Endocrinology — MCQs
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Which of the following clinical features of diabetes insipidus is false?
A 63-year-old woman with Type 2 diabetes is seen for follow-up after a fasting lipid profile. She has no other medical conditions and feels well. Her diabetes is well controlled and the last hemoglobin A1c value was 6.5%. Her total cholesterol is 240 mg/dL, HDL is 50 mg/dL, low-density lipoprotein is 160 mg/dL, and triglycerides are 150 mg/dL. For this patient with dyslipidemia, what is the most appropriate treatment?
Which type of thyroiditis is also known as "Painless Thyroiditis"?
A 60-year-old man with small cell carcinoma of the lung presents to the emergency room in a coma after a clonic-tonic seizure. His temperature is 37°C, blood pressure is 100/50 mm Hg, and pulse is 88 per minute. Laboratory studies show a serum sodium of 103 mmol/L, normal serum levels of BUN and creatinine, and a dilute but otherwise normal urine. A CT scan of the head is normal. What is the most likely cause of seizures in this patient?
A 40-year-old lady presents with weight loss and palpitations, having a heart rate of 110/min, BP 130/70 mmHg, bilateral proptosis, and warm, moist skin. Investigations show undetectable TSH and normal free T4. What is the next best step in diagnosis?
Diffuse toxic goiter is characterized by:
Which of the following is NOT a complication arising out of the use of the medical device shown?
Obesity is associated with all the following conditions except?
A 53-year-old woman presents with weight loss, increased appetite, sweating, palpitations, and preference for cold weather, hot, moist palms, and tremors. What is the best investigation for the clinical diagnosis of this patient?
Eosinopenia occurs in which of the following conditions?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 451: Which of the following clinical features of diabetes insipidus is false?
- A. Daily urine volume is >50 mL/kg body weight
- B. Urine osmolarity is <300 mosmol/L
- C. Dehydration (Correct Answer)
- D. Enuresis
Explanation: **Explanation:** In Diabetes Insipidus (DI), the primary pathology is a deficiency of Antidiuretic Hormone (ADH) or resistance to its action. This leads to an inability of the kidneys to concentrate urine, resulting in massive polyuria. **Why "Dehydration" is the False Feature:** While patients with DI lose significant amounts of free water, **clinically significant dehydration is rare** in patients with an intact thirst mechanism and free access to water. These patients compensate for urinary losses by developing intense thirst (polydipsia). Dehydration only occurs if the patient is unable to communicate thirst (e.g., infants, elderly) or has a concomitant hypothalamic lesion affecting the thirst center (adipsic DI). **Analysis of Other Options:** * **A. Daily urine volume >50 mL/kg:** This is a diagnostic criterion for polyuria. In DI, urine output is typically massive, often ranging from 3 to 20 liters per day. * **B. Urine osmolarity <300 mosmol/L:** Since the kidneys cannot reabsorb water, the urine is characteristically dilute. In complete DI, urine osmolarity is usually <200 mOsm/kg, and it is always less than the plasma osmolarity (which is typically >290 mOsm/kg). * **D. Enuresis:** Nocturia is almost universal in DI. In children, this frequently manifests as bedwetting (enuresis) and is often a presenting complaint. **High-Yield NEET-PG Pearls:** * **Water Deprivation Test:** The gold standard for diagnosis. Central DI shows a >50% increase in urine osmolarity after Desmopressin; Nephrogenic DI shows little to no response. * **Most common cause of Central DI:** Idiopathic (30-50%), followed by trauma/surgery and tumors (Craniopharyngioma). * **Drug-induced Nephrogenic DI:** Lithium is the most common cause. * **Treatment:** Desmopressin (DDAVP) is the drug of choice for Central DI. Thiazide diuretics are used for Nephrogenic DI.
Question 452: A 63-year-old woman with Type 2 diabetes is seen for follow-up after a fasting lipid profile. She has no other medical conditions and feels well. Her diabetes is well controlled and the last hemoglobin A1c value was 6.5%. Her total cholesterol is 240 mg/dL, HDL is 50 mg/dL, low-density lipoprotein is 160 mg/dL, and triglycerides are 150 mg/dL. For this patient with dyslipidemia, what is the most appropriate treatment?
- A. Fibric acid derivatives
- B. Nicotinic acid
- C. Bile acid-binding resins
- D. HMG-CoA reductase inhibitors (Correct Answer)
Explanation: **Explanation:** The correct answer is **D. HMG-CoA reductase inhibitors (Statins).** The primary goal in managing dyslipidemia in a patient with Type 2 Diabetes Mellitus (T2DM) is the reduction of cardiovascular risk. According to current clinical guidelines (ADA and AHA/ACC), **statins are the first-line therapy** for diabetic patients aged 40–75 years, regardless of their baseline lipid levels, provided their LDL-C is $\geq$ 70 mg/dL. This patient is 63 years old with an LDL of 160 mg/dL, placing her in a high-risk category where statins have been proven to significantly reduce major adverse cardiovascular events (MACE) [1]. **Why other options are incorrect:** * **A. Fibric acid derivatives:** These are primarily used to lower triglycerides [2]. While they can be used in T2DM, they are second-line and indicated mainly when triglycerides are severely elevated (>500 mg/dL) to prevent pancreatitis. * **B. Nicotinic acid:** Niacin can increase HDL and lower LDL, but it is rarely used now due to side effects (flushing, hyperglycemia) and a lack of evidence showing improved cardiovascular outcomes when added to statins. * **C. Bile acid-binding resins:** These are less potent than statins and can actually increase triglyceride levels, making them unfavorable for many diabetic patients [2]. **NEET-PG High-Yield Pearls:** * **Statin Benefit Groups:** T2DM patients aged 40–75 are a major "statin benefit group." * **Intensity:** Patients with T2DM and multiple risk factors or aged 50-75 usually require **High-Intensity Statins** (e.g., Atorvastatin 40–80 mg or Rosuvastatin 20–40 mg) [3]. * **Pleiotropic Effects:** Statins do more than lower LDL; they stabilize atherosclerotic plaques and have anti-inflammatory properties [1]. * **Rule of 6:** Each doubling of the statin dose leads to an additional 6% reduction in LDL-C.
Question 453: Which type of thyroiditis is also known as "Painless Thyroiditis"?
- A. Subacute lymphocytic thyroiditis (Correct Answer)
- B. Subacute granulomatous thyroiditis
- C. Hashimoto's thyroiditis
- D. Riedel's thyroiditis
Explanation: **Explanation:** **Subacute lymphocytic thyroiditis** (Option A) is the correct answer. It is also known as **"Painless Thyroiditis"** or "Silent Thyroiditis." Pathologically, it is characterized by a lymphocytic infiltration of the thyroid gland. Clinically, it presents with a transient phase of thyrotoxicosis (due to the release of stored hormones from damaged follicles) followed by hypothyroidism, eventually returning to a euthyroid state [1]. Crucially, unlike other inflammatory thyroid conditions, there is **no thyroid tenderness** on palpation. **Why other options are incorrect:** * **Subacute granulomatous thyroiditis (de Quervain’s):** This is the most common cause of a **painful** thyroid gland. It typically follows a viral upper respiratory tract infection and presents with exquisite tenderness and an elevated ESR. * **Hashimoto's thyroiditis:** While it is a lymphocytic thyroiditis, it is chronic and typically presents with a firm, non-tender goiter and permanent hypothyroidism. It is not referred to as "painless thyroiditis" in clinical nomenclature. * **Riedel's thyroiditis:** This is a rare manifestation of IgG4-related disease characterized by dense fibrous replacement of the thyroid ("stony hard" thyroid). While painless, it presents with obstructive symptoms (dysphagia, hoarseness). **High-Yield NEET-PG Pearls:** * **Postpartum Thyroiditis:** A variant of subacute lymphocytic thyroiditis occurring within one year of delivery. * **Radioactive Iodine Uptake (RAIU):** In the thyrotoxic phase of painless thyroiditis, RAIU is **low** (distinguishing it from Graves' disease where RAIU is high) [1]. * **Treatment:** Since the thyrotoxicosis is due to "leakage" and not overproduction, antithyroid drugs (PTU/Methimazole) are **not** used; beta-blockers are used for symptomatic relief [1].
Question 454: A 60-year-old man with small cell carcinoma of the lung presents to the emergency room in a coma after a clonic-tonic seizure. His temperature is 37°C, blood pressure is 100/50 mm Hg, and pulse is 88 per minute. Laboratory studies show a serum sodium of 103 mmol/L, normal serum levels of BUN and creatinine, and a dilute but otherwise normal urine. A CT scan of the head is normal. What is the most likely cause of seizures in this patient?
- A. Central diabetes insipidus
- B. Diabetes mellitus
- C. Renal metastases
- D. Syndrome of inappropriate ADH secretion (Correct Answer)
Explanation: The patient presents with severe hyponatremia (103 mmol/L) and neurological symptoms (coma, seizures) in the setting of Small Cell Carcinoma of the Lung (SCLC) [1]. This is a classic presentation of Syndrome of Inappropriate Antidiuretic Hormone (SIADH), a common paraneoplastic syndrome associated with SCLC [1]. Why SIADH is correct: In SIADH, ectopic production of ADH leads to excessive water reabsorption in the renal collecting ducts [4]. This results in euvolemic hyponatremia due to water retention and secondary natriuresis [3]. When serum sodium drops rapidly or falls below 120 mmol/L, it causes cerebral edema, leading to headache, confusion, seizures, and coma [2]. The normal BUN and creatinine levels support a non-renal, euvolemic state [3]. Why other options are incorrect: * Central Diabetes Insipidus: This involves a deficiency of ADH, leading to polyuria and hypernatremia, not hyponatremia. * Diabetes Mellitus: While severe hyperglycemia can cause osmotic diuresis or pseudohyponatremia, it would not typically present with a sodium level as low as 103 mmol/L without significant glucose elevation or ketoacidosis. * Renal Metastases: While possible in advanced cancer, they usually cause hematuria or renal failure (elevated BUN/Creatinine) rather than isolated, profound hyponatremia. NEET-PG High-Yield Pearls: * SCLC Associations: SIADH and Lambert-Eaton Myasthenic Syndrome are the most common paraneoplastic syndromes [1]. * Diagnosis of SIADH: Characterized by hyponatremia, low serum osmolality (<275 mOsm/kg), and inappropriately high urine osmolality (>100 mOsm/kg). * Management: For severe symptomatic hyponatremia (seizures/coma), the treatment of choice is Hypertonic Saline (3% NaCl). * Caution: Avoid rapid correction (>8–10 mmol/L in 24 hours) to prevent Osmotic Demyelination Syndrome (Central Pontine Myelinolysis) [5].
Question 455: A 40-year-old lady presents with weight loss and palpitations, having a heart rate of 110/min, BP 130/70 mmHg, bilateral proptosis, and warm, moist skin. Investigations show undetectable TSH and normal free T4. What is the next best step in diagnosis?
- A. Radioactive iodine uptake scan
- B. Thyroid peroxidase antibody screen
- C. Thyroid stimulating antibody screen
- D. Free T3 levels (Correct Answer)
Explanation: ### **Explanation** **1. Why Free T3 levels is the correct answer:** The patient presents with classic symptoms of hyperthyroidism (weight loss, palpitations, tachycardia, warm skin) and pathognomonic signs of **Graves' disease** (bilateral proptosis) [1]. Laboratory findings show a suppressed TSH with a normal Free T4. This biochemical pattern suggests one of two possibilities: * **Subclinical Hyperthyroidism:** (TSH low, both T3 and T4 normal). * **T3 Toxicosis:** (TSH low, T4 normal, but **T3 is elevated**). In early Graves' disease or toxic multinodular goiter, T3 often rises before T4. Since the patient is clinically symptomatic (tachycardia, weight loss), we must rule out **T3 Toxicosis** by measuring Free T3 levels before labeling it as subclinical disease. **2. Why other options are incorrect:** * **A. Radioactive iodine uptake (RAIU) scan:** While useful to differentiate causes of hyperthyroidism (e.g., Graves' vs. Thyroiditis), the diagnosis of hyperthyroidism must first be biochemically confirmed (elevated T3 or T4) before performing a scan [2]. * **B. Thyroid peroxidase (TPO) antibody:** These are markers for Hashimoto’s thyroiditis. While they can be present in Graves', they are not the primary diagnostic step for thyrotoxicosis [3]. * **C. Thyroid stimulating antibody (TRAb):** These are specific for Graves' disease [4]. However, the immediate priority in a symptomatic patient with normal T4 is to confirm the biochemical state (T3 levels) rather than the etiology. --- ### **High-Yield Pearls for NEET-PG** * **T3 Toxicosis:** Seen in ~5% of hyperthyroid patients. It is often the earliest stage of Graves' disease or seen in autonomous thyroid nodules. * **Apathetic Hyperthyroidism:** Seen in the elderly; presents with depression and atrial fibrillation rather than classic "hyper" symptoms. * **Graves' Disease Triad:** Hyperthyroidism + Diffuse Goiter + Exophthalmos (Proptosis) [4]. * **Diagnostic Algorithm:** Always check **TSH first**. If TSH is low, check **Free T4**. If Free T4 is normal, the next step is always **Free T3**.
Question 456: Diffuse toxic goiter is characterized by:
- A. Primary thyroid disease (Correct Answer)
- B. Secondary thyroid disease
- C. It is due to an autoimmune thyroid stimulating hormone (TSH) antibody
- D. It is due to the TSH receptor
Explanation: **Explanation:** **Diffuse Toxic Goiter (Graves’ Disease)** is the most common cause of hyperthyroidism [2]. It is classified as a **Primary Thyroid Disease** because the pathology originates within the thyroid gland itself, leading to the autonomous overproduction of thyroid hormones (T3 and T4) [1]. * **Why Option A is correct:** In primary thyroid disorders, the gland produces excess hormone despite low levels of stimulating hormones from the pituitary. In Graves’ disease, the thyroid gland is the direct site of overactivity, resulting in elevated T3/T4 and suppressed TSH [3]. * **Why Option B is incorrect:** Secondary thyroid disease refers to pathology in the anterior pituitary (e.g., a TSH-secreting adenoma). In such cases, both TSH and thyroid hormones would be elevated. * **Why Option C is incorrect:** While Graves' is autoimmune, it is not caused by a "TSH antibody" (which implies an antibody against the TSH molecule itself). It is caused by **Thyroid Stimulating Immunoglobulins (TSI)** [1]. * **Why Option D is incorrect:** This is a distractor. The disease is due to antibodies *binding to* the TSH receptor, not a defect in the receptor itself [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Type II Hypersensitivity reaction where IgG antibodies (TSI) mimic TSH and bind to the **TSH Receptor**, stimulating the follicular cells [1]. * **Classic Triad:** Hyperthyroidism with diffuse goiter, Ophthalmopathy (Exophthalmos), and Dermopathy (Pretibial myxedema) [1][2]. * **Diagnosis:** Low TSH, High T3/T4, and **diffuse, increased uptake** on Radioactive Iodine Uptake (RAIU) scan. * **Histology:** Tall columnar epithelium with "scalloping" of colloid.
Question 457: Which of the following is NOT a complication arising out of the use of the medical device shown?
- A. Lipo-hypertrophy
- B. Neuro-glucopenia
- C. Pre-breakfast hyperglycemia
- D. Molar ratio of insulin/C-peptide < 1 (Correct Answer)
Explanation: ***Molar ratio of insulin/C-peptide < 1*** - **Exogenous insulin therapy** (via insulin pump) suppresses endogenous **C-peptide** production, resulting in a **high insulin/C-peptide ratio (>1)**, not less than 1. - A **molar ratio < 1** suggests **insulinoma** where endogenous insulin and C-peptide are co-secreted in equimolar amounts, which is unrelated to insulin pump complications. *Lipo-hypertrophy* - **Repeated injections** at the same infusion site can cause **subcutaneous fat hypertrophy**, leading to lumpy skin areas. - This is a **common complication** of insulin pump therapy and affects **insulin absorption** at affected sites. *Neuro-glucopenia* - **Hypoglycemia** from insulin pump malfunction or incorrect dosing can cause **neuroglycopenic symptoms** like confusion, seizures, or coma. - This is a **serious complication** requiring immediate glucose administration and pump adjustment. *Pre-breakfast hyperglycemia* - Can result from **Dawn phenomenon** (physiological cortisol rise) or **Somogyi effect** (rebound hyperglycemia after nocturnal hypoglycemia). - **Insulin pump programming** may need adjustment to address these **circadian glucose variations**.
Question 458: Obesity is associated with all the following conditions except?
- A. Growth hormone deficiency
- B. Thyroid hormone deficiency
- C. Diabetes mellitus
- D. Estrogen deficiency (Correct Answer)
Explanation: Obesity is a complex metabolic state characterized by significant hormonal alterations. The correct answer is **Estrogen deficiency** because obesity is actually associated with **estrogen excess**, not deficiency. **1. Why Estrogen Deficiency is the Correct Answer (The Exception):** In obese individuals, adipose tissue acts as an active endocrine organ. It contains high levels of the enzyme **aromatase**, which converts adrenal androgens (like androstenedione) into estrogens (estrone). Consequently, obesity leads to hyperestrogenemia. In females, this increases the risk of endometrial hyperplasia and breast cancer; in males, it can lead to gynecomastia. **2. Analysis of Incorrect Options:** * **Growth Hormone (GH) Deficiency:** Obesity is associated with "acquired" GH deficiency. High levels of free fatty acids and hyperinsulinemia suppress GH secretion from the pituitary. However, IGF-1 levels often remain normal, and linear growth in obese children is typically not impaired. * **Thyroid Hormone Deficiency:** Hypothyroidism is a well-known secondary cause of obesity due to a decreased basal metabolic rate (BMR) and accumulation of glycosaminoglycans. Conversely, even in simple obesity, mild elevations in TSH are often seen as a compensatory mechanism. * **Diabetes Mellitus:** This is the most classic association [1]. Obesity (especially visceral) leads to increased TNF-̑, resistin, and free fatty acids, which cause **insulin resistance**, eventually leading to Type 2 Diabetes Mellitus [2, 3]. **Clinical Pearls for NEET-PG:** * **Pickwickian Syndrome:** Obesity Hypoventilation Syndrome characterized by BMI >30, daytime hypercapnia, and sleep apnea. * **Adiponectin Paradox:** While most adipokines (like Leptin) increase with obesity, **Adiponectin** (which is cardioprotective and insulin-sensitizing) **decreases** in obese individuals [3]. * **Polycystic Ovary Syndrome (PCOS):** Obesity worsens the hyperinsulinemia-hyperandrogenism cycle in PCOS.
Question 459: A 53-year-old woman presents with weight loss, increased appetite, sweating, palpitations, and preference for cold weather, hot, moist palms, and tremors. What is the best investigation for the clinical diagnosis of this patient?
- A. TSH levels (Correct Answer)
- B. Autoimmune panel
- C. Plasma catecholamines
- D. Plasma Cortisol
Explanation: ### Explanation **1. Why TSH levels is the correct answer:** The patient presents with classic symptoms of **hyperthyroidism** (thyrotoxicosis): weight loss despite increased appetite, heat intolerance, diaphoresis (sweating), palpitations, and tremors [2], [3]. In clinical practice, the **Serum TSH level** is the single most sensitive and best initial screening test for diagnosing thyroid dysfunction. In primary hyperthyroidism, TSH will be suppressed (usually <0.01 mU/L) due to negative feedback from elevated thyroid hormones (T3/T4) on the pituitary gland [2]. **2. Why the other options are incorrect:** * **Autoimmune panel (e.g., Anti-TPO, TRAb):** While these help determine the *etiology* (e.g., Graves' disease), they are not the first-line investigation for establishing the *clinical diagnosis* of thyrotoxicosis [2]. * **Plasma catecholamines:** These are used to diagnose Pheochromocytoma. While pheochromocytoma can cause palpitations and sweating, it typically presents with episodic hypertension and does not explain the preference for cold weather or increased appetite [3]. * **Plasma Cortisol:** This is used to evaluate adrenal disorders (Cushing’s or Addison’s). It does not correlate with the hypermetabolic symptoms described. **3. NEET-PG High-Yield Pearls:** * **Best Screening Test for Thyroid Disorders:** Serum TSH. * **Most Sensitive Indicator of Thyroid Status:** TSH (except in secondary/central hypothyroidism). * **Apathetic Hyperthyroidism:** Seen in elderly patients; they may present only with atrial fibrillation or depression rather than classic hypermetabolic symptoms [1]. * **Thyroid Storm:** A life-threatening exacerbation of hyperthyroidism; the first-line drug to inhibit peripheral conversion of T4 to T3 is **Propylthiouracil (PTU)**. * **Wolff-Chaikoff Effect:** Autoregulation where high iodine intake leads to a transient *reduction* in thyroid hormone synthesis.
Question 460: Eosinopenia occurs in which of the following conditions?
- A. Asthma
- B. Hookworm infestation
- C. Chronic myeloid leukemia
- D. Cushing's disease (Correct Answer)
Explanation: Cushing’s Disease is the correct answer because it is characterized by an excess of endogenous cortisol [1]. Glucocorticoids cause eosinopenia (a decrease in the number of circulating eosinophils) by promoting their sequestration in the spleen and lungs and inducing apoptosis of eosinophils. This is part of the classic "steroid-induced leukogram," which typically shows neutrophilia alongside lymphopenia, monocytopenia, and eosinopenia. Analysis of Incorrect Options: * Asthma: This is a Type I hypersensitivity reaction. Eosinophils are recruited to the airway mucosa, and peripheral eosinophilia is a common finding, reflecting the Th2-driven inflammatory response. * Hookworm Infestation: Helminthic infections are classic causes of eosinophilia. Eosinophils play a crucial role in the immune response against parasites by releasing major basic protein (MBP) and eosinophil cationic protein (ECP). * Chronic Myeloid Leukemia (CML): CML is a myeloproliferative neoplasm. It typically presents with a "leukemoid" picture involving an increase in all granulocytic cell lines, including neutrophils, basophils, and eosinophils. Basophilia and eosinophilia are important diagnostic clues for CML. High-Yield Clinical Pearls for NEET-PG: * Mnemonic for Eosinophilia (NAACP): Neoplasia, Allergy/Asthma, Addison’s disease, Connective tissue disorders, Parasites. * Addison’s vs. Cushing’s: While Cushing’s (high cortisol) causes eosinopenia, Addison’s disease (low cortisol) causes eosinophilia [1]. * Steroid Effect: Glucocorticoids "kick" neutrophils out of the marginated pool into the blood (neutrophilia) but "hide" eosinophils and lymphocytes (eosinopenia/lymphopenia).
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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