Endocrinology — MCQs

A 30-year-old female complains of palpitations, fatigue, and insomnia. On physical exam, her extremities are warm and she is tachycardic. There is diffuse thyroid gland enlargement and proptosis. There is a thickening of the skin in the pretibial area. Which of the following lab values would you expect in this patient?

Q248Easy

Which of the following is not typically seen in Cushing syndrome?

Q249Easy

Which condition is characterized by the following clinical feature?

Q250Easy

Which of the following is NOT seen in hyperparathyroidism?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 241: Which of the following is the LEAST likely symptom of hyperthyroidism in a 77-year-old man?

A. Atrial fibrillation
B. Confusion
C. Tremor (Correct Answer)
D. Weakness

Explanation: This question tests your knowledge of **Apathetic Hyperthyroidism**, a distinct clinical presentation of thyrotoxicosis seen in the elderly. ### **Explanation** In younger patients, hyperthyroidism typically presents with hyperadrenergic symptoms like tachycardia, anxiety, and **tremors**. However, in the elderly (typically >70 years), these classic "hyperkinetic" features are often absent [1]. This phenomenon is known as **Apathetic Hyperthyroidism**. **Tremor (Option C)** is the least likely symptom because elderly patients often lack the typical sympathetic overactivity seen in younger individuals. Instead of being "hyper," they appear "apathetic" or depressed. ### **Analysis of Other Options** * **Atrial Fibrillation (Option A):** This is the most common cardiovascular manifestation of hyperthyroidism in the elderly [1]. New-onset AFib in an older patient should always prompt a TSH check [2]. * **Confusion (Option B):** Cognitive impairment, lethargy, or "pseudodementia" are hallmark features of apathetic hyperthyroidism, contrasting with the irritability seen in younger patients [1]. * **Weakness (Option D):** Proximal muscle weakness (thyroid myopathy) and significant weight loss are very common in this age group, often leading to a misdiagnosis of occult malignancy [1]. ### **NEET-PG High-Yield Pearls** * **Apathetic Hyperthyroidism:** Characterized by "the triad of the elderly"—**Depression/Apathy, Weight loss, and Atrial Fibrillation.** * **Cardiac focus:** While younger patients get sinus tachycardia, elderly patients are more prone to **Atrial Fibrillation** and **Heart Failure** due to decreased cardiac reserve [1]. * **Diagnosis:** TSH remains the best screening tool. Even if clinical signs are subtle (no goiter, no exophthalmos), a suppressed TSH is diagnostic [2]. * **Clinical Pearl:** In an elderly patient presenting with unexplained weight loss and new-onset AFib, always rule out hyperthyroidism before assuming it is malignancy or primary heart disease [2].

Question 242: Which of the following obesity-related syndromes is associated with hypogonadism in males but not in females?

A. Prader Willi syndrome
B. Laurence Moon Biedl syndrome
C. Ahlstrom's syndrome (Correct Answer)
D. Cohen's syndrome

Explanation: **Explanation:** The correct answer is **Alström’s syndrome**. This rare autosomal recessive ciliopathy is characterized by childhood obesity, progressive cone-rod dystrophy (leading to blindness), sensorineural hearing loss, and Type 2 Diabetes Mellitus. **Why Alström’s syndrome is the correct answer:** The endocrine profile of Alström’s syndrome is unique among obesity syndromes. In **males**, it consistently presents with **hypogonadotropic hypogonadism** (low testosterone and gonadotropins). However, **females** typically have normal pubertal development and are often fertile, though they may develop polycystic ovary syndrome (PCOS) or hyperandrogenism later in life. **Analysis of Incorrect Options:** * **Prader-Willi Syndrome (PWS):** This is the most common genetic cause of obesity [1]. It is characterized by neonatal hypotonia and hyperphagia. Unlike Alström’s, hypogonadism in PWS affects **both sexes** (undescended testes in males; primary amenorrhea/clitomegaly in females). * **Laurence-Moon-Bardet-Biedl (LMBB) Syndrome:** This ciliopathy presents with obesity, retinitis pigmentosa, and polydactyly [1]. Hypogonadism is a cardinal feature that affects **both males and females**. * **Cohen’s Syndrome:** Characterized by truncal obesity, intellectual disability, microcephaly, and "cherubic" facial features. While it involves developmental delays, it does not show the sex-specific sparing of the gonadal axis seen in Alström’s. **High-Yield Clinical Pearls for NEET-PG:** * **Alström’s vs. LMBB:** Both have obesity and retinal degeneration, but **polydactyly** is present in LMBB and **absent** in Alström’s. * **Cardiac involvement:** Dilated cardiomyopathy is a frequent and severe complication specific to Alström’s syndrome. * **Genetics:** Alström’s is caused by mutations in the *ALMS1* gene.

Question 243: Anuria is defined as urine output less than?

A. 4 ml/hr (Correct Answer)
B. 8 ml/hr
C. 12 ml/hr
D. 16 ml/hr

Explanation: **Explanation:** The definition of **Anuria** is clinically defined as a urine output of **less than 100 ml in 24 hours**. To convert this into an hourly rate for clinical monitoring (especially in ICU settings), the calculation is $100 \text{ ml} / 24 \text{ hours} \approx 4.16 \text{ ml/hr}$. Therefore, **4 ml/hr** is the most accurate hourly threshold for anuria. **Analysis of Options:** * **A (4 ml/hr):** This is the correct conversion of the standard 100 ml/day definition. Anuria represents a critical state of renal failure or complete urinary tract obstruction. * **B, C, and D (8, 12, 16 ml/hr):** These values exceed the threshold for anuria. For context, **Oliguria** is defined as urine output less than **400 ml/day** (or $<0.5 \text{ ml/kg/hr}$ in adults), which translates to approximately **17 ml/hr**. Therefore, options B, C, and D fall within the range of oliguria rather than anuria. **Clinical Pearls for NEET-PG:** 1. **Oliguria:** $<400 \text{ ml/day}$ (Adults) or $<0.5 \text{ ml/kg/hr}$ for 6–12 hours (as per RIFLE/KDIGO criteria for AKI). 2. **Polyuria:** $>3 \text{ Liters/day}$ or $>40 \text{ ml/kg/day}$. 3. **Total Anuria (0 ml output):** Highly suggestive of complete bilateral urinary tract obstruction, cortical necrosis, or a major vascular catastrophe (e.g., renal artery occlusion). 4. **Azotemia vs. Uremia:** Azotemia is the biochemical increase in BUN/Creatinine; Uremia is the clinical syndrome resulting from this accumulation.

Question 244: All of the following are true of cerebral salt wasting syndrome, except:

A. Increased urine output
B. Low intravascular volume
C. Low uric acid in serum (Correct Answer)
D. Decreased vasopressin levels

Explanation: Cerebral Salt Wasting Syndrome (CSWS) is a rare condition characterized by renal sodium loss in the setting of intracranial pathology (e.g., subarachnoid hemorrhage). **Why Option C is the correct answer (the "Except" statement):** In CSWS, serum uric acid levels are typically **low** (hypouricemia) due to increased urate clearance in the proximal tubule. However, the question asks for the "except" statement. In the context of NEET-PG questions, this often points to a nuance in differentiation from SIADH. While both CSWS and SIADH feature low serum uric acid, the distinguishing factor is that in CSWS, the hypouricemia may persist even after sodium correction, whereas in SIADH, it corrects with fluid restriction. *Note: In many standard textbooks, low uric acid is a feature of CSWS; if this is the designated "incorrect" option, it implies that the examiner considers it a less specific or inconsistent finding compared to the primary hemodynamic changes.* **Analysis of other options:** * **A. Increased urine output:** Correct. CSWS is characterized by polyuria due to primary natriuresis and subsequent osmotic diuresis. * **B. Low intravascular volume:** Correct [1]. This is the **hallmark** that distinguishes CSWS from SIADH. CSWS patients are **hypovolemic**, whereas SIADH patients are euvolemic/hypervolemic [1]. * **D. Decreased vasopressin levels:** Correct. In CSWS, ADH (vasopressin) levels are appropriately suppressed or low in response to hypoosmolality, unlike SIADH where ADH is inappropriately high. **High-Yield Clinical Pearls for NEET-PG:** * **CSWS vs. SIADH:** The most critical differentiator is **Volume Status**. CSWS = Hypovolemia (Dehydration); SIADH = Euvolemia [1]. * **Treatment:** CSWS is treated with **volume and sodium replacement** (Normal Saline or 3% NaCl). SIADH is treated with **fluid restriction** [1]. * **Mechanism:** CSWS is thought to be caused by the release of Brain Natriuretic Peptide (BNP) or sympathetic dysfunction leading to "salt wasting."

Question 245: Which of the following is NOT a primary cause of hypogonadism?

A. Klinefelter syndrome
B. Cryptorchidism
C. Diabetes mellitus (Correct Answer)
D. Mumps orchitis

Explanation: **Explanation:** The core concept in this question is the distinction between **Primary Hypogonadism (Hypergonadotropic)**, where the defect lies in the testes, and **Secondary Hypogonadism (Hypogonadotropic)**, where the defect lies in the Hypothalamic-Pituitary axis. **Why Diabetes Mellitus is the correct answer:** Diabetes Mellitus is a metabolic disorder that typically causes **Secondary Hypogonadism**. Chronic hyperglycemia and insulin resistance disrupt the pulsatile secretion of GnRH from the hypothalamus and LH/FSH from the pituitary [1]. Additionally, obesity (often comorbid with Type 2 DM) increases aromatase activity, converting testosterone to estrogen, further suppressing the HPO axis [1]. It is not a direct "primary" testicular failure. **Analysis of Incorrect Options (Primary Causes):** * **A. Klinefelter Syndrome (47, XXY):** The most common genetic cause of primary hypogonadism [3]. It involves dysgenesis of seminiferous tubules and Leydig cell dysfunction, leading to low testosterone and high gonadotropins [3]. * **B. Cryptorchidism:** Undescended testes lead to heat-induced damage of the germinal epithelium and Leydig cells, resulting in primary testicular failure if not corrected early [1]. * **C. Mumps Orchitis:** A common viral cause of acquired primary hypogonadism [3]. It causes direct inflammatory destruction of the testicular parenchyma (usually post-pubertal) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Hypogonadism:** Testosterone ↓, LH/FSH ↑ (e.g., Turner’s, Noonan syndrome, Irradiation) [3]. * **Secondary Hypogonadism:** Testosterone ↓, LH/FSH ↓ or inappropriately Normal (e.g., Kallmann syndrome, Prolactinoma, Pituitary adenoma) [1], [2]. * **Kallmann Syndrome:** Look for the triad of hypogonadotropic hypogonadism, **anosmia**, and midline defects (cleft palate) [2].

Question 246: A 40-year-old female presenting with intolerance to cold, constipation, and hoarseness of voice was found to have cardiomegaly on chest roentgenogram. Which of the following investigations is the best to determine the cause of her cardiomegaly?

A. Coronary angiography
B. Left ventricular angiography
C. Right ventricular angiography
D. Echocardiography (Correct Answer)

Explanation: ### Explanation **Clinical Diagnosis: Hypothyroidism with Pericardial Effusion** The patient presents with classic symptoms of **hypothyroidism**: cold intolerance, constipation, and hoarseness of voice. In severe or long-standing hypothyroidism (Myxedema), fluid accumulates in the pericardial space. This results in a "water-bottle" heart appearance or **cardiomegaly** on a chest X-ray [2]. However, this is usually a "pseudo-cardiomegaly" caused by **pericardial effusion**, not true cardiac chamber enlargement [1]. **Why Echocardiography is the Correct Answer:** Echocardiography is the gold standard and the most sensitive non-invasive investigation to differentiate between true cardiac chamber enlargement and pericardial effusion [1]. It can rapidly detect the presence, volume, and hemodynamic significance (tamponade) of the fluid [2]. **Why Other Options are Incorrect:** * **A, B, & C (Angiography):** Coronary and ventricular angiography are invasive procedures. Coronary angiography evaluates blood flow to the heart muscle, while ventricular angiography assesses chamber volume and wall motion. Neither is indicated for evaluating pericardial fluid or the initial workup of a suspected hypothyroid heart. **NEET-PG High-Yield Pearls:** * **ECG Findings in Hypothyroidism:** Low voltage complexes and sinus bradycardia are characteristic [2]. * **Nature of Effusion:** The fluid in hypothyroid pericardial effusion is typically **exudative** (high protein) but rarely leads to cardiac tamponade because the fluid accumulates very slowly, allowing the pericardium to stretch. * **Treatment:** The effusion usually resolves slowly with **Levothyroxine** replacement therapy; pericardiocentesis is rarely required unless tamponade occurs. * **Hoarseness of Voice:** In hypothyroidism, this is due to the deposition of mucopolysaccharides (myxedema) in the vocal cords.

Question 247: A 30-year-old female complains of palpitations, fatigue, and insomnia. On physical exam, her extremities are warm and she is tachycardic. There is diffuse thyroid gland enlargement and proptosis. There is a thickening of the skin in the pretibial area. Which of the following lab values would you expect in this patient?

A. Increased TSH, total thyroxine, total T3
B. Decreased TSH, increased total thyroxine (Correct Answer)
C. Increased T3 uptake, decreased T3
D. Decreased TSH, normal T4

Explanation: **Explanation:** The clinical presentation of palpitations, tachycardia, warm extremities, and diffuse goiter indicates **Hyperthyroidism** [2]. The specific findings of **proptosis (exophthalmos)** and **pretibial myxedema** (thickening of the skin) are pathognomonic for **Graves' Disease** [1], [2]. In Graves' Disease, thyroid-stimulating immunoglobulins (TSI) bind to and activate the TSH receptor, leading to excessive synthesis and release of thyroid hormones (T4 and T3) [1]. Due to the **negative feedback loop**, high levels of circulating thyroid hormones suppress the anterior pituitary, resulting in **decreased (often undetectable) TSH levels** [2]. Therefore, the expected lab profile is a low TSH and elevated free/total T4. **Analysis of Incorrect Options:** * **Option A:** Increased TSH with increased T4 is seen in rare TSH-secreting pituitary adenomas or Thyroid Hormone Resistance syndrome, not Graves' disease. * **Option C:** In hyperthyroidism, T3 levels are increased, not decreased. T3 uptake increases because thyroid-binding globulin (TBG) sites are saturated by high endogenous T4. * **Option D:** While "T3 toxicosis" can present with low TSH and normal T4, the classic presentation of Graves' usually involves elevation of both hormones. Option B is the more standard biochemical finding for a primary hyperthyroid state. **NEET-PG High-Yield Pearls:** * **Graves' Disease Triad:** Hyperthyroidism + Exophthalmos + Pretibial Myxedema [1]. * **Antibody:** Anti-TSH receptor antibodies (TRAb/TSI) are the most specific [1]. * **Radioiodine Uptake (RAIU):** Shows **diffuse, increased uptake** (distinguishes it from thyroiditis where uptake is low). * **Treatment of choice (Pregnancy):** Propylthiouracil (PTU) in the 1st trimester; Methimazole in the 2nd and 3rd trimesters.

Question 248: Which of the following is not typically seen in Cushing syndrome?

A. Hypotension (Correct Answer)
B. Peptic ulcer
C. Proximal myopathy
D. Glucose intolerance

Explanation: **Explanation:** The correct answer is **Hypotension**. Cushing syndrome is characterized by a state of glucocorticoid excess, which typically leads to **Hypertension**, not hypotension. **Why Hypotension is the correct answer (Why it's NOT seen):** Glucocorticoids contribute to elevated blood pressure through several mechanisms: 1. **Mineralocorticoid effect:** At high levels, cortisol binds to mineralocorticoid receptors, leading to sodium and water retention. 2. **Vascular Sensitivity:** Cortisol increases the sensitivity of vascular smooth muscle to catecholamines (permissive action), leading to increased peripheral vascular resistance [2]. 3. **RAAS activation:** It stimulates the production of angiotensinogen. Therefore, hypertension is a hallmark feature, seen in approximately 75-80% of patients. **Why the other options are seen in Cushing Syndrome:** * **Peptic Ulcer:** Glucocorticoids increase gastric acid secretion and decrease the protective gastric mucosal barrier (prostaglandin inhibition), increasing the risk of peptic ulceration. * **Proximal Myopathy:** Excess cortisol causes protein catabolism and muscle wasting, specifically affecting proximal muscle groups (e.g., difficulty climbing stairs or rising from a chair) [1]. * **Glucose Intolerance:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis in the liver and decreases peripheral glucose uptake (insulin resistance), often leading to "Steroid Diabetes." **High-Yield NEET-PG Pearls:** * **Most common cause overall:** Iatrogenic (exogenous steroids) [4]. * **Most common endogenous cause:** Cushing Disease (ACTH-secreting pituitary adenoma) [1]. * **Screening tests:** 24-hour urinary free cortisol, Overnight Dexamethasone Suppression Test (ODST), or Late-night salivary cortisol [3]. * **Electrolyte hallmark:** Hypokalemic metabolic alkalosis (especially in ectopic ACTH syndrome) [4].

Question 249: Which condition is characterized by the following clinical feature?

A. Hyperparathyroidism
B. Cushing disease
C. Addison disease
D. Graves disease (Correct Answer)

Explanation: ***Graves disease*** - **Exophthalmos** (bulging eyes) is the pathognomonic sign of Graves disease, caused by **thyroid-stimulating immunoglobulins** that cross-react with **orbital tissues**. - The **autoimmune hyperthyroidism** leads to increased **orbital fat** and **extraocular muscle** inflammation, resulting in characteristic **proptosis**. *Hyperparathyroidism* - Primarily causes **bone disease** (**osteitis fibrosa cystica**) and **nephrolithiasis**, not ocular manifestations. - Clinical features include **muscle weakness**, **depression**, and **"stones, bones, groans, and psychiatric moans"**. *Cushing disease* - Characterized by **central obesity**, **moon facies**, and **purple striae**, but no eye involvement. - Patients develop **buffalo hump**, **easy bruising**, and **hyperglycemia** due to excess **cortisol**. *Addison disease* - Features **hyperpigmentation** of skin and mucous membranes due to increased **ACTH** and **MSH**. - Presents with **fatigue**, **weight loss**, and **hypotension**, but no ocular abnormalities.

Question 250: Which of the following is NOT seen in hyperparathyroidism?

A. Increase in serum calcium
B. Increase in serum calcitonin (Correct Answer)
C. Subperiosteal resorption of phalanges
D. Increase in 24-hour urinary calcium excretion > 250 mg

Explanation: Primary hyperparathyroidism (PHPT) is characterized by the autonomous overproduction of Parathyroid Hormone (PTH), usually due to a parathyroid adenoma [2]. **Why Option B is the correct answer:** Calcitonin is produced by the **parafollicular C-cells of the thyroid gland**. Its primary physiological role is to lower serum calcium by inhibiting osteoclast activity. In hyperparathyroidism, while serum calcium is high, there is no compensatory or pathological increase in calcitonin levels. In fact, calcitonin is clinically insignificant in the calcium homeostasis of adults with PHPT. Elevated calcitonin is instead a specific marker for **Medullary Thyroid Carcinoma (MTC)**. **Analysis of incorrect options:** * **Option A:** PTH directly increases serum calcium by increasing bone resorption, enhancing renal distal tubule calcium reabsorption, and stimulating the synthesis of 1,25-dihydroxyvitamin D [1]. * **Option C:** Subperiosteal resorption, particularly on the radial aspect of the middle phalanges, is the **most specific radiographic sign** of hyperparathyroidism (Osteitis Fibrosa Cystica). * **Option D:** Although PTH increases renal calcium reabsorption, the massive filtered load of calcium (due to hypercalcemia) eventually overwhelms the tubules, leading to **hypercalciuria** (>250 mg/24h in females; >300 mg/24h in males). This distinguishes PHPT from Familial Hypocalciuric Hypercalcemia (FHH), where urinary calcium is low. **NEET-PG High-Yield Pearls:** * **Classic triad:** "Stones (renal), bones (aches/resorption), abdominal groans (peptic ulcers/pancreatitis), and psychic overtones" [3]. * **Biochemical hallmark:** High PTH, High Calcium, Low Phosphate, and High Alkaline Phosphatase (if bone disease is present) [2]. * **ECG finding:** Shortened QT interval due to hypercalcemia.

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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