Endocrinology — MCQs

A 75-year-old woman presents with mild congestive heart failure 6 weeks after a myocardial infarction. She has a history of neck surgery for parathyroid adenoma 5 years ago and her ECG shows slow atrial fibrillation. Her serum calcium is 13.0 mg/dL and urinary calcium is 300 mg/24 h. Examination reveals a small mass in the paratracheal region behind the right clavicle. What is the most appropriate management at this time?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 901: All of the following conditions are known to cause diabetes insipidus except?

A. Multiple sclerosis (Correct Answer)
B. Head injury
C. Histiocytosis
D. Viral encephalitis

Explanation: Diabetes Insipidus (DI) results from either a deficiency of Antidiuretic Hormone (ADH/Vasopressin) due to hypothalamic-pituitary pathology (**Central DI**) or resistance to its action in the kidneys (**Nephrogenic DI**). **Why Multiple Sclerosis (Option A) is the correct answer:** Multiple Sclerosis is a demyelinating disease primarily affecting the white matter of the brain and spinal cord. While it can involve various CNS regions, it **rarely, if ever**, involves the hypothalamic-pituitary axis significantly enough to cause Diabetes Insipidus. Clinical manifestations are typically sensory, motor, or visual (optic neuritis), making it the "odd one out" in this list. **Why the other options are incorrect:** * **Head Injury (Option B):** Traumatic brain injury is a leading cause of Central DI. [1] Shearing forces can damage the pituitary stalk or the hypothalamic nuclei (supraoptic and paraventricular), disrupting ADH production or transport. * **Histiocytosis (Option C):** Langerhans Cell Histiocytosis (LCH) is a classic infiltrative cause of Central DI. [1] It often involves the pituitary stalk, leading to thickening and subsequent ADH deficiency. * **Viral Encephalitis (Option D):** Inflammatory and infectious processes (like encephalitis or meningitis) can cause transient or permanent damage to the hypothalamus or posterior pituitary, resulting in Central DI. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Central DI:** Idiopathic (30-50%), followed by neurosurgery and trauma. * **Triad of Hand-Schüller-Christian disease (a form of LCH):** Diabetes insipidus, exophthalmos, and lytic bone lesions. * **Diagnosis:** The **Water Deprivation Test** is the gold standard. [2] Central DI shows a >50% increase in urine osmolality after exogenous desmopressin administration, whereas Nephrogenic DI shows little to no response. * **Drug of Choice:** Desmopressin (DDAVP) for Central DI; [2] Thiazide diuretics for Nephrogenic DI.

Question 902: Which of the following causes of gynecomastia is not associated with androgen deficiency?

A. Klinefelter's syndrome
B. Kallmann syndrome
C. Cryptorchidism
D. Alcoholic Liver cirrhosis (Correct Answer)

Explanation: The core pathophysiology of gynecomastia involves an **imbalance between free estrogen and free androgen** action on breast tissue. This can occur via three mechanisms: decreased androgen production, increased estrogen production, or androgen receptor insensitivity. [1] **Why Alcoholic Liver Cirrhosis is the correct answer:** In liver cirrhosis, gynecomastia is primarily driven by **increased estrogen levels** rather than a primary androgen deficiency. The mechanisms include: 1. **Increased Peripheral Conversion:** Decreased hepatic clearance of adrenal androgens (androstenedione) leads to increased peripheral aromatization into estrogens. 2. **Increased SHBG:** Cirrhosis triggers an increase in Sex Hormone Binding Globulin (SHBG), which binds testosterone more tightly than estrogen, further reducing the ratio of free testosterone to free estrogen. 3. **Direct Effect:** Alcohol itself may have a direct stimulatory effect on estrogen receptors. **Analysis of Incorrect Options (Causes of Androgen Deficiency):** * **Klinefelter’s Syndrome (47, XXY):** This is the most common cause of primary hypogonadism [1]. It features testicular atrophy and Leydig cell dysfunction, leading to **low testosterone** and high gonadotropins [2]. * **Kallmann Syndrome:** A form of hypogonadotropic hypogonadism (secondary hypogonadism) characterized by GnRH deficiency and anosmia. The lack of LH/FSH leads to **androgen deficiency**. * **Cryptorchidism:** Undescended testes often undergo atrophy or dysgenesis, resulting in impaired testosterone production (**androgen deficiency**) and an increased risk of malignancy [1]. **High-Yield NEET-PG Pearls:** * **Most common physiological cause:** Pubertal gynecomastia (usually resolves spontaneously) [1]. * **Drugs causing gynecomastia (Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone, **C**imetidine, **O**estrogens/Ketoconazole. * **Spironolactone** is the most common drug-related cause; it acts by displacing androgens from their receptors and increasing metabolic clearance of testosterone.

Question 903: Which statement is true regarding the treatment of hypertensive crisis with encephalopathy in a patient with a pheochromocytoma?

A. Immediate surgical removal of the mass is indicated.
B. High-dose phenoxybenzamine should be used to control blood pressure with surgery in 24 to 48 hours.
C. Treatment with phentolamine should be started with low-dose phenoxybenzamine to be titrated upward. Surgery should be done in 2 to 3 weeks once blood pressure is below 160/100 mmHg. (Correct Answer)
D. Beta blockade is contraindicated.

Explanation: ### Explanation **1. Why Option C is Correct:** In a hypertensive crisis due to pheochromocytoma (especially with encephalopathy), the immediate goal is rapid reduction of blood pressure using **IV Phentolamine** (a competitive, short-acting alpha-blocker). Once the crisis is stabilized, the patient requires **preoperative medical optimization** with oral alpha-blockers (e.g., Phenoxybenzamine) to restore intravascular volume and prevent intraoperative "catecholamine storms." Surgery is never an emergency; it is ideally performed **2 to 3 weeks** later, once the patient is normotensive and the plasma volume is expanded [1]. **2. Why Other Options are Wrong:** * **Option A:** Immediate surgery is contraindicated. Handling a tumor in an unprepared patient leads to massive catecholamine release, causing fatal arrhythmias or stroke. * **Option B:** While phenoxybenzamine is used preoperatively, surgery within 24–48 hours is too soon. It does not allow enough time for adequate volume expansion, leading to severe refractory hypotension post-resection. * **Option D:** Beta-blockade is **not** contraindicated, but it must **never be used alone**. It should only be started *after* adequate alpha-blockade. If used first, it causes "unopposed alpha-stimulation," leading to a paradoxical worsening of hypertension. **3. NEET-PG High-Yield Pearls:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), 10% pediatric, 10% familial. * **Drug of Choice (Pre-op):** Phenoxybenzamine (Irreversible alpha-blocker). * **Roizen Criteria:** Used to determine if a patient is ready for surgery (BP <160/90 mmHg, no ST-T changes, no more than 1 PVC every 5 mins). * **Post-op Complication:** The most common cause of death post-surgery is **hypotension** (due to sudden drop in catecholamines and persistent alpha-blockade).

Question 904: Which of the following drugs is NOT used in the management of SIADH?

A. Fludrocortisone
B. Demeclocycline
C. Desmopressin (Correct Answer)
D. Hypertonic saline

Explanation: The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is characterized by excessive release of ADH (Vasopressin), leading to water retention, dilutional hyponatremia, and concentrated urine. **Why Desmopressin is the Correct Answer:** Desmopressin (dDAVP) is a **synthetic analogue of ADH** [1]. Since SIADH is a state of ADH excess, administering Desmopressin would worsen water retention and exacerbate life-threatening hyponatremia. Desmopressin is actually the treatment of choice for *Diabetes Insipidus*, which is the physiological opposite of SIADH [1]. **Analysis of Incorrect Options:** * **Hypertonic Saline (3% NaCl):** Used in the emergency management of severe or symptomatic hyponatremia in SIADH to acutely raise serum sodium levels. * **Demeclocycline:** An antibiotic that acts as an ADH antagonist at the renal collecting duct (induces nephrogenic diabetes insipidus) [2]. It is used in chronic SIADH management when fluid restriction fails [2]. * **Fludrocortisone:** A mineralocorticoid that increases sodium reabsorption in the distal tubule. It is sometimes used off-label in SIADH to help limit urinary sodium loss and maintain sodium balance. **NEET-PG High-Yield Pearls:** 1. **First-line treatment** for SIADH is always **Fluid Restriction** (<800ml/day) [2]. 2. **Vaptans (Tolvaptan, Conivaptan):** These are "Aquaretics" (V2 receptor antagonists) and are now preferred over Demeclocycline for chronic SIADH. 3. **Correction Rate:** In symptomatic hyponatremia, do not exceed a sodium rise of **8–10 mEq/L in 24 hours** to avoid **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)** [2].

Question 905: Obesity is associated with which of the following conditions?

A. Cushing's syndrome
B. Pheochromocytoma
C. Insulinoma
D. Hypothalamic lesion (Correct Answer)

Explanation: Obesity is a complex metabolic state often linked to endocrine and neurological dysfunctions. [1] **Why Hypothalamic Lesion is Correct:** The hypothalamus is the primary regulatory center for energy homeostasis. [2] It contains the **ventromedial nucleus (VMN)**, known as the "satiety center," and the **lateral hypothalamus**, known as the "hunger center." Damage to the hypothalamus (due to tumors like craniopharyngioma, trauma, or inflammation) disrupts these pathways, leading to **"Hypothalamic Obesity."** [2] This is characterized by hyperphagia (excessive eating) and a decreased metabolic rate, often accompanied by hyperinsulinemia. [3] **Analysis of Incorrect Options:** * **Cushing’s Syndrome:** While Cushing’s is classically associated with **centripetal (trunkal) obesity**, the question asks for the condition most fundamentally "associated" with the development of obesity in a physiological/regulatory context. [5] In many exams, if "Hypothalamic lesion" is an option, it is prioritized as a direct cause of primary regulatory failure. * **Pheochromocytoma:** This catecholamine-secreting tumor typically causes a hypermetabolic state. Patients usually present with **weight loss**, hypertension, palpitations, and diaphoresis. * **Insulinoma:** While insulin is an anabolic hormone, patients with insulinoma often present with fasting hypoglycemia. While some patients may gain weight because they eat frequently to avoid hypoglycemic symptoms, it is not a classic or primary cause of obesity compared to hypothalamic damage. **NEET-PG High-Yield Pearls:** * **Prader-Willi Syndrome:** The most common genetic cause of obesity, involving hypothalamic dysfunction. [4] * **Leptin:** Produced by adipocytes; it acts on the arcuate nucleus of the hypothalamus to inhibit hunger. [3] Resistance to leptin is a hallmark of common obesity. * **Fröhlich Syndrome (Adiposogenital dystrophy):** A classic triad of hypothalamic obesity, growth retardation, and hypogonadotropic hypogonadism. [2]

Question 906: Which of the following is not seen in subacute thyroiditis?

A. Raised T4 levels
B. Raised ESR
C. Pain
D. High Radioiodine uptake (Correct Answer)

Explanation: **Explanation:** Subacute thyroiditis (also known as De Quervain’s or Granulomatous thyroiditis) is a self-limiting inflammatory condition of the thyroid, often following a viral upper respiratory tract infection. **Why "High Radioiodine Uptake" is the correct answer:** In subacute thyroiditis, the primary pathology is the **destruction of thyroid follicles** due to inflammation. This leads to the leakage of pre-formed thyroid hormones into the bloodstream [1]. Because the follicular cells are damaged and inflamed, they are unable to actively trap iodine. Consequently, the **Radioactive Iodine Uptake (RAIU) is characteristically low (<5%)**, despite the patient being in a thyrotoxic state [1], [2]. This "thyrotoxicosis with low uptake" is a classic diagnostic hallmark. **Analysis of Incorrect Options:** * **Raised T4 levels:** During the initial "thyrotoxic phase," the release of stored hormones leads to elevated serum T4 and T3 levels and suppressed TSH [1]. * **Raised ESR:** Subacute thyroiditis is an inflammatory process. A markedly elevated Erythrocyte Sedimentation Rate (ESR), often >50–100 mm/hr, is a key diagnostic feature [1]. * **Pain:** This is the most common clinical presentation. Patients typically present with a **painful, tender thyroid gland**, often radiating to the jaw or ears [1]. **NEET-PG High-Yield Pearls:** * **Triad:** Painful goiter + Suppressed TSH + Low RAIU. * **Pathology:** Characterized by **multinucleated giant cells** and granulomatous inflammation. * **Treatment:** NSAIDs for mild cases; Glucocorticoids (Prednisone) for severe pain [1]. * **Biphasic Course:** Thyrotoxic phase → Hypothyroid phase → Recovery (Euthyroid).

Question 907: What is the most likely diagnosis in a full-term neonate with electrolyte abnormalities and specific exam findings?

A. Congenital adrenal hyperplasia (Correct Answer)
B. Hypospadias with cryptorchidism
C. Preterm ovarian hyperstimulation syndrome
D. Turner syndrome

Explanation: ***Congenital adrenal hyperplasia*** - Classic **21-hydroxylase deficiency** presents with **salt-wasting** electrolyte abnormalities (**hyponatremia**, **hyperkalemia**) and **ambiguous genitalia** in virilized females. - **Elevated 17-hydroxyprogesterone** levels and **decreased cortisol** and **aldosterone** production confirm the diagnosis in full-term neonates. *Hypospadias with cryptorchidism* - These are **isolated genital anomalies** in males that do not cause **electrolyte disturbances** or systemic metabolic abnormalities. - **Normal adrenal function** is maintained, so **salt-wasting** and **hyperkalemia** would not be present. *Preterm ovarian hyperstimulation syndrome* - This condition occurs in **reproductive-age women** undergoing **fertility treatments**, not in **neonates**. - Presents with **ovarian enlargement** and **fluid retention**, completely unrelated to neonatal electrolyte abnormalities. *Turner syndrome* - Typically presents with **normal female external genitalia** and **streak gonads**, not **virilized ambiguous genitalia**. - Associated with **cardiac defects** and **lymphedema**, but does not cause **salt-wasting** electrolyte abnormalities in neonates.

Question 908: A 72-year-old man is prescribed hydrochlorothiazide for hypertension. Which of the following is the most likely symptomatic side effect?

A. Increased serum potassium
B. Metabolic acidosis
C. Sexual impotence (Correct Answer)
D. Respiratory alkalosis

Explanation: Thiazide diuretics, such as hydrochlorothiazide (HCTZ), are a cornerstone of hypertension management but are associated with several metabolic and symptomatic side effects [3]. Among the options provided, **sexual impotence (erectile dysfunction)** is a well-documented symptomatic side effect of thiazides [1]. While the exact mechanism is multifactorial, it is attributed to decreased peripheral vascular resistance and the depletion of zinc, which is essential for testosterone production [2]. **Analysis of Options:** * **A. Increased serum potassium:** Incorrect. Thiazides cause **hypokalemia** (decreased potassium) [4] by increasing sodium delivery to the distal tubule, which enhances potassium excretion. * **B. Metabolic acidosis:** Incorrect. Thiazides typically cause **metabolic alkalosis** (contraction alkalosis) [4] due to the loss of hydrogen ions and chloride alongside potassium. * **D. Respiratory alkalosis:** Incorrect. This is a primary respiratory pathology (hyperventilation) and is not a direct metabolic consequence of diuretic therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Thiazide Side Effects (Hyper-GLUC):** Hyper**G**lycemia (impaired insulin release), Hyper**L**ipidemia, Hyper**U**ricemia (can precipitate Gout), and Hyper**C**alcemia (useful in patients with osteoporosis/nephrolithiasis). * **Electrolyte Profile:** Hypokalemia, Hyponatremia, and Hypomagnesemia. * **Clinical Note:** If a patient develops erectile dysfunction on a thiazide, switching to an ACE inhibitor or ARB may be beneficial, as these classes are generally "neutral" or even positive regarding sexual function.

Question 909: A patient presents to a clinic with complaints of headache and fatigue. Lab data show serum sodium, 122 mEq/L; serum osmolality, 240 mOsm/L; urine osmolality, 455 mOsm/L. Which condition best correlates with these data?

A. Neurogenic diabetes insipidus
B. Nephrogenic diabetes insipidus
C. Diabetes mellitus
D. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) (Correct Answer)

Explanation: ### Explanation The laboratory findings in this patient are characteristic of **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)**. The diagnosis is based on the following triad: 1. **Hypotonic Hyponatremia:** Serum sodium is 122 mEq/L (Normal: 135–145) and serum osmolality is 240 mOsm/L (Normal: 275–295). 2. **Inappropriately Concentrated Urine:** Urine osmolality is 455 mOsm/L. In the presence of low serum osmolality, the kidneys should normally excrete dilute urine (<100 mOsm/L). A value >100 mOsm/L indicates ADH is present and active despite low serum tonicity [2]. 3. **Euvolemia:** Clinically, these patients lack signs of fluid overload (edema) or dehydration [1]. #### Analysis of Incorrect Options: * **A & B (Diabetes Insipidus):** Both Neurogenic (central) and Nephrogenic DI are characterized by a lack of ADH effect [3]. This leads to **hypernatremia** and the excretion of large volumes of **dilute urine** (low urine osmolality), which is the opposite of this clinical picture. * **C (Diabetes Mellitus):** Uncontrolled DM typically causes osmotic diuresis, leading to dehydration. While it can cause "dilutional hyponatremia" due to hyperglycemia (translocational hyponatremia), the urine osmolality would be high due to glucose, but the serum osmolality would be **elevated**, not low. #### NEET-PG High-Yield Pearls: * **Diagnostic Criteria:** SIADH requires normal renal, adrenal, and thyroid function. Always rule out hypothyroidism and adrenal insufficiency first. * **Urine Sodium:** In SIADH, urine sodium is typically **>40 mEq/L** due to pressure natriuresis (the body’s attempt to maintain euvolemia). * **Treatment:** Fluid restriction is the first-line treatment. For severe symptomatic hyponatremia, use 3% hypertonic saline. * **Caution:** Avoid rapid correction of chronic hyponatremia (>8–10 mEq/L in 24 hours) to prevent **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).**

Question 910: A 75-year-old woman presents with mild congestive heart failure 6 weeks after a myocardial infarction. She has a history of neck surgery for parathyroid adenoma 5 years ago and her ECG shows slow atrial fibrillation. Her serum calcium is 13.0 mg/dL and urinary calcium is 300 mg/24 h. Examination reveals a small mass in the paratracheal region behind the right clavicle. What is the most appropriate management at this time?

A. Repeat neck surgery
B. Treatment with Technetium-99
C. Observation and repeat serum calcium in two months
D. Ultrasound-guided alcohol injection of the mass (Correct Answer)

Explanation: The patient presents with **persistent/recurrent primary hyperparathyroidism (PHPT)** (Calcium 13.0 mg/dL) and a localized parathyroid mass. The key to this question is the patient’s **recent myocardial infarction (6 weeks ago)** and current **congestive heart failure (CHF)**. [1] 1. **Why Option D is Correct:** In patients with symptomatic hypercalcemia who are **high-risk surgical candidates** (due to recent MI and CHF), invasive surgery is contraindicated. **Ultrasound-guided percutaneous ethanol injection (PEI)** is a minimally invasive alternative to ablate the overactive parathyroid tissue. It effectively reduces PTH and calcium levels without the risks of general anesthesia or complex neck re-exploration. 2. **Why Other Options are Incorrect:** * **Option A:** Repeat neck surgery is the definitive treatment for recurrent PHPT but is contraindicated here. Surgery within 6 months of an MI carries a high risk of perioperative mortality and cardiac complications. * **Option B:** Technetium-99m (Sestamibi) is a **diagnostic imaging modality** used for localization, not a treatment. [1] Radioactive iodine is used for thyroid, not parathyroid, ablation. * **Option C:** Observation is inappropriate. A calcium level of 13.0 mg/dL is significantly elevated (hypercalcemic crisis threshold is >14) and is likely exacerbating her cardiac issues (atrial fibrillation and CHF). **Clinical Pearls for NEET-PG:** * **Surgical Criteria for PHPT:** Serum Ca >1 mg/dL above normal, age <50, T-score <-2.5, or creatinine clearance <60 mL/min. [1] * **Localization:** Sestamibi scan is the gold standard for localizing adenomas before re-operation. [1] * **Post-MI Surgery:** Elective non-cardiac surgery should ideally be delayed **6 months** post-MI to minimize risk. * **ECG in Hypercalcemia:** Characterized by a **shortened QT interval**.

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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