Endocrinology — MCQs

A 43-year-old woman with chronic alcoholism presents with shortness of breath and edema. On examination, her blood pressure is 100/60 mm Hg, pulse 110/min, JVP is 8 cm, the cardiac apex is displaced and enlarged, there are bilateral inspiratory crackles, and there is pedal edema. For this patient with a potential vitamin deficiency, what is the most likely diagnosis?

Q1206Easy

Which of the following does NOT precipitate ulcers in diabetes?

Q1207Easy

Edema of the feet is not a feature of which of the following conditions?

Q1208Easy

Cushing syndrome is characterized by all of the following except?

Q1209Medium

All of the following forms of porphyria are associated with peripheral neuropathy except?

Q1210Medium

A 45-year-old male presents with palpitations, tachycardia, and anxiety. His blood pressure is 158/90 mmHg. He has mild depression and is currently taking citalopram, labetalol, and amlodipine for blood pressure control. 24-hour urine total metanephrines show an elevation of 1.5 times the upper limit of normal. What is the next best step?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1201: A patient presents with intermittent headache. On examination, there is hypertension and a thyroid nodule. Which of the following steps is to be taken next?

A. Urine HIAA levels
B. Urine VMA and aspiration of the thyroid nodule (Correct Answer)
C. Ultrasound abdomen
D. Echocardiography

Explanation: ### Explanation The clinical presentation of **intermittent headaches, hypertension, and a thyroid nodule** strongly suggests **Multiple Endocrine Neoplasia Type 2 (MEN 2)**. This syndrome is characterized by the association of **Pheochromocytoma** (causing paroxysmal hypertension and headaches) and **Medullary Thyroid Carcinoma (MTC)** (presenting as a thyroid nodule). **1. Why Option B is Correct:** * **Urine VMA (Vanillylmandelic Acid):** This is a screening test for Pheochromocytoma. In a patient suspected of MEN 2, it is **mandatory** to rule out or treat Pheochromocytoma *before* any surgical intervention on the thyroid to prevent a lethal intraoperative hypertensive crisis. Medical therapy is required to prepare the patient for surgery, often for a minimum of time to allow restoration of normal plasma volume [1]. * **Aspiration (FNAC) of the thyroid nodule:** This is the gold standard for investigating a thyroid nodule to confirm Medullary Thyroid Carcinoma (MTC). **2. Why Other Options are Incorrect:** * **Option A (Urine HIAA):** 5-Hydroxyindoleacetic acid is used to diagnose **Carcinoid Syndrome**, which typically presents with flushing and diarrhea, not hypertension and thyroid nodules. * **Option C (Ultrasound Abdomen):** While an ultrasound or CT can localize an adrenal mass [1], biochemical confirmation (VMA/Metanephrines) is the prioritized first step in diagnosing Pheochromocytoma. * **Option D (Echocardiography):** This assesses cardiac structure/function but does not aid in the diagnosis of the underlying endocrine tumors. **Clinical Pearls for NEET-PG:** * **MEN 2A:** MTC + Pheochromocytoma + Parathyroid Hyperplasia. * **MEN 2B:** MTC + Pheochromocytoma + Mucosal Neuromas/Marfanoid habitus. * **Rule of Thumb:** Always exclude Pheochromocytoma first in any patient with a thyroid mass and hypertension to avoid a hypertensive crisis during surgery. * **MTC Marker:** Serum **Calcitonin** is the specific tumor marker for Medullary Thyroid Carcinoma.

Question 1202: Which of the following is considered a silent thyroiditis?

A. Acute thyroiditis
B. Subacute thyroiditis
C. Hashimoto thyroiditis
D. Postpartum thyroiditis (Correct Answer)

Explanation: **Explanation:** **Postpartum thyroiditis (Option D)** is a variant of **painless (silent) thyroiditis**. It is an autoimmune-mediated destructive thyroiditis occurring within one year of delivery. Pathologically, it is characterized by a lymphocytic infiltration similar to Hashimoto’s, but clinically it presents with a transient thyrotoxic phase (due to the release of preformed hormones) followed by a hypothyroid phase, eventually returning to euthyroidism in most cases. It is "silent" because it lacks the thyroid pain and tenderness seen in inflammatory types. **Why other options are incorrect:** * **Acute thyroiditis (Option A):** Also known as Suppurative Thyroiditis, it is usually bacterial (e.g., *S. aureus*). It presents with high fever, redness, and severe localized pain. * **Subacute thyroiditis (Option B):** Also known as **De Quervain’s thyroiditis**, it is typically post-viral [1]. It is the most common cause of a **painful** thyroid gland. * **Hashimoto thyroiditis (Option C):** While it is an autoimmune lymphocytic thyroiditis, it typically presents as a chronic, progressive goitrous hypothyroidism rather than the transient, self-limiting "silent" episodes characteristic of postpartum or sporadic painless thyroiditis. **High-Yield Clinical Pearls for NEET-PG:** * **Radioactive Iodine Uptake (RAIU):** In the thyrotoxic phase of silent/postpartum thyroiditis, **RAIU is low** (distinguishing it from Graves' disease where RAIU is high) [1]. * **ESR:** Markedly elevated in Subacute (De Quervain’s) thyroiditis but usually normal or mildly elevated in silent thyroiditis [1]. * **Treatment:** Since the thyrotoxicosis is due to "leakage" and not overproduction, **Propranolol** is used for symptom control; Antithyroid drugs (PTU/Methimazole) have no role [1].

Question 1203: Hyperparathyroidism is characterized by the following except?

A. Generalised osteoporosis
B. Renal calculi
C. Hypercalcemia
D. Osteosclerosis (Correct Answer)

Explanation: **Explanation:** Hyperparathyroidism (specifically Primary Hyperparathyroidism) is characterized by the overproduction of Parathyroid Hormone (PTH). PTH acts to increase serum calcium levels by stimulating bone resorption (osteoclast activity), increasing renal calcium reabsorption, and enhancing intestinal calcium absorption via Vitamin D activation [1]. **Why Osteosclerosis is the correct answer:** Osteosclerosis refers to an abnormal increase in bone density. In hyperparathyroidism, the primary skeletal effect is **bone resorption** (loss of bone density) due to excessive osteoclast activity [1]. Therefore, osteosclerosis is not a feature of hyperparathyroidism; rather, its opposite—osteopenia or osteoporosis—is characteristic. *(Note: "Rugger-jersey spine" is a form of osteosclerosis seen in Secondary Hyperparathyroidism/Renal Osteodystrophy, but it is not a feature of classic Primary Hyperparathyroidism). **Analysis of Incorrect Options:** * **A. Generalised osteoporosis:** Chronic elevation of PTH leads to systemic bone loss, particularly in cortical bone, making generalized osteoporosis a hallmark [3]. * **B. Renal calculi:** Hypercalcemia leads to hypercalciuria (as the filtered load exceeds reabsorption capacity), resulting in the formation of calcium oxalate or phosphate stones [2], [4]. * **C. Hypercalcemia:** This is the biochemical hallmark of primary hyperparathyroidism due to increased bone mobilization and renal retention of calcium [2], [4]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Classic Mnemonic:** "Stones (renal), bones (osteitis fibrosa cystica), abdominal groans (peptic ulcers/pancreatitis), and psychic moans (depression/delirium)." 2. **Radiological Sign:** Subperiosteal resorption of phalanges (most sensitive) and "Salt and pepper" appearance of the skull. 3. **Brown Tumors:** These are non-neoplastic cystic lesions of the bone caused by rapid osteoclast activity (Osteitis fibrosa cystica). 4. **Biochemical Profile:** High PTH, High Calcium, Low Phosphate, and High Alkaline Phosphatase [2].

Question 1204: A 30-year-old female presents with visual defects, breast engorgement, and amenorrhea. What is the investigation of choice?

A. CT brain
B. Serum prolactin (Correct Answer)
C. Biopsy
D. MR angiography

Explanation: ### Explanation The clinical presentation of **amenorrhea** and **breast engorgement (galactorrhea)** in a young female strongly suggests **hyperprolactinemia**. The addition of **visual defects** (typically bitemporal hemianopia) indicates a space-occupying lesion in the sella turcica, most likely a **Prolactinoma** (a pituitary adenoma), which is compressing the optic chiasm [1]. **Why Serum Prolactin is the Investigation of Choice:** In any patient presenting with the triad of galactorrhea, amenorrhea, and suspected pituitary pathology, the **initial biochemical investigation** is measuring **Serum Prolactin levels**. This confirms the hormonal diagnosis and often correlates with tumor size (levels >200 ng/mL are highly suggestive of a macroprolactinoma) [1]. While an MRI of the brain (specifically the sella) is the gold standard for *imaging*, the first step in the diagnostic workup is biochemical confirmation [1]. **Analysis of Incorrect Options:** * **A. CT Brain:** While CT can detect large masses, **MRI with gadolinium contrast** is the imaging modality of choice for the pituitary gland due to superior soft-tissue resolution. * **C. Biopsy:** Pituitary tumors are diagnosed via clinical, biochemical, and radiological findings. Surgical biopsy is never the first step and is usually reserved for cases requiring resection. * **D. MR Angiography:** This is used to visualize vascular structures (e.g., aneurysms). It is not indicated for evaluating secretory pituitary adenomas. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-induced hyperprolactinemia:** Always rule out drugs like antipsychotics (dopamine antagonists), metoclopramide, and methyldopa [1]. * **Hook Effect:** In extremely high prolactin levels, a lab error may show falsely low results; serial dilution is required. * **Treatment:** Unlike other pituitary tumors, the first-line treatment for prolactinomas (even large ones causing visual loss) is **Medical Management** with Dopamine agonists (**Cabergoline** > Bromocriptine) [1]. Surgery is reserved for refractory cases.

Question 1205: A 43-year-old woman with chronic alcoholism presents with shortness of breath and edema. On examination, her blood pressure is 100/60 mm Hg, pulse 110/min, JVP is 8 cm, the cardiac apex is displaced and enlarged, there are bilateral inspiratory crackles, and there is pedal edema. For this patient with a potential vitamin deficiency, what is the most likely diagnosis?

A. Niacin deficiency
B. Thiamine deficiency (Correct Answer)
C. Pyridoxine deficiency
D. Vitamin C deficiency

Explanation: The clinical presentation of shortness of breath, edema, tachycardia, displaced apex beat (indicating cardiomegaly), and pulmonary crackles in a patient with chronic alcoholism points toward **Wet Beriberi**, which is caused by **Thiamine (Vitamin B1) deficiency**. [2] **Why Thiamine deficiency is correct:** Thiamine is a crucial cofactor for carbohydrate metabolism (specifically for enzymes like pyruvate dehydrogenase). [2] Deficiency leads to impaired aerobic metabolism and the accumulation of lactate, causing peripheral vasodilation. This results in a **high-output heart failure** state characterized by: 1. **Peripheral vasodilation:** Leading to warm extremities and low systemic vascular resistance. 2. **Salt and water retention:** Mediated by the kidneys, leading to edema and elevated JVP. 3. **Myocardial failure:** Eventually, the heart cannot keep up with the high demand, leading to pulmonary congestion (crackles) and cardiomegaly. **Why incorrect options are wrong:** * **Niacin (B3) deficiency:** Causes **Pellagra**, characterized by the "3 Ds": Dermatitis, Diarrhea, and Dementia. It does not typically cause high-output heart failure. * **Pyridoxine (B6) deficiency:** Primarily manifests as sideroblastic anemia, peripheral neuropathy, or seborrheic dermatitis. * **Vitamin C deficiency:** Causes **Scurvy**, characterized by perifollicular hemorrhages, bleeding gums, and poor wound healing. While it can cause "scurvy heart" in rare, extreme cases, it is not the classic association with alcoholism and acute heart failure. **NEET-PG High-Yield Pearls:** * **Dry Beriberi:** Symmetrical peripheral neuropathy (sensory and motor). * **Wet Beriberi:** Cardiovascular involvement (High-output heart failure). * **Wernicke-Korsakoff Syndrome:** Triad of Ataxia, Ophthalmoplegia, and Confusion (Wernicke) + Confabulation/Memory loss (Korsakoff). [3] * **Management:** Always administer Thiamine **before** Glucose in alcoholic patients to prevent precipitating Wernicke Encephalopathy. [1]

Question 1206: Which of the following does NOT precipitate ulcers in diabetes?

A. Microangiopathic changes in blood vessels (Correct Answer)
B. Neuropathy
C. Trophic ulcers
D. Macroangiopathy

Explanation: The pathogenesis of diabetic foot ulcers is primarily driven by a triad of **neuropathy, ischemia, and infection.** [1] **Explanation of the Correct Answer:** **Option A (Microangiopathic changes)** is the correct answer because, while microangiopathy (thickening of the capillary basement membrane) is a hallmark of diabetes leading to nephropathy and retinopathy, it is **not** a primary cause of skin ulceration. [1] Studies have shown that despite basement membrane thickening, the microcirculation in the skin remains functionally adequate to prevent spontaneous ulceration. Ulcers are instead driven by large vessel disease (macroangiopathy) and nerve damage. **Explanation of Incorrect Options:** * **B. Neuropathy:** This is the most common precursor. **Sensory neuropathy** leads to loss of protective sensation (LOPS), allowing repetitive trauma to go unnoticed. [1] **Motor neuropathy** causes muscle atrophy and foot deformities (e.g., claw toes), creating abnormal pressure points. [1] **Autonomic neuropathy** leads to dry, cracked skin (anhidrosis), providing an entry point for infection. [1] * **C. Trophic ulcers:** These are chronic ulcers caused by repeated trauma to an insensitive limb (neuropathic origin). In diabetes, these typically occur at pressure-bearing areas like the metatarsal heads. [1] * **D. Macroangiopathy:** Peripheral Arterial Disease (PAD) involving large vessels (e.g., femoral, popliteal) leads to ischemia. [1] This reduces the delivery of oxygen and nutrients required for wound healing, directly precipitating ischemic ulcers. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site:** Plantar aspect of the first metatarsal head. * **Wagner Classification:** Used to grade the severity of diabetic foot ulcers (Grade 0 to 5). * **Monofilament Test:** The 10g Semmes-Weinstein monofilament is the gold standard for screening for Loss of Protective Sensation (LOPS). [1] * **Charcot’s Arthropathy:** A complication of neuropathy leading to "rocker-bottom foot" deformity. [1]

Question 1207: Edema of the feet is not a feature of which of the following conditions?

A. Conn syndrome (Correct Answer)
B. Hypothyroidism
C. Congestive Heart Failure (CHF)
D. Nephrotic syndrome

Explanation: **Explanation:** The correct answer is **Conn Syndrome** (Primary Hyperaldosteronism). **1. Why Conn Syndrome is the correct answer:** In Conn syndrome, there is an overproduction of aldosterone, which leads to sodium and water retention. While this initially increases extracellular fluid volume, it does not result in clinical edema due to a phenomenon known as **"Aldosterone Escape."** When the volume expands, the body compensates by increasing the secretion of **Atrial Natriuretic Peptide (ANP)** and increasing the pressure natriuresis in the kidneys. This leads to the excretion of excess sodium and water, preventing the formation of edema while maintaining hypertension. **2. Why the other options are incorrect:** * **Hypothyroidism:** Characteristically causes **Myxedema** (non-pitting edema) due to the accumulation of glycosaminoglycans (hyaluronic acid) in the interstitial space, which traps water. * **Congestive Heart Failure (CHF):** Causes pitting edema due to increased capillary hydrostatic pressure resulting from venous congestion and reduced cardiac output. * **Nephrotic Syndrome:** Leads to severe generalized edema (Anasarca) due to decreased plasma oncotic pressure (hypoalbuminemia) and secondary activation of the Renin-Angiotensin-Aldosterone System (RAAS). **Clinical Pearls for NEET-PG:** * **Aldosterone Escape:** This is the hallmark reason why patients with Primary Hyperaldosteronism have hypertension and hypokalemia but **no edema**. * **Triad of Conn Syndrome:** Hypertension, Hypokalemia, and Metabolic Alkalosis. * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio >20-30 is suggestive. * **Confirmatory Test:** Saline infusion test or Oral salt loading test (failure to suppress aldosterone).

Question 1208: Cushing syndrome is characterized by all of the following except?

A. Hypoglycemia (Correct Answer)
B. Hypertension
C. Proximal myopathy
D. Centripetal obesity

Explanation: **Explanation:** Cushing syndrome results from chronic exposure to excessive levels of glucocorticoids (cortisol). To identify the correct answer, one must understand the metabolic and physiological actions of cortisol. **Why Hypoglycemia is the correct answer:** Cortisol is a "stress hormone" that acts as a **counter-regulatory hormone** to insulin. It stimulates gluconeogenesis in the liver and decreases peripheral glucose uptake in muscles and adipose tissue. Therefore, Cushing syndrome leads to **Hyperglycemia** (or impaired glucose tolerance/Diabetes Mellitus), not hypoglycemia. **Analysis of incorrect options:** * **Hypertension:** Cortisol causes hypertension through several mechanisms: mineralocorticoid activity (sodium and water retention), increased sensitivity to catecholamines, and activation of the Renin-Angiotensin-Aldosterone System (RAAS). * **Proximal Myopathy:** Excess cortisol has a catabolic effect on proteins. It causes muscle wasting, particularly in the proximal limb muscles (shoulders and hips), leading to difficulty climbing stairs or rising from a chair [1]. * **Centripetal Obesity:** Cortisol redistributes fat from the extremities to the trunk and face [1]. This results in the classic "Cushingoid" habitus: moon facies, buffalo hump (suvaclavicular/dorsocervical fat pads), and truncal obesity with thin extremities. **NEET-PG High-Yield Pearls:** * **Most common cause overall:** Iatrogenic (exogenous steroid use) [4]. * **Most common endogenous cause:** Cushing’s Disease (ACTH-secreting pituitary adenoma) [1], [4]. * **Electrolyte profile:** Hypokalemic metabolic alkalosis (due to mineralocorticoid effects, especially common in ectopic ACTH syndrome). * **Screening tests:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or Late-night salivary cortisol [2], [3].

Question 1209: All of the following forms of porphyria are associated with peripheral neuropathy except?

A. Acute intermittent porphyria
B. Hereditary coproporphyria
C. Porphyria cutanea tarda (Correct Answer)
D. Variegate porphyria

Explanation: **Explanation:** Porphyrias are metabolic disorders caused by deficiencies in the enzymes of the heme biosynthetic pathway [2]. They are broadly classified into **Acute Porphyrias** (neurovisceral symptoms) and **Cutaneous Porphyrias** (photosensitivity). **1. Why Porphyria Cutanea Tarda (PCT) is the correct answer:** PCT is the most common form of porphyria and is strictly a **cutaneous porphyria** [2]. It is caused by a deficiency of *uroporphyrinogen decarboxylase*. Unlike the acute forms, PCT presents with skin fragility, blistering, and hypertrichosis on sun-exposed areas [3]. It **does not** involve the accumulation of neurotoxic precursors like delta-aminolevulinic acid (ALA); therefore, it is **never associated with peripheral neuropathy** or acute abdominal pain [3]. **2. Why the other options are incorrect:** Options A, B, and D are the **Acute Porphyrias**. These are characterized by life-threatening "acute attacks" triggered by drugs, fasting, or hormones [1]. * **Acute Intermittent Porphyria (AIP):** The most severe acute form; lacks skin findings. * **Hereditary Coproporphyria (HCP) & Variegate Porphyria (VP):** These are "mixed" porphyrias, presenting with both neurovisceral attacks and skin photosensitivity [3]. All three involve the elevation of **ALA and PBG**, which are neurotoxic. The resulting neuropathy is typically a progressive, symmetric **motor neuropathy** (often involving the proximal muscles or cranial nerves) that can mimic Guillain-Barré Syndrome [1]. **NEET-PG High-Yield Pearls:** * **The "3 Ps" of Acute Porphyria:** **P**ain (Abdominal), **P**olyneuropathy, and **P**sychosis [1]. * **Urine finding:** In AIP, urine turns "port-wine" colored upon standing due to the oxidation of porphobilinogen. * **Enzyme Deficiencies:** AIP (*PBG Deaminase*); PCT (*uroporphyrinogen decarboxylase*). * **Treatment:** Acute attacks are managed with **IV Hemin** and **Glucose** (which inhibits ALA synthase).

Question 1210: A 45-year-old male presents with palpitations, tachycardia, and anxiety. His blood pressure is 158/90 mmHg. He has mild depression and is currently taking citalopram, labetalol, and amlodipine for blood pressure control. 24-hour urine total metanephrines show an elevation of 1.5 times the upper limit of normal. What is the next best step?

A. Hold labetalol for 1 week and repeat testing (Correct Answer)
B. Hold citalopram for 1 week and repeat testing
C. Refer immediately for surgical evaluation
D. Measure 24-hour urine vanillylmandelic acid level

Explanation: **Explanation:** The patient presents with symptoms suggestive of **Pheochromocytoma** (palpitations, tachycardia, hypertension). However, his biochemical testing shows only a mild elevation (1.5x upper limit of normal) of urinary metanephrines. In clinical practice, a diagnosis of pheochromocytoma typically requires metanephrine levels to be **>3 times the upper limit of normal** [1]. **1. Why Option A is Correct:** The most common cause of mildly elevated metanephrines is **medication interference**. **Labetalol** (a combined alpha and beta-blocker) is notorious for causing **false-positive** elevations in catecholamines and metanephrines because it interferes with the analytical assays (HPLC) and inhibits the reuptake of norepinephrine. To ensure diagnostic accuracy, labetalol must be discontinued for at least **4–7 days** before repeating the test. **2. Why Incorrect Options are Wrong:** * **Option B:** While some antidepressants (like TCAs or SNRIs) can interfere with testing, **SSRIs like Citalopram** generally do not cause significant false-positive elevations in metanephrines compared to labetalol. * **Option C:** Surgical referral is premature. Imaging (CT/MRI) and surgery should only be pursued after biochemical confirmation (levels >3x normal or confirmed after stopping interfering drugs) [1]. * **Option D:** Vanillylmandelic acid (VMA) has lower sensitivity and specificity compared to metanephrines and is no longer the preferred screening test. **Clinical Pearls for NEET-PG:** * **Rule of 3:** Metanephrines >3x normal = Highly suggestive of Pheochromocytoma. * **Drugs causing False Positives:** Labetalol, Tricyclic Antidepressants (TCAs), Levodopa, and Decongestants (Pseudoephedrine). * **Best Initial Screening Test:** Plasma free metanephrines (highest sensitivity) or 24-hour urinary fractionated metanephrines. * **Pre-op Management:** Always give **Alpha-blockers first** (e.g., Phenoxybenzamine) followed by Beta-blockers to avoid a hypertensive crisis [1].

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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