Endocrinology — MCQs
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What is the first step in the diagnosis of pheochromocytoma?
A 70-year-old female presents with symptoms of hyperthyroidism. Investigations show increased radioactive iodine uptake (RAI), and elevated serum T3 and T4 levels. What is the most probable diagnosis?
A 32-year-old woman presents with symptoms of heat intolerance, palpitations, diarrhea, weakness, and 10 lb weight loss. The symptoms started gradually but worsened over the past week. She has no other medical history and is not taking any medications. Her family history is negative for thyroid diseases. On physical examination, her blood pressure is 90/60 mmHg, heart rate is 110/min, and she has a fine tremor in her hands. The TSH level is suppressed, and T3 and T4 are elevated. Which of the following is most likely to precipitate this condition?
Which of the following is characteristic of diabetes mellitus?
A 35-year-old man has had recurrent attacks of abdominal pain and proximal motor neuropathy since puberty. The episodes are precipitated by infections and certain medications. During one of the attacks, the plasma porphobilinogen levels were increased. Which of the following medications is not considered safe in patients with this condition?
What is the cause of nephrocalcinosis in granulomatous diseases?
Bone pain, bone cysts, fractures, and renal stones are characteristic of which condition?
A 46-year-old man presents with mild renal failure and hypertension that is difficult to manage. A CT scan reveals both a small adrenal tumor and bilateral hyperplasia. Which of the following is the best test to make a definitive diagnosis?
Which is least likely to be elevated in patients with a pheochromocytoma?
Which of the following is the best diagnostic test for pheochromocytoma?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1061: What is the first step in the diagnosis of pheochromocytoma?
- A. 24-hour urinary metanephrines (Correct Answer)
- B. 24-hour urinary VMA
- C. CT scan
- D. MRI scan
Explanation: **Explanation:** The diagnosis of pheochromocytoma follows a strict biochemical-first approach. The correct answer is **24-hour urinary metanephrines** (or plasma free metanephrines) because they are the most sensitive screening tests. **1. Why 24-hour urinary metanephrines?** Pheochromocytomas continuously metabolize catecholamines into **metanephrines** (metanephrine and normetanephrine) within the tumor cells. This process occurs independently of catecholamine release. Therefore, metanephrines are more stable markers than catecholamines themselves. A 24-hour urine collection provides a cumulative measure, minimizing the risk of missing a diagnosis due to the episodic nature of hormone secretion. **2. Why other options are incorrect:** * **B. 24-hour urinary VMA:** Vanillylmandelic acid (VMA) is the end-metabolite of catecholamines. While specific, it has **low sensitivity** compared to metanephrines, leading to a high rate of false negatives. It is no longer the preferred first-line test. * **C & D. CT and MRI scans:** Imaging should **never** be the first step [2]. Localization via CT or MRI is only performed *after* biochemical confirmation of the disease [3]. "Biochemical first, imaging second" prevents the accidental discovery of non-functional adrenal incidentalomas [1]. **Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% extra-adrenal (paragangliomas), 10% pediatric, and 10% familial. * **High Sensitivity vs. Specificity:** Plasma free metanephrines have the highest sensitivity (best for high-risk patients), while 24-hour urinary metanephrines have high specificity. * **Clonidine Suppression Test:** Used if biochemical results are equivocal (borderline). * **MIBG Scan:** Used for localizing extra-adrenal tumors or metastatic disease when CT/MRI are negative [2].
Question 1062: A 70-year-old female presents with symptoms of hyperthyroidism. Investigations show increased radioactive iodine uptake (RAI), and elevated serum T3 and T4 levels. What is the most probable diagnosis?
- A. Benign Colloid Nodule
- B. Solitary Nodule
- C. Follicular Adenoma
- D. Toxic Multinodular Goiter (Correct Answer)
Explanation: ### Explanation The patient presents with clinical and biochemical evidence of hyperthyroidism (elevated T3/T4) and increased Radioactive Iodine (RAI) uptake [1]. **1. Why Toxic Multinodular Goiter (TMNG) is correct:** TMNG (Plummer’s Disease) is the second most common cause of hyperthyroidism after Graves' disease and is the **most common cause in the elderly** [4]. It occurs when multiple nodules in a long-standing multinodular goiter [3] become autonomous, secreting excess thyroid hormone independent of TSH. On a thyroid scan, RAI uptake is increased, typically showing a "patchy" or "heterogeneous" distribution (areas of high uptake interspersed with suppressed tissue) [1]. **2. Why the other options are incorrect:** * **Benign Colloid Nodule:** These are non-functional (non-secretory) nodules. They do not cause hyperthyroidism and typically appear as "cold" nodules on RAI scans. * **Solitary Nodule:** While a "Toxic Adenoma" is a solitary nodule that causes hyperthyroidism, the term "Solitary Nodule" is a general anatomical description. In an elderly patient with hyperthyroidism, multiple autonomous nodules (TMNG) are statistically more likely than a single toxic adenoma. * **Follicular Adenoma:** This is a histological diagnosis of a benign neoplasm. Most follicular adenomas are non-functional. If it were "toxic," it would present as a single hot nodule, not the generalized hyperthyroid state typically associated with the elderly demographic described. **3. NEET-PG High-Yield Pearls:** * **Graves' Disease:** Most common cause of hyperthyroidism overall; characterized by **diffuse** RAI uptake and exophthalmos [2]. * **Toxic Multinodular Goiter:** Most common cause in **elderly** and iodine-deficient areas; characterized by **patchy** RAI uptake. * **Jod-Basedow Phenomenon:** Hyperthyroidism induced by iodine administration (e.g., contrast or amiodarone) in a patient with underlying TMNG [3]. * **Treatment of Choice for TMNG:** Radioactive Iodine ($I^{131}$) ablation or surgery (Total Thyroidectomy) if the goiter is large.
Question 1063: A 32-year-old woman presents with symptoms of heat intolerance, palpitations, diarrhea, weakness, and 10 lb weight loss. The symptoms started gradually but worsened over the past week. She has no other medical history and is not taking any medications. Her family history is negative for thyroid diseases. On physical examination, her blood pressure is 90/60 mmHg, heart rate is 110/min, and she has a fine tremor in her hands. The TSH level is suppressed, and T3 and T4 are elevated. Which of the following is most likely to precipitate this condition?
- A. Propylthiouracil administration
- B. High-dose prednisone therapy
- C. Beta-adrenergic blockade
- D. Pneumonia (Correct Answer)
Explanation: The patient presents with classic symptoms of **thyrotoxicosis** (heat intolerance, palpitations, weight loss, tremors) and biochemical evidence of hyperthyroidism (suppressed TSH, elevated T3/T4) [3]. However, the presence of hypotension (90/60 mmHg) and tachycardia suggests a progression toward **Thyroid Storm**, a life-threatening hypermetabolic state [1]. **1. Why Pneumonia is correct:** Thyroid storm is rarely spontaneous; it is typically triggered by an acute "stressor" in a patient with underlying, often untreated or poorly controlled, hyperthyroidism. **Infection (such as pneumonia)** is the most common precipitating factor [1]. Other triggers include surgery, trauma, myocardial infarction, or parturition. These stressors cause a sudden surge in catecholamine sensitivity and a rapid increase in free thyroid hormone levels. **2. Why the other options are incorrect:** * **Propylthiouracil (PTU):** This is a treatment for hyperthyroidism that inhibits thyroid peroxidase and the peripheral conversion of T4 to T3. It would improve, not precipitate, the condition. * **High-dose prednisone:** Glucocorticoids are actually used in the management of thyroid storm because they inhibit the peripheral conversion of T4 to T3 and treat potential relative adrenal insufficiency [1]. * **Beta-adrenergic blockade (e.g., Propranolol):** This is a mainstay of treatment to control the sympathomimetic symptoms (tachycardia, tremors) of thyrotoxicosis [2]. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Thyroid storm is a clinical diagnosis (often using the **Burch-Wartofsky Point Scale**); thyroid function tests cannot distinguish between uncomplicated thyrotoxicosis and thyroid storm [1]. * **Management Sequence:** 1. Beta-blockers (symptom control) → 2. Thionamides (PTU/Methimazole) → 3. Iodine (Lugol’s solution/SSKI - *must be given 1 hour after thionamides*) [1] → 4. Glucocorticoids. * **Key Sign:** Hyperpyrexia (high fever) is often the hallmark sign that differentiates storm from simple thyrotoxicosis [1].
Question 1064: Which of the following is characteristic of diabetes mellitus?
- A. Encephalopathy
- B. Myelopathy
- C. Neuropathy (Correct Answer)
- D. Myopathy
Explanation: **Explanation:** **Diabetes Mellitus (DM)** is a chronic metabolic disorder characterized by hyperglycemia, which leads to long-term microvascular and macrovascular complications [2]. Among the options provided, **Neuropathy** is a hallmark microvascular complication of DM [1]. **1. Why Neuropathy is Correct:** Diabetic neuropathy is the most common complication of DM, affecting up to 50% of patients [1]. The underlying pathophysiology involves the **polyol pathway** (accumulation of sorbitol), increased **Advanced Glycation End-products (AGEs)**, and oxidative stress, leading to nerve ischemia and axonal degeneration [1]. The most common presentation is **Distal Symmetric Polyneuropathy** (length-dependent "stocking-and-glove" pattern) [1]. **2. Why the other options are incorrect:** * **Encephalopathy:** While acute metabolic crises (DKA or HHS) can cause altered sensorium, chronic encephalopathy is not a primary characteristic of DM. It is more typical of hepatic or uremic failure. * **Myelopathy:** Spinal cord involvement (myelopathy) is rare in diabetes [4]. DM primarily affects the peripheral nervous system, not the central nervous system (spinal cord). * **Myopathy:** Muscle weakness in DM is usually secondary to neuropathy (denervation atrophy) rather than a primary muscle disease (myopathy). **High-Yield Clinical Pearls for NEET-PG:** * **Earliest sign of Diabetic Nephropathy:** Microalbuminuria (30–300 mg/day). * **Most common cranial nerve involved in DM:** CN III (Oculomotor nerve), typically presenting with **pupillary sparing**. * **Mononeuritis Multiplex:** DM is a leading cause of this condition (asymmetric involvement of multiple nerves) [4]. * **Autonomic Neuropathy:** Can manifest as gastroparesis, resting tachycardia, and orthostatic hypotension [3].
Question 1065: A 35-year-old man has had recurrent attacks of abdominal pain and proximal motor neuropathy since puberty. The episodes are precipitated by infections and certain medications. During one of the attacks, the plasma porphobilinogen levels were increased. Which of the following medications is not considered safe in patients with this condition?
- A. Chlorpromazine
- B. Sulfonamide antibiotics (Correct Answer)
- C. Penicillin and derivatives
- D. Narcotics
Explanation: **Explanation:** The clinical presentation of recurrent abdominal pain, proximal motor neuropathy, and elevated plasma porphobilinogen (PBG) levels strongly indicates **Acute Intermittent Porphyria (AIP)** [3]. AIP is an autosomal dominant disorder caused by a deficiency of the enzyme **porphobilinogen deaminase** [1]. **1. Why Sulfonamides are the Correct Answer:** Sulfonamides are potent **inducers of the cytochrome P450 system** [2]. Induction of these enzymes increases the demand for heme synthesis in the liver. This stimulates **ALA synthase-1** (the rate-limiting enzyme), leading to a massive accumulation of toxic heme precursors (ALA and PBG). This "porphyrinogenic" effect triggers or worsens acute attacks [3]. **2. Analysis of Incorrect Options:** * **Chlorpromazine (A):** This is considered a **safe** antipsychotic/antiemetic in porphyria and is often used to manage agitation or nausea during attacks. * **Penicillin and derivatives (C):** Most penicillins (including amoxicillin and ampicillin) are classified as **safe** and do not induce the heme biosynthetic pathway. * **Narcotics (D):** Opiates like Morphine and Fentanyl are **safe** and are the mainstay for managing the severe abdominal pain associated with AIP. **3. NEET-PG High-Yield Pearls:** * **The "3 Ps" of AIP:** **P**ain (Abdominal), **P**olyneuropathy, and **P**sychiatric manifestations [3]. * **Urine Finding:** Urine may turn "port-wine" colored upon standing due to the oxidation of PBG to porphobilin [2]. * **Common Triggers:** Barbiturates, Sulfonamides, Alcohol, Starvation (fasting), and Progesterone [3]. * **Management:** Intravenous **Hemin** (suppresses ALA synthase via negative feedback) and high-dose **Glucose** (inhibits ALA synthase induction).
Question 1066: What is the cause of nephrocalcinosis in granulomatous diseases?
- A. Increased absorption of calcium
- B. Increased conversion to 1,25-dihydroxyvitamin D (Correct Answer)
- C. Dystrophic calcification
- D. Mutation in calcium-sensing receptor
Explanation: **Explanation:** In granulomatous diseases such as **Sarcoidosis** and **Tuberculosis**, hypercalcemia and subsequent nephrocalcinosis occur due to the dysregulated metabolism of Vitamin D. 1. **Mechanism (Why B is correct):** Normally, the conversion of 25-hydroxyvitamin D to its active form, **1,25-dihydroxyvitamin D (Calcitriol)**, is strictly regulated by the enzyme **1-alpha-hydroxylase** in the kidneys, under the control of PTH [2]. However, in granulomatous diseases, the **activated macrophages** within the granulomas express 1-alpha-hydroxylase independently of PTH. This leads to the autonomous, excessive production of calcitriol, which increases intestinal calcium absorption and bone resorption, resulting in hypercalcemia, hypercalciuria, and nephrocalcinosis. 2. **Analysis of Incorrect Options:** * **Option A:** While increased calcium absorption occurs, it is the *consequence* of the primary pathology (elevated 1,25-dihydroxyvitamin D), not the root cause. * **Option C:** Dystrophic calcification occurs in necrotic or damaged tissues with normal serum calcium levels. In granulomatous disease, the calcification is **metastatic** (due to high serum calcium). * **Option D:** Mutations in the calcium-sensing receptor (CaSR) are associated with Familial Hypocalciuric Hypercalcemia (FHH), not granulomatous disease [1]. **High-Yield NEET-PG Pearls:** * **Classic Presentation:** A patient with bilateral hilar lymphadenopathy (Sarcoidosis) presenting with kidney stones or polyuria. * **Lab Findings:** High Calcium, High Phosphate, **Low PTH** (suppressed by high Ca), and **High 1,25-(OH)₂D**. * **Treatment:** Glucocorticoids are the mainstay as they inhibit the 1-alpha-hydroxylase enzyme in macrophages.
Question 1067: Bone pain, bone cysts, fractures, and renal stones are characteristic of which condition?
- A. Hyperparathyroidism (Correct Answer)
- B. Cushing's syndrome
- C. Multiple myeloma
- D. Marfan's syndrome
Explanation: ### Explanation **Correct Option: A. Hyperparathyroidism** The clinical triad of bone pain, bone cysts, and renal stones is the classic presentation of **Primary Hyperparathyroidism (PHPT)**, often summarized by the mnemonic: *"Stones, bones, abdominal groans, and psychic overtones."* [1] * **Pathophysiology:** Excess Parathyroid Hormone (PTH) increases osteoclast activity, leading to bone resorption. This results in **Osteitis Fibrosa Cystica**, characterized by subperiosteal bone resorption, bone cysts, and "Brown tumors." * **Renal Involvement:** PTH increases calcium reabsorption in the kidneys but also causes significant hypercalcemia, leading to hypercalciuria (once the renal threshold is exceeded), which results in **nephrolithiasis** (calcium oxalate/phosphate stones) [1]. **Why other options are incorrect:** * **B. Cushing’s Syndrome:** While it causes osteoporosis and fractures due to cortisol-induced bone loss, it does not typically present with bone cysts or a high incidence of renal stones. It is more characterized by "buffalo hump," striae, and hypertension. * **C. Multiple Myeloma:** Presents with "punched-out" lytic lesions and bone pain, but it is a plasma cell dyscrasia. While it causes hypercalcemia, it lacks the specific cystic bone changes (Osteitis Fibrosa Cystica) seen in PHPT. * **D. Marfan’s Syndrome:** A connective tissue disorder characterized by tall stature, arachnodactyly, and ectopia lentis. It does not involve hypercalcemia or renal stones. **NEET-PG High-Yield Pearls:** * **Radiology:** Look for **subperiosteal resorption** (pathognomonic), especially on the radial aspect of the middle phalanges, and a **"Salt and pepper" skull** appearance. * **Biochemistry:** PHPT shows **↑ Serum Calcium, ↓ Serum Phosphate, and ↑ PTH.** [1] * **Most Common Cause:** A single parathyroid adenoma (85% of cases).
Question 1068: A 46-year-old man presents with mild renal failure and hypertension that is difficult to manage. A CT scan reveals both a small adrenal tumor and bilateral hyperplasia. Which of the following is the best test to make a definitive diagnosis?
- A. Dexamethasone suppression test
- B. NP-59 adrenal scintigraphy
- C. Adrenal MRI
- D. Selective adrenal vein sampling (Correct Answer)
Explanation: The clinical presentation of hypertension and a CT scan showing both a small adrenal tumor and bilateral hyperplasia suggests **Primary Aldosteronism (Conn’s Syndrome)**. In this scenario, the diagnostic challenge is distinguishing between a unilateral aldosterone-producing adenoma (which is surgically curable) and bilateral adrenal hyperplasia (which requires medical management). **1. Why Selective Adrenal Vein Sampling (AVS) is the Correct Answer:** CT and MRI often fail to differentiate between functional and non-functional adrenal nodules, especially in patients over 40 where "incidentalomas" are common [1]. **AVS is the gold standard** for lateralization [1]. It involves measuring aldosterone and cortisol levels from both adrenal veins [1]. A significant gradient between the two sides confirms unilateral disease, making it the definitive test before considering surgery [1]. **2. Why the Other Options are Incorrect:** * **A. Dexamethasone suppression test:** This is the screening test for Cushing’s syndrome (hypercortisolism), not primary aldosteronism [2]. * **B. NP-59 adrenal scintigraphy:** While used historically for functional imaging, it has low sensitivity and poor spatial resolution compared to AVS and is rarely used in modern practice. * **C. Adrenal MRI:** Like CT, MRI provides anatomical detail but cannot determine if a lesion is hormonally active or distinguish a functional adenoma from bilateral hyperplasia [1]. **Clinical Pearls for NEET-PG:** * **Screening:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio > 20-30. * **Confirmatory Test:** Oral/IV Salt Loading test or Fludrocortisone suppression test. * **Localization:** CT scan is the first-line imaging, but **AVS is the most accurate** for lateralization [1]. * **Treatment:** Unilateral disease = Laparoscopic Adrenalectomy; Bilateral disease = Spironolactone [1].
Question 1069: Which is least likely to be elevated in patients with a pheochromocytoma?
- A. Systemic arterial diastolic pressure
- B. Systemic arterial systolic pressure
- C. Serum norepinephrine
- D. Intravascular volume (Correct Answer)
Explanation: **Explanation:** **Why Intravascular Volume is the Correct Answer:** In patients with pheochromocytoma, chronic and excessive secretion of catecholamines (epinephrine and norepinephrine) leads to persistent **alpha-1 adrenergic stimulation**. This causes profound, generalized vasoconstriction. Over time, this "tightening" of the vascular bed, combined with pressure natriuresis (loss of sodium and water due to high blood pressure), results in a **contraction of the intravascular volume**. This is why these patients are often volume-depleted and can develop profound orthostatic hypotension despite being hypertensive. **Analysis of Incorrect Options:** * **A & B (Systolic and Diastolic Pressure):** Catecholamines increase peripheral vascular resistance (via alpha-receptors) and cardiac output/heart rate (via beta-receptors). This typically results in sustained or paroxysmal elevations of both systolic and diastolic blood pressure. * **C (Serum Norepinephrine):** Pheochromocytomas are catecholamine-secreting tumors of the chromaffin cells [1]. Elevated levels of norepinephrine (and its metabolite normetanephrine) are the biochemical hallmark of the disease. **NEET-PG High-Yield Pearls:** * **The Rule of 10s:** 10% are bilateral, 10% are extra-adrenal (Paragangliomas), 10% are malignant, and 10% occur in children. * **Clinical Triad:** Episodic headache, sweating (diaphoresis), and tachycardia. * **Pre-operative Management:** Always follow the **"Alpha before Beta"** rule. Start alpha-blockers (e.g., Phenoxybenzamine) first to expand the contracted intravascular volume [1]. Giving beta-blockers first can lead to an unopposed alpha-agonistic crisis, causing a fatal spike in blood pressure. * **Diagnosis:** Best initial screening test is **Plasma free metanephrines**; most specific is 24-hour urinary metanephrines.
Question 1070: Which of the following is the best diagnostic test for pheochromocytoma?
- A. Urinary catecholamines and their metabolites (Correct Answer)
- B. Serum catecholamines and their metabolites
- C. CT scan
- D. Surgery
Explanation: Explanation: Pheochromocytoma is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla. **Why Option A is correct:** The diagnosis of pheochromocytoma relies on demonstrating catecholamine excess. **24-hour urinary fractionated metanephrines and catecholamines** are considered the gold standard for diagnosis due to their high sensitivity and specificity [1]. While plasma free metanephrines are often used as a screening tool (due to high sensitivity), urinary metabolites provide a more stable assessment of hormone production over a full day, compensating for the episodic secretion characteristic of these tumors. **Why other options are incorrect:** * **Option B:** Serum catecholamine levels are highly volatile and can be falsely elevated by the stress of venipuncture, pain, or anxiety, making them less reliable than urinary metabolites. Serum chromogranin A is sometimes used, but primarily as a tumor marker for non-secretory or metastatic disease [1]. * **Option C:** CT scan (and MRI) is a **localization tool**, not a diagnostic one [1]. Imaging should only be performed *after* biochemical confirmation of the disease to prevent the accidental discovery of non-secreting adrenal incidentalomas. Biopsy of a mass should be avoided if pheochromocytoma is suspected to prevent hypertensive crisis [2]. * **Option D:** Surgery is the definitive **treatment**, not a diagnostic test. Performing surgery without biochemical confirmation and proper alpha-blockade can trigger a fatal hypertensive crisis. Medical therapy with alpha-blockers is required for a minimum of 6 weeks to restore plasma volume prior to surgery [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paragangliomas), and 10% familial. * **Pre-operative Management:** Always start **Alpha-blockers first** (e.g., Phenoxybenzamine) followed by Beta-blockers to avoid "unopposed alpha stimulation" which leads to severe hypertension [1]. * **Genetic Associations:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL) syndrome, and Neurofibromatosis type 1 (NF1). * **Classic Triad:** Episodic headache, sweating, and tachycardia.
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