Endocrinology — MCQs

A 40-year-old woman presents with an 8-month history of severe headaches, weakness, and dizziness. Her blood pressure is 180/110 mm Hg. Physical examination shows diminished tendon reflexes. An abdominal CT scan reveals a 4-cm mass in the right adrenal gland. Laboratory studies include serum potassium of 2.3 mEq/L, serum sodium of 155 mEq/L, plasma cortisol of 25 mg/dL (8 AM) and 20 mg/dL (4 PM), and low plasma renin. These clinical and laboratory findings are consistent with an adrenal tumor that secretes which of the following hormones?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 601: Which of the following findings would help to differentiate between SIADH and psychogenic polydipsia?

A. Blood urea nitrogen (BUN) 16 mg/dL
B. Serum osmolality 265 mOsm/L
C. Serum potassium 4 meq/L
D. Urine osmolality 500 mOsm/L (Correct Answer)

Explanation: In both **SIADH** and **Psychogenic Polydipsia**, patients present with **hypotonic hyponatremia** (low serum sodium and low serum osmolality). [2] The key to differentiating them lies in the body's physiological response to water excess, specifically the suppression of Antidiuretic Hormone (ADH). ### Why Option D is Correct * **Psychogenic Polydipsia:** Excessive water intake suppresses ADH. In the absence of ADH, the kidneys maximally dilute the urine to excrete the excess water. [1] Therefore, urine osmolality is typically **very low (<100 mOsm/L)**. [3] * **SIADH:** There is "inappropriate" secretion of ADH despite low serum osmolality. ADH causes water reabsorption in the collecting ducts, leading to concentrated urine. [1] Therefore, urine osmolality is **inappropriately high (>100 mOsm/L, often >300-500 mOsm/L)**. * A urine osmolality of **500 mOsm/L** is concentrated, which is consistent with SIADH and rules out psychogenic polydipsia. ### Why Other Options are Incorrect * **A & B (BUN and Serum Osmolality):** Both conditions are characterized by **euvolemic hyponatremia**. [2] Dilutional effects lead to low serum osmolality and often low-to-normal BUN in both cases. They do not help in differentiation. * **C (Serum Potassium):** Potassium levels are typically normal in both SIADH and psychogenic polydipsia. Abnormal potassium would point toward other causes like diuretics or adrenal insufficiency. ### NEET-PG High-Yield Pearls * **Diagnostic Criteria for SIADH:** Hyponatremia, low serum osmolality (<275), high urine osmolality (>100), and high urine sodium (>40 mEq/L) in a euvolemic patient. * **Uric Acid:** Low serum uric acid (<4 mg/dL) is a classic finding in SIADH due to increased urate excretion. * **Treatment:** Fluid restriction is the first-line treatment for both; however, Vaptans (ADH antagonists) are specific for SIADH.

Question 602: Addison's disease is caused by?

A. Tuberculosis
B. HIV
C. Metastatic carcinomas
D. All of the above (Correct Answer)

Explanation: **Explanation:** Addison’s disease (Primary Adrenal Insufficiency) results from the bilateral destruction of the adrenal cortex [2], leading to a deficiency in cortisol, aldosterone, and androgens. For clinical symptoms to manifest, typically >90% of the adrenal cortex must be destroyed. **Why "All of the above" is correct:** * **Tuberculosis (TB):** Historically the most common cause worldwide and still a leading cause in developing nations like India [2]. It typically causes adrenal calcification, visible on imaging [1]. * **HIV/AIDS:** HIV can cause adrenal insufficiency through multiple mechanisms, including opportunistic infections; an HIV test should be performed if risk factors are present [1]. * **Metastatic Carcinomas:** The adrenal glands are highly vascular, making them a common site for metastases. While bilateral involvement is common, clinical Addison’s only occurs if the destruction is near-total, though adrenal metastases are a rare cause of insufficiency compared to other factors [1]. **Clinical Pearls for NEET-PG:** 1. **Autoimmune Adrenalitis:** Currently the **most common cause** of Addison’s disease in developed countries (associated with adrenal autoantibodies) [1]. 2. **Waterhouse-Friderichsen Syndrome:** Acute adrenal destruction due to hemorrhagic infarction, most commonly associated with *Neisseria meningitidis* sepsis. 3. **Diagnosis:** The gold standard screening test is the **ACTH Stimulation Test** (Cosyntropin test) [3]. A subnormal rise in cortisol confirms the diagnosis. 4. **Hyperpigmentation:** A hallmark sign of primary (but not secondary) adrenal insufficiency due to increased ACTH and its precursor POMC, which stimulates melanocytes [1].

Question 603: What is the criterion for diagnosing diabetes mellitus based on fasting blood glucose levels?

A. Greater than 110 mg/dL
B. Greater than 116 mg/dL
C. Greater than 100 mg/dL
D. Greater than 126 mg/dL (Correct Answer)

Explanation: The diagnosis of Diabetes Mellitus (DM) is standardized globally based on criteria established by the American Diabetes Association (ADA) and WHO [1]. **Explanation of the Correct Answer:** **Option D (Greater than or equal to 126 mg/dL)** is the correct diagnostic threshold for Fasting Plasma Glucose (FPG) [1]. "Fasting" is defined as no caloric intake for at least 8 hours. This specific cutoff is chosen because the risk of microvascular complications, particularly diabetic retinopathy, increases significantly once fasting glucose levels exceed this limit [1]. To confirm a diagnosis in an asymptomatic patient, the test should be repeated on a subsequent day [1]. **Analysis of Incorrect Options:** * **Option A (110 mg/dL):** This was previously used in older WHO criteria for Impaired Fasting Glucose (IFG) but is not the diagnostic threshold for diabetes. * **Option B (116 mg/dL):** This value has no specific clinical significance in current diagnostic guidelines. * **Option C (100 mg/dL):** This is the upper limit of "Normal." A fasting glucose between **100–125 mg/dL** is categorized as **Impaired Fasting Glucose (IFG)**, a state of pre-diabetes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **HbA1c Criteria:** $\geq$ 6.5% is diagnostic of DM; 5.7–6.4% is pre-diabetes. * **OGTT (2-hr post-load):** $\geq$ 200 mg/dL is diagnostic; 140–199 mg/dL is Impaired Glucose Tolerance (IGT). * **Random Blood Glucose:** $\geq$ 200 mg/dL **plus** classic symptoms (polyuria, polydipsia, weight loss) is diagnostic without needing a repeat test [1]. * **Gold Standard for Diagnosis:** While HbA1c is convenient, the **75g Oral Glucose Tolerance Test (OGTT)** remains the most sensitive test.

Question 604: Anti-thyroglobulin antibodies are seen in which of the following conditions?

A. Hashimoto thyroiditis (Correct Answer)
B. Graves disease
C. De Quervain thyroiditis
D. Subacute lymphocytic thyroiditis

Explanation: **Explanation:** **Hashimoto Thyroiditis (Correct Answer):** Hashimoto thyroiditis (chronic lymphocytic thyroiditis) is an autoimmune disorder characterized by the destruction of thyroid follicles by cellular and humoral immunity. **Anti-thyroglobulin (Anti-Tg)** antibodies are present in approximately 60-80% of patients, while **Anti-thyroid peroxidase (Anti-TPO)** antibodies are even more sensitive, appearing in over 95% of cases. These antibodies serve as markers of thyroid autoimmunity and are central to the diagnosis. **Analysis of Incorrect Options:** * **Graves Disease:** While Anti-Tg and Anti-TPO can be present in Graves disease, the hallmark and pathognomonic antibody is the **TSH Receptor Antibody (TRAb/TSI)**, which stimulates the gland to cause hyperthyroidism [1]. * **De Quervain Thyroiditis (Subacute Granulomatous):** This is a post-viral inflammatory condition, not an autoimmune one. It is characterized by a high ESR and painful thyroid; thyroid antibodies are typically absent or only transiently/weakly positive due to follicle leakage [2]. * **Subacute Lymphocytic Thyroiditis (Painless Thyroiditis):** Although this is an autoimmune variant (often postpartum), the question asks for the primary association. Hashimoto is the classic and most frequent association for high-titer Anti-Tg antibodies in medical examinations. **High-Yield Clinical Pearls for NEET-PG:** * **Most Sensitive Marker:** Anti-TPO is the most sensitive antibody for Hashimoto thyroiditis. * **Anti-Tg Significance:** Anti-Tg must be measured alongside Serum Thyroglobulin when monitoring **Thyroid Cancer** patients, as the presence of these antibodies can falsely interfere with thyroglobulin assays. * **Histology:** Look for **Hurthle cells** (Askanazy cells) and lymphoid follicles with germinal centers on FNAC/Biopsy in Hashimoto patients. * **Risk:** Hashimoto thyroiditis increases the risk of **B-cell Non-Hodgkin Lymphoma** of the thyroid.

Question 605: What is the most common cause of hypoparathyroidism?

A. Idiopathic
B. Familial
C. Postradiation
D. Surgical removal (Correct Answer)

Explanation: The most common cause of hypoparathyroidism (responsible for approximately 75% of cases) is **iatrogenic injury or accidental removal** during neck surgery. This typically occurs during total thyroidectomy, parathyroidectomy, or radical neck dissection for malignancy. The mechanism involves either the inadvertent removal of the glands or, more commonly, the disruption of their delicate blood supply (primarily from the inferior thyroid artery). **2. Why Other Options are Incorrect:** * **Idiopathic:** This is a rare cause, often associated with autoimmune destruction of the parathyroid glands. It can occur in isolation or as part of **Autoimmune Polyglandular Syndrome Type 1 (APS-1)**. * **Familial:** Genetic causes, such as mutations in the *GCM2* gene or DiGeorge Syndrome (22q11.2 deletion), are significant in pediatric populations but are far less common than surgical causes in the general population. * **Postradiation:** While external beam radiation to the neck or radioactive iodine therapy for hyperthyroidism can theoretically damage the glands, it is an extremely rare clinical cause of permanent hypoparathyroidism. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hungry Bone Syndrome:** A state of profound hypocalcemia following parathyroidectomy for hyperparathyroidism, caused by rapid bone remineralization. * **Clinical Signs:** Look for **Chvostek sign** (facial twitching on tapping the facial nerve) and **Trousseau sign** (carpal spasm on inflating a BP cuff). * **ECG Finding:** The classic finding in hypocalcemia/hypoparathyroidism is **QT interval prolongation** [1]. * **Biochemical Profile:** Low Calcium, High Phosphate, and Low PTH [1].

Question 606: What is the most common malignancy of the endocrine system?

A. Thyroid cancer (Correct Answer)
B. Pancreatic cancer
C. Pituitary adenoma
D. Adrenal malignancy

Explanation: **Explanation:** **Thyroid cancer** is the most common malignancy of the endocrine system, accounting for approximately 90% of all endocrine cancers. Among thyroid malignancies, **Papillary Thyroid Carcinoma (PTC)** is the most frequent subtype (80-85%). The incidence of thyroid cancer has been rising globally, primarily due to increased detection of small papillary microcarcinomas via high-resolution ultrasound. **Analysis of Incorrect Options:** * **Pancreatic cancer:** While the pancreas has endocrine functions (Islets of Langerhans), the vast majority (>95%) of pancreatic cancers are **exocrine** (adenocarcinomas). Endocrine tumors of the pancreas (PanNETs) are relatively rare. * **Pituitary adenoma:** These are common, but they are almost always **benign**. True pituitary carcinomas (malignancies with systemic metastasis) are exceedingly rare, representing less than 0.2% of pituitary tumors. * **Adrenal malignancy:** Adrenocortical carcinoma (ACC) is a rare and aggressive tumor with an incidence of only 1-2 per million population per year, making it far less common than thyroid cancer. **High-Yield Clinical Pearls for NEET-PG:** * **Most common thyroid cancer:** Papillary Carcinoma (associated with *BRAF* mutations and Psammoma bodies). * **Most common thyroid cancer post-radiation:** Papillary Carcinoma. * **Medullary Thyroid Carcinoma (MTC):** Arises from parafollicular C-cells; secretes Calcitonin; associated with **MEN 2A and 2B**. * **Anaplastic Carcinoma:** The most aggressive thyroid malignancy with the worst prognosis. * **Orphan Annie Eye nuclei:** Pathognomonic histological feature of Papillary Thyroid Carcinoma.

Question 607: Wolfram disease includes all of the following except?

A. Diabetes insipidus
B. Optic glioma (Correct Answer)
C. Diabetes mellitus
D. Neural deafness

Explanation: **Explanation:** Wolfram syndrome is a rare, autosomal recessive neurodegenerative disorder caused by mutations in the **WFS1 gene** (encoding the protein Wolframin). It is classically defined by the mnemonic **DIDMOAD**, which represents its four core clinical features. **Why Optic Glioma is the correct answer:** Optic glioma is a benign tumor of the optic nerve most commonly associated with **Neurofibromatosis Type 1 (NF1)**, not Wolfram syndrome. While Wolfram syndrome involves the optic nerve, it presents as **Optic Atrophy** (progressive loss of vision), not a neoplastic growth like a glioma. **Analysis of incorrect options (Features of DIDMOAD):** * **Diabetes Insipidus (A):** Specifically Central Diabetes Insipidus, occurring in about 70% of patients due to vasopressin deficiency. * **Diabetes Mellitus (C):** Typically the first manifestation (usually diagnosed around age 6). It is non-autoimmune (insulin-dependent but antibody-negative). * **Neural Deafness (D):** Sensorineural hearing loss, often affecting high frequencies, typically developing in the second decade of life. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Recessive (WFS1 gene on Chromosome 4p). * **Mnemonic (DIDMOAD):** **D**iabetes **I**nsipidus, **D**iabetes **M**ellitus, **O**ptic **A**trophy, and **D**eafness. * **Additional Features:** Urinary tract abnormalities (dilated renal pelvis, neurogenic bladder) and neurological/psychiatric symptoms (ataxia, depression). * **Prognosis:** It is a progressive disease; the median age of death is usually in the 30s, often due to central apnea or renal failure.

Question 608: Symptoms of hyperthyroidism include which of the following?

A. Intolerance to cold
B. Decreased appetite
C. Weight gain
D. Palpitations (Correct Answer)

Explanation: **Explanation:** Hyperthyroidism is a clinical state resulting from excessive circulating thyroid hormones ($T_3$ and $T_4$), which leads to a hypermetabolic state and increased sensitivity to catecholamines. **Why Palpitations is Correct:** Thyroid hormones have a direct stimulatory effect on the myocardium and upregulate $\beta$-adrenergic receptors. This increases heart rate (tachycardia) and myocardial contractility. Patients frequently experience **palpitations**, and in elderly patients or severe cases, this can progress to atrial fibrillation or high-output heart failure [1]. **Analysis of Incorrect Options:** * **A. Intolerance to cold:** This is a classic symptom of **hypothyroidism**. In hyperthyroidism, increased basal metabolic rate (BMR) leads to excessive heat production, resulting in **heat intolerance** and increased sweating [2]. * **B. Decreased appetite:** Hyperthyroidism typically causes an **increased appetite (polyphagia)** due to the high metabolic demand [2]. A decreased appetite is more characteristic of hypothyroidism or systemic illness. * **C. Weight gain:** Despite increased food intake, patients with hyperthyroidism usually experience **weight loss** because the metabolic rate exceeds caloric intake [2]. Weight gain is a hallmark of hypothyroidism. **NEET-PG High-Yield Pearls:** * **Most common cause:** Graves' Disease (associated with exophthalmos and pretibial myxedema) [2]. * **Cardiovascular signs:** Sinus tachycardia is the most common sign; Atrial Fibrillation occurs in 10-15% of patients [1]. * **Neuromuscular:** Look for fine tremors of outstretched hands and proximal muscle weakness (thyrotoxic myopathy) [2]. * **Apathetic Hyperthyroidism:** In elderly patients, typical hypermetabolic features may be absent; they may present only with depression, weight loss, or atrial fibrillation.

Question 609: Which of the following is NOT a life-threatening complication of diabetes mellitus?

A. Malignant otitis externa
B. Rhinocerebral mucormycosis
C. Emphysematous pyelonephritis
D. Emphysematous appendicitis (Correct Answer)

Explanation: This question tests your knowledge of specific, life-threatening infections that occur with significantly higher frequency and severity in patients with Diabetes Mellitus (DM). [1] ### **Explanation of the Correct Answer** **D. Emphysematous appendicitis:** While emphysematous infections (caused by gas-forming organisms like *E. coli* or *Clostridium*) are classic diabetic complications in the gallbladder or kidneys, **emphysematous appendicitis** is an extremely rare clinical entity. It is not traditionally classified as a "diabetic-specific" life-threatening complication in standard medical textbooks (like Harrison’s). In contrast, the other three options are "classic" diabetic emergencies. ### **Analysis of Incorrect Options** * **A. Malignant Otitis Externa:** An invasive infection of the external auditory canal, usually caused by *Pseudomonas aeruginosa*. It occurs almost exclusively in elderly diabetics and can lead to osteomyelitis of the skull base and cranial nerve palsies. It is a surgical emergency. * **B. Rhinocerebral Mucormycosis:** A fungal infection (Rhizopus/Mucor) seen typically in patients with **Diabetic Ketoacidosis (DKA)**. It is highly aggressive, spreading from the sinuses to the orbit and brain. It requires urgent debridement and Amphotericin B. * **C. Emphysematous Pyelonephritis:** A severe, necrotizing renal parenchymal infection characterized by gas in the renal tissues. Approximately **90% of cases occur in diabetics**. It carries a high mortality rate and often requires nephrectomy. ### **High-Yield NEET-PG Pearls** * **Emphysematous Cholecystitis:** Another life-threatening infection to remember; it is much more common in diabetic men than the general population. * **Fournier’s Gangrene:** A necrotizing fasciitis of the perineum that is frequently associated with DM. * **Papillary Necrosis:** DM is the most common cause of non-analgesic-related renal papillary necrosis. * **Mucormycosis Key Sign:** Look for "black eschar" on the nasal turbinates or palate in a patient with DKA.

Question 610: A 40-year-old woman presents with an 8-month history of severe headaches, weakness, and dizziness. Her blood pressure is 180/110 mm Hg. Physical examination shows diminished tendon reflexes. An abdominal CT scan reveals a 4-cm mass in the right adrenal gland. Laboratory studies include serum potassium of 2.3 mEq/L, serum sodium of 155 mEq/L, plasma cortisol of 25 mg/dL (8 AM) and 20 mg/dL (4 PM), and low plasma renin. These clinical and laboratory findings are consistent with an adrenal tumor that secretes which of the following hormones?

A. Aldosterone (Correct Answer)
B. Cortisol
C. Epinephrine
D. Renin

Explanation: ### Explanation This patient presents with the classic triad of **Conn’s Syndrome** (Primary Hyperaldosteronism): **Hypertension, Hypokalemia, and Metabolic Alkalosis.** [1] **1. Why Aldosterone is Correct:** The adrenal mass, combined with hypertension and significant hypokalemia (2.3 mEq/L), points toward excess mineralocorticoid activity. Aldosterone acts on the distal convoluted tubule and collecting duct to [4]: * **Reabsorb Sodium:** Leading to hypernatremia (155 mEq/L) and hypertension. * **Excrete Potassium:** Leading to hypokalemia and diminished tendon reflexes (a clinical sign of low potassium). [5] * **Suppress Renin:** The high sodium/volume status causes a feedback inhibition of the renin-angiotensin system, resulting in the **low plasma renin** levels characteristic of primary hyperaldosteronism. **2. Why Other Options are Incorrect:** * **Cortisol (Cushing’s Syndrome):** While cortisol can cause hypertension, the patient’s levels (25 mg/dL AM, 20 mg/dL PM) show a preserved (though slightly blunted) diurnal rhythm and are not high enough to explain the severe hypokalemia without other signs like striae or buffalo hump. [4] * **Epinephrine (Pheochromocytoma):** Presents with episodic hypertension, palpitations, and diaphoresis. It does not typically cause profound, persistent hypokalemia or suppressed renin. [3] * **Renin:** A renin-secreting tumor (Robertson-Kihara syndrome) would cause **high** plasma renin levels, not low. [3] **3. NEET-PG High-Yield Pearls:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20-30** is highly suggestive. * **Confirmatory Test:** Saline infusion test (failure to suppress aldosterone) or Oral Salt Loading test. * **Management:** Surgical excision for unilateral adenoma (Conn's); Spironolactone (Aldosterone antagonist) for bilateral adrenal hyperplasia. [1] * **The "Aldosterone Escape" Phenomenon:** Patients with Conn’s syndrome rarely have significant edema because hypervolemia triggers ANP release, leading to some sodium excretion. [2]

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

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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