Endocrinology — MCQs

A 35-year-old woman presents with fatigue, weakness, and weight gain. Her blood pressure is 155/90 mm Hg, pulse 80/min, and there is central obesity with skin striae. Investigations are as follows: Plasma ACTH < 150 pg/mL (normal < 50), Plasma cortisol 17 mcg/dL (normal 35 - note: this seems inverted or mislabeled in the original), Urine 17-OHCS 25 mg/24 h (normal 2-10), Urine 17-KS 10 mg/24 h (normal 5-15). Following ACTH IV stimulation, there is a five-fold increase in plasma cortisol. No response to 0.5 mg or 2.0 mg Dexamethasone. No response to Metyrapone 750 mg (cortisol increased 2-fold). What is the most likely diagnosis?

Q1087Medium

All are used in the treatment of hypercalcemia, except?

Q1088Medium

Which of the following can cause magnesium deficiency?

Q1089Medium

Intensive management of diabetes is needed in all situations except:

Q1090Easy

Beta-blockers are used in hyperthyroidism:

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1081: Which of the following thyroid diseases is associated with pain?

A. Hashimoto's thyroiditis
B. De Quervain's thyroiditis (Correct Answer)
C. Simple nontoxic goiter
D. Graves' disease

Explanation: **Explanation:** The hallmark clinical feature of **De Quervain’s thyroiditis** (also known as Subacute Granulomatous Thyroiditis) is **exquisite anterior neck pain**. This condition is typically post-viral in origin (often following an upper respiratory tract infection) and involves inflammatory destruction of the thyroid parenchyma. The pain is often sudden in onset, localized to the thyroid gland, and may radiate to the jaw or ears [2]. It is frequently accompanied by systemic symptoms like fever and malaise. **Analysis of Incorrect Options:** * **Hashimoto’s thyroiditis:** This is an autoimmune, chronic lymphocytic thyroiditis. It typically presents as a **painless**, firm, diffuse goiter. While it is the most common cause of hypothyroidism, it rarely causes discomfort. * **Simple nontoxic goiter:** This refers to a diffuse enlargement of the thyroid gland without hyperthyroidism, hypothyroidism, or inflammation. It is characteristically **painless** and asymptomatic unless it becomes large enough to cause compressive symptoms (e.g., dysphagia). * **Graves’ disease:** This is an autoimmune condition causing hyperthyroidism. While the gland is diffusely enlarged and hypervascular (often with an audible bruit), it is **painless** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of De Quervain’s:** Painful thyroid + Elevated ESR + Low Radioactive Iodine Uptake (RAIU) [2]. * **Histology:** Characterized by **multinucleated giant cells** and granulomatous inflammation. * **Treatment:** Primarily symptomatic with NSAIDs; steroids are used for severe pain [2]. * **Differential for Painful Thyroid:** Subacute thyroiditis (most common), Infectious (Suppurative) thyroiditis, and occasionally, hemorrhage into a thyroid cyst.

Question 1082: Which of the following is the drug of choice for adrenal insufficiency?

A. Hydrocortisone (Correct Answer)
B. Adrenaline
C. Dexamethasone
D. Fludrocortisone

Explanation: ### Explanation **Correct Answer: A. Hydrocortisone** **Why it is the Correct Choice:** Hydrocortisone is the drug of choice for adrenal insufficiency (both primary and secondary) because it most closely mimics the natural physiological secretion and activity of endogenous cortisol [1]. It possesses both **glucocorticoid** and **mineralocorticoid** activity (in a ratio of 1:1). Its short half-life allows for split dosing (usually twice or thrice daily), which helps replicate the normal diurnal rhythm of cortisol—higher in the morning and lower in the evening. **Analysis of Incorrect Options:** * **B. Adrenaline:** This is the drug of choice for anaphylaxis and cardiac arrest. While the adrenal medulla produces adrenaline, adrenal insufficiency primarily involves a deficiency of steroids from the adrenal cortex. * **C. Dexamethasone:** This is a potent, long-acting pure glucocorticoid with **zero mineralocorticoid activity**. While useful in an acute adrenal crisis (because it does not interfere with serum cortisol assays during a dynamic stimulation test) [1], it is not preferred for long-term maintenance due to a higher risk of iatrogenic Cushing’s syndrome and lack of salt-retaining properties. * **D. Fludrocortisone:** This is a potent mineralocorticoid. While it is used as an **adjunct** in primary adrenal insufficiency (Addison’s disease) to replace aldosterone [1], it cannot be used as monotherapy because it lacks sufficient glucocorticoid effect. **Clinical Pearls for NEET-PG:** * **Primary vs. Secondary:** In primary AI (Addison’s), you need both Hydrocortisone and Fludrocortisone [1]. In secondary AI (Pituitary cause), only Hydrocortisone is needed as the Renin-Angiotensin-Aldosterone system remains intact. * **Sick Day Rules:** Patients must double or triple their steroid dose during periods of minor illness or stress to prevent an adrenal crisis. * **Diagnosis:** The gold standard for diagnosis is the **ACTH Stimulation Test** (Cosyntropin test) [1].

Question 1083: A man presents with weakness, pain in the upper abdomen, hyperpigmentation, arthritis, hyperglycemia, and an enlarged palpable liver. What is the most probable diagnosis?

A. Hemochromatosis (Correct Answer)
B. Addison's disease
C. Insulin-dependent diabetes mellitus
D. Cushing's syndrome

Explanation: **Explanation:** The clinical presentation described is the classic "Bronze Diabetes" triad seen in **Hereditary Hemochromatosis**, a disorder of iron overload [1]. **Why Hemochromatosis is correct:** Excessive iron deposition (hemosiderin) occurs in various organs, leading to multi-system dysfunction: * **Liver:** Iron deposition leads to hepatomegaly, cirrhosis, and abdominal pain [1]. * **Pancreas:** Damage to beta cells causes secondary diabetes mellitus (**Hyperglycemia**) [1]. * **Skin:** Increased melanin and iron deposition result in a metallic/slate-gray **hyperpigmentation** [1]. * **Joints:** Calcium pyrophosphate deposition (CPPD) leads to **arthritis**, typically involving the 2nd and 3rd metacarpophalangeal joints. * **Heart:** Can lead to restrictive cardiomyopathy or arrhythmias. **Why other options are incorrect:** * **Addison’s Disease:** While it causes hyperpigmentation and weakness, it typically presents with *hypoglycemia* and hypotension, not hyperglycemia or hepatomegaly. * **Insulin-dependent Diabetes Mellitus (IDDM):** While it explains hyperglycemia, it does not account for hyperpigmentation, arthritis, or hepatomegaly. * **Cushing’s Syndrome:** Presents with hyperglycemia and weakness, but skin changes involve striae and easy bruising rather than generalized hyperpigmentation. It also lacks the characteristic arthritis of iron overload. **NEET-PG High-Yield Pearls:** * **Gene Mutation:** Most commonly the **HFE gene** (C282Y mutation) on Chromosome 6 [1], [2]. * **Screening Test:** Transferrin saturation (Best initial test; >45% is suggestive). * **Gold Standard:** Liver biopsy with Prussian Blue staining (to quantify the Hepatic Iron Index) [2]. * **Treatment:** Therapeutic phlebotomy is the mainstay of management [2]. * **Complication:** Significantly increased risk of **Hepatocellular Carcinoma (HCC)** [1].

Question 1084: What is the gold standard test for diagnosing insulinoma?

A. 72-hour fasting test (Correct Answer)
B. Plasma insulin levels
C. C-peptide levels
D. Low glucose levels < 30 mg/dL

Explanation: ### Explanation **1. Why Option A is Correct:** The **72-hour supervised fasting test** is the gold standard for diagnosing insulinoma. The physiological hallmark of an insulinoma is the **failure to suppress insulin secretion** in the presence of hypoglycemia [1]. In a healthy individual, as blood glucose drops, insulin levels should become undetectable. In patients with insulinoma, insulin remains inappropriately high despite hypoglycemia. The test is terminated when the patient develops symptoms of neuroglycopenia and plasma glucose is **≤ 54 mg/dL**. **2. Why Other Options are Incorrect:** * **Option B & C:** While elevated plasma insulin (≥3 μU/mL) and C-peptide (≥0.6 ng/mL) are essential components of the diagnosis, they must be interpreted **simultaneously** with low blood glucose during the fast [1]. A random insulin or C-peptide level without concurrent hypoglycemia has no diagnostic value. * **Option D:** While a low glucose level is part of the diagnostic criteria, the threshold for terminating the 72-hour fast is typically **≤ 54 mg/dL** (not 30 mg/dL). Waiting for 30 mg/dL is clinically dangerous and unnecessary for diagnosis. **3. NEET-PG High-Yield Clinical Pearls:** * **Whipple’s Triad:** (1) Symptoms of hypoglycemia, (2) Low plasma glucose at the time of symptoms, (3) Relief of symptoms when glucose is raised. * **Biochemical Diagnosis:** During the fast, look for: Glucose < 55 mg/dL, Insulin ≥ 3 μU/mL, C-peptide ≥ 0.6 ng/mL, and **Proinsulin ≥ 5.0 pmol/L** [1]. * **Localization:** Once biochemically confirmed, **Endoscopic Ultrasound (EUS)** is the most sensitive imaging modality for localizing the tumor. * **Association:** Insulinomas are usually small, solitary, and benign, but they are the most common pancreatic endocrine tumor associated with **MEN-1 syndrome**.

Question 1085: Which of the following statements regarding diabetes mellitus is NOT true?

A. Free fatty acids in the blood increase the risk of DM.
B. Patients may have high insulin levels in some conditions.
C. The commonest cause of death is renal failure. (Correct Answer)
D. Regular physical activity improves glycemic control.

Explanation: ### Explanation **1. Why Option C is the Correct (False) Statement:** While Diabetic Nephropathy is a major complication and the leading cause of End-Stage Renal Disease (ESRD) globally, it is **not** the most common cause of death in patients with Diabetes Mellitus. The leading cause of mortality in both Type 1 and Type 2 DM is **Cardiovascular Disease (CVD)**, specifically Myocardial Infarction and Stroke [1]. Approximately 70-80% of diabetic patients die from macrovascular complications rather than microvascular ones like renal failure [1]. **2. Analysis of Other Options:** * **Option A (True):** Elevated levels of **Free Fatty Acids (FFAs)** contribute to insulin resistance via "lipotoxicity." They inhibit glucose utilization in muscles and stimulate gluconeogenesis in the liver (the Randle Cycle), significantly increasing the risk of Type 2 DM. * **Option B (True):** In the early stages of Type 2 DM, there is significant **insulin resistance** [2]. To compensate, the pancreas produces excess insulin, leading to **Hyperinsulinemia** [2]. High levels are also seen in conditions like PCOS and Metabolic Syndrome. * **Option C (True):** Physical activity increases the expression of **GLUT-4 receptors** on skeletal muscle membranes and enhances insulin sensitivity, directly improving glycemic control and reducing HbA1c levels. **3. NEET-PG High-Yield Pearls:** * **Most common cause of death in DM:** Cardiovascular Disease (MI) [1]. * **Most common cause of ESRD:** Diabetes Mellitus. * **Earliest clinical sign of diabetic nephropathy:** Microalbuminuria (30–300 mg/day). * **Pathognomonic biopsy finding in Diabetic Nephropathy:** Kimmelstiel-Wilson (KW) nodules (Nodular glomerulosclerosis). * **Metabolic Syndrome (Syndrome X):** Defined by abdominal obesity, hypertension, hyperglycemia, and dyslipidemia (High TG, Low HDL) [1].

Question 1086: A 35-year-old woman presents with fatigue, weakness, and weight gain. Her blood pressure is 155/90 mm Hg, pulse 80/min, and there is central obesity with skin striae. Investigations are as follows: Plasma ACTH < 150 pg/mL (normal < 50), Plasma cortisol 17 mcg/dL (normal 35 - note: this seems inverted or mislabeled in the original), Urine 17-OHCS 25 mg/24 h (normal 2-10), Urine 17-KS 10 mg/24 h (normal 5-15). Following ACTH IV stimulation, there is a five-fold increase in plasma cortisol. No response to 0.5 mg or 2.0 mg Dexamethasone. No response to Metyrapone 750 mg (cortisol increased 2-fold). What is the most likely diagnosis?

A. Adrenal hyperplasia secondary to hypothalamic dysfunction
B. Adrenal adenoma with complete autonomy (Correct Answer)
C. Exogenous steroid use, iatrogenic
D. Pituitary tumor

Explanation: ### Explanation The clinical presentation of central obesity, hypertension, and striae is classic for **Cushing’s Syndrome** [1]. To differentiate the etiology, we must analyze the biochemical markers and dynamic tests. **1. Why Adrenal Adenoma is Correct:** * **ACTH Levels:** The plasma ACTH is elevated/detachable (though the question's provided range is slightly atypical, the key is the response to stimulation). Measurement of plasma ACTH is the key to establishing the differential diagnosis [2]. * **Dexamethasone Suppression Test (DST):** The failure to suppress cortisol with both low-dose (0.5 mg) and high-dose (2.0 mg) dexamethasone indicates **autonomy** [1]. In pituitary-dependent Cushing’s (Cushing’s Disease), high-dose dexamethasone usually suppresses cortisol by >50%. * **ACTH Stimulation Test:** A five-fold increase in cortisol following exogenous ACTH is highly characteristic of an **adrenal adenoma**, as the neoplastic cells often retain ACTH receptors and hyper-respond compared to the suppressed normal adrenal tissue or a carcinoma. * **Metyrapone Test:** Metyrapone blocks 11-β-hydroxylase. In an autonomous adrenal tumor, the negative feedback loop is broken; therefore, there is no compensatory rise in ACTH or 11-deoxycortisol (and subsequently no significant cortisol rise). **2. Why Other Options are Incorrect:** * **Pituitary Tumor/Hypothalamic Dysfunction:** These would typically show suppression with High-Dose DST and a significant response to Metyrapone (as the feedback loop is intact at the pituitary level). * **Exogenous Steroids:** This would cause adrenal atrophy, leading to **low** baseline cortisol and **no response** to ACTH stimulation [2]. **3. NEET-PG High-Yield Pearls:** * **Screening:** Overnight 1mg DST or 24-hour Urinary Free Cortisol [1]. * **Localization:** If ACTH is suppressed (<5 pg/mL), perform an Adrenal CT [2]. If ACTH is high (>20 pg/mL), perform a Pituitary MRI. * **Metyrapone Test:** Used to differentiate Pituitary (response) from Ectopic/Adrenal (no response) causes. * **Adrenal Carcinoma vs. Adenoma:** Carcinomas usually produce high levels of androgens (elevated 17-KS), whereas adenomas primarily produce cortisol [3].

Question 1087: All are used in the treatment of hypercalcemia, except?

A. Phosphate
B. Mithramycin (Correct Answer)
C. Vitamin D in high dose
D. Any of the above

Explanation: **Explanation:** The management of hypercalcemia focuses on increasing renal calcium excretion and inhibiting bone resorption. **Why Mithramycin is the correct answer (Contextual Note):** There appears to be a discrepancy in the provided key. **Mithramycin (Plicamycin)** is actually a potent inhibitor of osteoclastic bone resorption and was historically used to treat refractory hypercalcemia of malignancy. However, in the context of this question, **Vitamin D in high dose (Option C)** is the most clinically logical "except" choice, as high doses of Vitamin D *cause* hypercalcemia by increasing intestinal calcium absorption and bone resorption. If the provided key insists on Mithramycin, it may be due to its high toxicity profile (hepatotoxicity, nephrotoxicity, and thrombocytopenia), which has led to its replacement by safer bisphosphonates in modern practice. **Analysis of Options:** * **Phosphate (Option A):** Oral or intravenous phosphate can be used to treat hypercalcemia. It works by forming calcium-phosphate complexes that are deposited in tissues (soft tissue calcification) and bone, thereby lowering serum calcium levels. * **Mithramycin (Option B):** An antibiotic that acts as a cytotoxic agent. It inhibits DNA-directed RNA synthesis in osteoclasts, effectively lowering calcium levels in patients with malignancy. * **Vitamin D (Option C):** This is a **cause**, not a treatment. High doses lead to Vitamin D toxicity, characterized by severe hypercalcemia. **NEET-PG High-Yield Pearls:** 1. **First-line treatment:** Aggressive IV hydration with Normal Saline (0.9% NaCl) is the initial step to restore volume and promote calciuresis. 2. **Loop Diuretics:** Furosemide is used *only after* volume repletion to prevent fluid overload and further enhance calcium excretion. 3. **Bisphosphonates (e.g., Zoledronic acid):** The drug of choice for hypercalcemia of malignancy due to long-term efficacy. 4. **Calcitonin:** Used for rapid, short-term reduction of calcium (works within hours) but is limited by tachyphylaxis. 5. **Glucocorticoids:** Highly effective for hypercalcemia caused by Vitamin D toxicity, sarcoidosis, or lymphomas.

Question 1088: Which of the following can cause magnesium deficiency?

A. Prolonged artificial ventilation
B. Small bowel resection (Correct Answer)
C. Renal disease
D. Liver cirrhosis

Explanation: **Explanation:** Magnesium (Mg²⁺) homeostasis is primarily maintained through a balance between intestinal absorption (mainly in the distal small bowel) and renal excretion. [1] **Why Small Bowel Resection is Correct:** The ileum and jejunum are the primary sites for magnesium absorption via both passive diffusion and active transport (TRPM6/7 channels). **Small bowel resection** (Short Bowel Syndrome) leads to a significant reduction in the surface area available for absorption. Furthermore, unabsorbed fatty acids in these patients bind to magnesium, forming insoluble "soaps" that are excreted in the stool (steatorrhea-induced malabsorption), leading to profound hypomagnesemia. **Analysis of Incorrect Options:** * **A. Prolonged artificial ventilation:** This does not directly affect magnesium levels. However, respiratory *alkalosis* (often seen in over-ventilation) can cause a transient intracellular shift of magnesium, but not a true deficiency. * **C. Renal disease:** Chronic Kidney Disease (CKD) typically causes **hypermagnesemia** because the kidneys are the primary route for magnesium excretion. As GFR falls below 30 mL/min, magnesium retention occurs. * **D. Liver cirrhosis:** While alcoholics often have low magnesium due to poor intake and tubular dysfunction, cirrhosis itself is not a primary cause of magnesium deficiency unless associated with diuretic use or chronic diarrhea. **High-Yield Clinical Pearls for NEET-PG:** * **Refractory Hypokalemia:** If a patient’s potassium levels do not normalize despite supplementation, always check and correct **Magnesium** first. [1] Low Mg²⁺ removes the inhibition on ROMK channels in the kidney, leading to excessive K⁺ secretion. * **Hypocalcemia Connection:** Severe hypomagnesemia causes functional hypoparathyroidism by inhibiting PTH release and inducing PTH resistance at the bone level. * **ECG Findings:** Hypomagnesemia can lead to **Torsades de Pointes** (prolonged QT interval). The treatment of choice for Torsades is IV Magnesium Sulfate.

Question 1089: Intensive management of diabetes is needed in all situations except:

A. Autonomic neuropathy causing hypotension (Correct Answer)
B. Pregnancy
C. Post kidney transplant in diabetic nephropathy
D. Diabetes Mellitus with acute myocardial infarction

Explanation: **Explanation:** The goal of intensive glycemic control (HbA1c < 6.5–7.0%) is to prevent microvascular complications [1]. However, intensive management carries a high risk of **hypoglycemia**, which can be life-threatening in specific clinical scenarios. **Why Option A is the Correct Answer:** In patients with **Autonomic Neuropathy**, the body’s "fight or flight" response to falling blood glucose is impaired. This leads to **Hypoglycemia Unawareness**, where the patient does not experience warning signs like tremors or palpitations. If these patients also have **orthostatic hypotension**, aggressive insulin therapy can trigger severe syncopal episodes or cardiovascular collapse. In such cases, glycemic targets are relaxed to prioritize safety over strict control. **Why the other options are incorrect:** * **B. Pregnancy:** Strict euglycemia is mandatory to prevent congenital malformations, macrosomia, and pre-eclampsia [2]. Targets are much tighter than in non-pregnant adults. * **C. Post-Kidney Transplant:** Hyperglycemia increases the risk of graft rejection, opportunistic infections, and "New-Onset Diabetes After Transplantation" (NODAT). Intensive control helps preserve the life of the new graft. * **D. Acute Myocardial Infarction:** Stress hyperglycemia during an MI is associated with poor outcomes and increased mortality. Maintaining controlled glucose levels (typically via insulin infusion) is standard cardiac critical care. **High-Yield Clinical Pearls for NEET-PG:** * **DCCT and UKPDS Trials:** Established that intensive control reduces microvascular (retinopathy, nephropathy) but has less immediate impact on macrovascular (stroke, MI) outcomes [1]. * **ACCORD Trial Warning:** Showed that overly aggressive glucose lowering in high-risk elderly patients with long-standing T2DM actually *increased* mortality [1]. * **Relaxed Targets:** Indications for less stringent control (HbA1c < 8%) include limited life expectancy, advanced micro/macrovascular complications, and history of severe hypoglycemia [1].

Question 1090: Beta-blockers are used in hyperthyroidism:

A. As short-term symptomatic therapy until the effect of carbimazole develops (Correct Answer)
B. As long-term therapy after subtotal thyroidectomy
C. In patients not responding to carbimazole
D. To potentiate the effect of radioactive iodine

Explanation: **Explanation:** **1. Why Option A is Correct:** In hyperthyroidism, many clinical manifestations (tachycardia, palpitations, tremors, and anxiety) are due to increased beta-adrenergic sensitivity. Antithyroid drugs like **Carbimazole** or Methimazole inhibit thyroid hormone synthesis but take **3–6 weeks** to achieve a clinical effect because they do not affect pre-formed hormones already in circulation. Beta-blockers (specifically **Propranolol**) provide rapid symptomatic relief within hours, acting as a "bridge" or short-term therapy until the patient reaches a euthyroid state via definitive treatment [1]. **2. Why Other Options are Incorrect:** * **Option B:** After subtotal thyroidectomy, the source of excess hormone is removed. Long-term beta-blockers are unnecessary unless the patient develops permanent arrhythmias or has underlying cardiac disease. * **Option C:** If a patient does not respond to carbimazole, the next steps are usually radioactive iodine (RAI) or surgery, not just beta-blockers, which do not treat the underlying hyperthyroid state [1]. * **Option D:** Beta-blockers do not potentiate the mechanism of RAI. However, they are used to prevent the symptomatic "thyroid storm" that can occasionally be triggered by the release of stored hormones following RAI treatment. **3. High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Propranolol is the preferred beta-blocker because it also inhibits the **peripheral conversion of T4 to T3** (at high doses). * **Contraindication:** Avoid beta-blockers in hyperthyroid patients with **bronchial asthma**; use cardioselective blockers (e.g., Atenolol) or Calcium Channel Bookers (Diltiazem/Verapamil) instead. * **Thyroid Storm:** Beta-blockers are a cornerstone of management in thyroid storm to control life-threatening sympathetic overactivity.

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