hypercalcemia appropriately **suppresses the parathyroid glands**, leading to low or low-normal PTH levels (PTH-independent hypercalcemia) [2]. **2. Why the Other Options are Incorrect:** * **A & C (Parathyroid Adenoma/Hyperplasia):** These are causes of **Primary Hyperparathyroidism** [1]. Here, the pathology lies within the parathyroid gland itself, which autonomously secretes high levels of PTH despite elevated serum calcium [1]. * **B (Familial Hypocalciuric Hypercalcemia - FHH):** This is caused by an inactivating mutation in the **Calcium-Sensing Receptor (CaSR)** [1]. The parathyroid glands "perceive" normal calcium levels as low, leading to inappropriately **normal or mildly elevated PTH** levels in the presence of hypercalcemia [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **PTH-Independent Hypercalcemia (Low PTH):** Think of Malignancy (PTHrP), Sarcoidosis/Tuberculosis (Vitamin D mediated), Multiple Myeloma, and Vitamin D toxicity [2]. * **PTH-Dependent Hypercalcemia (High/Normal PTH):** Think of Primary Hyperparathyroidism and FHH [2]. * **Distinguishing FHH from Primary Hyperparathyroidism:** FHH presents with a **Urinary Calcium/Creatinine Clearance Ratio < 0.01**, whereas it is > 0.02 in Primary Hyperparathyroidism. * **Sarcoidosis Triad:** Bilateral hilar lymphadenopathy, hypercalcemia, and elevated ACE (Angiotensin-Converting Enzyme) levels.

Question 140: A 45-year-old man, a known case of chronic renal failure, develops rugger jersey spine. What is the probable cause?

A. Aluminium intoxication
B. Secondary hyperparathyroidism (Correct Answer)
C. Osteoporosis
D. Osteomalacia

Explanation: **Explanation:** The **Rugger Jersey Spine** is a classic radiological sign pathognomonic for **Renal Osteodystrophy**, specifically caused by **Secondary Hyperparathyroidism**. **1. Why Secondary Hyperparathyroidism is correct:** In chronic renal failure (CRF), the kidneys fail to excrete phosphate and cannot convert Vitamin D to its active form (1,25-dihydroxyvitamin D). This leads to hyperphosphatemia and hypocalcemia, which chronically stimulate the parathyroid glands [3]. The resulting excess Parathyroid Hormone (PTH) increases osteoclastic activity [1]. Radiologically, this manifests as alternating bands of sclerotic (dense) bone at the superior endplates of the vertebrae and radiolucent (decalcified) bone in the center, mimicking the stripes on a British rugby jersey. **2. Why other options are incorrect:** * **Aluminium intoxication:** Previously common due to aluminium-containing phosphate binders, it typically causes **Adynamic Bone Disease** or osteomalacia [1], not the sclerotic bands seen in rugger jersey spine. * **Osteoporosis:** Characterized by a generalized decrease in bone mass. Radiologically, it shows "codfish vertebrae" or wedge fractures, but not the distinct banded sclerosis [2]. * **Osteomalacia:** Involves defective mineralization of the bone matrix [4]. While it occurs in CRF, its hallmark radiological features are **Looser’s zones** (pseudofractures), not vertebral sclerosis. **Clinical Pearls for NEET-PG:** * **Rugger Jersey Spine:** Secondary Hyperparathyroidism (Renal Osteodystrophy). * **Salt and Pepper Skull:** Another classic sign of Hyperparathyroidism (granular decalcification). * **Brown Tumors:** Osteoclastoma-like lesions found in primary or secondary hyperparathyroidism. * **Ivory Vertebrae:** Differential includes Hodgkin’s Lymphoma, Paget’s disease, and Metastatic Prostatic Carcinoma (distinct from Rugger Jersey as the entire vertebra is dense).

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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