Endocrinology — MCQs

A 29-year-old woman complains of nervousness and muscle weakness of 6 months' duration. She is intolerant of heat and sweats excessively. She has lost 9 kg over the past 6 months despite an increased caloric intake. She frequently experiences a racing heart and palpitations. She has also missed several menstrual periods in the past few months. Physical examination reveals warm, moist skin and exophthalmos. What endocrine abnormality is most likely present in this patient?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1001: Medullary thyroid carcinoma is associated with which of the following syndromes?

A. Multiple Endocrine Neoplasia type I (MEN I)
B. Multiple Endocrine Neoplasia type II (MEN II) (Correct Answer)
C. Multiple Endocrine Neoplasia type IV (MEN IV)
D. All of the above

Explanation: Medullary Thyroid Carcinoma (MTC) is a tumor arising from the parafollicular C-cells of the thyroid, which secrete calcitonin. While most cases are sporadic, approximately 25% are familial and occur as a component of **Multiple Endocrine Neoplasia type 2 (MEN 2)**. **1. Why MEN II is correct:** MEN 2 is an autosomal dominant syndrome caused by a germline mutation in the **RET proto-oncogene**. It is subdivided into: * **MEN 2A (Sipple Syndrome):** MTC (100%), Pheochromocytoma (50%), and Parathyroid hyperplasia (20%). * **MEN 2B:** MTC (100%, more aggressive), Pheochromocytoma, Marfanoid habitus, and Mucosal neuromas. MTC is the most consistent feature and often the presenting manifestation of both subtypes. **2. Why other options are incorrect:** * **MEN I (Wermer Syndrome):** Characterized by the "3 Ps"—**P**arathyroid adenoma, **P**ituitary adenoma, and **P**ancreatic neuroendocrine tumors (e.g., Gastrinoma). It is caused by mutations in the *MEN1* gene (Menin protein) and is not associated with MTC. * **MEN IV:** A rare syndrome caused by *CDKN1B* mutations. It presents similarly to MEN I (primarily parathyroid and pituitary tumors) but does not typically include MTC. **High-Yield Clinical Pearls for NEET-PG:** * **Screening:** In patients with a known *RET* mutation, prophylactic thyroidectomy is often indicated. * **Tumor Marker:** Calcitonin is used for both diagnosis and monitoring recurrence of MTC. Carcinoembryonic antigen (CEA) is also a useful marker. * **Rule of Thumb:** Always exclude a **Pheochromocytoma** (via urinary/plasma metanephrines) before performing surgery on a patient with MEN 2 to prevent a hypertensive crisis during anesthesia.

Question 1002: Which of the following is the most likely cause of hirsutism, when associated with anovulation, obesity, and amenorrhea?

A. Drug-induced hirsutism
B. Adrenal tumor
C. Polycystic ovarian disease (PCOD) (Correct Answer)
D. Idiopathic hirsutism

Explanation: ### Explanation **Correct Answer: C. Polycystic ovarian disease (PCOD)** The clinical tetrad of **hirsutism, anovulation (leading to infertility), obesity, and amenorrhea/oligomenorrhea** is the classic presentation of Polycystic Ovarian Syndrome (PCOS/PCOD), also known as Stein-Leventhal Syndrome [1]. The underlying pathophysiology involves **insulin resistance** and an imbalance in the hypothalamic-pituitary-ovarian axis [1]. Elevated Luteinizing Hormone (LH) stimulates the ovarian theca cells to produce excess androgens (androstenedione and testosterone). These androgens cause hirsutism and inhibit follicular maturation, leading to chronic anovulation and menstrual irregularities. Obesity further exacerbates the condition by decreasing Sex Hormone Binding Globulin (SHBG), increasing the levels of free, active testosterone. **Why other options are incorrect:** * **A. Drug-induced hirsutism:** Usually presents with generalized hair growth (hypertrichosis) rather than a male-pattern distribution. Common culprits like Minoxidil or Phenytoin do not typically cause the systemic metabolic and ovulatory disturbances seen here. * **B. Adrenal tumor:** While these cause severe hirsutism, the onset is usually **rapid and virilizing** (clitoromegaly, deepening of voice). PCOS is typically a slow, progressive process starting at puberty [1]. * **D. Idiopathic hirsutism:** This is a diagnosis of exclusion where patients have hirsutism but **normal ovulatory cycles** and normal androgen levels. The presence of amenorrhea and obesity points specifically toward a systemic endocrine disorder like PCOS [1]. **NEET-PG High-Yield Pearls:** * **Rotterdam Criteria:** Diagnosis requires 2 out of 3: (1) Clinical/biochemical hyperandrogenism, (2) Ovulatory dysfunction, (3) Polycystic ovaries on ultrasound ("String of pearls" appearance) [1]. * **LH:FSH Ratio:** Classically elevated (>2:1 or 3:1), though no longer a primary diagnostic criterion. * **First-line Management:** Weight loss and lifestyle modification. For hirsutism, Combined Oral Contraceptive Pills (COCPs) are the first-line pharmacological choice.

Question 1003: In Conn's syndrome, which of the following statements are true?

A. Diastolic hypertension without edema
B. Systolic hypertension without edema (Correct Answer)
C. Pseudotetany
D. Hyperkalemia

Explanation: **Explanation:** **Conn’s Syndrome (Primary Hyperaldosteronism)** is characterized by the autonomous overproduction of aldosterone, usually due to an adrenal adenoma [1]. **1. Why the Correct Answer is Right:** Aldosterone acts on the principal cells of the collecting duct to increase sodium and water reabsorption and promote potassium excretion. This leads to volume expansion and **hypertension**. A hallmark of Conn’s syndrome is **Hypertension without edema**. This occurs due to the **"Aldosterone Escape" phenomenon**: the initial volume expansion triggers the release of Atrial Natriuretic Peptide (ANP) and increases pressure natriuresis, leading to the excretion of excess sodium and water [2]. This prevents the formation of overt edema while maintaining a high-pressure state (systolic hypertension). **2. Analysis of Incorrect Options:** * **A. Diastolic hypertension:** While both systolic and diastolic pressures rise, systolic hypertension is the more prominent clinical feature of the volume-expanded state. * **C. Pseudotetany:** While hypokalemia can cause muscle weakness, "pseudotetany" is not a classic or defining feature of Conn’s. True tetany is associated with hypocalcemia. * **D. Hyperkalemia:** This is incorrect. Aldosterone causes **Hypokalemia** due to increased potassium secretion in the distal tubules. **3. NEET-PG High-Yield Pearls:** * **Classic Triad:** Hypertension, Hypokalemia, and Metabolic Alkalosis. * **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 adenoma (Conn’s); Spironolactone or Eplerenone (Aldosterone antagonists) for bilateral adrenal hyperplasia [1].

Question 1004: Whipple's triad is seen in which of the following conditions?

A. Gastrinoma
B. Insulinoma (Correct Answer)
C. Vipomas
D. Somatostatinoma

Explanation: **Explanation:** **Whipple’s Triad** is the classic clinical diagnostic criterion for **Insulinoma**, a neuroendocrine tumor of the pancreatic beta cells that results in the autonomous secretion of insulin. The triad consists of: 1. **Symptoms of hypoglycemia** (e.g., sweating, palpitations, confusion, or seizures) usually triggered by fasting or exercise. 2. **Low plasma glucose levels** (typically <55 mg/dL) measured at the time of symptoms. 3. **Relief of symptoms** promptly after the administration of glucose. **Why the other options are incorrect:** * **Gastrinoma:** Causes Zollinger-Ellison Syndrome, characterized by refractory peptic ulcers and diarrhea due to excessive gastric acid secretion. * **VIPoma:** Causes WDHA syndrome (Watery Diarrhea, Hypokalemia, and Achlorhydria), also known as Verner-Morrison syndrome. * **Somatostatinoma:** Presents with a "inhibitory syndrome" including diabetes mellitus, cholelithiasis, and steatorrhea due to the suppression of multiple gastrointestinal hormones. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The gold standard for diagnosing insulinoma is the **72-hour supervised fast**. * **Biochemical Profile:** During a hypoglycemic episode, patients with insulinoma will show **elevated Insulin**, **elevated C-peptide**, and **elevated Pro-insulin** levels, with an absence of sulfonylureas in the urine/blood. * **Localization:** Most insulinomas are small, benign, and solitary. Endoscopic ultrasound (EUS) is highly sensitive for localization. * **Association:** While most are sporadic, insulinomas can be associated with **MEN1 syndrome** (3Ps: Pituitary, Parathyroid, Pancreas).

Question 1005: Chovstek's sign is seen in which of the following conditions?

A. Hypocalcemia (Correct Answer)
B. Hypercalcemia
C. Hypokalemia
D. Hyperkalemia

Explanation: **Explanation:** **Chvostek’s sign** is a clinical indicator of **latent tetany** caused by **hypocalcemia** [1]. It is elicited by tapping the facial nerve at the angle of the jaw (anterior to the external auditory meatus). A positive sign is characterized by twitching of the facial muscles (ipsilateral) due to neuromuscular irritability. **Why Hypocalcemia is the correct answer:** Calcium ions normally stabilize neuronal membranes by inhibiting sodium channels. In hypocalcemia, the threshold for depolarization is lowered, making the nerve membranes "hyperexcitable." Even minor mechanical stimulation (like tapping) triggers spontaneous action potentials, leading to muscle contraction. **Why other options are incorrect:** * **Hypercalcemia:** This leads to decreased neuromuscular excitability, typically presenting with muscle weakness, constipation, and "moans, stones, and groans," rather than twitching. * **Hypokalemia:** Usually presents with muscle weakness, paralysis, or U-waves on ECG, but does not cause Chvostek’s sign. * **Hyperkalemia:** Primarily affects cardiac conduction (peaked T-waves) and can cause muscle weakness, but not tetany. **High-Yield Clinical Pearls for NEET-PG:** 1. **Trousseau’s Sign:** More sensitive and specific than Chvostek’s sign. It involves carpal spasm induced by inflating a BP cuff above systolic pressure for 3 minutes. 2. **Hypomagnesemia:** Can also cause a positive Chvostek’s sign because low magnesium often leads to refractory hypocalcemia [1]. 3. **Respiratory Alkalosis:** Hyperventilation can trigger these signs because increased pH causes more calcium to bind to albumin, reducing the ionized (active) fraction of calcium [1]. 4. **False Positives:** Chvostek’s sign can be present in approximately 10% of healthy individuals with normal calcium levels.

Question 1006: Thyrotoxic periodic paralysis (TPP) is usually due to hypokalemia. What is the best treatment?

A. Potassium
B. Magnesium
C. Hydration
D. Propranolol (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Propranolol** **Mechanism and Rationale:** Thyrotoxic periodic paralysis (TPP) is characterized by sudden muscle weakness due to an **intracellular shift of potassium**, rather than a true total-body potassium deficit. Excess thyroid hormone increases **Na+/K+-ATPase pump activity**, a process mediated by **beta-adrenergic stimulation**. **Propranolol** (a non-selective beta-blocker) is the treatment of choice because it directly antagonizes the hyper-adrenergic state, reversing the intracellular shift and normalizing serum potassium levels without the risk of rebound hyperkalemia [1]. **Why other options are incorrect:** * **A. Potassium:** While hypokalemia is present, giving intravenous potassium is risky. Since there is no actual loss of potassium from the body, as the attack resolves, the potassium shifts back into the extracellular space. Exogenous administration often leads to **rebound hyperkalemia** (seen in up to 40% of cases). If used, it must be given in very low doses and with extreme caution. * **B. Magnesium:** Magnesium deficiency can coexist with hypokalemia, but it is not the primary pathophysiology of TPP. * **C. Hydration:** While supportive, hydration does not address the underlying ion shift or the thyrotoxic state [1]. **NEET-PG High-Yield Pearls:** * **Demographics:** TPP is most common in **Asian males**, despite hyperthyroidism being more common in females. * **Triggers:** High carbohydrate meals (insulin release) and strenuous exercise followed by rest. * **Definitive Treatment:** Achieving a **euthyroid state** (e.g., antithyroid drugs, radioactive iodine, or surgery) is the only way to prevent recurrence [1]. * **Key Distinction:** Unlike Familial Periodic Paralysis, TPP patients will show signs of hyperthyroidism (tachycardia, tremors, low TSH).

Question 1007: Impaired oral glucose tolerance test (OGTT) is indicated by which of the following criteria?

A. Fasting plasma glucose > 126 mg/dL
B. Random blood glucose > 200 mg/dL
C. Fasting blood glucose < 90 mg/dL
D. Fasting blood glucose < 126 mg/dL and two hours after glucose load 140-199 mg/dL (Correct Answer)

Explanation: The diagnosis of glycemic status is based on specific thresholds defined by the American Diabetes Association (ADA). **Impaired Glucose Tolerance (IGT)** is a state of "Pre-diabetes" where blood glucose levels are higher than normal but do not yet meet the criteria for a diagnosis of Diabetes Mellitus [1]. **1. Why Option D is Correct:** The Oral Glucose Tolerance Test (OGTT) involves administering 75g of anhydrous glucose. IGT is specifically defined as a **2-hour post-load plasma glucose between 140 mg/dL and 199 mg/dL**. To fit the definition of IGT (rather than overt diabetes), the fasting plasma glucose must also be below the diabetic threshold (< 126 mg/dL) [1]. **2. Analysis of Incorrect Options:** * **Option A (Fasting > 126 mg/dL):** This is the diagnostic threshold for **Diabetes Mellitus**, not impaired tolerance [1]. * **Option B (Random > 200 mg/dL):** A random plasma glucose ≥ 200 mg/dL in a symptomatic patient (polyuria, polydipsia) is diagnostic of **Diabetes Mellitus**. * **Option C (Fasting < 90 mg/dL):** This represents a normal fasting glucose level (Normal is < 100 mg/dL). **3. NEET-PG High-Yield Pearls:** * **Impaired Fasting Glucose (IFG):** Fasting plasma glucose between **100–125 mg/dL**. * **HbA1c Criteria:** Normal (< 5.7%), Pre-diabetes (5.7–6.4%), and Diabetes (≥ 6.5%). * **Gold Standard:** While HbA1c is convenient, the **OGTT** is considered more sensitive for diagnosing early glucose intolerance. * **Pregnancy (GDM):** Note that the Carpenter-Coustan or DIPSI criteria used in pregnancy have different thresholds than the general population.

Question 1008: What are the diagnostic criteria for Diabetes Mellitus?

A. Fasting blood glucose is 100 mg/dL and post prandial 140 mg/dL
B. Fasting blood sugar is 125 mg/dL and 2-hour postprandial blood sugar is 199 mg/dL
C. Elevated insulin level
D. HbA1c > 6.5% (Correct Answer)

Explanation: The diagnosis of Diabetes Mellitus (DM) is based on specific glycemic thresholds established by the American Diabetes Association (ADA). [1] **Explanation of the Correct Answer:** **Option D (HbA1c ≥ 6.5%)** is a primary diagnostic criterion. HbA1c reflects the average blood glucose over the preceding 2–3 months. A value of **≥ 6.5%** (using a standardized assay) is diagnostic of DM. In the absence of unequivocal hyperglycemia, the diagnosis requires two abnormal test results from the same sample or in two separate test samples. **Analysis of Incorrect Options:** * **Option A:** These values (Fasting 100 mg/dL, PP 140 mg/dL) represent the upper limit of **normal** glycemic status. * **Option B:** These values (Fasting 125 mg/dL, 2-hr PP 199 mg/dL) fall into the **Prediabetes** category. For a DM diagnosis, Fasting Plasma Glucose (FPG) must be **≥ 126 mg/dL** and 2-hour Oral Glucose Tolerance Test (OGTT) must be **≥ 200 mg/dL**. [1] * **Option C:** Insulin levels are not used to diagnose DM. While they may help distinguish between Type 1 (low insulin/C-peptide) and Type 2 (high insulin/insulin resistance), they do not define the disease. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Criteria Summary:** 1. **FPG:** ≥ 126 mg/dL (8-hour fast). [1] 2. **2-hr OGTT:** ≥ 200 mg/dL (using 75g anhydrous glucose). 3. **HbA1c:** ≥ 6.5%. 4. **Random Plasma Glucose:** ≥ 200 mg/dL **PLUS** classic symptoms of hyperglycemia (polyuria, polydipsia, weight loss). [1] * **Prediabetes Ranges:** HbA1c: 5.7–6.4%; FPG: 100–125 mg/dL (Impaired Fasting Glucose); 2-hr OGTT: 140–199 mg/dL (Impaired Glucose Tolerance). [1] * **Note:** HbA1c may be unreliable in conditions with high red cell turnover (e.g., hemolytic anemia, pregnancy, recent hemorrhage).

Question 1009: What is the most diagnostic test for Addison's disease?

A. Serum Na+, K+, and renin levels
B. Serum Na+, K+, and saline suppression test
C. Serum creatinine/urea ratio
D. ACTH stimulation test (Correct Answer)

Explanation: **Explanation:** **Addison’s Disease (Primary Adrenocortical Insufficiency)** is characterized by the failure of the adrenal cortex to produce cortisol and aldosterone [1] [2]. 1. **Why the ACTH Stimulation Test is the Correct Answer:** The **Short Synacthen (ACTH) Stimulation Test** is the gold standard for diagnosing adrenal insufficiency. In a healthy individual, administering synthetic ACTH (Synacthen) should trigger the adrenal glands to produce a significant rise in serum cortisol (typically >18–20 μg/dL). In Addison’s disease, the adrenal cortex is damaged; therefore, even with high levels of exogenous ACTH, the glands fail to respond, and cortisol levels remain low [1]. This confirms the diagnosis of primary adrenal failure. 2. **Why Other Options are Incorrect:** * **Option A & B:** While hyponatremia, hyperkalemia, and elevated renin are classic biochemical features of Addison’s (due to mineralocorticoid deficiency), they are **non-specific** and can occur in other conditions (e.g., renal failure, diuretic use) [2]. They are suggestive but not diagnostic. * **Option B (Saline Suppression Test):** This is used to diagnose **Primary Hyperaldosteronism (Conn’s Syndrome)**, not adrenal insufficiency. * **Option C:** Serum creatinine/urea ratios are markers of renal function and hydration status, providing no specific information regarding adrenal steroidogenesis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Autoimmune adrenalitis (developed countries); Tuberculosis (developing countries like India) [2]. * **Screening Test:** Early morning (8 AM) serum cortisol. If <3 μg/dL, it strongly suggests insufficiency. * **Differentiation:** In Primary AI (Addison’s), ACTH is **high** and skin hyperpigmentation is present [1]. In Secondary AI (Pituitary failure), ACTH is **low** and there is no hyperpigmentation. * **Acute Crisis Management:** Do not wait for the ACTH test results; treat immediately with IV fluids and **Hydrocortisone** (or Dexamethasone if the test is to be performed concurrently) [1].

Question 1010: A 29-year-old woman complains of nervousness and muscle weakness of 6 months' duration. She is intolerant of heat and sweats excessively. She has lost 9 kg over the past 6 months despite an increased caloric intake. She frequently experiences a racing heart and palpitations. She has also missed several menstrual periods in the past few months. Physical examination reveals warm, moist skin and exophthalmos. What endocrine abnormality is most likely present in this patient?

A. Increased anti-thyroid DNA antibodies
B. Increased anti-TSH receptor antibodies (Correct Answer)
C. Decreased uptake of radioactive iodine in the thyroid
D. Increased serum TSH

Explanation: ### Explanation The clinical presentation of weight loss despite increased appetite, heat intolerance, palpitations, and menstrual irregularities points toward **hyperthyroidism** [1]. The presence of **exophthalmos** (proptosis) is a pathognomonic finding for **Graves' disease**, the most common cause of hyperthyroidism in young women [1], [3]. **1. Why the correct answer is right:** Graves' disease is an autoimmune disorder caused by the production of **Thyroid-Stimulating Immunoglobulins (TSI)**, also known as **anti-TSH receptor antibodies (TRAb)** [3]. These antibodies bind to and activate the TSH receptors on thyroid follicular cells, mimicking the action of TSH. This leads to autonomous overproduction of thyroid hormones (T3 and T4) and diffuse hyperplasia of the gland [1]. **2. Why the incorrect options are wrong:** * **Option A:** Anti-thyroid DNA antibodies are not associated with thyroid disease (Anti-dsDNA is seen in SLE). Anti-thyroid peroxidase (TPO) antibodies are seen in Hashimoto’s and Graves', but they are not the primary drivers of hyperthyroidism. * **Option C:** In Graves' disease, the radioactive iodine uptake (RAIU) is **increased** and diffuse because the entire gland is overactive [2]. Decreased uptake is seen in thyroiditis or factitious thyrotoxicosis [2]. * **Option D:** Due to the high levels of circulating T3 and T4, there is a strong negative feedback on the anterior pituitary, resulting in **decreased (suppressed) serum TSH** [1]. **Clinical Pearls for NEET-PG:** * **Graves' Triad:** Hyperthyroidism + Exophthalmos + Pretibial Myxedema (Dermopathy) [3]. * **Diagnosis:** Low TSH, High Free T4, and positive TRAb. * **Treatment of choice (Pregnancy):** Propylthiouracil (PTU) in the 1st trimester; Methimazole in the 2nd and 3rd trimesters. * **Specific Sign:** Lid lag and lid retraction are due to sympathetic overactivity, but **exophthalmos** is due to autoimmune-mediated inflammation of retro-orbital tissues [1].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

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