Endocrinology — MCQs

A 40-year-old non-alcoholic male patient presented with jaundice, lethargy, arthralgia, skin pigmentation, loss of libido, polyuria, polydipsia, and exertional dyspnea. On examination, hepatosplenomegaly, increased pigmentation, spider angiomas, arthropathy, ascites, loss of body hair, and testicular atrophy were noted. Liver function tests were deranged, and insulin levels were raised. Liver biopsy was performed. The patient had no history of long-term medication intake. Iron studies revealed: Plasma iron - 200 microgm/dL, TIBC - 300 microgm/dL, Transferrin saturation - 90%, Serum ferritin - 5000 microgm/L, Liver iron - 10000 microgm/gm of dry weight, Hepatic iron index - 3. What is the most common mutation seen in this condition?

Q1167Medium

All of the following are features of acromegaly, except?

Q1168Medium

Which of the sulfonylureas is the best choice in patients with chronic kidney disease?

Q1169Easy

Hypoglycemia is an important feature of which of the following conditions?

Q1170Medium

A 50-year-old male presents with severe refractory hypertension, weakness, muscle cramps, and hypokalemia. What is the most likely diagnosis?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1161: Hypophosphatemia is seen in all except?

A. Acute renal failure (Correct Answer)
B. Rickets
C. Respiratory alkalosis/COPD
D. Chronic alcoholism

Explanation: **Explanation:** The correct answer is **Acute Renal Failure (ARF)**. In ARF, particularly during the oliguric phase, the kidneys fail to excrete phosphate, leading to **Hyperphosphatemia**, not hypophosphatemia. This occurs due to a decreased Glomerular Filtration Rate (GFR), which causes phosphate retention in the blood. [1] **Analysis of Options:** * **Rickets (Option B):** Whether due to Vitamin D deficiency or Vitamin D-resistant types, Rickets leads to decreased intestinal absorption of calcium and phosphate. Secondary hyperparathyroidism (in response to low calcium) further increases renal phosphate excretion, causing **hypophosphatemia**. * **Respiratory Alkalosis/COPD (Option C):** Acute respiratory alkalosis (often seen in COPD patients during hyperventilation or treatment) triggers intracellular pH changes. This activates phosphofructokinase, stimulating glycolysis, which shifts inorganic phosphate from the extracellular space into the cells, resulting in **transcellular hypophosphatemia**. * **Chronic Alcoholism (Option D):** This is a classic cause of hypophosphatemia due to multiple factors: poor dietary intake, decreased intestinal absorption, and alcohol-induced tubular dysfunction leading to phosphaturia. **NEET-PG High-Yield Pearls:** 1. **Refeeding Syndrome:** A high-yield cause of severe hypophosphatemia. Insulin release causes a massive shift of phosphate into cells. [1] 2. **Hungry Bone Syndrome:** Seen post-parathyroidectomy; rapid bone mineralization "consumes" serum phosphate. 3. **Fanconi Syndrome:** Proximal tubular defect leading to significant renal phosphate wasting. [1] 4. **Rule of Thumb:** Renal failure is the most common cause of *high* phosphate; almost all other metabolic crises (alkalosis, malnutrition, Vitamin D deficiency) lead to *low* phosphate.

Question 1162: Pseudo Cushing's syndrome is seen in which of the following conditions?

A. Obesity
B. Alcoholism
C. Depression
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Pseudo-Cushing’s syndrome** refers to a group of conditions that exhibit clinical features and biochemical evidence of hypercortisolism (elevated cortisol levels) but are not caused by a primary pathology of the hypothalamic-pituitary-adrenal (HPA) axis. **Why "All of the above" is correct:** The underlying mechanism in Pseudo-Cushing’s is the **activation of the HPA axis** due to external physiological or psychological stress, rather than an autonomous tumor [1]. * **Alcoholism:** Chronic alcohol abuse stimulates CRH secretion and impairs liver clearance of cortisol. It is the most common cause of a "Cushingoid" appearance that resolves with abstinence. * **Depression:** Major depressive disorder leads to hypercortisolemia due to increased central CRH drive. These patients often fail the Dexamethasone Suppression Test (DST) but do not show the physical stigmata of true Cushing’s (like thinning of skin or proximal myopathy). * **Obesity:** Severe obesity is associated with increased cortisol production rates and urinary free cortisol (UFC), though serum levels usually remain normal. **Clinical Pearls for NEET-PG:** 1. **Differentiation:** The most reliable way to differentiate Pseudo-Cushing's from true Cushing’s Syndrome is the **Insulin Tolerance Test (ITT)**. Patients with true Cushing’s show no rise in ACTH/Cortisol during hypoglycemia, whereas those with Pseudo-Cushing’s show a normal response. 2. **Dexamethasone-CRH Test:** This is another high-yield test; patients with Pseudo-Cushing’s will show suppressed cortisol levels compared to those with Cushing’s disease. 3. **Key Fact:** Clinical features like **easy bruising, supraclavicular fat pads, and proximal myopathy** are rare in Pseudo-Cushing’s and strongly point toward true Cushing’s Syndrome [2].

Question 1163: What is the most common cause of hyperthyroidism?

A. Thyroid hyperplasia
B. Thyroid adenoma
C. Thyroid carcinoma
D. Graves' disease (Correct Answer)

Explanation: **Explanation:** **Graves’ disease** is the most common cause of hyperthyroidism worldwide, accounting for approximately 60–80% of all cases [2]. It is an autoimmune disorder characterized by the production of **Thyroid Stimulating Immunoglobulins (TSI)** [1]. These autoantibodies act as agonists to the TSH receptor on thyroid follicular cells, leading to continuous stimulation of the gland, excessive synthesis of thyroid hormones (T3 and T4), and diffuse glandular enlargement [1], [2]. **Analysis of Incorrect Options:** * **Thyroid hyperplasia (A):** While Graves' disease involves diffuse hyperplasia of the thyroid gland, "hyperplasia" is a pathological description rather than a specific disease entity. In the context of hyperthyroidism, the underlying autoimmune process (Graves') is the primary clinical cause [1]. * **Thyroid adenoma (B):** Specifically, a "Toxic Adenoma" (Plummer’s disease) is a common cause of hyperthyroidism, but it ranks second to Graves' disease. It involves a solitary hyperfunctioning nodule that acts independently of TSH [3]. * **Thyroid carcinoma (C):** Most thyroid cancers (like papillary or follicular) are "cold" nodules and do not produce excess thyroid hormone. Hyperthyroidism due to functioning thyroid carcinoma is extremely rare. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad of Graves’:** Hyperthyroidism, Diffuse Goiter, and Ophthalmopathy (Exophthalmos) [2]. * **Specific Sign:** **Pretibial Myxedema** (Dermopathy) is pathognomonic for Graves’ disease [1]. * **Diagnosis:** Low TSH, High Free T4, and **diffuse increased uptake** on Radioactive Iodine Uptake (RAIU) scan. * **Antibody:** Anti-TSH receptor antibody (TRAb) is the most specific marker [1].

Question 1164: Diabetes control is best monitored by?

A. Serum glucose
B. Post prandial blood glucose
C. HbA1c (Correct Answer)
D. HbA2c

Explanation: **Explanation:** **HbA1c (Glycated Hemoglobin)** is the gold standard for monitoring long-term glycemic control in diabetic patients [3]. It reflects the average blood glucose levels over the preceding **8 to 12 weeks** (the average lifespan of a red blood cell) [4]. The underlying medical concept is the **non-enzymatic glycosylation** of hemoglobin. Glucose molecules attach to the N-terminal valine of the beta chain of hemoglobin A at a rate proportional to the glucose concentration in the blood [3]. Because this process is irreversible, HbA1c provides a stable "weighted average" that is not affected by recent meals, exercise, or acute stress [4]. **Why other options are incorrect:** * **Serum Glucose & Post-Prandial Blood Glucose (PPBG):** These provide only a "snapshot" of the blood sugar at a specific moment [1]. They are highly variable and can be influenced by the patient's last meal, physical activity, or medication adherence on the day of the test [2]. They are useful for acute management but not for assessing overall long-term control. * **HbA2c:** This is a distractor. HbA2 is a normal variant of hemoglobin (comprising two alpha and two delta chains), but "HbA2c" is not a standard clinical marker used for monitoring diabetes. **Clinical Pearls for NEET-PG:** * **Target HbA1c:** For most non-pregnant adults, the goal is **<7%** [5]. * **Falsely Low HbA1c:** Seen in conditions with high RBC turnover (e.g., Hemolytic anemia, recent blood transfusion, pregnancy, or treatment with Erythropoietin). * **Falsely High HbA1c:** Seen in conditions that prolong RBC lifespan (e.g., Iron deficiency anemia, Vitamin B12 deficiency, or Splenectomy). * **Fructosamine Test:** Used to monitor control over a shorter period (**2–3 weeks**) in patients where HbA1c is unreliable (e.g., Hemoglobinopathies).

Question 1165: Which one of the following is NOT an endocrine myopathy?

A. Addison's disease
B. Cushing's disease
C. Myasthenia gravis (Correct Answer)
D. Primary Hypoparathyroidism

Explanation: **Explanation:** The core concept here is distinguishing between **endocrine myopathies** (muscle weakness caused by hormonal imbalances) and **neuromuscular junction disorders**. [1] **Why Myasthenia Gravis is the correct answer:** Myasthenia Gravis (MG) is an **autoimmune disorder** caused by antibodies against the post-synaptic nicotinic acetylcholine receptors (AChR) at the neuromuscular junction. [1] While it presents with muscle weakness and fatigability, it is not caused by a primary endocrine gland dysfunction. [1] Therefore, it is classified as a neuromuscular disorder, not an endocrine myopathy. **Why the other options are incorrect (Endocrine Myopathies):** * **Addison’s Disease (Adrenal Insufficiency):** Chronic deficiency of cortisol and aldosterone leads to significant muscle fatigue, cramping, and generalized weakness, often exacerbated by electrolyte imbalances (hyponatremia and hyperkalemia). * **Cushing’s Disease:** Excess glucocorticoids cause **proximal muscle wasting** and weakness (steroid myopathy) due to increased catabolism of muscle proteins. [2] * **Primary Hypoparathyroidism:** Low parathyroid hormone leads to hypocalcemia, which increases neuromuscular irritability. This can manifest as muscle cramps, tetany, and in chronic cases, a specific myopathy. **NEET-PG High-Yield Pearls:** * **Thyroid Disorders:** Both Hyperthyroidism (proximal weakness, periodic paralysis) and Hypothyroidism (Hoffman’s syndrome—pseudohypertrophy) are common causes of endocrine myopathy. [2] * **Cushing’s Myopathy:** Characteristically affects the **proximal muscles** (difficulty climbing stairs or rising from a chair) while sparing the facial and distal muscles. [2] * **Electrolytes:** Always check Potassium levels in endocrine weakness; both hyperkalemia (Addison’s) and hypokalemia (Conn’s syndrome) can cause muscle paralysis.

Question 1166: A 40-year-old non-alcoholic male patient presented with jaundice, lethargy, arthralgia, skin pigmentation, loss of libido, polyuria, polydipsia, and exertional dyspnea. On examination, hepatosplenomegaly, increased pigmentation, spider angiomas, arthropathy, ascites, loss of body hair, and testicular atrophy were noted. Liver function tests were deranged, and insulin levels were raised. Liver biopsy was performed. The patient had no history of long-term medication intake. Iron studies revealed: Plasma iron - 200 microgm/dL, TIBC - 300 microgm/dL, Transferrin saturation - 90%, Serum ferritin - 5000 microgm/L, Liver iron - 10000 microgm/gm of dry weight, Hepatic iron index - 3. What is the most common mutation seen in this condition?

A. C282Y (Correct Answer)
B. H63D
C. H62D
D. C283Y

Explanation: The clinical presentation of jaundice, skin pigmentation ("bronze" skin), diabetes mellitus (polyuria/polydipsia), arthropathy, and hypogonadism (loss of libido/testicular atrophy), combined with iron studies showing high transferrin saturation (>45%) and ferritin (>200 ng/mL), is diagnostic of Hereditary Hemochromatosis (HH) [2]. The Hepatic Iron Index (HII) > 1.9 further confirms the diagnosis [1]. **1. Why C282Y is correct:** Hereditary Hemochromatosis is most commonly an autosomal recessive disorder involving the **HFE gene** located on chromosome 6 [2]. The **C282Y mutation** (substitution of tyrosine for cysteine at amino acid position 282) is the most common and significant mutation [1]. It is found in approximately 85-90% of patients with classic HH. This mutation prevents the HFE protein from reaching the cell surface, leading to inappropriately low levels of **hepcidin**, which results in uncontrolled intestinal iron absorption. **2. Why other options are incorrect:** * **H63D:** This is the second most common HFE mutation (aspartate for histidine at position 63) [1]. While it can cause iron overload when inherited as a compound heterozygote (C282Y/H63D), it rarely causes significant clinical disease on its own. * **H62D and C283Y:** These are not recognized pathogenic mutations associated with Hereditary Hemochromatosis and are likely included as distractors. **Clinical Pearls for NEET-PG:** * **Classic Triad:** "Bronze Diabetes" (Cirrhosis, Diabetes, and Skin Pigmentation) [2]. * **Arthropathy:** Classically involves the 2nd and 3rd metacarpophalangeal (MCP) joints with "hook-like" osteophytes. * **Cardiac involvement:** Can present as restrictive or dilated cardiomyopathy. * **Screening:** Transferrin saturation is the most sensitive initial test. * **Gold Standard:** Liver biopsy with Perl’s Prussian blue stain (though genetic testing has largely replaced it) [1]. * **Treatment:** Therapeutic phlebotomy is the mainstay of management [1].

Question 1167: All of the following are features of acromegaly, except?

A. Glucose intolerance
B. Nonsuppressibility of growth hormone by glucose ingestion
C. Raised levels of plasma somatomedin C
D. Low serum phosphate (Correct Answer)

Explanation: In Acromegaly, excessive Growth Hormone (GH) leads to characteristic metabolic and biochemical changes. The correct answer is **D (Low serum phosphate)** because Acromegaly actually causes **hyperphosphatemia**, not low phosphate. [1] ### Why Option D is correct: Growth hormone has a direct effect on the kidneys, where it **increases the renal tubular reabsorption of phosphate**. This leads to elevated serum phosphate levels in patients with active acromegaly. [1] Therefore, "Low serum phosphate" is the incorrect feature. ### Why other options are incorrect: * **A. Glucose intolerance:** GH is a potent counter-regulatory hormone that antagonizes insulin action and increases hepatic gluconeogenesis. [1] Approximately 50% of patients have glucose intolerance, and 10-15% develop overt Diabetes Mellitus. * **B. Nonsuppressibility of GH:** This is the physiological hallmark. In healthy individuals, an oral glucose load (75g) suppresses GH to <1 µg/L. In acromegaly, the autonomous secretion from a pituitary adenoma fails to suppress [2], which is the **Gold Standard diagnostic test**. * **C. Raised Somatomedin C (IGF-1):** GH stimulates the liver to produce IGF-1 (Somatomedin C). Since GH secretion is pulsatile, a single GH measurement is unreliable; however, IGF-1 levels are stable and serve as the **best screening test**. [3] ### NEET-PG High-Yield Pearls: * **Best Screening Test:** Serum IGF-1 levels. * **Confirmatory Test:** Oral Glucose Tolerance Test (OGTT) for GH suppression. * **Most Common Cause:** Pituitary Adenoma (Somatotroph adenoma). [3] * **Radiological Investigation of Choice:** MRI of the Brain (Sella turcica). * **Metabolic Associations:** Hypercalciuria (due to increased Vitamin D activation) and Hyperphosphatemia. [1]

Question 1168: Which of the sulfonylureas is the best choice in patients with chronic kidney disease?

A. Glimipride
B. Glibenclamide
C. Glipizide (Correct Answer)
D. Glyburide

Explanation: **Explanation:** The primary concern when using sulfonylureas in patients with chronic kidney disease (CKD) is the risk of **severe, prolonged hypoglycemia**. This occurs because many sulfonylureas or their active metabolites are excreted renally. [1] **Why Glipizide is the Correct Choice:** Glipizide is considered the safest sulfonylurea in CKD because it is primarily metabolized by the **liver** into **inactive metabolites**. These inactive metabolites are then excreted in the urine, posing no risk of hypoglycemia even if they accumulate due to a low Glomerular Filtration Rate (GFR). It also has a shorter half-life compared to other agents in its class. **Analysis of Incorrect Options:** * **Glibenclamide (Glyburide):** These are the same drug (Option B and D). It is **contraindicated** in CKD (especially if GFR <60 mL/min). It has active metabolites that are cleared by the kidneys; accumulation leads to profound, life-threatening hypoglycemia. * **Glimepiride:** While it is a second/third-generation agent, it possesses active metabolites that are renally cleared. It should be used with extreme caution or avoided in advanced CKD. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** While Glipizide is the best *sulfonylurea* for CKD, the overall oral hypoglycemic agent of choice in advanced CKD is typically a **DPP-4 inhibitor** (like Linagliptin, which requires no renal adjustment) or **Insulin**. [2] * **Metformin:** Must be discontinued if **eGFR <30 mL/min** due to the risk of lactic acidosis. [1] * **Gliclazide:** Another preferred sulfonylurea in mild-to-moderate CKD as it has inactive metabolites, but Glipizide remains the classic textbook answer for safety. * **Rule of Thumb:** "Glipizide stays in the liver, Glyburide gets stuck in the kidney."

Question 1169: Hypoglycemia is an important feature of which of the following conditions?

A. Hypoparathyroidism
B. Addison disease (Correct Answer)
C. Pheochromocytoma
D. All of the above

Explanation: ### Explanation **Correct Option: B. Addison disease** **Mechanism of Hypoglycemia in Addison Disease:** Addison disease (Primary Adrenal Insufficiency) is characterized by the destruction of the adrenal cortex [1], leading to a deficiency of both mineralocorticoids and glucocorticoids (cortisol) [3]. Cortisol is a potent **counter-regulatory hormone** that maintains blood glucose levels by: 1. **Stimulating Gluconeogenesis:** Increasing the synthesis of glucose from non-carbohydrate sources in the liver [2]. 2. **Antagonizing Insulin:** Decreasing peripheral glucose uptake in tissues [2]. 3. **Promoting Lipolysis and Proteolysis:** Providing substrates for glucose production. In the absence of cortisol, these processes are impaired, leading to fasting hypoglycemia, especially during periods of stress or illness. **Analysis of Incorrect Options:** * **A. Hypoparathyroidism:** This condition is characterized by low levels of Parathyroid Hormone (PTH), leading to **hypocalcemia** and hyperphosphatemia. It has no direct effect on glucose metabolism. * **C. Pheochromocytoma:** This catecholamine-secreting tumor typically causes **hyperglycemia**. Catecholamines (epinephrine/norepinephrine) stimulate glycogenolysis and inhibit insulin secretion, leading to elevated blood sugar levels [2]. **NEET-PG High-Yield Pearls:** * **Classic Triad of Addison’s:** Hyponatremia, Hyperkalemia, and Hypoglycemia [3]. * **Hyperpigmentation:** Seen in primary adrenal insufficiency (due to increased ACTH/MSH) but *absent* in secondary adrenal insufficiency. * **Waterhouse-Friderichsen Syndrome:** Acute adrenal insufficiency due to hemorrhagic necrosis of adrenal glands, often secondary to Meningococcemia. * **Diagnostic Gold Standard:** ACTH Stimulation Test (Cosyntropin test) [3].

Question 1170: A 50-year-old male presents with severe refractory hypertension, weakness, muscle cramps, and hypokalemia. What is the most likely diagnosis?

A. Hypoaldosteronism
B. Hyperaldosteronism (Correct Answer)
C. Cushing syndrome
D. Pheochromocytoma

Explanation: ### Explanation **Correct Answer: B. Hyperaldosteronism** The clinical triad of **refractory hypertension, hypokalemia, and muscle weakness** is the classic presentation of Primary Hyperaldosteronism (Conn’s Syndrome). **Pathophysiology:** Excess aldosterone acts on the principal cells of the renal collecting ducts, leading to: 1. **Sodium and water retention:** Resulting in hypertension (often resistant to standard therapy) [1]. 2. **Potassium excretion:** Leading to hypokalemia, which manifests clinically as muscle weakness, cramps, and occasionally cardiac arrhythmias [1], [2]. 3. **Hydrogen ion excretion:** Often causing metabolic alkalosis [1]. --- ### Why the other options are incorrect: * **A. Hypoaldosteronism:** This would present with hypotension and **hyperkalemia**, the exact opposite of this patient's presentation [1]. * **C. Cushing Syndrome:** While it can cause hypertension and hypokalemia (due to mineralocorticoid cross-reactivity of cortisol), it is typically accompanied by distinct physical features like truncal obesity, moon facies, striae, and hyperglycemia. * **D. Pheochromocytoma:** This presents with "paroxysmal" hypertension associated with the classic triad of **palpitations, perspiration, and headache**, rather than primary electrolyte disturbances like profound hypokalemia. --- ### NEET-PG High-Yield Pearls: * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20–30** is highly suggestive. * **Confirmatory Test:** Saline infusion test or Oral salt loading test (failure to suppress aldosterone). * **Most Common Cause:** Adrenal adenoma (Conn’s) or Bilateral adrenal hyperplasia. * **Spironolactone** (Aldosterone antagonist) is the medical treatment of choice for bilateral hyperplasia.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free