Endocrinology — MCQs
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Gynaecomastia is seen in all of the following conditions except?
Cardiovascular manifestations are more dominant in which of the following conditions?
A 33-year-old man presents with complaints of polydipsia and polyuria. Physical examination reveals a normal JVP at the sternal angle. Laboratory findings include serum sodium of 150 mEq/L, glucose of 120 mg/dL, and serum osmolality of 315 mOsm/kg. Urine studies show urine sodium of 20 mEq/L and urine osmolality of 260 mOsm/kg. Which of the following drugs is most likely to cause this clinical presentation?
Conn's disease is characterized by an excess of which hormone?
Ketoacidosis without glycosuria is seen in which of the following conditions?
A man presents with gynecomastia and infertility. What is the most likely cause?
A 40-year-old female with a known history of ischemic heart disease (IHD) is diagnosed with hypothyroidism. Which of the following would be the most appropriate line of management for her?
Which of the following conditions is associated with pretibial myxedema?
Which of the following is contraindicated in diabetics with Congestive Heart Failure?
Which of the following signs is NOT seen in Cushing's syndrome?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 1131: Gynaecomastia is seen in all of the following conditions except?
- A. Prolactinoma (Correct Answer)
- B. TSH secreting adenoma
- C. HCG secreting tumor
- D. Estrogen secreting tumor
Explanation: The correct answer is **A. Prolactinoma**. **1. Why Prolactinoma is the correct answer:** While hyperprolactinemia causes galactorrhea (milky nipple discharge), it does **not** directly cause gynecomastia (proliferation of glandular breast tissue) [1]. Prolactinoma leads to hypogonadotropic hypogonadism by inhibiting GnRH [2]. While the resulting low testosterone can theoretically alter the estrogen/androgen ratio, clinical gynecomastia is rarely seen in pure prolactinomas unless there is significant secondary estrogen elevation or co-secretion [1]. In the context of NEET-PG, prolactinoma is the classic "distractor" often tested against gynecomastia. **2. Analysis of Incorrect Options:** * **TSH secreting adenoma:** Hyperthyroidism increases the production of **Sex Hormone Binding Globulin (SHBG)**. SHBG binds testosterone more avidly than estrogen, leading to an increase in "free estrogen," which stimulates breast tissue. * **HCG secreting tumor:** (e.g., Choriocarcinoma, Germ cell tumors). HCG is structurally similar to LH and stimulates testicular **Leydig cells** to produce both testosterone and estrogen. However, the aromatization to estrogen is disproportionately high, leading to gynecomastia. * **Estrogen secreting tumor:** (e.g., Sertoli or Leydig cell tumors). These directly secrete excess estradiol, shifting the hormonal balance in favor of breast tissue proliferation [3]. **Clinical Pearls for NEET-PG:** * **Physiological Gynecomastia:** Seen in neonates, at puberty (most common), and in the elderly [1]. * **Drug-induced Gynecomastia (High Yield):** Remember the mnemonic **"DISCO"** – **D**igoxin, **I**soniazid, **S**pironolactone (most common drug cause), **C**imetidine, **O**estrogens/Ketoconazole. * **Key Distinction:** Gynecomastia is a proliferation of **glandular** tissue; "Pseudogynecomastia" refers to fat deposition (lipomastia) seen in obese individuals [1].
Question 1132: Cardiovascular manifestations are more dominant in which of the following conditions?
- A. Primary thyrotoxicosis
- B. Secondary thyrotoxicosis (Correct Answer)
- C. Simple goitre
- D. All of the above
Explanation: **Explanation:** The correct answer is **Secondary thyrotoxicosis** (Toxic Multinodular Goitre). **1. Why Secondary Thyrotoxicosis is correct:** Secondary thyrotoxicosis occurs when a pre-existing simple or multinodular goitre becomes toxic (Plummer’s disease). This condition typically affects **elderly patients**. Because the cardiovascular system in older individuals often has underlying degenerative changes or reduced reserve, the excess thyroid hormone triggers significant cardiac manifestations [1]. In these patients, the classic signs of hyperthyroidism (like tremors or exophthalmos) are often absent, while **atrial fibrillation, heart failure, and palpitations** dominate the clinical picture [1]. This is sometimes referred to as "masked" or "apathetic" hyperthyroidism. **2. Why other options are incorrect:** * **Primary Thyrotoxicosis (Graves' Disease):** This typically affects younger patients (20–40 years) [1]. While tachycardia and increased cardiac output occur, the clinical presentation is usually dominated by **neuromuscular symptoms** (tremors, nervousness) and **ophthalmopathy** (exophthalmos) rather than primary cardiac failure or arrhythmias [1]. * **Simple Goitre:** This is a euthyroid state where thyroid hormone levels are normal [1]. Therefore, there are no thyrotoxic cardiovascular manifestations. **3. High-Yield Clinical Pearls for NEET-PG:** * **Graves' Disease:** Most common cause of hyperthyroidism in the young; characterized by diffuse uptake on scan and presence of TSI (Thyroid Stimulating Immunoglobulins) [1]. * **Plummer’s Disease:** Most common cause of hyperthyroidism in the elderly; characterized by "hot nodules" on scan. * **Cardiac Sign:** Atrial fibrillation is the most common arrhythmia associated with thyrotoxicosis, especially in the elderly [1]. * **Treatment Note:** In secondary thyrotoxicosis, radioactive iodine or surgery is often preferred over long-term antithyroid drugs due to the autonomous nature of the nodules.
Question 1133: A 33-year-old man presents with complaints of polydipsia and polyuria. Physical examination reveals a normal JVP at the sternal angle. Laboratory findings include serum sodium of 150 mEq/L, glucose of 120 mg/dL, and serum osmolality of 315 mOsm/kg. Urine studies show urine sodium of 20 mEq/L and urine osmolality of 260 mOsm/kg. Which of the following drugs is most likely to cause this clinical presentation?
- A. lithium (Correct Answer)
- B. cyclophosphamide
- C. barbiturates
- D. nicotine
Explanation: **Explanation:** The patient presents with the classic triad of **Diabetes Insipidus (DI)**: polyuria, polydipsia, and hypernatremia (150 mEq/L) with high serum osmolality (315 mOsm/kg) and inappropriately dilute urine (260 mOsm/kg). The normal JVP indicates a state of euvolemic hypernatremia, typical of DI [1]. **Why Lithium is correct:** Lithium is the most common cause of **drug-induced Nephrogenic Diabetes Insipidus**. It enters the principal cells of the collecting duct through epithelial sodium channels (ENaC) and inhibits glycogen synthase kinase-3 ̧. This interferes with the action of ADH (Vasopressin) on V2 receptors, preventing the insertion of **Aquaporin-2 channels** into the apical membrane [2]. Consequently, the kidneys cannot concentrate urine despite high serum osmolality. **Why other options are incorrect:** * **Cyclophosphamide, Barbiturates, and Nicotine:** These drugs are associated with **SIADH** (Syndrome of Inappropriate Antidiuretic Hormone). SIADH presents with the exact opposite biochemical profile: hyponatremia, low serum osmolality, and inappropriately concentrated urine [3]. **NEET-PG High-Yield Pearls:** * **Diagnosis:** If urine osmolality remains low after Desmopressin administration, it confirms Nephrogenic DI. If it increases by >50%, it is Central DI [1]. * **Management of Lithium-induced DI:** The drug of choice is **Amiloride**, which blocks ENaC channels, preventing lithium from entering the collecting duct cells. * **Other causes of Nephrogenic DI:** Hypercalcemia, hypokalemia, and drugs like Demeclocycline or Amphotericin B [1].
Question 1134: Conn's disease is characterized by an excess of which hormone?
- A. Adrenaline
- B. Aldosterone (Correct Answer)
- C. Cortisol
- D. Noradrenaline
Explanation: **Explanation:** **Conn’s Syndrome** (Primary Hyperaldosteronism) is caused by an aldosterone-secreting adenoma of the adrenal cortex (specifically the *zona glomerulosa*) [2]. **Why Aldosterone is Correct:** Aldosterone is a mineralocorticoid that acts on the distal convoluted tubules and collecting ducts of the kidney. It promotes **sodium and water reabsorption** in exchange for **potassium and hydrogen ion excretion** [1]. Consequently, an excess of aldosterone leads to the classic clinical triad of: 1. **Hypertension** (due to sodium/water retention) 2. **Hypokalemia** (due to potassium wasting) 3. **Metabolic Alkalosis** (due to hydrogen ion loss) **Why Other Options are Incorrect:** * **Adrenaline & Noradrenaline (Options A & D):** These are catecholamines secreted by the adrenal medulla [3]. Excess levels are characteristic of **Pheochromocytoma**, which presents with episodic hypertension, palpitations, and diaphoresis. * **Cortisol (Option B):** Excess cortisol leads to **Cushing’s Syndrome**. While it can cause hypertension, it is also associated with distinct features like truncal obesity, striae, and hyperglycemia [2]. **High-Yield NEET-PG 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 or Oral salt loading test (failure to suppress aldosterone). * **Gold Standard for Lateralization:** Adrenal Venous Sampling (AVS) to distinguish between a unilateral adenoma (Conn's) and bilateral adrenal hyperplasia [4]. * **Treatment:** Surgical excision for unilateral adenoma; **Spironolactone** (aldosterone antagonist) for bilateral hyperplasia.
Question 1135: Ketoacidosis without glycosuria is seen in which of the following conditions?
- A. Aspirin poisoning
- B. Renal tubular acidosis
- C. Prolonged starvation (Correct Answer)
- D. Paracetamol poisoning
Explanation: The presence of **ketoacidosis without glycosuria** is a classic biochemical hallmark of **Prolonged Starvation**. **1. Why Prolonged Starvation is Correct:** During starvation, the body exhausts its glycogen stores (within 24 hours) and shifts to lipolysis for energy [1]. Fatty acids are converted into ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) in the liver to provide fuel for the brain [1, 3, 4]. Since the blood glucose levels remain low or normal (euglicemia), the renal threshold for glucose (180 mg/dL) is not exceeded. Consequently, ketones appear in the urine (ketonuria) and blood, but glucose does not [1]. **2. Analysis of Incorrect Options:** * **Aspirin (Salicylate) Poisoning:** While it causes a high anion gap metabolic acidosis (and sometimes ketosis due to interference with Krebs cycle), it typically presents with a complex mixed acid-base picture. It does not characteristically present with isolated ketoacidosis without glycosuria in the same physiological context as starvation. * **Renal Tubular Acidosis (RTA):** This causes a **normal** anion gap (hyperchloremic) metabolic acidosis. It does not involve the production of ketone bodies. * **Paracetamol Poisoning:** Severe toxicity leads to lactic acidosis due to liver failure, not ketoacidosis. (Note: 5-oxoprolinuria is a rare cause of acidosis in chronic paracetamol use, but not ketoacidosis). **3. High-Yield Clinical Pearls for NEET-PG:** * **Diabetic Ketoacidosis (DKA):** Characterized by the triad of Hyperglycemia, Ketosis, and Acidosis. Unlike starvation, DKA presents with **heavy glycosuria** due to extreme hyperglycemia [4]. * **Euglycemic DKA:** Seen with **SGLT-2 inhibitors** (e.g., Empagliflozin). Here, you see ketoacidosis with minimal or no glycosuria, mimicking starvation biochemistry. * **Alcoholic Ketoacidosis:** Occurs in chronic alcoholics after a binge followed by vomiting/starvation; glucose levels are usually low or normal, and glycosuria is absent.
Question 1136: A man presents with gynecomastia and infertility. What is the most likely cause?
- A. Cimetidine (Correct Answer)
- B. Omeprazole
- C. Erythromycin
- D. Digitalis
Explanation: The correct answer is **Cimetidine**. This is a classic high-yield topic in endocrinology and pharmacology for NEET-PG. **Why Cimetidine is Correct:** Cimetidine, an H2-receptor antagonist, is a notorious cause of drug-induced gynecomastia and infertility through three distinct mechanisms: 1. **Anti-androgenic effects:** It acts as a competitive antagonist at the androgen receptor, blocking testosterone action. 2. **Inhibition of Cytochrome P450:** It inhibits the metabolism of estradiol, leading to increased estrogen levels. 3. **Hyperprolactinemia:** It can stimulate prolactin release, which suppresses the hypothalamic-pituitary-gonadal (HPG) axis, leading to decreased LH/FSH and subsequent infertility. **Analysis of Incorrect Options:** * **B. Omeprazole:** While Proton Pump Inhibitors (PPIs) are used for similar indications as H2 blockers, they do not possess anti-androgenic properties and are not typically associated with gynecomastia. * **C. Erythromycin:** This is a macrolide antibiotic. While it is a potent CYP450 inhibitor, it does not affect sex steroid receptors or prolactin levels. * **D. Digitalis:** Digoxin *can* cause gynecomastia because its steroid nucleus mimics estrogen; however, it is not typically associated with infertility in the same clinical context as cimetidine. **Clinical Pearls for NEET-PG:** * **Mnemonic for Gynecomastia (DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common cause), **C**imetidine, **O**estrogens [1]. * **Ketoconazole** is another common culprit that inhibits steroid synthesis (17,20-desmolase). * When a patient presents with both gynecomastia and infertility, always look for drugs that interfere with the **Androgen:Estrogen ratio** [1].
Question 1137: A 40-year-old female with a known history of ischemic heart disease (IHD) is diagnosed with hypothyroidism. Which of the following would be the most appropriate line of management for her?
- A. Start levothyroxine at a low dose (Correct Answer)
- B. Do not start levothyroxine
- C. Use levothyroxine
- D. Thyroid extract is a better option
Explanation: ### Explanation **Correct Option: A. Start levothyroxine at a low dose** The management of hypothyroidism in patients with underlying **Ischemic Heart Disease (IHD)** or the elderly requires extreme caution [1]. Thyroid hormones increase the metabolic rate, heart rate, and myocardial contractility, which in turn increases **myocardial oxygen demand**. In a patient with compromised coronary circulation (IHD), a rapid increase in thyroid hormone levels can precipitate angina, myocardial infarction, or fatal arrhythmias [1]. Therefore, the standard clinical practice is to **"start low and go slow."** The typical starting dose for such patients is **12.5 to 25 µg/day**, with gradual increments every 4–6 weeks based on TSH levels and cardiac tolerance. --- ### Why other options are incorrect: * **B. Do not start levothyroxine:** Untreated hypothyroidism can worsen cardiovascular risk factors (like dyslipidemia and hypertension) and lead to myxedema coma. Treatment is necessary but must be cautious. * **C. Use levothyroxine:** While technically correct regarding the drug of choice, this option is incomplete. In the context of IHD, the *method* of administration (low starting dose) is the critical clinical distinction required for the exam. * **D. Thyroid extract is a better option:** Desiccated thyroid extracts are outdated and not recommended. They contain unpredictable ratios of T3 and T4, which can cause dangerous fluctuations in heart rate compared to the stable kinetics of synthetic Levothyroxine (T4). --- ### NEET-PG High-Yield Pearls: * **Standard Adult Dose:** 1.6 µg/kg/day. * **Elderly/IHD Starting Dose:** 12.5–25 µg/day. * **Drug of Choice:** Levothyroxine (T4) is preferred over Liothyronine (T3) due to its longer half-life (7 days) and smoother peak levels [1]. * **Monitoring:** TSH is the gold standard for monitoring. Check 6–8 weeks after dose adjustment [1]. * **Absorption:** Best taken on an empty stomach (30–60 mins before breakfast). Absorption is decreased by iron, calcium, and proton pump inhibitors (PPIs) [1].
Question 1138: Which of the following conditions is associated with pretibial myxedema?
- A. Thyrotoxicosis (Correct Answer)
- B. Hypothyroidism
- C. Hyperparathyroidism
- D. All of the above
Explanation: **Explanation:** **Pretibial Myxedema** (also known as Thyroid Dermopathy) is a classic extrathyroidal manifestation of **Graves' Disease**, the most common cause of **Thyrotoxicosis** [1]. 1. **Why Thyrotoxicosis is Correct:** The underlying mechanism is autoimmune. In Graves' disease, Thyroid Stimulating Immunoglobulins (TSI) bind to TSH receptors located on fibroblasts in the pretibial dermis [1]. This stimulates the overproduction of glycosaminoglycans (primarily hyaluronic acid). The accumulation of these substances leads to non-pitting edema, skin thickening, and an "orange-peel" (peau d'orange) appearance [2]. It is almost exclusively seen in Graves' thyrotoxicosis and is often associated with Graves' ophthalmopathy [1], [3]. 2. **Why Other Options are Incorrect:** * **Hypothyroidism:** While hypothyroidism is associated with "Generalized Myxedema" (due to systemic deposition of mucopolysaccharides), it does **not** cause the localized, infiltrative dermopathy known as pretibial myxedema. * **Hyperparathyroidism:** This condition involves calcium metabolism (stones, bones, abdominal groans, and psychic moans) and has no pathophysiological link to dermal fibroblast stimulation or TSH-receptor antibodies. **High-Yield Clinical Pearls for NEET-PG:** * **The Graves' Triad:** Hyperthyroidism (Goiter), Ophthalmopathy (Exophthalmos), and Dermopathy (Pretibial Myxedema) [1], [3]. * **Location:** Despite the name, it can occasionally occur on the dorsum of the foot or shoulders, though the pretibial area is most common. * **Biopsy Finding:** Increased dermal hyaluronic acid and chondroitin sulfate. * **Management:** Topical glucocorticoids under occlusive dressings are the first-line treatment for symptomatic cases.
Question 1139: Which of the following is contraindicated in diabetics with Congestive Heart Failure?
- A. Empagliflozin
- B. Metformin
- C. Linagliptin
- D. Pioglitazone (Correct Answer)
Explanation: **Explanation:** The correct answer is **Pioglitazone**. **1. Why Pioglitazone is Contraindicated:** Pioglitazone belongs to the **Thiazolidinedione (TZD)** class. Its primary mechanism involves activating the PPAR-gamma receptor, which leads to increased sodium and water reabsorption in the renal collecting ducts. This results in **fluid retention, peripheral edema, and plasma volume expansion** [1]. In patients with pre-existing Congestive Heart Failure (CHF), this volume overload can precipitate acute decompensation. According to clinical guidelines (NYHA Class III or IV), TZDs are strictly contraindicated in symptomatic heart failure. **2. Analysis of Incorrect Options:** * **Empagliflozin (SGLT2 Inhibitor):** Far from being contraindicated, these are now a **gold standard** treatment for patients with both Diabetes and CHF (HFrEF and HFpEF). They promote osmotic diuresis and natriuresis, significantly reducing heart failure hospitalizations. * **Metformin (Biguanide):** Historically avoided in HF due to fears of lactic acidosis; however, current guidelines state it is safe in stable CHF if renal function is preserved (eGFR >30 mL/min) [2]. * **Linagliptin (DPP-4 Inhibitor):** Most DPP-4 inhibitors are safe in CHF [1]. While *Saxagliptin* is associated with increased HF hospitalizations, Linagliptin has shown cardiovascular safety (CARMELINA trial) and is safe to use. **Clinical Pearls for NEET-PG:** * **SGLT2 inhibitors** (Empagliflozin, Dapagliflozin) are the drugs of choice for Diabetics with HF. * **Saxagliptin** is the specific DPP-4 inhibitor to avoid in HF (mnemonic: "S" for Saxagliptin, "S" for Stay away in HF). * **TZDs** (Pioglitazone) also increase the risk of **osteoporotic fractures** and are associated with a potential risk of **bladder cancer**.
Question 1140: Which of the following signs is NOT seen in Cushing's syndrome?
- A. Hypertension
- B. Weight gain
- C. Hirsutism
- D. Hypoglycemia (Correct Answer)
Explanation: Cushing’s syndrome results from chronic exposure to excessive levels of glucocorticoids (cortisol). Cortisol is a "stress hormone" that fundamentally opposes the actions of insulin. **Why Hypoglycemia is the correct answer:** Cortisol is a potent **diabetogenic** hormone. It increases blood glucose levels by stimulating gluconeogenesis in the liver and decreasing peripheral glucose uptake in muscles and adipose tissue. Therefore, Cushing’s syndrome is characterized by **hyperglycemia** (or impaired glucose tolerance), not hypoglycemia. **Analysis of Incorrect Options:** * **Hypertension:** Cortisol causes hypertension through several mechanisms: mineralocorticoid cross-reactivity (retaining sodium and water), increased sensitivity to catecholamines, and activation of the renin-angiotensin system. * **Weight Gain:** This is the most common clinical feature [3]. It typically presents as **centripetal obesity** (trunk, neck, and face) with "moon facies" and a "buffalo hump," due to the redistribution of fat [1]. * **Hirsutism:** In many cases (especially ACTH-dependent Cushing’s or adrenal carcinomas), there is a concomitant increase in adrenal androgens, leading to male-pattern hair growth in women [1], [3]. **NEET-PG High-Yield Pearls:** 1. **Screening Tests:** Overnight Dexamethasone Suppression Test (ONDST) or 24-hour urinary free cortisol [2]. 2. **Hypokalemic Metabolic Alkalosis:** Often seen in ectopic ACTH syndrome due to massive mineralocorticoid effects. 3. **Proximal Myopathy:** Cortisol causes protein catabolism, leading to thin extremities and difficulty climbing stairs [1]. 4. **Purple Striae:** Broad (>1 cm), reddish-purple streaks on the abdomen are highly specific for Cushing’s.
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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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