Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 361: Gynaecomastia may be seen in all of the following conditions except?

A. Klinefelter syndrome
B. Cirrhosis of liver
C. Cryptorchidism (Correct Answer)
D. Sex cord tumour of Sertoli cells

Explanation: Gynecomastia is the benign proliferation of glandular breast tissue in males, caused by an imbalance between estrogen and androgen action [1]. **Why Cryptorchidism is the correct answer:** Cryptorchidism (undescended testes) is a developmental defect where the testes fail to descend into the scrotum. While it is a major risk factor for **testicular germ cell tumors** and **infertility**, it does not inherently cause an endocrine imbalance (excess estrogen or low testosterone) sufficient to produce gynecomastia unless it is part of a broader syndrome [1]. **Analysis of other options:** * **Klinefelter Syndrome (47, XXY):** This is the most common congenital cause of primary hypogonadism [2]. Elevated gonadotropins (LH/FSH) lead to increased aromatization of testosterone to estrogen, making gynecomastia a hallmark clinical feature (seen in ~80% of cases) [1]. * **Cirrhosis of Liver:** The liver is responsible for metabolizing estrogen and producing Sex Hormone Binding Globulin (SHBG). In cirrhosis, decreased estrogen clearance and increased peripheral conversion of androgens to estrogens lead to gynecomastia. * **Sertoli Cell Tumors:** These are sex cord-stromal tumors that can actively secrete estrogens or increase aromatase activity, directly leading to feminizing symptoms including gynecomastia [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs causing Gynecomastia (Mnemonic: DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common), **C**imetidine, **O**estrogens/Ketoconazole. * **Physiological Gynecomastia:** Occurs in three peaks—Neonatal, Pubertal, and Senile (old age) [1]. * **Spironolactone** causes gynecomastia by displacing androgens from their receptors and increasing peripheral conversion to estrogen. * **Reassurance** is the management of choice for pubertal gynecomastia as it usually resolves spontaneously within 1–2 years [1].

Question 362: What is the most common cause of death in acromegaly?

A. Obstructive Sleep Apnea
B. Impaired glucose Tolerance
C. Colonic malignancy
D. Cardiovascular causes (Correct Answer)

Explanation: Acromegaly is characterized by the chronic hypersecretion of Growth Hormone (GH), which stimulates the liver to produce Insulin-like Growth Factor-1 (IGF-1) [2]. While the disease presents with multisystem involvement, **Cardiovascular disease** is the leading cause of mortality, accounting for approximately 60% of deaths. **1. Why Cardiovascular causes are correct:** Chronic elevation of GH and IGF-1 leads to "Acromegalic Cardiomyopathy." This involves biventricular concentric hypertrophy, interstitial fibrosis, and myofibrillar derangement. These structural changes result in congestive heart failure, arrhythmias, and valvular heart disease. Additionally, associated hypertension and dyslipidemia further accelerate atherosclerotic cardiovascular disease. **2. Analysis of Incorrect Options:** * **Obstructive Sleep Apnea (OSA):** Extremely common (up to 70% of patients) due to soft tissue macroglossia and pharyngeal narrowing. While it increases morbidity and CV risk, it is rarely the direct primary cause of death. * **Impaired Glucose Tolerance:** GH is a counter-regulatory hormone that causes insulin resistance. While "Pituitary Diabetes" occurs in 25% of patients, it is a metabolic complication rather than a primary cause of mortality [1]. * **Colonic Malignancy:** There is an increased risk of colonic polyps and adenocarcinoma in acromegaly [1]. While it is a significant cause of late morbidity, it ranks lower than cardiovascular and respiratory causes in terms of mortality statistics. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum IGF-1 levels (stable throughout the day) [2]. * **Gold Standard Diagnostic Test:** Oral Glucose Tolerance Test (OGTT) showing failure to suppress GH <1 ng/mL [1]. * **Most common cause of death:** Cardiovascular (1st), Respiratory (2nd), Malignancy (3rd). * **Treatment of choice:** Transsphenoidal surgery (except in prolactin-secreting tumors where medical management is first) [1].

Question 363: A 65-year-old woman with a history of type 2 diabetes mellitus for the last 8 years dies in a hospital. She had no other significant medical history. Which of the following is the most likely cause of her death?

A. Diabetic ketoacidosis
B. Myocardial infarction (Correct Answer)
C. Renal failure
D. Stroke

Explanation: In patients with Type 2 Diabetes Mellitus (T2DM), **cardiovascular disease (CVD)** is the leading cause of morbidity and mortality [2]. Approximately 65–70% of deaths in diabetic patients are attributed to macrovascular complications, with **Myocardial Infarction** being the single most common cause [2], [3]. Diabetes is considered a **"Coronary Artery Disease (CAD) equivalent,"** meaning a diabetic patient without a prior MI has the same cardiovascular risk as a non-diabetic patient who has already suffered one. **2. Why the other options are incorrect:** * **Diabetic Ketoacidosis (DKA):** This is an acute metabolic complication more common in Type 1 DM. While it can occur in T2DM (especially during severe stress), it is rarely the primary cause of death in an elderly patient with long-standing T2DM compared to vascular events. * **Renal Failure:** While diabetic nephropathy is the leading cause of End-Stage Renal Disease (ESRD) globally, most diabetic patients with chronic kidney disease actually die from cardiovascular events *before* they reach the stage of terminal renal failure [2]. * **Stroke:** Cerebrovascular accidents are a significant macrovascular complication of DM, but statistically, they occur less frequently as a cause of death than ischemic heart disease [2]. **3. Clinical Pearls for NEET-PG:** * **Silent MI:** Diabetic patients often present with "painless" or silent MI due to **autonomic neuropathy**, leading to delayed diagnosis and higher mortality [1]. * **Leading cause of death in T1DM:** In young patients (<30 years), it is often acute complications (DKA) or renal disease; however, as they age, CVD becomes the leading cause here as well. * **The "Legacy Effect":** Early intensive glycemic control reduces long-term macrovascular risks (UKPDS study).

Question 364: All of the following are associated with pituitary apoplexy except?

A. Hyperthyroidism (Correct Answer)
B. Diabetes mellitus
C. Sickle cell anemia
D. Hypertension

Explanation: **Explanation:** Pituitary apoplexy is a clinical syndrome caused by sudden hemorrhage or infarction of the pituitary gland, usually occurring within a pre-existing pituitary adenoma [3]. **Why Hyperthyroidism is the correct answer:** Hyperthyroidism is **not** a recognized risk factor for pituitary apoplexy. In fact, the relationship is often the opposite: pituitary apoplexy leads to sudden secondary **hypothyroidism** due to the destruction of thyrotrophs and the loss of TSH production [2]. **Why the other options are incorrect (Risk Factors):** * **Diabetes Mellitus:** Chronic hyperglycemia causes microvascular changes and endothelial dysfunction, which predisposes the pituitary vessels to rupture or infarction [4]. * **Sickle Cell Anemia:** Vaso-occlusive crises can lead to infarction of the pituitary gland, similar to how it affects other end-organs. * **Hypertension:** This is one of the most common predisposing factors. Sudden fluctuations in blood pressure can lead to hemorrhagic transformation within a fragile pituitary adenoma. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** Sudden onset "thunderclap" headache, visual field defects (bitemporal hemianopia), ophthalmoplegia (CN III, IV, VI involvement), and altered mental status [3]. * **Most Common Risk Factor:** Underlying pituitary macroadenoma [1]. * **Precipitating Factors:** Pregnancy (Sheehan’s syndrome is a form of postpartum apoplexy), major surgery (especially CABG), head trauma, and anticoagulation therapy [1]. * **Immediate Management:** The most life-threatening complication is **acute secondary adrenal insufficiency**. Immediate administration of high-dose intravenous corticosteroids (Hydrocortisone) is the priority before surgical decompression [2]. * **Imaging of Choice:** MRI of the brain/sella is more sensitive than CT for detecting hemorrhage in the acute phase [3].

Question 365: Which of the following statements about Diabetes Insipidus is true?

A. Urine osmolality should be > 300 mosm/L
B. Plasma osmolality should be < 280 mmol/L
C. Water deprivation test is required (Correct Answer)
D. Plasma osmolality should be > 300 mosm/L prior to water deprivation test

Explanation: **Explanation:** Diabetes Insipidus (DI) is characterized by the inability to concentrate urine due to either a deficiency of Antidiuretic Hormone (ADH) (Central DI) [1] or resistance to its action (Nephrogenic DI). [2] **Why Option C is Correct:** The **Water Deprivation Test (Miller-Moses Test)** is the gold-standard diagnostic tool to differentiate between Central DI, Nephrogenic DI, and Primary Polydipsia. [1] By withholding fluids, the body is forced to concentrate urine. If the urine remains dilute despite rising plasma osmolality, DI is confirmed. Subsequent administration of exogenous ADH (Desmopressin) then differentiates Central from Nephrogenic types. **Why the Other Options are Incorrect:** * **Option A:** In DI, urine is characteristically dilute. Urine osmolality is typically **< 300 mOsm/kg** (often < 200 mOsm/kg). A value > 300 suggests the kidneys are still capable of concentrating urine. * **Option B:** Patients with DI lose free water, leading to hemoconcentration. Therefore, plasma osmolality is usually **elevated (> 295 mOsm/kg)**, not low. [1] Low plasma osmolality (< 280) is more suggestive of Primary Polydipsia or SIADH. [1] * **Option D:** The water deprivation test is initiated when the patient is stable. If the baseline plasma osmolality is already **> 295–300 mOsm/kg** and the urine is still dilute, the diagnosis of DI is already established, and the deprivation phase is unnecessary (and potentially dangerous); one should proceed directly to the Desmopressin challenge. **High-Yield Clinical Pearls for NEET-PG:** * **Central DI:** Responds to Desmopressin (Urine osmolality increases by >50%). [1] * **Nephrogenic DI:** No response to Desmopressin (Urine osmolality increases <10%). * **Drug of Choice:** Desmopressin (Central DI); Thiazides/Amiloride (Nephrogenic DI). [1] * **Most common cause of Nephrogenic DI in adults:** Lithium therapy.

Question 366: Which of the following is NOT a cause of thyrotoxicosis?

A. Graves' disease
B. Struma ovarii
C. Toxic adenoma
D. None of the above (Correct Answer)

Explanation: ### Explanation The correct answer is **D (None of the above)** because all three listed conditions (Graves' disease, Struma ovarii, and Toxic adenoma) are established causes of **thyrotoxicosis**. Thyrotoxicosis is a clinical state resulting from inappropriate high levels of circulating thyroid hormones ($T_3$ and/or $T_4$), regardless of the source. #### Breakdown of Options: * **Graves' Disease (Option A):** This is the most common cause of hyperthyroidism [1], [2]. It is an autoimmune disorder where TSH-receptor antibodies (TRAb) stimulate the thyroid gland to overproduce thyroid hormones [1]. * **Struma Ovarii (Option B):** This is a rare form of **ectopic thyrotoxicosis**. It occurs when a specialized ovarian teratoma contains functional thyroid tissue that secretes thyroid hormones independently of the pituitary-thyroid axis. * **Toxic Adenoma (Option C):** Also known as Plummer’s disease when multiple (Toxic Multinodular Goiter), this involves a solitary functioning thyroid nodule that produces excess thyroid hormone autonomously, typically due to somatic mutations in the TSH receptor. #### NEET-PG High-Yield Pearls: 1. **Hyperthyroidism vs. Thyrotoxicosis:** Hyperthyroidism is a subset of thyrotoxicosis caused specifically by *increased synthesis* by the thyroid gland [2]. Struma ovarii and Factitious thyrotoxicosis are examples of thyrotoxicosis *without* hyperthyroidism [3]. 2. **Radioactive Iodine Uptake (RAIU):** * **High Uptake:** Graves', Toxic Adenoma, TMG. * **Low/Absent Uptake:** Thyroiditis, Struma ovarii (uptake will be in the pelvis), and Factitious intake [3]. 3. **Jod-Basedow Phenomenon:** Iodine-induced thyrotoxicosis (often after contrast media or Amiodarone). 4. **Amiodarone:** Can cause both hypothyroidism (Wolff-Chaikoff effect) and thyrotoxicosis (Type 1 or Type 2).

Question 367: What clinical features are characteristic of acromegaly?

A. Large tongue (Correct Answer)
B. Hypoglycemia
C. Crowding of teeth
D. Micrognathia

Explanation: **Explanation:** Acromegaly is caused by the excessive secretion of **Growth Hormone (GH)** after the closure of epiphyseal plates, usually due to a pituitary adenoma [3]. GH stimulates the liver to produce **Insulin-like Growth Factor-1 (IGF-1)**, which promotes the overgrowth of bone and soft tissues [1]. **Why Option A is Correct:** **Macroglossia (Large tongue)** is a classic hallmark of acromegaly. It occurs due to the generalized hypertrophy of soft tissues [3]. This can lead to functional issues such as obstructive sleep apnea (OSA) and deepening of the voice. **Analysis of Incorrect Options:** * **B. Hypoglycemia:** Incorrect. GH is a counter-regulatory hormone that antagonizes insulin action. Therefore, acromegaly typically causes **secondary diabetes mellitus** or impaired glucose tolerance (hyperglycemia), not hypoglycemia. * **C. Crowding of teeth:** Incorrect. Due to the overgrowth of the mandible, patients develop **widely spaced teeth** (diastema) rather than crowding. * **D. Micrognathia:** Incorrect. Acromegaly causes **Prognathism** (protrusion of the lower jaw) due to mandibular overgrowth, leading to a prominent chin and malocclusion. Micrognathia (a small jaw) is the opposite. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum IGF-1 levels (stable throughout the day) [2]. * **Gold Standard Diagnostic Test:** Oral Glucose Tolerance Test (OGTT)—failure to suppress GH levels below 1 ng/mL after 75g of glucose [2]. * **Most Common Cause of Death:** Cardiovascular disease (specifically dilated cardiomyopathy/congestive heart failure). * **Radiological Sign:** "Heel pad thickness" >25 mm on X-ray. * **Visual Field Defect:** Bitemporal hemianopia (due to optic chiasm compression by the pituitary tumor).

Question 368: Which of the following is/are a symptom of Pheochromocytoma?

A. Palpitation
B. Headache
C. Diaphoresis
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Pheochromocytoma** is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla (or extra-adrenal paraganglia) [1]. The clinical presentation is primarily driven by the episodic or continuous release of epinephrine and norepinephrine into the circulation. **Why "All of the above" is correct:** The classic presentation of Pheochromocytoma is characterized by the **"Classic Triad"** of symptoms, which occurs in paroxysms (spells): 1. **Headache (Option B):** The most common symptom (up to 90% of cases), usually sudden and severe due to abrupt surges in blood pressure. 2. **Diaphoresis (Option C):** Excessive sweating occurs as the body attempts to dissipate heat generated by a catecholamine-induced hypermetabolic state. 3. **Palpitations (Option A):** Resulting from the chronotropic and inotropic effects of catecholamines on the heart, often accompanied by tachycardia. When these three symptoms occur alongside **Hypertension** (the most common clinical sign), the specificity for Pheochromocytoma exceeds 90% [2]. **Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% are bilateral, 10% are extra-adrenal (paragangliomas), 10% are malignant, and 10% are familial. * **Diagnosis:** The best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. * **Localization:** CT or MRI of the abdomen is the initial imaging [2]; **123I-MIBG scan** is used if CT/MRI is negative or to detect metastatic disease [2]. * **Management:** Pre-operative stabilization requires **Alpha-blockade first** (e.g., Phenoxybenzamine) followed by Beta-blockade to avoid a hypertensive crisis (unopposed alpha-stimulation) [2].

Question 369: Which of the following is not a clinical feature of hypothyroidism?

A. Edema
B. Cold skin
C. Diastolic hypertension
D. Atrial fibrillation (Correct Answer)

Explanation: **Explanation:** In hypothyroidism, the metabolic rate and sympathetic activity are significantly decreased. **Atrial Fibrillation (AF)** is a classic feature of **hyperthyroidism** (thyrotoxicosis) [1], where excess thyroid hormone increases the expression of beta-adrenergic receptors in the heart, leading to tachycardia and arrhythmias. In contrast, hypothyroidism is typically associated with **sinus bradycardia** and low-voltage complexes on ECG. **Analysis of Options:** * **Edema:** Hypothyroidism leads to the accumulation of glycosaminoglycans (like hyaluronic acid) in the interstitial space, which traps water. This results in non-pitting edema, classically termed **myxedema**. * **Cold skin:** Decreased thermogenesis and peripheral vasoconstriction (to conserve heat) result in skin that is characteristically cold, dry, and rough. * **Diastolic hypertension:** While hyperthyroidism causes systolic hypertension (due to increased stroke volume), hypothyroidism often causes **diastolic hypertension** due to increased systemic vascular resistance and stiffness of the arterial wall. **Clinical Pearls for NEET-PG:** * **Wolff-Chaikoff Effect:** Autoregulatory inhibition of thyroid hormone synthesis after ingestion of a large amount of iodine. * **Most common cause:** Globally, iodine deficiency; in iodine-sufficient areas, **Hashimoto’s Thyroiditis** (associated with anti-TPO antibodies). * **Hoffman’s Syndrome:** A rare form of hypothyroid myopathy characterized by muscle stiffness and pseudohypertrophy. * **Hungry Bone Syndrome** is a complication of parathyroid surgery, but **Delayed relaxation of deep tendon reflexes** (Woltman sign) is a pathognomonic physical finding in hypothyroidism.

Question 370: Cardiac manifestations of Grave's disease would include all of the following except?

A. Wide pulse pressure
B. Atrial fibrillation
C. Pleuropericardial scratch
D. Aortic insufficiency (Correct Answer)

Explanation: Explanation: Graves' disease (Hyperthyroidism) induces a hyperdynamic circulatory state due to the direct effects of thyroid hormones on the myocardium and the upregulation of beta-adrenergic receptors. Why Aortic Insufficiency is the correct answer: Aortic insufficiency (AI) is a structural valvular abnormality. While Graves' disease causes functional murmurs due to increased flow [3], it does not cause structural damage to the aortic valve leaflets. Therefore, AI is not a manifestation of thyrotoxicosis. Analysis of other options: * Wide pulse pressure: Thyroid hormones decrease systemic vascular resistance (vasodilation) and increase systolic blood pressure (increased stroke volume), leading to a characteristic wide pulse pressure [4]. * Atrial fibrillation: This is the most common rhythm disturbance in hyperthyroidism, occurring in approximately 10–15% of patients, especially in the elderly [1]. * Pleuropericardial scratch (Means-Lerman scratch): This is a high-yield clinical sign. It is a systolic scratchy sound heard over the left second intercostal space during expiration. It is thought to result from the rubbing of the hyperdynamic heart against the pleura, not from pericarditis. NEET-PG High-Yield Pearls: 1. Most common arrhythmia: Sinus tachycardia [1]; however, Atrial Fibrillation is the most significant supraventricular tachyarrhythmia. 2. Means-Lerman Scratch: A classic physical sign of hyperthyroidism mimicking a friction rub. 3. Heart Failure: Graves' can lead to "High-Output Heart Failure." 4. Treatment of choice for cardiac symptoms: Propranolol (Beta-blockers) to control adrenergic overactivity [2].

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

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Pituitary Disorders

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Calcium and Bone Metabolism

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Reproductive Endocrinology

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Lipid Disorders

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Endocrine Hypertension

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Multiple Endocrine Neoplasia

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Obesity and Metabolic Syndrome

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Neuroendocrine Tumors

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Endocrine Emergencies

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