Endocrinology — MCQs
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A 25-year-old male reports episodic spells characterized by palpitations, sweating, nervousness, and feelings of anxiety. On examination, the man's blood pressure is 165/95 mm Hg. Plasma norepinephrine is 450 pg/mL (normal, 150-400 pg/mL), plasma epinephrine is 115 pg/mL (normal, 25-100 pg/mL), and 24-hour urinary VMA is 11 mg (normal, < 8 mg). Which of the following is the most likely cause of the patient's hypertension?
A perimenopausal woman presents with increasing swallowing difficulty and fatigue. Physical examination reveals a palpable goiter. Laboratory examination of her serum reveals T4 of 4.9 mg/dL, free T4 of 2.5 ng/dL, and TSH of 5.5 mIU/mL. No thyroid-stimulating immunoglobulins are identified in the serum, but antimicrosomal antibodies are present. Which one of the listed histologic findings, if present in a thyroid biopsy from this individual, would be most consistent with a diagnosis of Hashimoto's thyroiditis?
Tolvaptan is approved for use in which of the following conditions?
A 49-year-old man presents with recurrent episodes of drowsiness, sweating, and palpitations. During one episode, his blood glucose level was 52 mg/dL, and he recovered with intravenous 10% dextrose. His C-peptide levels are below the normal range. What is the most likely diagnosis?
What is true about Klinefelter syndrome?
Gestational hyperthyroidism occurs due to which of the following?
Which of the following has NOT been proven to delay or prevent diabetes in individuals with impaired glucose tolerance?
What is the insulin of choice in a patient with Diabetic ketoacidosis?
A patient presents with a nodular thyroid swelling and signs suggestive of hyperthyroidism. On examination, the patient shows absence of wrinkling on the forehead when looking upwards with the face inclined downwards. Which sign does this finding represent?
All of the following are true about Graves disease except?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1141: A 25-year-old male reports episodic spells characterized by palpitations, sweating, nervousness, and feelings of anxiety. On examination, the man's blood pressure is 165/95 mm Hg. Plasma norepinephrine is 450 pg/mL (normal, 150-400 pg/mL), plasma epinephrine is 115 pg/mL (normal, 25-100 pg/mL), and 24-hour urinary VMA is 11 mg (normal, < 8 mg). Which of the following is the most likely cause of the patient's hypertension?
- A. 11-beta-hydroxylase deficiency
- B. Conn's syndrome
- C. Pheochromocytoma (Correct Answer)
- D. Renin-secreting tumor
Explanation: The clinical presentation of episodic palpitations, sweating, anxiety, and hypertension forms the classic triad of **Pheochromocytoma**. This catecholamine-secreting tumor (usually arising from the adrenal medulla) leads to an excess of epinephrine and norepinephrine. The laboratory findings in this case—elevated plasma catecholamines and increased 24-hour urinary Vanillylmandelic acid (VMA)—confirm the diagnosis [2]. VMA is the end-stage metabolite of catecholamines, and its elevation is a high-yield diagnostic marker. **Why the other options are incorrect:** * **11-beta-hydroxylase deficiency:** This form of Congenital Adrenal Hyperplasia (CAH) causes hypertension due to the buildup of 11-deoxycorticosterone (a mineralocorticoid). However, it is typically associated with virilization (excess androgens) and would not cause elevated catecholamines or VMA. * **Conn’s Syndrome (Primary Hyperaldosteronism):** This presents with hypertension and hypokalemia due to excess aldosterone [1]. It does not cause episodic "spells" or elevated urinary VMA. * **Renin-secreting tumor:** This rare tumor leads to secondary hyperaldosteronism. While it causes severe hypertension, it is driven by the Renin-Angiotensin-Aldosterone System (RAAS), not the sympathetic nervous system. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% are bilateral, 10% are extra-adrenal (Paragangliomas), 10% are malignant, and 10% occur in children. * **Diagnosis:** The most sensitive initial screening test is **Plasma free metanephrines**. 24-hour urinary metanephrines and VMA are highly specific. * **Management:** Always start **Alpha-blockers (e.g., Phenoxybenzamine)** before Beta-blockers to avoid an "unopposed alpha" hypertensive crisis [2]. * **Associations:** Often linked with **MEN 2A/2B**, von Hippel-Lindau (VHL) syndrome, and Neurofibromatosis type 1 [2].
Question 1142: A perimenopausal woman presents with increasing swallowing difficulty and fatigue. Physical examination reveals a palpable goiter. Laboratory examination of her serum reveals T4 of 4.9 mg/dL, free T4 of 2.5 ng/dL, and TSH of 5.5 mIU/mL. No thyroid-stimulating immunoglobulins are identified in the serum, but antimicrosomal antibodies are present. Which one of the listed histologic findings, if present in a thyroid biopsy from this individual, would be most consistent with a diagnosis of Hashimoto's thyroiditis?
- A. Lymphocytic infiltrate without follicle formation
- B. Intense lymphoplasmacytic infiltrate with lymphoid follicles and scattered oxyphilic cells (Correct Answer)
- C. Hyperplasia of follicular cells with scalloping of colloid at the margin of follicles
- D. Granulomatous inflammation with multinucleated giant cells surrounding fragments of colloid
Explanation: ### Explanation **Hashimoto’s Thyroiditis (Chronic Lymphocytic Thyroiditis)** is the most common cause of hypothyroidism in iodine-sufficient regions. It is an autoimmune destruction of the thyroid gland mediated by T-cells and antibody-dependent cytotoxicity. #### Why Option B is Correct: The hallmark histological features of Hashimoto’s thyroiditis include: 1. **Intense Lymphoplasmacytic Infiltrate:** A dense collection of lymphocytes and plasma cells. 2. **Germinal Centers:** Well-developed lymphoid follicles with germinal centers (similar to a lymph node). 3. **Hürthle Cells (Oxyphilic Cells):** These are follicular epithelial cells that have undergone metaplasia. They appear enlarged with abundant, granular, eosinophilic (pink) cytoplasm due to an increased number of mitochondria. #### Why Other Options are Incorrect: * **Option A:** While lymphocytic infiltration occurs, the absence of follicle formation is not characteristic of Hashimoto’s; the presence of organized lymphoid follicles is a defining feature. * **Option C:** This describes **Graves’ Disease**. Hyperplasia with "scalloping" of the colloid indicates an overactive gland where the colloid is being rapidly consumed. * **Option D:** This describes **De Quervain’s (Subacute Granulomatous) Thyroiditis**, which typically follows a viral infection and presents with a painful thyroid. #### NEET-PG High-Yield Pearls: * **Serology:** Most patients have high titers of **Anti-TPO (antimicrosomal)** and **Anti-thyroglobulin** antibodies. * **Clinical Presentation:** Often presents as a painless goiter in middle-aged women. Patients may initially have transient "Hashitoxicosis" before progressing to permanent hypothyroidism (elevated TSH, low T4). * **Risk Factor:** Associated with HLA-DR3 and HLA-DR5. * **Malignancy Risk:** Patients have an increased risk of developing **Primary Thyroid B-cell Lymphoma** and Papillary Thyroid Carcinoma.
Question 1143: Tolvaptan is approved for use in which of the following conditions?
- A. Hypernatremia
- B. Hyperkalemia
- C. Hypercupruria
- D. Hyponatremia (Correct Answer)
Explanation: Explanation: **Tolvaptan** is a selective, oral **Vasopressin V2-receptor antagonist** (often referred to as an "Aquaretic"). By blocking the V2 receptors in the renal collecting ducts, it prevents the insertion of aquaporin-2 channels, thereby increasing the excretion of free water without significant loss of electrolytes [1]. **Why Hyponatremia is Correct:** Tolvaptan is specifically FDA-approved for the treatment of **clinically significant hypervolemic and euvolemic hyponatremia** (Serum Na <125 mEq/L). It is commonly used in conditions like **SIADH** (Syndrome of Inappropriate Antidiuretic Hormone secretion), Heart Failure, and Cirrhosis, where free water restriction has failed [1]. By promoting "aquaresis," it raises serum sodium levels. **Why Other Options are Incorrect:** * **A. Hypernatremia:** Tolvaptan would worsen hypernatremia by further increasing free water loss. * **B. Hyperkalemia:** Tolvaptan does not significantly affect potassium excretion; hyperkalemia is typically managed with insulin/dextrose, calcium gluconate, or potassium binders. * **C. Hypercupruria:** This refers to excess copper in urine (seen in Wilson’s disease), which is treated with chelating agents like Penicillamine or Trientine, not vaptans. **High-Yield Clinical Pearls for NEET-PG:** * **Black Box Warning:** Tolvaptan should be initiated only in a hospital setting to monitor the rate of sodium correction. Rapid correction can lead to **Osmotic Demyelination Syndrome (ODS)**. * **Hepatotoxicity:** Use is limited to 30 days due to the risk of liver injury. * **Other Vaptans:** **Conivaptan** is a non-selective (V1a and V2) antagonist administered intravenously. * **Other Indications:** Tolvaptan is also used to slow the progression of cyst formation in **Autosomal Dominant Polycystic Kidney Disease (ADPKD)**.
Question 1144: A 49-year-old man presents with recurrent episodes of drowsiness, sweating, and palpitations. During one episode, his blood glucose level was 52 mg/dL, and he recovered with intravenous 10% dextrose. His C-peptide levels are below the normal range. What is the most likely diagnosis?
- A. Factitious insulin use (Correct Answer)
- B. Gastrinoma
- C. Glucagonoma
- D. Insulinoma
Explanation: The patient presents with **Whipple’s Triad**: symptoms of hypoglycemia (drowsiness, sweating, palpitations), a documented low blood glucose level (52 mg/dL), and relief of symptoms upon glucose administration [2]. The key to differentiating the cause lies in the **C-peptide level**. **1. Why Factitious Insulin Use is Correct:** Insulin is synthesized as proinsulin, which is cleaved into equal amounts of active insulin and C-peptide. **Exogenous (injected) insulin** contains only the insulin hormone and lacks C-peptide. Therefore, in cases of factitious insulin use, the patient will have high circulating insulin levels but **suppressed/low C-peptide levels** due to the negative feedback of exogenous insulin on endogenous beta-cell secretion [1]. **2. Why Incorrect Options are Wrong:** * **Insulinoma (Option D):** This is an endogenous insulin-secreting tumor. Since the body is producing the insulin, both **insulin and C-peptide levels would be elevated** [1]. * **Gastrinoma (Option B):** This tumor secretes gastrin, leading to Zollinger-Ellison Syndrome (severe peptic ulcers and diarrhea), not hypoglycemia. * **Glucagonoma (Option C):** This tumor secretes glucagon, which causes **hyperglycemia** (diabetes mellitus), necrolytic migratory erythema, and weight loss. **3. NEET-PG High-Yield Pearls:** * **Whipple’s Triad:** 1. Symptoms of hypoglycemia; 2. Low plasma glucose; 3. Relief of symptoms after raising glucose. * **C-peptide:** The best marker for endogenous insulin production [1]. * **Factitious Hypoglycemia:** If C-peptide is low but insulin is high, suspect **Exogenous Insulin**. If both C-peptide and insulin are high, but a screen for oral hypoglycemics is positive, suspect **Sulfonylurea abuse** [1]. * **Insulinoma Diagnosis:** 72-hour supervised fast is the gold standard; look for high Insulin (>3 μU/mL) and high C-peptide (>0.6 ng/mL) during hypoglycemia [1].
Question 1145: What is true about Klinefelter syndrome?
- A. Height is greater than arm span
- B. Karyotype is 45, X
- C. Testes and sperm count are normal
- D. Puberty is attained at a normal age (Correct Answer)
Explanation: **Explanation:** **Klinefelter Syndrome (47, XXY)** is the most common cause of congenital hypogonadism in males [1]. **Why Option D is Correct:** In Klinefelter syndrome, the onset of puberty typically occurs at the **normal age**. However, as puberty progresses, the primary testicular failure becomes evident. The seminiferous tubules undergo hyalinization and fibrosis [3], leading to a failure in testosterone production and a compensatory rise in gonadotropins (FSH and LH). This results in the failure of secondary sexual characteristic completion rather than a delay in the initiation of puberty. **Analysis of Incorrect Options:** * **Option A:** Patients typically exhibit **eunuchoid body proportions**, where the **arm span is greater than the height** (by >2 cm) [3] and the lower segment is longer than the upper segment. This is due to delayed epiphyseal closure caused by testosterone deficiency. * **Option B:** The classic karyotype is **47, XXY** [1]. 45, X is the karyotype for Turner Syndrome. * **Option C:** Characteristically, patients have **small, firm testes** (usually <2 cm or <6 mL) and **azoospermia** (absence of sperm) due to tubular atrophy [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Hormonal Profile:** High FSH, High LH, Low/Low-normal Testosterone, and High Estradiol [3]. * **Clinical Features:** Gynecomastia (increased risk of male breast cancer), female-type hair distribution, and mitral valve prolapse. * **Diagnosis:** Karyotyping is the gold standard [3]. Barr bodies are present on buccal smear (due to the extra X chromosome). * **Comorbidities:** Increased risk of Germ Cell Tumors (specifically mediastinal), Type 2 Diabetes, and autoimmune disorders (like SLE) [2]. * **Treatment:** patients with Klinefelter syndrome are often supplemented with androgens to improve virilization and libido [4].
Question 1146: Gestational hyperthyroidism occurs due to which of the following?
- A. Beta HCG from placenta (Correct Answer)
- B. Trans-placental transfer of TSH
- C. TPO antibodies
- D. Anti thyroglobulin antibody
Explanation: **Explanation:** **Gestational Hyperthyroidism** (also known as Gestational Transient Thyrotoxicosis) is a physiological phenomenon occurring primarily in the first trimester of pregnancy. **1. Why Option A is Correct:** The underlying mechanism is the **structural homology** between Human Chorionic Gonadotropin (hCG) and Thyroid Stimulating Hormone (TSH). Both are glycoprotein hormones that share an identical **alpha-subunit**. Because of this similarity, hCG acts as a weak agonist at the TSH receptor. During the first trimester, hCG levels peak (around 10–12 weeks), leading to a transient stimulation of the thyroid gland, increased Free T4 levels, and a compensatory suppression of serum TSH. This is most pronounced in conditions with very high hCG, such as multiple gestations or molar pregnancies. **2. Why Other Options are Incorrect:** * **Option B:** TSH does not cross the placenta in significant amounts; moreover, maternal TSH is typically suppressed, not elevated, in this condition. * **Options C & D:** TPO (Thyroid Peroxidase) and Anti-thyroglobulin antibodies are markers for **autoimmune** thyroid diseases like Hashimoto’s thyroiditis or Graves' disease [2]. Gestational hyperthyroidism is a non-autoimmune, HCG-mediated condition. **Clinical Pearls for NEET-PG:** * **Hyperemesis Gravidarum:** This is the most common clinical association with gestational hyperthyroidism due to high hCG levels. * **Differentiation:** Unlike Graves' disease, gestational hyperthyroidism lacks clinical signs like ophthalmopathy (exophthalmos), pretibial myxedema, or a diffuse goiter [2]. * **Management:** It is usually self-limiting and resolves by 18–20 weeks as hCG levels decline. Anti-thyroid drugs (PTU/Methimazole) are generally **not** indicated [1]. * **Thyroid Function Tests in Pregnancy:** Normal pregnancy sees an increase in Total T3/T4 (due to increased Thyroid Binding Globulin) but Free T4 remains within or slightly above the high-normal range.
Question 1147: Which of the following has NOT been proven to delay or prevent diabetes in individuals with impaired glucose tolerance?
- A. Lifestyle modification
- B. Metformin
- C. Orlistat
- D. Atorvastatin (Correct Answer)
Explanation: ### Explanation The prevention of Type 2 Diabetes Mellitus (T2DM) in high-risk individuals with Impaired Glucose Tolerance (IGT) focuses on improving insulin sensitivity and reducing beta-cell exhaustion. **Why Atorvastatin is the Correct Answer:** Statins, including **Atorvastatin**, are primarily used for lipid management [3], [4]. However, large-scale clinical trials (such as JUPITER) and meta-analyses have shown that statins are actually associated with a **slight increase in the risk of developing new-onset diabetes**. This is thought to occur via the inhibition of glucose-stimulated insulin secretion and a reduction in peripheral insulin sensitivity. While their cardiovascular benefits outweigh this risk, they do *not* prevent diabetes [4]. **Analysis of Other Options:** * **Lifestyle Modification:** The landmark **Diabetes Prevention Program (DPP)** study proved that intensive lifestyle intervention (weight loss of 7% and 150 minutes of exercise/week) reduced the risk of T2DM by **58%**, making it the most effective intervention [2]. * **Metformin:** The DPP study also showed that Metformin reduced the risk by **31%**, particularly in younger, more obese individuals (BMI >35) [1]. * **Orlistat:** The **XENDOS study** demonstrated that Orlistat, by promoting weight loss through gastric/pancreatic lipase inhibition, significantly reduced the progression to T2DM in obese patients with IGT. **High-Yield Clinical Pearls for NEET-PG:** * **DPP Study Gold Standard:** Lifestyle modification > Metformin for diabetes prevention. * **Other proven drugs:** Alpha-glucosidase inhibitors (Acarbose - STOP-NIDDM trial), Thiazolidinediones (Pioglitazone), and GLP-1 receptor agonists (Liraglutide). * **Statin Paradox:** Statins increase the risk of T2DM but are still indicated in diabetic patients due to their significant reduction in Major Adverse Cardiovascular Events (MACE).
Question 1148: What is the insulin of choice in a patient with Diabetic ketoacidosis?
- A. Lispro
- B. Deterimer
- C. Aspart
- D. Regular Insulin (Correct Answer)
Explanation: **Explanation:** The management of Diabetic Ketoacidosis (DKA) requires a rapid-acting insulin that can be administered intravenously to quickly suppress ketogenesis and lower blood glucose. [1] **Why Regular Insulin is the Correct Choice:** Regular (Short-acting) Insulin is the **gold standard** for DKA management. Its primary advantage in an acute setting is its compatibility with intravenous (IV) administration. [2] When given as a continuous IV infusion, it has a rapid onset of action and a short half-life (approx. 5–10 minutes), allowing for precise, minute-to-minute titration based on hourly bedside glucose and anion gap monitoring. **Analysis of Incorrect Options:** * **Lispro and Aspart (Options A & C):** These are rapid-acting insulin analogs. While they can be used subcutaneously in very mild cases of DKA, they are not the standard of care for IV infusion in moderate-to-severe DKA. [2] They offer no clinical advantage over Regular insulin when given intravenously and are significantly more expensive. * **Detemir (Option B):** This is a long-acting (basal) insulin analog. It has a slow onset and a prolonged duration of action, making it entirely unsuitable for the acute, dynamic management required in DKA. **High-Yield Clinical Pearls for NEET-PG:** * **Route:** IV infusion is preferred over bolus. The standard dose is **0.1 unit/kg/hour**. * **The "Rule of 200":** When blood glucose reaches ~200–250 mg/dL, switch the IV fluid to 5% Dextrose to prevent hypoglycemia while continuing insulin to close the anion gap. [1] * **Potassium Warning:** Never start insulin if serum $K^+$ is **<3.3 mEq/L**, as insulin shifts potassium intracellularly, potentially causing fatal arrhythmias. [1] * **Resolution Criteria:** DKA is considered resolved when the pH >7.3, bicarbonate $\geq$18 mEq/L, and the anion gap is closed. [1]
Question 1149: A patient presents with a nodular thyroid swelling and signs suggestive of hyperthyroidism. On examination, the patient shows absence of wrinkling on the forehead when looking upwards with the face inclined downwards. Which sign does this finding represent?
- A. Von Graefe's sign
- B. Joffroy's sign (Correct Answer)
- C. Stellwag's sign
- D. Moebius sign
Explanation: **Explanation:** The clinical presentation describes a patient with hyperthyroidism (likely Graves' disease or toxic multinodular goiter) exhibiting specific ocular signs [1]. The correct answer is **Joffroy’s sign**. **1. Why Joffroy’s sign is correct:** Joffroy’s sign is characterized by the **absence of forehead wrinkling** when the patient attempts to look upwards while the head is tilted downwards. In a healthy individual, the frontalis muscle contracts to wrinkle the forehead during upward gaze. In hyperthyroidism, sympathetic overactivity and infiltrative ophthalmopathy can lead to a lack of this compensatory movement. **2. Analysis of Incorrect Options:** * **Von Graefe’s sign:** This refers to **lid lag** [1]. When the patient is asked to look slowly downwards, the upper eyelid fails to follow the movement of the globe, exposing the white sclera above the iris. * **Stellwag’s sign:** This refers to **infrequent or incomplete blinking**, which contributes to the characteristic "staring look" seen in thyrotoxicosis. * **Moebius sign:** This is the **inability to maintain convergence** of the eyeballs when looking at a near object, resulting from weakness of the medial rectus muscles. **Clinical Pearls for NEET-PG:** * **Dalrymple’s sign:** Widening of the palpebral fissure (staring look) due to upper lid retraction. * **Pathophysiology:** These signs occur due to increased sympathetic stimulation of the Müller’s muscle (lid retraction) and inflammatory changes in the extraocular muscles (infiltrative ophthalmopathy). * **Graves' Ophthalmopathy:** While many signs are due to sympathetic overactivity (seen in any thyrotoxicosis), true proptosis (exophthalmos) is specific to Graves' disease due to retro-orbital fibroblast proliferation [1].
Question 1150: All of the following are true about Graves disease except?
- A. Cardiac failure is common.
- B. Hypertrophy and hyperplasia of the thyroid gland are due to TSH receptor antibodies.
- C. Remissions and exacerbations are not infrequent. (Correct Answer)
- D. It is highly vascular with audible bruit.
Explanation: ### Explanation **Graves’ Disease** is an autoimmune disorder and the most common cause of hyperthyroidism [2]. It is characterized by the triad of hyperthyroidism with diffuse goiter, ophthalmopathy, and dermopathy [1]. **Why Option C is the "Except" (Correct Answer):** In Graves' disease, **spontaneous remissions are rare**. Once the autoimmune process is triggered, the disease typically follows a progressive or persistent course unless treated with antithyroid drugs (ATDs), radioactive iodine, or surgery. While ATDs can induce remission in about 30-50% of patients after a prolonged course (12-18 months), the natural history of the untreated disease is not characterized by frequent spontaneous fluctuations [1]. **Analysis of Other Options:** * **Option A (Cardiac Failure):** High-output cardiac failure is a recognized complication, especially in elderly patients or those with underlying heart disease. T3 has direct toxic effects on the myocardium and increases heart rate and stroke volume. * **Option B (Pathophysiology):** The hallmark of Graves is the presence of **Thyroid Stimulating Immunoglobulins (TSI)** [1]. These are IgG antibodies that bind to and activate the **TSH receptor**, leading to follicular cell hypertrophy, hyperplasia, and excessive thyroid hormone synthesis [2]. * **Option D (Vascularity):** Due to the intense metabolic activity and increased blood flow (angiogenesis), the gland becomes highly vascular. On clinical examination, a **systolic bruit** or a palpable thrill is a pathognomonic sign. **NEET-PG High-Yield Pearls:** * **Most common cause** of hyperthyroidism worldwide [2]. * **HLA Associations:** HLA-DR3 and HLA-B8. * **Diagnosis:** Low TSH, High T3/T4, and **diffuse uptake** on Technetium-99m pertechnetate scan. * **Specific Sign:** Exophthalmos (due to TSH receptor expression on orbital fibroblasts) is specific to Graves and not seen in other forms of hyperthyroidism [2].
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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