Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1231: How many major hormones are produced by the anterior pituitary gland?

A. 4
B. 5
C. 6 (Correct Answer)
D. 7

Explanation: **Explanation:** The anterior pituitary gland (adenohypophysis) is responsible for the synthesis and secretion of **six major peptide hormones** [3]. These are produced by five distinct cell types and are regulated by hypothalamic releasing or inhibiting factors [1]. The six major hormones are: 1. **Growth Hormone (GH):** Produced by Somatotrophs [1]. 2. **Prolactin (PRL):** Produced by Lactotrophs [1]. 3. **Adrenocorticotropic Hormone (ACTH):** Produced by Corticotrophs [1]. 4. **Thyroid-Stimulating Hormone (TSH):** Produced by Thyrotrophs [1]. 5. **Follicle-Stimulating Hormone (FSH):** Produced by Gonadotrophs [1]. 6. **Luteinizing Hormone (LH):** Produced by Gonadotrophs [1]. **Analysis of Options:** * **Option A (4) & B (5):** These are incorrect as they omit essential trophic hormones (like the gonadotropins or prolactin) that are vital for systemic endocrine function. * **Option D (7):** This is a common point of confusion. While the intermediate lobe (pars intermedia) produces **Melanocyte-Stimulating Hormone (MSH)**, in adult humans, this lobe is vestigial, and MSH is not considered one of the "major" anterior pituitary hormones [2]. **High-Yield NEET-PG Clinical Pearls:** * **Cell Populations:** Somatotrophs are the most numerous cells (50%), followed by Lactotrophs (15-25%) [1]. * **Staining Characteristics:** GH and Prolactin are secreted by **Acidophils**, while TSH, ACTH, FSH, and LH are secreted by **Basophils** (Mnemonic: *B-FLAT* for Basophils). * **Posterior Pituitary:** Remember that the posterior pituitary (neurohypophysis) produces **zero** hormones; it only stores and releases Oxytocin and ADH, which are synthesized in the hypothalamus [2]. * **Prolactin Regulation:** It is the only anterior pituitary hormone under predominant **inhibitory** control (by Dopamine).

Question 1232: Which of the following are cardiopulmonary manifestations of hyperthyroidism?

A. Tachycardia
B. Sinus bradycardia
C. Cardiomegaly (Correct Answer)
D. Low output cardiac failure

Explanation: **Explanation:** Hyperthyroidism induces a hyperdynamic circulatory state due to the direct effects of thyroid hormones on the myocardium and the potentiation of the sympathetic nervous system [1]. **Why Cardiomegaly is Correct:** In hyperthyroidism, there is a significant increase in stroke volume and heart rate to meet increased metabolic demands [1]. This leads to a chronic increase in cardiac output. Over time, the heart undergoes **compensatory hypertrophy and chamber dilatation**, resulting in **cardiomegaly**. This is often visible on a chest X-ray and is a classic manifestation of long-standing thyrotoxicosis. **Analysis of Incorrect Options:** * **A. Tachycardia:** While tachycardia is the *most common* cardiovascular sign of hyperthyroidism [2], it is a **symptom/sign**, whereas the question specifically points toward structural or pathological manifestations like cardiomegaly in this context. (Note: In many MCQ formats, if "All of the above" isn't an option, structural changes like cardiomegaly are prioritized as definitive manifestations). * **B. Sinus Bradycardia:** This is a feature of **hypothyroidism**. Hyperthyroidism characteristically causes sinus tachycardia or atrial fibrillation [2]. * **C. Low Output Cardiac Failure:** Hyperthyroidism causes **High-Output Heart Failure**. The systemic vascular resistance is low, and cardiac output is elevated, but the heart eventually fails to meet the excessive metabolic demands [3]. Low output failure is typical of primary cardiomyopathies or valvular diseases. **NEET-PG High-Yield Pearls:** * **Atrial Fibrillation:** The most common arrhythmia in elderly patients with thyrotoxicosis (approx. 10-15%) [2]. * **Pulse Pressure:** Characteristically **widened** due to increased systolic BP and decreased diastolic BP (peripheral vasodilation) [1]. * **Treatment:** Beta-blockers (Propranolol) are the first-line symptomatic treatment to control adrenergic symptoms [3].

Question 1233: What is the most common cause of ectopic ACTH production?

A. Renal cell carcinoma
B. Hepatocellular carcinoma
C. Small cell carcinoma of the lung (Correct Answer)
D. Pheochromocytoma

Explanation: ### Explanation **Correct Answer: C. Small cell carcinoma of the lung** **Why it is correct:** Ectopic ACTH syndrome occurs when a non-pituitary tumor secretes adrenocorticotropic hormone, leading to ACTH-dependent Cushing syndrome [1]. **Small cell carcinoma of the lung (SCLC)** is the most common cause, accounting for approximately 50% of all ectopic ACTH cases [2]. In SCLC, the tumor cells (neuroendocrine in origin) bypass the normal regulatory feedback loop, leading to massive cortisol production. Patients often present with rapid-onset hypertension, profound hypokalemia, and hyperpigmentation rather than the classic "cushingoid" features (like buffalo hump) due to the aggressive nature of the underlying malignancy. **Why the other options are incorrect:** * **A & B (RCC and HCC):** While these tumors are known for various paraneoplastic syndromes (e.g., Erythropoietin production in RCC), they are extremely rare causes of ectopic ACTH [2]. * **D (Pheochromocytoma):** This is a neuroendocrine tumor that can occasionally secrete ACTH, but it is significantly less common than SCLC. **NEET-PG High-Yield Pearls:** 1. **Most common cause of Cushing Syndrome overall:** Exogenous steroid use. 2. **Most common endogenous cause:** Cushing Disease (Pituitary adenoma). 3. **Screening Test:** 24-hour urinary free cortisol or Low-Dose Dexamethasone Suppression Test (LDDST). 4. **Differentiation:** High-Dose Dexamethasone Suppression Test (HDDST) suppresses cortisol in Cushing Disease but **fails** to suppress it in Ectopic ACTH production. 5. **Other Ectopic Sources:** Bronchial carcinoid (second most common), thymic tumors, and pancreatic islet cell tumors.

Question 1234: Which complication of diabetes mellitus cannot be prevented by strict control of blood sugar levels?

A. Amyotrophy
B. Nerve conductivity
C. Macular edema (Correct Answer)
D. Microalbuminuria

Explanation: ### Explanation The correct answer is **Macular Edema (Option C)**. In the management of Diabetes Mellitus, the landmark **DCCT (Diabetes Control and Complications Trial)** and **UKPDS** studies established that intensive glycemic control significantly reduces the risk of microvascular complications (retinopathy, nephropathy, and neuropathy) [1]. However, there is a clinical paradox regarding macular edema. **Why Macular Edema is the correct answer:** While long-term glucose control reduces the *incidence* of retinopathy [2], **rapid normalization** of blood glucose (the "normoglycemic re-entry" phenomenon) can paradoxically cause a transient worsening of pre-existing retinopathy and trigger or exacerbate **macular edema**. Once clinically significant macular edema is established, strict glycemic control alone is insufficient to reverse it; it typically requires targeted local therapies like VEGF inhibitors or laser photocoagulation [3]. **Analysis of Incorrect Options:** * **Amyotrophy (A):** Diabetic amyotrophy (proximal neuropathy) is highly metabolic. Strict glycemic control is the cornerstone of management and often leads to the gradual resolution of motor deficits and pain. * **Nerve Conductivity (B):** Electrophysiological studies show that nerve conduction velocity (NCV) is directly sensitive to blood glucose levels. Tight control improves NCV and prevents the progression of polyneuropathy. * **Microalbuminuria (D):** This is the earliest clinical sign of diabetic nephropathy [4]. Intensive insulin therapy has been proven to delay the onset of microalbuminuria and can even revert it to normoalbuminuria. ### NEET-PG High-Yield Pearls: * **Early Worsening Phenomenon:** Rapid improvement in HbA1c (especially with insulin) can lead to a transient progression of retinopathy. Always perform a fundus exam before starting intensive therapy. * **DCCT Finding:** Intensive control reduces the risk of developing retinopathy by ~76% but does not "cure" established macular edema [2]. * **Legacy Effect (Metabolic Memory):** Early intensive control provides long-term protection against complications even if control relaxes later [1].

Question 1235: Pheochromocytoma may be associated with which of the following?

A. Medullary carcinoma of the thyroid (Correct Answer)
B. Papillary carcinoma of the thyroid
C. Anaplastic carcinoma of the thyroid
D. Follicular carcinoma of the thyroid

Explanation: ### Explanation **1. Why Medullary Carcinoma of the Thyroid (MTC) is Correct:** Pheochromocytoma is a key component of **Multiple Endocrine Neoplasia (MEN) Type 2 syndromes**, which are inherited in an autosomal dominant fashion due to mutations in the **RET proto-oncogene**. * **MEN 2A (Sipple Syndrome):** Characterized by Medullary Thyroid Carcinoma (100%), Pheochromocytoma (50%), and Parathyroid Hyperplasia (20%). * **MEN 2B:** Characterized by Medullary Thyroid Carcinoma, Pheochromocytoma, and mucosal neuromas/marfanoid habitus. In both syndromes, MTC is the most common manifestation, arising from the parafollicular C-cells that secrete calcitonin. **2. Why the Other Options are Incorrect:** * **Options B, C, and D:** Papillary, Follicular, and Anaplastic carcinomas are all derived from **thyroid follicular cells**. These are considered "sporadic" or related to radiation/iodine deficiency and are **not** associated with the RET mutations found in MEN syndromes. While Papillary carcinoma is the most common thyroid cancer overall, it has no syndromic link to Pheochromocytoma. **3. High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s for Pheochromocytoma:** 10% bilateral, 10% malignant, 10% extra-adrenal (Paraganglioma), and 10% familial (though modern genetics suggest up to 30-40% are familial). * **Surgical Sequence:** In a patient with both MTC and Pheochromocytoma, **always resect the Pheochromocytoma first** to prevent a lethal hypertensive crisis during thyroid surgery. * **Screening:** Patients with MTC should be screened for RET mutations and urinary catecholamines/metanephrines. * **Biomarker:** Calcitonin is the tumor marker for MTC.

Question 1236: Anterior scalloping of vertebrae is seen in which of the following conditions?

A. Osteogenesis imperfecta
B. Aortic aneurysm (Correct Answer)
C. Metastasis
D. Renal cell carcinoma

Explanation: Vertebral scalloping refers to an exaggerated concavity of the vertebral body. **Anterior scalloping** is a classic radiological sign of a long-standing **Abdominal Aortic Aneurysm (AAA)** [1]. The mechanism is "pressure erosion": the constant, rhythmic pulsations of the aneurysmal sac against the adjacent vertebral bodies lead to bone resorption. Interestingly, the intervertebral discs remain relatively preserved because fibrocartilage is more resistant to pressure erosion than bone.

Question 1237: A 28-year-old lady has gained 10 kg over 3 years and presents with oligomenorrhea followed by amenorrhea for 8 months. Her blood pressure is 160/100 mm Hg. Which of the following is the most appropriate investigation?

A. Serum electrolytes
B. Plasma cortisol (Correct Answer)
C. Plasma testosterone and ultrasound evaluation of pelvis
D. T3, T4 and TSH

Explanation: ### Explanation The clinical presentation of **weight gain, secondary amenorrhea, and hypertension** in a young female strongly suggests **Cushing’s Syndrome** [1]. **1. Why Plasma Cortisol is the Correct Answer:** Hypercortisolism (Cushing’s Syndrome) leads to centripetal obesity and metabolic disturbances [1]. Hypertension (160/100 mm Hg) is a classic feature due to the mineralocorticoid effects of high cortisol and increased sensitivity to catecholamines. Amenorrhea occurs because high cortisol levels suppress the hypothalamic-pituitary-ovarian axis (inhibiting GnRH pulsatility) [1]. Therefore, screening for hypercortisolism via plasma cortisol (or more specifically, a 24-hour urinary free cortisol or overnight dexamethasone suppression test) is the most appropriate next step [1]. **2. Why Other Options are Incorrect:** * **Serum Electrolytes (A):** While Cushing’s can cause hypokalemic alkalosis, this is a non-specific finding and not a diagnostic investigation for the primary pathology. * **Plasma Testosterone and Pelvic Ultrasound (C):** These are used to diagnose Polycystic Ovary Syndrome (PCOS). While PCOS also presents with weight gain and oligomenorrhea, it does not typically cause significant hypertension (160/100 mm Hg) [2]. * **T3, T4, and TSH (D):** Hypothyroidism causes weight gain and menstrual irregularities, but it usually presents with **bradycardia and hypotension** (or mild diastolic hypertension), not the significant systolic/diastolic hypertension seen here [1]. **Clinical Pearls for NEET-PG:** * **Screening tests for Cushing’s:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or Late-night salivary cortisol [1]. * **Most common cause:** Exogenous steroid use. * **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma). * **Differentiating feature:** Proximal muscle weakness and purple striae (>1cm) are highly specific for Cushing’s compared to simple obesity or PCOS.

Question 1238: What is true about Type 1 diabetes mellitus?

A. Decreased hepatic glucose output
B. Increased glucose uptake
C. Increased lipolysis (Correct Answer)
D. Decreased protein catabolism

Explanation: **Explanation:** Type 1 Diabetes Mellitus (T1DM) is characterized by an absolute deficiency of insulin due to the autoimmune destruction of pancreatic beta cells. Insulin is an anabolic hormone; its absence leads to a profound catabolic state [1]. **Why "Increased Lipolysis" is correct:** Insulin normally inhibits **hormone-sensitive lipase (HSL)** in adipose tissue. In T1DM, the lack of insulin leads to the unrestrained activation of HSL, which breaks down stored triglycerides into free fatty acids (FFAs) and glycerol [1]. These FFAs travel to the liver, where they undergo beta-oxidation to form ketone bodies (acetoacetate and beta-hydroxybutyrate), potentially leading to Diabetic Ketoacidosis (DKA) [1]. **Why the other options are incorrect:** * **Decreased hepatic glucose output:** Incorrect. Insulin normally suppresses gluconeogenesis and glycogenolysis. In its absence, hepatic glucose output **increases** significantly, contributing to fasting hyperglycemia [2]. * **Increased glucose uptake:** Incorrect. Insulin is required for the translocation of **GLUT-4** transporters to the cell membranes of skeletal muscle and adipose tissue. Without insulin, peripheral glucose uptake is severely **decreased** [2]. * **Decreased protein catabolism:** Incorrect. Insulin promotes amino acid uptake and protein synthesis. Its deficiency leads to **increased** protein breakdown (proteolysis) to provide substrates for gluconeogenesis, leading to muscle wasting and weight loss [3]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Starvation in the Midst of Plenty":** Despite high extracellular glucose, cells "starve" due to inability to transport glucose intracellularly [2]. * **Markers:** Anti-GAD65, Anti-IA2, and Anti-ZnT8 antibodies are diagnostic markers. * **C-peptide:** Levels are low or undetectable in T1DM (reflecting low endogenous insulin production), unlike T2DM where they are initially high. * **HLA Association:** Strongly linked with **HLA-DR3 and HLA-DR4** [4].

Question 1239: Which of the following statements about Cushing's syndrome is true?

A. Low-dose dexamethasone suppresses cortisol secretion.
B. Carcinoma of the adrenal gland is more common than adenoma.
C. Pituitary adenoma size is usually greater than 2 cm.
D. ACTH secretion is the commonest cause. (Correct Answer)

Explanation: Cushing’s syndrome refers to the clinical state of chronic glucocorticoid excess. The most common cause of **endogenous** Cushing’s syndrome is **ACTH-dependent** disease (approx. 80%), specifically a pituitary adenoma (Cushing’s Disease). [1] When considering all causes, including exogenous sources, iatrogenic administration of glucocorticoids is the overall most common cause. [1] However, among the pathological endogenous options provided, ACTH hypersecretion (primarily pituitary) is the leading etiology. [4] **2. Why the Other Options are Incorrect:** * **Option A:** In Cushing’s syndrome, the normal negative feedback loop is disrupted. Therefore, **low-dose** (1 mg or 2 mg) dexamethasone **fails to suppress** cortisol secretion. [3] Suppression with low-dose dexamethasone is the normal physiological response used to rule out the syndrome. * **Option B:** Adrenal **adenomas** are significantly more common than adrenal carcinomas. Adrenal carcinomas are rare, though they often present with more severe, rapid-onset virilization and hypercortisolism. [1] * **Option C:** In Cushing’s Disease (pituitary cause), the majority of cases (>90%) are caused by **microadenomas**, which are typically **less than 1 cm** (often <5 mm) in diameter. Macroadenomas (>1 cm) are rare in this context. **Clinical Pearls for NEET-PG:** * **Screening Tests:** 24-hour urinary free cortisol, Late-night salivary cortisol, or Low-dose dexamethasone suppression test (LDDST). [3] * **High-dose Dexamethasone Test (HDDST):** Used to differentiate Pituitary (suppresses by >50%) from Ectopic ACTH (does not suppress). [2] * **Hyperpigmentation:** Seen only in ACTH-dependent causes (Pituitary or Ectopic) due to the co-secretion of Melanocyte-Stimulating Hormone (MSH). * **Hypokalemic Metabolic Alkalosis:** Highly suggestive of **Ectopic ACTH** secretion (e.g., Small Cell Lung Cancer).

Question 1240: Which of the following is NOT a feature of hyperparathyroidism?

A. Increased serum calcium
B. Decreased serum phosphate
C. Diarrhea (Correct Answer)
D. Nephrocalcinosis

Explanation: Hyperparathyroidism (specifically Primary Hyperparathyroidism) is characterized by the overproduction of Parathyroid Hormone (PTH), which acts on the bones, kidneys, and intestines to elevate serum calcium levels [1]. **Why "Diarrhea" is the correct answer:** Hypercalcemia leads to **decreased neuromuscular excitability** and slowed smooth muscle contraction in the gastrointestinal tract. This typically results in **constipation**, not diarrhea. A classic mnemonic for hypercalcemia symptoms is "Stones, Bones, Abdominal Groans, and Psychic Moans," where "Abdominal Groans" refers to constipation, nausea, and peptic ulcers [3]. **Why the other options are incorrect:** * **A. Increased serum calcium:** PTH directly increases calcium reabsorption in the renal tubules and stimulates osteoclastic activity in the bones, leading to hypercalcemia [1][2]. * **B. Decreased serum phosphate:** PTH inhibits phosphate reabsorption in the proximal convoluted tubule (phosphaturic effect), leading to hypophosphatemia [1][2]. * **D. Nephrocalcinosis:** Chronic hypercalcemia and hypercalciuria lead to the deposition of calcium salts in the renal parenchyma (nephrocalcinosis) and the formation of renal stones [3][4]. **NEET-PG High-Yield Pearls:** * **Most common cause:** Solitary adenoma (85%). * **Biochemical Hallmark:** High Serum Calcium + High/Inappropriately Normal PTH + Low Serum Phosphate [2]. * **Radiological sign:** Subperiosteal bone resorption (most common in the radial aspect of middle phalanges) and "Salt and pepper" appearance of the skull. * **Brown Tumors:** These are non-neoplastic cystic lesions (Osteitis fibrosa cystica) caused by intense osteoclastic activity.

Practice by Chapter

Diabetes Mellitus

Practice Questions

Thyroid Disorders

Practice Questions

Adrenal Gland Disorders

Practice Questions

Pituitary Disorders

Practice Questions

Calcium and Bone Metabolism

Practice Questions

Reproductive Endocrinology

Practice Questions

Lipid Disorders

Practice Questions

Endocrine Hypertension

Practice Questions

Multiple Endocrine Neoplasia

Practice Questions

Obesity and Metabolic Syndrome

Practice Questions

Neuroendocrine Tumors

Practice Questions

Endocrine Emergencies

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free