Endocrinology — MCQs
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A patient presents with bilateral proptosis, heat intolerance, and palpitations. What is the most likely diagnosis?
A 25-year-old man presents with 3 months of polyuria and increased thirst. The patient suffered trauma to the base of the skull in a motorcycle accident 4 months ago. A 24-hour urine collection shows polyuria but no evidence of hematuria, glucosuria, or proteinuria. The pathogenesis of polyuria in this patient is most likely caused by a lesion in which of the following areas of the brain?
High T3, high T4, low TSH, and low radioiodine uptake is seen in which condition?
Which of the following is NOT a risk factor for severe hypoglycemia?
Which drug is given for painful tingling of diabetic neuropathy?
A 65-year-old woman with a history of multinodular goiter complains of increasing nervousness, insomnia, and heart palpitations. She has lost 9 kg over the past 6 months. There is no evidence of exophthalmos. Laboratory studies show elevated serum levels of free T3 and T4. Serologic tests for antithyroid antibodies are negative. Which of the following is the likely endocrinopathy in this patient?
A 20-year-old male presents with chronic constipation, headache, Marfanoid habitus, neuromas of the tongue, medullated corneal nerve fibers, and a 2x2 cm nodule in the left lobe of the thyroid. What is the most probable diagnosis?
Migratory necrolytic erythema is seen in which condition?
Conn's syndrome is characterized by diastolic hypertension without edema. Which of the following is a characteristic electrolyte imbalance seen in Conn's syndrome?
Which of the following clinical features of diabetes insipidus is false?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 441: A patient presents with bilateral proptosis, heat intolerance, and palpitations. What is the most likely diagnosis?
- A. Hashimoto's thyroiditis
- B. Thyroid adenoma
- C. Diffuse thyroid goitre (Correct Answer)
- D. Reidel's thyroiditis
Explanation: The clinical triad of **bilateral proptosis** (exophthalmos), **heat intolerance**, and **palpitations** is pathognomonic for **Graves' disease** [1], [2], which is the most common cause of a **Diffuse Toxic Goitre**. [1], [2] **1. Why the Correct Answer is Right:** Graves' disease is an autoimmune disorder where TSH-receptor antibodies (TRAb) stimulate the thyroid gland [1], leading to hyperthyroidism (causing heat intolerance and palpitations). [2] The **proptosis** is a specific feature of Graves' ophthalmopathy, caused by the activation of orbital fibroblasts by these same antibodies. [1], [2] In this condition, the thyroid gland is typically enlarged symmetrically and non-nodular, hence the term "Diffuse Thyroid Goitre." **2. Why the Other Options are Wrong:** * **A. Hashimoto’s Thyroiditis:** This is an autoimmune destruction of the thyroid leading to **hypothyroidism** (cold intolerance, weight gain). While it causes a diffuse goitre, it does not cause proptosis or hyperthyroid symptoms (except in the transient 'Hashitoxicosis' phase, which lacks ophthalmopathy). * **B. Thyroid Adenoma:** This is a solitary nodule. While a "toxic adenoma" can cause palpitations and heat intolerance, it **does not cause proptosis**, as ophthalmopathy is unique to the autoimmune process of Graves' disease. [1], [2] * **C. Riedel’s Thyroiditis:** This is a rare chronic thyroiditis characterized by dense fibrous tissue replacing the thyroid parenchyma. It presents as a "stony hard" fixed goitre and usually results in hypothyroidism or euthyroidism, not hyperthyroidism or proptosis. **3. Clinical Pearls for NEET-PG:** * **Graves' Disease Triad:** Hyperthyroidism + Diffuse Goitre + Exophthalmos (and occasionally Pretibial Myxedema). [1] * **Specific Sign:** A **thyroid bruit** heard on auscultation is highly suggestive of Graves' due to increased vascularity. * **Diagnosis:** Best initial test is **TSH** (suppressed); most specific test is **TSH-receptor antibody (TRAb)**. [1], [2] * **Radioiodine Uptake (RAIU):** Shows **diffuse, increased uptake** in Graves' disease.
Question 442: A 25-year-old man presents with 3 months of polyuria and increased thirst. The patient suffered trauma to the base of the skull in a motorcycle accident 4 months ago. A 24-hour urine collection shows polyuria but no evidence of hematuria, glucosuria, or proteinuria. The pathogenesis of polyuria in this patient is most likely caused by a lesion in which of the following areas of the brain?
- A. Adenohypophysis
- B. Brain stem
- C. Mammillothalamic tract
- D. Neurohypophysis (Correct Answer)
Explanation: ### Explanation **1. Why the Correct Answer is Right:** The patient presents with classic symptoms of **Central Diabetes Insipidus (CDI)**—polyuria and polydipsia—following a traumatic brain injury (TBI). CDI is caused by a deficiency of **Antidiuretic Hormone (ADH/Vasopressin)** [2]. ADH is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and is transported via the hypothalamic-hypophyseal tract to the **Neurohypophysis (Posterior Pituitary)**, where it is stored and released into the systemic circulation [2][3]. Trauma to the base of the skull or the pituitary stalk disrupts this transport or release mechanism, leading to an inability to concentrate urine, resulting in dilute polyuria. **2. Why the Other Options are Wrong:** * **Adenohypophysis (Anterior Pituitary):** This gland secretes hormones like GH, ACTH, TSH, LH, and FSH. While trauma can cause hypopituitarism [1], a lesion here does not cause polyuria, as it does not produce or store ADH. Removal of both the anterior and posterior pituitary may actually ameliorate polyuria by decreasing osmotic load [2]. * **Brain Stem:** This area controls vital functions (respiration, heart rate) and cranial nerves. While a lesion here is life-threatening, it is not involved in ADH regulation or water homeostasis. * **Mammillothalamic Tract:** This is part of the limbic system (Papez circuit) involved in memory. Damage here (often seen in Wernicke-Korsakoff syndrome) leads to anterograde amnesia, not polyuria. **3. High-Yield Clinical Pearls for NEET-PG:** * **Triphasic Response:** Post-traumatic DI often follows a pattern: 1) Initial polyuric phase (axonal shock), 2) Intermittent antidiuretic phase (leakage of stored ADH), and 3) Permanent polyuric phase (depletion of ADH). * **Diagnosis:** Water deprivation test followed by Desmopressin (DDAVP) administration [3]. In CDI, urine osmolality increases by >50% after DDAVP. * **Site of Lesion:** For **permanent** DI to occur, the lesion must be high enough to involve the hypothalamic nuclei or the upper pituitary stalk [2]. Lesions limited to the neurohypophysis alone may be transient as ADH can still leak from the proximal stalk.
Question 443: High T3, high T4, low TSH, and low radioiodine uptake is seen in which condition?
- A. Hashimoto's thyroiditis
- B. Graves' disease
- C. Subacute thyroiditis (Correct Answer)
- D. Toxic nodule
Explanation: ### Explanation The clinical scenario describes **primary hyperthyroidism** (High T3/T4, Low TSH) [3] with **low radioactive iodine uptake (RAIU)** [1]. This combination indicates that the excess thyroid hormone is not being newly synthesized by the gland, but is instead leaking from pre-formed stores due to follicular destruction or coming from an exogenous source. #### Why Subacute Thyroiditis is Correct: In **Subacute (De Quervain’s) Thyroiditis**, a viral prodrome leads to inflammation and destruction of thyroid follicles. This causes a massive release of stored T3 and T4 into the bloodstream (**thyrotoxic phase**). Because the gland is damaged and the TSH is suppressed, the uptake of iodine is paradoxically low despite the high circulating hormone levels [2]. #### Why the Other Options are Incorrect: * **Graves’ Disease:** Characterized by **high RAIU** with a diffuse pattern, as TSH-receptor antibodies (TRAb) stimulate the gland to actively synthesize new hormones [4]. * **Toxic Nodule:** Characterized by **high RAIU** localized to a specific "hot" area, with the rest of the gland suppressed. * **Hashimoto’s Thyroiditis:** Typically presents with hypothyroidism (High TSH, Low T4). While a transient "Hashitoxicosis" can occur, the classic presentation and long-term profile involve high RAIU in early stages or low uptake in late fibrotic stages, but it is not the classic answer for this biochemical triad. #### NEET-PG High-Yield Pearls: * **Low RAIU Hyperthyroidism Differential:** Subacute thyroiditis, Silent/Painless thyroiditis, Factitious thyrotoxicosis (exogenous intake), and Iodine-induced (Jod-Basedow phenomenon) [1]. * **Subacute Thyroiditis Hallmark:** Extremely high **ESR** and a **painful/tender** thyroid gland [2]. * **Treatment:** Subacute thyroiditis is self-limiting; management involves NSAIDs for pain and Beta-blockers for symptoms. Antithyroid drugs (PTU/Methimazole) are **not** indicated as there is no new hormone synthesis [2].
Question 444: Which of the following is NOT a risk factor for severe hypoglycemia?
- A. Sleep (Correct Answer)
- B. Short duration of diabetes mellitus
- C. ACE genotype
- D. Strict control of blood sugar level
Explanation: The risk of severe hypoglycemia is primarily determined by the duration of diabetes, the intensity of glycemic control, and genetic predispositions. **1. Why "Sleep" is the correct answer:** While hypoglycemia often occurs during sleep (nocturnal hypoglycemia), **sleep itself is not a risk factor for "severe" hypoglycemia.** In fact, the physiological response to hypoglycemia is typically **blunted during sleep**, making it harder to detect [1], but the risk factors for a *severe* event (requiring third-party assistance) are rooted in the failure of counter-regulatory mechanisms (glucagon and epinephrine) rather than the state of sleep. **2. Why the other options are incorrect:** * **Short duration of diabetes mellitus (Option B):** This is the correct "incorrect" choice in the context of the question's logic. **Long duration** of diabetes is a major risk factor because it leads to "Hypoglycemia Associated Autonomic Failure" (HAAF) and loss of glucagon response. Therefore, a *short* duration is protective, making it the outlier in a list of risk factors. * **ACE Genotype (Option C):** Specific polymorphisms in the Angiotensin-Converting Enzyme (ACE) gene (specifically the **II genotype**) have been clinically linked to an increased risk of severe hypoglycemia in Type 1 Diabetes patients. * **Strict control of blood sugar level (Option D):** As demonstrated in the DCCT and UKPDS trials, intensive insulin therapy and lower HbA1c targets significantly increase the frequency of severe hypoglycemic episodes. **Clinical Pearls for NEET-PG:** * **Hypoglycemia Unawareness:** The most potent predictor of a future severe hypoglycemic attack is a history of previous frequent episodes, which shifts the glycemic threshold for autonomic symptoms to lower levels [1]. * **Whipple’s Triad:** (1) Symptoms of hypoglycemia, (2) Low plasma glucose, (3) Relief of symptoms after raising glucose. * **Counter-regulatory hormones:** Glucagon is the first line of defense, followed by Epinephrine. In long-standing T1DM, both responses are often impaired.
Question 445: Which drug is given for painful tingling of diabetic neuropathy?
- A. Gabapentin
- B. Duloxetine
- C. Pregabalin
- D. All of them (Correct Answer)
Explanation: **Explanation:** Diabetic Peripheral Neuropathy (DPN) often presents with "positive" symptoms like painful tingling, burning sensations, and electric-shock-like pain [1]. The management of painful DPN involves drugs that modulate neurotransmission to increase the pain threshold. **Why "All of them" is correct:** Current clinical guidelines (ADA and AAN) recommend several classes of drugs as first-line agents for painful diabetic neuropathy. * **Gabapentin and Pregabalin (Option A & C):** These are **Calcium Channel Alpha-2-Delta ($\alpha_2\delta$) ligands**. They bind to the voltage-gated calcium channels in the CNS, reducing the release of excitatory neurotransmitters (like glutamate and substance P), thereby dampening pain signals [2]. * **Duloxetine (Option B):** This is a **Serotonin-Norepinephrine Reuptake Inhibitor (SNRI)**. It enhances the descending inhibitory pain pathways in the spinal cord by increasing the synaptic concentration of serotonin and norepinephrine. Since all three drugs are FDA-approved and clinically effective first-line treatments for this condition, "All of them" is the correct choice. **High-Yield Clinical Pearls for NEET-PG:** * **First-line agents:** Pregabalin, Gabapentin, Duloxetine, and Tricyclic Antidepressants (TCAs like Amitriptyline). * **Pregabalin vs. Gabapentin:** Pregabalin has more predictable pharmacokinetics and quicker onset of action. * **Side Effects:** * Gabapentinoids: Sedation, dizziness, and peripheral edema. * Duloxetine: Nausea (most common), dry mouth, and insomnia. * **Avoid:** Opioids are generally not recommended as first-line therapy due to the risk of addiction and lack of long-term efficacy [2]. * **Aldose Reductase Inhibitors:** (e.g., Epalrestat) target the polyol pathway but are less commonly used than the above symptomatic treatments.
Question 446: A 65-year-old woman with a history of multinodular goiter complains of increasing nervousness, insomnia, and heart palpitations. She has lost 9 kg over the past 6 months. There is no evidence of exophthalmos. Laboratory studies show elevated serum levels of free T3 and T4. Serologic tests for antithyroid antibodies are negative. Which of the following is the likely endocrinopathy in this patient?
- A. Thyroid storm
- B. Thyrotoxicosis (Correct Answer)
- C. Graves disease
- D. Hypothyroidism
Explanation: ### Explanation **Correct Answer: B. Thyrotoxicosis** The patient presents with classic symptoms of hypermetabolism (nervousness, insomnia, palpitations, and significant weight loss) alongside biochemically confirmed elevated free T3 and T4 levels [3]. This clinical and biochemical state is defined as **thyrotoxicosis** [1]. In this specific case, the likely underlying cause is **Toxic Multinodular Goiter (Plummer Disease)**, suggested by her age (65), pre-existing multinodular goiter, and the absence of autoimmune markers or exophthalmos [3]. **Why other options are incorrect:** * **A. Thyroid storm:** This is a life-threatening, extreme manifestation of thyrotoxicosis characterized by decompensation (e.g., high fever, delirium, cardiac failure, or jaundice). While this patient is symptomatic, she is hemodynamically stable and lacks the systemic crisis required for this diagnosis. * **C. Graves disease:** Although it causes thyrotoxicosis, it is typically associated with extrathyroidal manifestations like **exophthalmos** (ophthalmopathy) and pretibial myxedema [2]. Furthermore, Graves is characterized by positive **TSH-receptor antibodies (TRAb)**, whereas this patient’s antibody tests were negative [2]. * **D. Hypothyroidism:** This would present with weight gain, lethargy, and bradycardia, with low levels of free T3 and T4—the exact opposite of this patient's profile [1]. **NEET-PG High-Yield Pearls:** * **Thyrotoxicosis vs. Hyperthyroidism:** Thyrotoxicosis is the clinical syndrome of excess thyroid hormone; Hyperthyroidism specifically refers to excess *synthesis* by the gland. * **Toxic Multinodular Goiter (TMNG):** The second most common cause of hyperthyroidism after Graves. It is more common in the elderly and in iodine-deficient regions. * **Jod-Basedow Phenomenon:** Thyrotoxicosis induced by iodine load (e.g., contrast media or amiodarone) in a patient with underlying multinodular goiter. * **Diagnostic Clue:** In an elderly patient with hyperthyroidism and no eye signs, always think of TMNG or Toxic Adenoma rather than Graves [3].
Question 447: A 20-year-old male presents with chronic constipation, headache, Marfanoid habitus, neuromas of the tongue, medullated corneal nerve fibers, and a 2x2 cm nodule in the left lobe of the thyroid. What is the most probable diagnosis?
- A. Sporadic medullary carcinoma of the thyroid
- B. Familial medullary carcinoma of the thyroid
- C. Multiple Endocrine Neoplasia (MEN) 2A
- D. Multiple Endocrine Neoplasia (MEN) 2B (Correct Answer)
Explanation: ### Explanation The correct diagnosis is **Multiple Endocrine Neoplasia (MEN) 2B**. [1] **1. Why MEN 2B is correct:** MEN 2B (formerly MEN 3) is characterized by a triad of **Medullary Thyroid Carcinoma (MTC)**, **Pheochromocytoma**, and distinctive **mucocutaneous manifestations**. [1] This patient exhibits the classic "phenotype" of MEN 2B: * **Marfanoid Habitus:** Long limbs and lax joints (without the lens dislocation or aortic issues seen in true Marfan syndrome). * **Mucosal Neuromas:** Fleshy bumps on the tongue, lips, and eyelids. * **Intestinal Ganglioneuromatosis:** This leads to chronic constipation or megacolon. * **Medullated Corneal Nerve Fibers:** A high-yield ophthalmological finding specific to this syndrome. * **Thyroid Nodule:** In MEN 2B, MTC occurs early (often in childhood) and is highly aggressive. [1] **2. Why other options are incorrect:** * **MEN 2A:** While it also features MTC and Pheochromocytoma, it is associated with **Primary Hyperparathyroidism** and *Lichen Amyloidosis*, not Marfanoid habitus or mucosal neuromas. * **Sporadic/Familial MTC:** These involve MTC without the associated syndromic features like neuromas, Marfanoid habitus, or other endocrine tumors (like pheochromocytoma). **3. NEET-PG High-Yield Pearls:** * **Genetics:** All MEN 2 syndromes are caused by a germline mutation in the **RET proto-oncogene** (Chromosome 10). [1] * **Management:** Due to the extreme aggressiveness of MTC in MEN 2B, prophylactic thyroidectomy is recommended **within the first year of life**. [1] * **Screening:** Always rule out **Pheochromocytoma** (via urinary/plasma metanephrines) before performing thyroid surgery to prevent a hypertensive crisis during anesthesia. [2]
Question 448: Migratory necrolytic erythema is seen in which condition?
- A. Glucagonoma syndrome (Correct Answer)
- B. Peutz-Jeghers syndrome
- C. Sarcoidosis
- D. Amyloidosis
Explanation: **Explanation:** **Migratory Necrolytic Erythema (MNE)** is the pathognomonic cutaneous manifestation of **Glucagonoma syndrome**, a rare neuroendocrine tumor of the pancreatic alpha cells [1]. 1. **Why Glucagonoma is correct:** MNE presents as pruritic, painful, erythematous plaques that blister and crust, typically involving the perineum, extremities, and perioral areas. The underlying mechanism involves hyperglucagonemia leading to increased gluconeogenesis and protein catabolism, resulting in hypoaminoacidemia. This nutritional deficiency, along with zinc and essential fatty acid depletion, is thought to trigger epidermal necrosis. 2. **Why other options are incorrect:** * **Peutz-Jeghers Syndrome:** Characterized by hamartomatous GI polyps and **mucocutaneous hyperpigmentation** (melanotic macules) on the lips and buccal mucosa. * **Sarcoidosis:** Classically associated with **Lupus Pernio** (violaceous plaques on the nose/cheeks) and Erythema Nodosum. * **Amyloidosis:** Skin findings typically include **waxy papules**, plaques, and "pinch purpura" (ecchymosis following minor trauma), especially in the periorbital area. **High-Yield Clinical Pearls for NEET-PG:** * **The "6Ds" of Glucagonoma:** **D**ermatitis (MNE), **D**iabetes (mild), **D**epression, **D**eclining weight, **D**eep vein thrombosis (DVT), and **D**iarrhea [1]. * **Diagnosis:** Markedly elevated fasting plasma glucagon levels (>1000 pg/mL). * **Treatment:** Surgical resection is definitive; Octreotide (somatostatin analog) is used to manage symptoms by inhibiting glucagon release.
Question 449: Conn's syndrome is characterized by diastolic hypertension without edema. Which of the following is a characteristic electrolyte imbalance seen in Conn's syndrome?
- A. Hypokalemia (Correct Answer)
- B. Hyperkalemia
- C. Sodium retention
- D. Hypertension
Explanation: **Explanation:** **Conn’s Syndrome** (Primary Hyperaldosteronism) is caused by an aldosterone-secreting adenoma of the adrenal cortex. The pathophysiology revolves against the excessive action of aldosterone on the **principal cells** of the renal collecting ducts. 1. **Why Hypokalemia is correct:** Aldosterone increases the activity of the ENaC (epithelial sodium channels), leading to sodium reabsorption. To maintain electrochemical neutrality, the kidney must excrete positive ions, specifically **Potassium (K+)** and Hydrogen (H+) [1]. This results in excessive urinary potassium loss, leading to **hypokalemia** and metabolic alkalosis [3]. 2. **Analysis of Incorrect Options:** * **B. Hyperkalemia:** This is the opposite of the expected finding. Hyperkalemia is seen in Addison’s disease (adrenal insufficiency) or Hypoaldosteronism. * **C. Sodium retention:** While sodium is indeed retained, it is **not** an electrolyte imbalance typically measured as "hypernatremia." Due to the **"Aldosterone Escape"** phenomenon (where increased ANP and pressure natriuresis prevent fluid overload), sodium levels usually remain at the high end of the normal range, and clinical edema is absent [2]. * **D. Hypertension:** While hypertension is a hallmark clinical feature of Conn’s syndrome, the question specifically asks for a characteristic **electrolyte imbalance**. **High-Yield Clinical Pearls for NEET-PG:** * **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). * **Aldosterone Escape:** Explains why patients with Conn’s syndrome do not develop overt volume overload or edema despite sodium retention [2]. * **Triad:** Hypertension + Hypokalemia + Metabolic Alkalosis.
Question 450: Which of the following clinical features of diabetes insipidus is false?
- A. Daily urine volume is >50 mL/kg body weight
- B. Urine osmolarity is <300 mosmol/L
- C. Dehydration (Correct Answer)
- D. Enuresis
Explanation: **Explanation:** In Diabetes Insipidus (DI), the primary pathology is a deficiency of Antidiuretic Hormone (ADH) or resistance to its action. This leads to an inability of the kidneys to concentrate urine, resulting in massive polyuria. **Why "Dehydration" is the False Feature:** While patients with DI lose significant amounts of free water, **clinically significant dehydration is rare** in patients with an intact thirst mechanism and free access to water. These patients compensate for urinary losses by developing intense thirst (polydipsia). Dehydration only occurs if the patient is unable to communicate thirst (e.g., infants, elderly) or has a concomitant hypothalamic lesion affecting the thirst center (adipsic DI). **Analysis of Other Options:** * **A. Daily urine volume >50 mL/kg:** This is a diagnostic criterion for polyuria. In DI, urine output is typically massive, often ranging from 3 to 20 liters per day. * **B. Urine osmolarity <300 mosmol/L:** Since the kidneys cannot reabsorb water, the urine is characteristically dilute. In complete DI, urine osmolarity is usually <200 mOsm/kg, and it is always less than the plasma osmolarity (which is typically >290 mOsm/kg). * **D. Enuresis:** Nocturia is almost universal in DI. In children, this frequently manifests as bedwetting (enuresis) and is often a presenting complaint. **High-Yield NEET-PG Pearls:** * **Water Deprivation Test:** The gold standard for diagnosis. Central DI shows a >50% increase in urine osmolarity after Desmopressin; Nephrogenic DI shows little to no response. * **Most common cause of Central DI:** Idiopathic (30-50%), followed by trauma/surgery and tumors (Craniopharyngioma). * **Drug-induced Nephrogenic DI:** Lithium is the most common cause. * **Treatment:** Desmopressin (DDAVP) is the drug of choice for Central DI. Thiazide diuretics are used for Nephrogenic DI.
Practice by Chapter
Diabetes Mellitus
Practice Questions
Thyroid Disorders
Practice Questions
Adrenal Gland Disorders
Practice Questions
Pituitary Disorders
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Calcium and Bone Metabolism
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Reproductive Endocrinology
Practice Questions
Lipid Disorders
Practice Questions
Endocrine Hypertension
Practice Questions
Multiple Endocrine Neoplasia
Practice Questions
Obesity and Metabolic Syndrome
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Neuroendocrine Tumors
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Endocrine Emergencies
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