Endocrinology — MCQs
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A 35-year-old man has fasting and postprandial blood sugar within normal limits, but urine sugar is 3 plus (+++). What is the diagnosis?
A 18-year-old male presents with severe weakness, dizziness, sleepiness, unquenchable thirst, and increased urination over the past 4 weeks. He has also experienced drowsiness and generalized tiredness in a previous episode 3 weeks earlier and has lost 4kg of weight. Laboratory findings on admission show a glucose of 560 mg/dl, urine that is 4+ for glucose and has "large" acetone, and an HbA1c of 14%. Which of the following is true regarding this patient?
Which of the following is NOT a cause of hypopituitarism?
High calcium uptake leads to which of the following conditions?
Atrial fibrillation is common in which of the following conditions?
The syndrome of inappropriate antidiuretic hormone (SIADH) is characterized by which of the following?
Which treatment is contraindicated in hypophosphatasia?
Which of the following is true about MEN-I?
Which of the following is a diagnostic criterion of Metabolic syndrome?
Shortening of the 4th metacarpal is a feature of which condition?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 851: A 35-year-old man has fasting and postprandial blood sugar within normal limits, but urine sugar is 3 plus (+++). What is the diagnosis?
- A. Renal glycosuria (Correct Answer)
- B. Pancreatic insufficiency
- C. Alimentary glycosuria
- D. High carbohydrate diet taken in the morning
Explanation: The clinical scenario describes **Renal Glycosuria**, a condition characterized by the excretion of glucose in the urine despite having normal blood glucose levels (euglycemia). **1. Why Renal Glycosuria is Correct:** Under normal physiological conditions, the kidney filters glucose at the glomerulus, and nearly 100% is reabsorbed in the proximal convoluted tubule (PCT) via **SGLT2 transporters** [1]. The "Renal Threshold" for glucose is typically **180 mg/dL** [1]. In renal glycosuria, there is a functional defect in these transporters or a reduced threshold, causing glucose to "leak" into the urine even when blood sugar levels are well within the normal range (Fasting <100 mg/dL; Postprandial <140 mg/dL). This deviation between the predicted and actual renal threshold is referred to as "splay" [1]. **2. Why Other Options are Incorrect:** * **Pancreatic Insufficiency:** This would lead to a deficiency in insulin secretion, resulting in **elevated** blood sugar levels (Diabetes Mellitus) alongside glycosuria [2]. * **Alimentary Glycosuria:** This occurs when rapid intestinal absorption of glucose causes a transient spike in blood sugar that exceeds the renal threshold (often seen after gastric surgery). Here, the postprandial blood sugar would be abnormally high, unlike in this patient. * **High Carbohydrate Diet:** In a healthy individual, the pancreas compensates for high carb intake by secreting insulin. Glycosuria would only occur if the blood glucose exceeded 180 mg/dL. **Clinical Pearls for NEET-PG:** * **Benign Nature:** Isolated renal glycosuria is usually an asymptomatic, benign condition (often autosomal dominant). * **Fanconi Syndrome:** If glycosuria is associated with phosphaturia, aminoaciduria, and uricosuria, suspect a generalized PCT defect (Fanconi Syndrome). * **Pregnancy:** A physiological decrease in the renal threshold for glucose is common during pregnancy, leading to glycosuria despite normal BSL. * **SGLT2 Inhibitors:** Drugs like Dapagliflozin intentionally induce "pharmacological renal glycosuria" to treat Diabetes.
Question 852: A 18-year-old male presents with severe weakness, dizziness, sleepiness, unquenchable thirst, and increased urination over the past 4 weeks. He has also experienced drowsiness and generalized tiredness in a previous episode 3 weeks earlier and has lost 4kg of weight. Laboratory findings on admission show a glucose of 560 mg/dl, urine that is 4+ for glucose and has "large" acetone, and an HbA1c of 14%. Which of the following is true regarding this patient?
- A. Increased glucose uptake
- B. Increased lipolysis (Correct Answer)
- C. Decreased hepatic glucose output
- D. Decreased protein catabolism
Explanation: ### Explanation **Diagnosis:** The patient is presenting with classic symptoms of **Type 1 Diabetes Mellitus (T1DM)** presenting as **Diabetic Ketoacidosis (DKA)**. This is evidenced by the triad of hyperglycemia (560 mg/dl), ketonuria ("large" acetone), and metabolic symptoms (polyuria, polydipsia, weight loss) [3]. An HbA1c of 14% indicates chronic, severe hyperglycemia. #### Why "Increased Lipolysis" is Correct: In T1DM, there is an absolute deficiency of insulin. Insulin is a potent inhibitor of **hormone-sensitive lipase (HSL)**. In its absence, HSL becomes hyperactive, leading to massive **increased lipolysis** in adipose tissue [2]. This breaks down triglycerides into glycerol and **Free Fatty Acids (FFAs)**. These FFAs travel to the liver, where they undergo beta-oxidation to form acetyl-CoA, which is then converted into **ketone bodies** (acetoacetate and beta-hydroxybutyrate), leading to ketosis and acidosis. #### Why Other Options are Incorrect: * **A. Increased glucose uptake:** In the absence of insulin, GLUT-4 transporters remain sequestered inside cells (muscle and fat), leading to **decreased** peripheral glucose uptake [2]. * **C. Decreased hepatic glucose output:** Insulin normally suppresses gluconeogenesis and glycogenolysis. Without insulin, the liver produces glucose unchecked, leading to **increased** hepatic glucose output [2]. * **D. Decreased protein catabolism:** Insulin is an anabolic hormone. Its deficiency leads to **increased** protein breakdown (catabolism) into amino acids to provide substrates for gluconeogenesis, contributing to weight loss and muscle wasting [1]. #### NEET-PG High-Yield Pearls: * **DKA Triad:** Hyperglycemia (>250 mg/dL), Ketosis (ketonemia/ketonuria), and Metabolic Acidosis (pH <7.3 or Bicarb <18). * **Rate-limiting step of Ketogenesis:** Controlled by the enzyme **HMG-CoA Synthase**. * **Most common precipitant of DKA:** Infection (often pneumonia or UTI) or non-compliance with insulin [3]. * **Initial Management:** The most critical first step in DKA management is **aggressive fluid resuscitation** (Normal Saline), followed by insulin infusion and potassium monitoring [4].
Question 853: Which of the following is NOT a cause of hypopituitarism?
- A. Breast cancer
- B. Bronchus cancer
- C. Chromophilic adenoma
- D. Acidophilic tumor (Correct Answer)
Explanation: **Explanation:** Hypopituitarism refers to the deficiency of one or more pituitary hormones, usually resulting from the destruction of the anterior pituitary gland [3]. **Why "Acidophilic tumor" is the correct answer:** Acidophilic tumors (also known as somatotroph adenomas) are **functioning adenomas**. They are characterized by the hypersecretion of Growth Hormone (GH), leading to Gigantism (in children) or Acromegaly (in adults). Because these tumors cause a **hyperstate** (excess hormone production) rather than a deficiency, they are not a cause of hypopituitarism. **Analysis of Incorrect Options:** * **Breast and Bronchus Cancer (A & B):** The pituitary gland is a common site for hematogenous metastasis. Breast and lung (bronchus) cancers are the most frequent primary malignancies that metastasize to the pituitary. These metastatic deposits destroy the normal pituitary parenchyma, leading to hypopituitarism and Diabetes Insipidus. * **Chromophilic Adenoma (C):** While the term is older, it refers to tumors that stain with dyes. Large, non-functioning chromophobe adenomas are the most common cause of hypopituitarism in adults because they compress the normal pituitary tissue and the pituitary stalk (mass effect) [2]. **NEET-PG High-Yield Pearls:** 1. **Most common cause of hypopituitarism:** Non-functioning pituitary adenomas (due to compression) [2]. 2. **Sheehan Syndrome:** Ischemic necrosis of the pituitary post-partum; the first clinical sign is usually failure to lactate [1]. 3. **Empty Sella Syndrome:** Can be primary (arachnoid herniation) or secondary (post-surgery/radiation), potentially leading to hormone deficiencies [1]. 4. **Order of hormone loss:** GH → LH/FSH → TSH → ACTH (mnemonic: **"Go Look For The Adenoma"**).
Question 854: High calcium uptake leads to which of the following conditions?
- A. Milk alkali syndrome (Correct Answer)
- B. Osteopoikilosis
- C. Osteopetrosis
- D. Cardiomyopathy
Explanation: ### Explanation **Correct Answer: A. Milk alkali syndrome** **Mechanism:** Milk-alkali syndrome (now often called **Calcium-alkali syndrome**) is characterized by the triad of **hypercalcemia, metabolic alkalosis, and renal insufficiency**. It occurs due to the excessive ingestion of calcium (usually as calcium carbonate) and absorbable alkali. High calcium intake leads to hypercalcemia, which causes renal vasoconstriction and inhibits the Na-K-2Cl cotransporter (solute diuresis), leading to volume depletion. This volume depletion stimulates bicarbonate reabsorption, maintaining the alkalosis. The alkalosis, in turn, enhances calcium reabsorption in the distal tubule, creating a vicious cycle that further elevates serum calcium levels. **Analysis of Incorrect Options:** * **B. Osteopoikilosis:** This is a rare, autosomal dominant sclerosing bone dysplasia characterized by multiple small, symmetric, radiopaque "islands" in the skeleton. It is an asymptomatic radiological finding and is not related to calcium intake. * **C. Ostepethrosis:** Also known as "Marble Bone Disease," this is a genetic disorder caused by **defective osteoclast function**. While it results in increased bone density, it is a failure of bone resorption, not a result of high dietary calcium uptake. * **D. Cardiomyopathy:** While severe hypercalcemia can cause ECG changes (shortened QT interval) and arrhythmias, "high calcium uptake" is not a primary or direct cause of cardiomyopathy. **NEET-PG High-Yield Pearls:** * **Modern Etiology:** Historically caused by milk/antacids for peptic ulcers; today, the most common cause is **calcium carbonate** supplements taken for osteoporosis prevention. * **Clinical Triad:** Hypercalcemia + Metabolic Alkalosis + Renal Failure. * **Lab Findings:** Low PTH (due to suppression by high calcium), low phosphate (usually), and elevated bicarbonate. * **Treatment:** Aggressive hydration with isotonic saline and cessation of calcium/alkali sources.
Question 855: Atrial fibrillation is common in which of the following conditions?
- A. Adrenogenital syndrome
- B. Addison's disease
- C. Hyperthyroidism (Correct Answer)
- D. Von-Willebrand's disease
Explanation: **Hyperthyroidism** is the correct answer because thyroid hormones (T3 and T4) have direct and indirect stimulatory effects on the cardiovascular system [1]. Excess thyroid hormone increases the expression of beta-adrenergic receptors in the myocardium, leading to a state of hyper-adrenergic sensitivity [4]. This results in increased heart rate (tachycardia), increased stroke volume, and shortened refractory periods of the atrial cardiomyocytes. These electrophysiological changes create a substrate for reentry, making **Atrial Fibrillation (AF)** the most common sustained arrhythmia in hyperthyroid patients (occurring in 10–15% of cases) [1], [3]. **Why other options are incorrect:** * **Adrenogenital Syndrome (CAH):** This involves enzyme deficiencies (like 21-hydroxylase) leading to cortisol deficiency and androgen excess. It typically presents with virilization or salt-wasting, not tachyarrhythmias. * **Addison’s Disease:** Primary adrenal insufficiency leads to hypotension and hyperkalemia. While severe hyperkalemia can cause peaked T-waves or bradycardia, AF is not a characteristic feature. * **Von-Willebrand’s Disease:** This is a qualitative or quantitative deficiency of Von-Willebrand factor leading to a bleeding diathesis. It has no direct pathophysiological link to cardiac rhythm disturbances. **Clinical Pearls for NEET-PG:** * **Apathetic Hyperthyroidism:** In elderly patients, AF may be the *only* presenting sign of hyperthyroidism [1]. * **Subclinical Hyperthyroidism:** Even a suppressed TSH with normal T3/T4 levels is a recognized risk factor for developing AF. * **Treatment:** In thyrotoxic AF, **Beta-blockers** (e.g., Propranolol) are the first-line treatment to control heart rate and inhibit the peripheral conversion of T4 to T3 [2]. Normal sinus rhythm often restores spontaneously once the patient becomes euthyroid.
Question 856: The syndrome of inappropriate antidiuretic hormone (SIADH) is characterized by which of the following?
- A. Hyponatremia and urine sodium excretion > 20 mEq/L (Correct Answer)
- B. Hypernatremia and urine sodium excretion > 20 mEq/L
- C. Hyponatremia and hyperkalemia
- D. Hypernatremia and hypokalemia
Explanation: **Explanation:** The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is a condition characterized by the excessive release of ADH (vasopressin) from the posterior pituitary or ectopic sources, regardless of serum osmolality. **1. Why Option A is Correct:** The core pathophysiology involves excessive water reabsorption in the collecting ducts [1], leading to **euvolemic hyponatremia** (dilutional) [2]. Despite the low serum sodium, the body’s volume-sensing mechanisms (atrial natriuretic peptide) are activated due to transient subclinical volume expansion. This leads to **natriuresis** (increased urinary sodium excretion, typically **> 20–40 mEq/L**) and inappropriately concentrated urine (Urine Osmolality > 100 mOsm/kg). **2. Why Other Options are Incorrect:** * **Options B & D:** SIADH is fundamentally a hyponatremic state. Hypernatremia is seen in conditions like Diabetes Insipidus, where there is a deficiency or resistance to ADH. * **Option C:** While hyponatremia is present, SIADH does not typically affect potassium levels. Hyperkalemia associated with hyponatremia is a hallmark of **Adrenal Insufficiency (Addison’s Disease)**, which must be ruled out before diagnosing SIADH. **Clinical Pearls for NEET-PG:** * **Diagnostic Criteria:** Hyponatremia, low serum osmolality (<275 mOsm/kg), high urine osmolality (>100 mOsm/kg), and clinical euvolemia [2]. * **Common Causes:** Small cell carcinoma of the lung (ectopic), CNS disorders (stroke, trauma), and drugs (SSRIs, Carbamazepine, Cyclophosphamide). * **Management:** Fluid restriction is the first-line treatment. For severe/symptomatic cases, hypertonic saline (3%) is used. **Vaptans** (Tolvaptan) are vasopressin receptor antagonists used in chronic cases [3]. * **Caution:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).**
Question 857: Which treatment is contraindicated in hypophosphatasia?
- A. Vitamin D (Correct Answer)
- B. Calcium chelating agent
- C. Enzyme replacement
- D. Renal dialysis
Explanation: **Explanation:** **Hypophosphatasia (HPP)** is a rare genetic disorder caused by a loss-of-function mutation in the **ALPL gene**, which encodes **Tissue-Nonspecific Alkaline Phosphatase (TNSALP)**. This deficiency leads to an accumulation of inorganic pyrophosphate (PPi), a potent inhibitor of mineralization. **Why Vitamin D is Contraindicated:** In HPP, patients typically present with **hypercalcemia** and **hypercalciuria** because calcium cannot be deposited into the bone matrix due to the lack of alkaline phosphatase. Administering **Vitamin D** (Option A) increases intestinal calcium absorption and bone resorption, which severely exacerbates hypercalcemia and hypercalciuria. This can lead to nephrocalcinosis, renal failure, and vitamin D toxicity. Therefore, Vitamin D and calcium supplements are strictly contraindicated unless a co-existing deficiency is proven. **Analysis of Other Options:** * **Calcium chelating agents (Option B):** These are not standard treatments but are not contraindicated; in cases of severe hypercalcemic crisis, they may be used to lower serum calcium. * **Enzyme Replacement (Option C):** **Asfotase alfa** is the definitive, FDA-approved treatment for HPP. It is a recombinant TNSALP that improves mineralization and survival. * **Renal Dialysis (Option D):** While not a primary treatment for HPP, it may be required if the patient develops end-stage renal disease due to chronic nephrocalcinosis. **NEET-PG High-Yield Pearls:** * **Biochemical Hallmark:** Low serum Alkaline Phosphatase (ALP) levels (age-adjusted) and elevated serum Pyridoxal-5'-Phosphate (Vitamin B6). * **Clinical Sign:** Premature loss of deciduous teeth (before age 5) is a classic pediatric presentation. * **Radiology:** "Copper beaten skull" (craniosynostosis) and metaphyseal lucencies (resembling rickets).
Question 858: Which of the following is true about MEN-I?
- A. Increased VMA in urine
- B. Increased Calcitonin
- C. Hypergastrinemia
- D. Hyperprolactinemia (Correct Answer)
Explanation: **Explanation:** Multiple Endocrine Neoplasia Type I (MEN-I), 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. **Why Hyperprolactinemia is Correct:** Pituitary adenomas occur in approximately 30–40% of MEN-I patients. Among these, **Prolactinoma** is the most common functional pituitary tumor. Therefore, elevated prolactin levels (hyperprolactinemia) are a hallmark clinical finding in these patients. **Analysis of Incorrect Options:** * **A. Increased VMA in urine:** Vanillylmandelic acid (VMA) is a metabolite of catecholamines. Increased VMA is seen in **Pheochromocytoma**, which is a feature of **MEN-2A and 2B**, not MEN-1. * **B. Increased Calcitonin:** Elevated calcitonin is a marker for **Medullary Thyroid Carcinoma (MTC)**. MTC is a defining component of **MEN-2A and 2B**. * **C. Hypergastrinemia:** While Gastrinomas (Zollinger-Ellison Syndrome) are the most common functional pancreatic neuroendocrine tumors in MEN-I, **Hyperprolactinemia** is considered a more direct "classic" answer in many competitive exams when distinguishing between the MEN syndromes, as pituitary involvement is unique to MEN-1. (Note: In some clinical contexts, both C and D could occur, but Prolactinoma remains the most frequent pituitary lesion). **NEET-PG High-Yield Pearls:** * **Most common presentation of MEN-I:** Primary Hyperparathyroidism (seen in >95% of patients). * **Most common Pancreatic tumor in MEN-I:** Gastrinoma (though non-functional tumors are also frequent). * **MEN-2A (Sipple Syndrome):** Medullary Thyroid CA + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN-2B:** Medullary Thyroid CA + Pheochromocytoma + Mucosal Neuromas + Marfanoid Habitus.
Question 859: Which of the following is a diagnostic criterion of Metabolic syndrome?
- A. High serum homocysteine
- B. High serum triglyceride (Correct Answer)
- C. High serum adiponectin
- D. Low HDL cholesterol
Explanation: **Explanation:** Metabolic Syndrome (Syndrome X) is a cluster of conditions that increase the risk of heart disease, stroke, and type 2 diabetes. While several organizations (NCEP-ATP III, IDF, WHO) have defined it, the **NCEP-ATP III criteria** are most frequently tested in NEET-PG. **Why Option B is Correct:** Hypertriglyceridemia is a core component of the metabolic syndrome. According to NCEP-ATP III, a **Serum Triglyceride level ≥ 150 mg/dL** (or being on treatment for high TGs) is one of the five diagnostic criteria. This reflects the underlying pathophysiology of insulin resistance and ectopic fat deposition. **Analysis of Incorrect Options:** * **Option A (High serum homocysteine):** While elevated homocysteine is an independent risk factor for cardiovascular disease (pro-thrombotic), it is **not** part of the formal diagnostic criteria for metabolic syndrome. * **Option C (High serum adiponectin):** Adiponectin is an "anti-inflammatory" adipokine. In metabolic syndrome, adiponectin levels are typically **low**, not high. Low levels correlate with insulin resistance. * **Option D (Low HDL cholesterol):** This is a tricky distractor. While Low HDL is indeed a criterion (< 40 mg/dL in men, < 50 mg/dL in women), the question asks for "a" diagnostic criterion. In many standardized keys, if both B and D are present, "High Triglycerides" is often the preferred answer if the question implies the most characteristic lipid abnormality, though technically both are components. [1] *Note: Always check if the question allows multiple correct answers; here, B is the classic primary lipid marker.* **High-Yield Clinical Pearls for NEET-PG:** * **NCEP-ATP III Criteria (Need 3 out of 5):** 1. **Waist Circumference:** >102 cm (M), >88 cm (F). 2. **Triglycerides:** ≥150 mg/dL. 3. **HDL-C:** <40 mg/dL (M), <50 mg/dL (F). 4. **Blood Pressure:** ≥130/85 mmHg. 5. **Fasting Glucose:** ≥100 mg/dL. [2] * **Modified Criteria for Indians:** Waist circumference cut-offs are lower (**>90 cm for men, >80 cm for women**) due to higher visceral adiposity at lower BMIs.
Question 860: Shortening of the 4th metacarpal is a feature of which condition?
- A. Hyperparathyroidism
- B. Hyperparathyroidism
- C. Pseudohypoparathyroidism (Correct Answer)
- D. Scleroderma
Explanation: The shortening of the 4th metacarpal (and often the 5th) is a classic clinical sign known as **Archibald’s sign**. This occurs due to premature closure of the epiphyses. **1. Why Pseudohypoparathyroidism (PHP) is correct:** PHP is characterized by end-organ resistance to Parathyroid Hormone (PTH). Specifically, **PHP Type 1a** is associated with a constellation of physical findings known as **Albright’s Hereditary Osteodystrophy (AHO)**. The hallmark features of AHO include short stature, round facies, obesity, subcutaneous calcifications, and **brachydactyly** (shortening of the 4th and 5th metacarpals) [1]. When you ask the patient to make a fist, the 4th knuckle appears as a dimple rather than a prominence (Knuckle-Knuckle-Dimple-Dimple sign). **2. Why other options are incorrect:** * **Hyperparathyroidism:** This condition is characterized by excessive PTH, leading to bone resorption. The classic radiological finding is **subperiosteal bone resorption**, most commonly seen on the radial aspect of the middle phalanges, not shortening of the metacarpals. * **Hypoparathyroidism:** This involves a deficiency of PTH. While it causes hypocalcemia and hyperphosphatemia, it does not typically present with the skeletal deformities (AHO) seen in PHP. * **Scleroderma:** This is a connective tissue disorder. While it can cause **acro-osteolysis** (resorption of the distal phalangeal tufts) leading to shortened fingertips, it does not cause congenital shortening of the metacarpals. **Clinical Pearls for NEET-PG:** * **Pseudopseudohypoparathyroidism (PPHP):** Patients have the physical features of AHO (including the short 4th metacarpal) but have **normal** calcium and PTH levels [1]. * **Genetics:** PHP Type 1a is caused by a mutation in the *GNAS1* gene and is inherited from the mother (Genomic Imprinting) [1]. * **Differential for short 4th metacarpal:** Turner Syndrome, PHP/PPHP, and occasionally Down Syndrome.
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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