Endocrinology — MCQs

A 63-year-old asymptomatic woman presents with a persistently elevated alkaline phosphatase (ALP) level as an isolated finding, with normal remaining liver enzymes. She reports no abdominal symptoms. Physical examination reveals normal vital signs, no icterus, normal heart sounds, clear lungs, and a soft abdomen with a liver span of 12 cm. X-rays of the pelvis show multiple porotic and sclerotic lesions with characteristic whorls of trabeculation. Her urinary hydroxyproline excretion is also elevated. Which of the following is the most likely diagnosis?

Q1120Easy

Which of the following tumors can secrete erythropoietin?

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 1111: Neutrophilic leukocytosis, lymphopenia, and eosinopenia are most likely associated with which of the following disorders?

A. Endotoxic shock
B. Typhoid fever
C. Whooping cough
D. Cushing syndrome (Correct Answer)

Explanation: The correct answer is **Cushing syndrome**. This hematological pattern is a classic manifestation of **hypercortisolism** (excess glucocorticoids). **Mechanism:** Glucocorticoids influence the distribution and count of various white blood cells through several mechanisms: 1. **Neutrophilic Leukocytosis:** Cortisol causes "demargination" of neutrophils. It decreases the expression of adhesion molecules (L-selectin) on neutrophils, preventing them from sticking to the vascular endothelium. This shifts neutrophils from the marginal pool into the circulating pool, increasing the count. 2. **Lymphopenia & Eosinopenia:** Cortisol induces apoptosis of lymphocytes (especially T-cells) and sequesters them in the bone marrow and spleen [1]. It also inhibits the release of eosinophils from the bone marrow and promotes their peripheral destruction. **Analysis of Incorrect Options:** * **Endotoxic Shock:** Typically presents with initial leucopenia followed by leukocytosis; however, it is often associated with a "left shift" (increased bands) rather than the specific triad mentioned. * **Typhoid Fever:** Characteristically causes **leukopenia** and **aneosinophilia** (disappearance of eosinophils), but not neutrophilic leukocytosis. * **Whooping Cough (Pertussis):** Classically associated with absolute **lymphocytosis** (due to pertussis toxin blocking lymphocyte entry into lymph nodes) [1], which is the opposite of the lymphopenia seen in Cushing’s. **NEET-PG High-Yield Pearls:** * **Steroid-induced Leukocytosis:** Always consider exogenous steroids or Cushing’s when you see high neutrophils with low eosinophils [1]. * **Aneosineophilia:** The complete absence of eosinophils is a sensitive marker for acute bacterial infections (e.g., Typhoid) or acute stress. * **Cushing’s Triad (Hematology):** Polycythemia, Neutrophilia, Lymphopenia, and Eosinopenia [2].

Question 1112: What is the treatment of choice for renal osteodystrophy?

A. Phosphorus
B. Olendronate
C. Calcium restriction
D. Phosphate binder (Correct Answer)

Explanation: **Explanation:** Renal Osteodystrophy is a complex alteration in bone morphology occurring in patients with Chronic Kidney Disease (CKD). The primary driver is **hyperphosphatemia** caused by decreased renal excretion of phosphorus [1]. High serum phosphate levels directly trigger the release of Fibroblast Growth Factor 23 (FGF-23) and indirectly stimulate Parathyroid Hormone (PTH) secretion by lowering serum ionized calcium and inhibiting Calcitriol (Vitamin D3) production [1]. This leads to **Secondary Hyperparathyroidism**, which causes high-bone-turnover lesions (Osteitis fibrosa cystica) [1]. **Why Phosphate Binders are the treatment of choice:** The cornerstone of management is controlling serum phosphorus levels. **Phosphate binders** (e.g., Calcium carbonate, Sevelamer, Lanthanum) bind dietary phosphorus in the gut, preventing its absorption [2]. By normalizing phosphate, the stimulus for PTH secretion is reduced, thereby halting the progression of bone resorption [2]. **Analysis of Incorrect Options:** * **A. Phosphorus:** Administering phosphorus would worsen the underlying hyperphosphatemia and exacerbate secondary hyperparathyroidism. * **B. Alendronate:** Bisphosphonates are generally avoided in advanced CKD (GFR <30-35 ml/min) due to the risk of adynamic bone disease and impaired renal clearance. * **C. Calcium restriction:** While hypercalcemia must be avoided, strict calcium restriction is not the primary treatment. In fact, calcium-based phosphate binders are often used to correct the hypocalcemia associated with CKD. **NEET-PG High-Yield Pearls:** * **First-line management:** Dietary phosphate restriction followed by phosphate binders [2]. * **Sevelamer:** A non-calcium, non-aluminum phosphate binder preferred in patients with hypercalcemia or vascular calcification [2]. * **Vitamin D:** Calcitriol is used only after phosphate levels are controlled to avoid metastatic calcification (Calcium x Phosphate product should be <55). * **Rugger-Jersey Spine:** A classic radiological sign of renal osteodystrophy showing sclerotic bands at the vertebral endplates.

Question 1113: Which of the following is a feature of primary adrenal cortical failure?

A. Hypopigmentation
B. Sodium and water depletion (Correct Answer)
C. Hypertension
D. Hypokalemia

Explanation: **Explanation:** Primary adrenal cortical failure (Addison’s disease) involves the destruction of the entire adrenal cortex, leading to a deficiency in both **cortisol** and **aldosterone** [1]. **1. Why "Sodium and water depletion" is correct:** Aldosterone is responsible for sodium reabsorption and potassium excretion in the distal renal tubules [3]. In primary adrenal failure, the lack of aldosterone leads to **renal salt wasting**. This results in hyponatremia, decreased intravascular volume, and dehydration (water depletion), which can progress to hypovolemic shock. **2. Analysis of Incorrect Options:** * **A. Hypopigmentation:** Incorrect. In primary failure, the low cortisol levels trigger a compensatory increase in ACTH [1]. Because ACTH shares a precursor with Melanocyte-Stimulating Hormone (POMC), patients develop **hyperpigmentation**, especially in skin creases and buccal mucosa. * **C. Hypertension:** Incorrect. Due to the loss of sodium and water, patients typically present with **hypotension** (often orthostatic). * **D. Hypokalemia:** Incorrect. Aldosterone deficiency prevents potassium excretion, leading to **hyperkalemia** and metabolic acidosis [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The gold standard is the **ACTH Stimulation Test** (Cosyntropin test) [2]. A failure of cortisol to rise indicates adrenal insufficiency. * **Electrolyte Triad:** Hyponatremia + Hyperkalemia + Azotemia (due to dehydration). * **Secondary vs. Primary:** Secondary adrenal failure (pituitary cause) does **not** feature hyperpigmentation (low ACTH) and usually has normal potassium levels (aldosterone is primarily regulated by the RAAS, not ACTH). * **Most Common Cause:** Worldwide, Tuberculosis; in developed nations, Autoimmune Adrenalitis [1].

Question 1114: Raised serum alkaline phosphatase is seen in all of the following conditions EXCEPT:

A. Paget's disease
B. Multiple myeloma (Correct Answer)
C. Osteomalacia
D. Hyperthyroidism

Explanation: Serum Alkaline Phosphatase (ALP) is a marker of **osteoblastic activity** (bone formation). In conditions where bone remodeling or bone formation is increased, ALP levels rise. **Why Multiple Myeloma is the correct answer:** In Multiple Myeloma, the bone lesions are characteristically **purely lytic**. The malignant plasma cells produce factors (like DKK-1 and sclerostin) that inhibit osteoblasts while activating osteoclasts. Because there is a lack of compensatory osteoblastic activity, the **ALP remains normal** despite extensive bone destruction. This is a classic diagnostic "negative" finding used to differentiate myeloma from other bone pathologies. **Analysis of incorrect options:** * **Paget’s Disease:** Characterized by focal areas of increased and disorganized bone remodeling [1]. It features the highest levels of serum ALP seen in clinical practice due to intense osteoblastic compensation. * **Osteomalacia:** Defective mineralization leads to an accumulation of unmineralized osteoid. This triggers a compensatory increase in osteoblastic activity, resulting in elevated ALP. * **Hyperthyroidism:** Thyroid hormones have a direct stimulatory effect on bone turnover. Increased bone resorption is coupled with increased bone formation, leading to mildly to moderately raised ALP. **NEET-PG High-Yield Pearls:** * **The "Cold" Scan:** Because Bone Scans (Technetium-99m) depend on osteoblastic activity, they are often negative in Multiple Myeloma. Skeletal surveys (X-rays) or MRI are preferred. * **Isolated ALP Elevation:** If ALP is raised with normal GGT, the source is bone; if GGT is also raised, the source is hepatobiliary. * **Hypercalcemia + Normal ALP:** Always consider Multiple Myeloma as a primary differential in an elderly patient [1].

Question 1115: A patient presents with arthritis, hyperpigmentation of the skin, and hypogonadism. What is the most likely diagnosis?

A. Hemochromatosis (Correct Answer)
B. Ectopic ACTH secreting tumor of the lung
C. Wilson's disease
D. Rheumatoid arthritis

Explanation: **Explanation:** The clinical triad of **arthritis, hyperpigmentation, and hypogonadism** is a classic presentation of **Hereditary Hemochromatosis (HH)**, often referred to as "Bronze Diabetes." [1] 1. **Why Hemochromatosis is correct:** Hemochromatosis is a disorder of iron overload where excess iron deposits in various organs, leading to multi-system dysfunction: * **Hyperpigmentation:** Iron deposition and increased melanin production give the skin a "bronze" or metallic grey appearance. * **Hypogonadism:** Iron deposition in the **pituitary gland** (siderosis) leads to secondary hypogonadotropic hypogonadism, causing decreased libido and impotence. * **Arthritis:** Characteristically involves the **2nd and 3rd metacarpophalangeal (MCP) joints** due to calcium pyrophosphate deposition. [1] * **Diabetes Mellitus:** Occurs due to iron deposition in the pancreas. 2. **Why other options are incorrect:** * **Ectopic ACTH Tumor:** While it causes hyperpigmentation (due to MSH-like activity), it typically presents with features of Cushing syndrome (hypertension, hypokalemia, muscle wasting) rather than arthritis or hypogonadism. * **Wilson’s Disease:** This is a disorder of copper metabolism. It primarily affects the liver and basal ganglia (Kayser-Fleischer rings, tremors), not typically presenting with the "bronze" triad. * **Rheumatoid Arthritis:** While it explains the arthritis, it does not account for hyperpigmentation or endocrine dysfunction like hypogonadism. **High-Yield NEET-PG Pearls:** * **Gene Mutation:** Most commonly the **HFE gene** (C282Y mutation) on Chromosome 6. * **Best Initial Test:** Transferrin saturation (>45%). * **Gold Standard Diagnosis:** Liver biopsy (Perls' Prussian blue stain) or MRI (T2*). * **Treatment of Choice:** Therapeutic phlebotomy. * **Classic Joint Finding:** "Hook-like" osteophytes on X-ray of the MCP joints.

Question 1116: Chronic adrenal insufficiency is characterized by all of the following EXCEPT:

A. Excess pigmentation
B. Asthenia
C. Weight gain (Correct Answer)
D. Hypoglycemic episodes

Explanation: **Explanation:** Chronic primary adrenal insufficiency (Addison’s disease) results from the destruction of the adrenal cortex, leading to a deficiency in cortisol, aldosterone, and adrenal androgens [1]. **Why Weight Gain is the Correct Answer:** Weight gain is **not** a feature of adrenal insufficiency. In fact, **weight loss** and anorexia are hallmark clinical signs [2]. The lack of cortisol leads to a catabolic state and gastrointestinal disturbances (nausea, vomiting), while the lack of aldosterone causes salt wasting and dehydration, further contributing to weight reduction. **Analysis of Incorrect Options:** * **Excess Pigmentation:** In primary adrenal insufficiency, low cortisol triggers a compensatory increase in ACTH [2]. ACTH is derived from Pro-opiomelanocortin (POMC), which also produces Melanocyte-Stimulating Hormone (MSH). High ACTH levels stimulate melanocytes, causing hyperpigmentation (especially in skin creases, scars, and buccal mucosa). * **Asthenia:** This refers to physical weakness or lack of energy. It is the most common presenting symptom (seen in nearly 100% of cases) due to cortisol deficiency and electrolyte imbalances [2]. * **Hypoglycemic Episodes:** Cortisol is a counter-regulatory hormone that promotes gluconeogenesis. Its absence leads to increased insulin sensitivity and decreased glucose production, resulting in fasting hypoglycemia. **NEET-PG High-Yield Pearls:** * **Most common cause:** Autoimmune adrenalitis (developed countries); Tuberculosis (developing countries/India) [3]. * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Diagnosis:** Best initial test is the Morning Serum Cortisol; Gold standard is the ACTH Stimulation Test (Cosyntropin test) [2]. * **Treatment:** Lifelong replacement of glucocorticoids (Hydrocortisone) and mineralocorticoids (Fludrocortisone) [3].

Question 1117: Which condition is characterized by insulin resistance leading to hyperglycemia?

A. Acromegaly (Correct Answer)
B. Osteomalacia
C. Liver cell carcinoma
D. Somatostatinoma

Explanation: **Explanation:** **Correct Option: A. Acromegaly** Acromegaly is characterized by the hypersecretion of Growth Hormone (GH), usually due to a pituitary adenoma [1]. GH is a potent **counter-regulatory hormone** that antagonizes the actions of insulin. It induces hyperglycemia through two primary mechanisms: 1. **Increased Gluconeogenesis:** It stimulates the liver to produce more glucose. 2. **Peripheral Insulin Resistance:** It reduces glucose uptake in skeletal muscle and adipose tissue by interfering with post-receptor insulin signaling. Approximately 30–50% of acromegalic patients develop impaired glucose tolerance or overt "Pituitary Diabetes" [2]. **Analysis of Incorrect Options:** * **B. Osteomalacia:** This is a metabolic bone disease characterized by defective mineralization of the osteoid, usually due to Vitamin D deficiency. It has no direct association with insulin resistance or hyperglycemia. * **C. Liver Cell Carcinoma (HCC):** HCC is more commonly associated with **hypoglycemia** (as a paraneoplastic syndrome) due to high metabolic demands of the tumor or the secretion of IGF-II ("Non-islet cell tumor hypoglycemia"). * **D. Somatostatinoma:** While this tumor causes hyperglycemia, it does so by **inhibiting the secretion of insulin** from pancreatic beta cells, rather than causing insulin resistance. **High-Yield Clinical Pearls for NEET-PG:** * **Secondary Diabetes:** Other endocrine causes of hyperglycemia include Cushing’s syndrome (excess cortisol) [3], Pheochromocytoma (excess catecholamines), and Glucagonoma. * **Screening for Acromegaly:** The best initial screening test is **Serum IGF-1** levels (stable throughout the day) [1]. * **Confirmatory Test:** The **Oral Glucose Tolerance Test (OGTT)**; failure to suppress GH levels below 1 ng/mL after 75g of glucose is diagnostic [2].

Question 1118: Which of the following can be present in hyperosmolar coma in a diabetic patient?

A. Low plasma glucose
B. Low plasma potassium
C. High plasma pH
D. High plasma ketones (Correct Answer)

Explanation: **Explanation:** Hyperosmolar Hyperglycemic State (HHS), formerly known as hyperosmolar coma, is a metabolic complication of Diabetes Mellitus (usually Type 2). The hallmark of HHS is extreme hyperglycemia and hyperosmolality without significant ketoacidosis. **Why Option D is Correct:** While HHS is characterized by the *absence* of significant ketosis (due to enough endogenous insulin being present to inhibit lipolysis), the term "High plasma ketones" in this specific question context refers to the fact that **mild ketonemia** can indeed be present. According to standard diagnostic criteria, while DKA has high ketones, HHS patients can still have small amounts of ketones (typically <3 mmol/L) or a small anion gap. In the context of this specific MCQ, it highlights that HHS and DKA exist on a spectrum, and "pure" HHS is rare. **Why the other options are incorrect:** * **A. Low plasma glucose:** Incorrect. HHS is defined by profound hyperglycemia, typically >600 mg/dL (often much higher than in DKA). * **B. Low plasma potassium:** Incorrect. While total body potassium is depleted due to osmotic diuresis, the **initial plasma potassium** is usually normal or high due to insulin deficiency and hypertonicity shifting K+ out of cells [1]. * **C. High plasma pH:** Incorrect. While HHS does not feature the profound metabolic acidosis seen in DKA, the pH is usually **normal (>7.30)** or slightly low. It is never "high" (alkalotic) as a primary feature of the condition. **NEET-PG High-Yield Pearls:** * **Diagnostic Triad of HHS:** Plasma glucose >600 mg/dL, Serum Osmolality >320 mOsm/kg, and absence of significant ketoacidosis [2]. * **Fluid Deficit:** HHS involves massive dehydration; the fluid deficit is typically 8–12 Liters (higher than DKA). * **Management:** Aggressive fluid resuscitation with Normal Saline is the priority, followed by insulin [2]. Always monitor for cerebral edema during treatment.

Question 1119: A 63-year-old asymptomatic woman presents with a persistently elevated alkaline phosphatase (ALP) level as an isolated finding, with normal remaining liver enzymes. She reports no abdominal symptoms. Physical examination reveals normal vital signs, no icterus, normal heart sounds, clear lungs, and a soft abdomen with a liver span of 12 cm. X-rays of the pelvis show multiple porotic and sclerotic lesions with characteristic whorls of trabeculation. Her urinary hydroxyproline excretion is also elevated. Which of the following is the most likely diagnosis?

A. Rickets and osteomalacia
B. Osteogenic sarcoma
C. Vitamin D deficiency
D. Paget disease of bone (Correct Answer)

Explanation: **Explanation:** The clinical presentation is classic for **Paget Disease of Bone (Osteitis Deformans)**. This condition is characterized by disordered bone remodeling, where excessive bone resorption is followed by disorganized, high-volume bone formation [1]. **Why Option D is correct:** 1. **Isolated Elevated ALP:** In asymptomatic elderly patients, an isolated rise in Alkaline Phosphatase (ALP) with normal GGT and bilirubin is the hallmark of Paget disease. 2. **Radiological Findings:** The description of "porotic and sclerotic lesions" with "whorls of trabeculation" (often called a "mosaic pattern" or "cotton wool appearance") is pathognomonic. 3. **Biochemical Markers:** Elevated **urinary hydroxyproline** and serum N-telopeptide reflect increased collagen breakdown due to high osteoclastic activity. **Why other options are incorrect:** * **A & C (Rickets/Osteomalacia/Vit D Deficiency):** These typically present with **low or low-normal serum calcium and phosphate**, and high PTH [2]. Radiologically, they show decreased bone density and Looser’s zones (pseudofractures), not the sclerotic/thickened bone seen here. * **B (Osteogenic Sarcoma):** While a known complication of Paget disease (occurring in <1%), it usually presents with localized pain, a soft tissue mass, and a "sunburst" appearance on X-ray, rather than generalized pelvic trabeculation in an asymptomatic patient. **NEET-PG High-Yield Pearls:** * **Most common site:** Pelvis, followed by the skull, femur, and tibia [1]. * **Hearing loss:** Occurs due to involvement of the skull (enlargement of the bone compressing CN VIII). * **High-output Heart Failure:** Can occur in extensive disease due to increased vascularity in the remodeling bone [1]. * **Treatment of choice:** Bisphosphonates (e.g., Zoledronic acid). * **Calcium/Phosphate levels:** Usually **normal** in Paget disease (unlike hyperparathyroidism or osteomalacia).

Question 1120: Which of the following tumors can secrete erythropoietin?

A. Cerebellar hemangioblastoma
B. Hepatoma
C. Renal cell carcinoma
D. All of the above (Correct Answer)

Explanation: The correct answer is **D. All of the above**. This question tests the concept of **Paraneoplastic Syndromes**, specifically the ectopic production of **Erythropoietin (EPO)**, which leads to secondary polycythemia (erythrocytosis). [1] **Underlying Medical Concept:** While EPO is physiologically produced by the peritubular interstitial cells of the kidney (and the liver in the fetus), certain tumors can undergo "ectopic" hormone production [2]. When these tumors secrete EPO, it stimulates the bone marrow to increase red blood cell production, resulting in an elevated hematocrit and hemoglobin level. **Analysis of Options:** * **Renal Cell Carcinoma (RCC):** This is the most common tumor associated with ectopic EPO production. It is a classic paraneoplastic manifestation of RCC [1]. * **Hepatoma (Hepatocellular Carcinoma):** The liver retains the genetic machinery for EPO production from fetal life; malignancy can reactivate this pathway [1]. * **Cerebellar Hemangioblastoma:** This is a high-yield association, often seen in **Von Hippel-Lindau (VHL) syndrome**. These vascular tumors are well-known secretors of EPO [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for EPO-secreting tumors (Potentially Really High Hematocrit):** **P**heochromocytoma, **R**enal Cell Carcinoma, **H**epatoma, **H**emangioblastoma (Cerebellar), and **U**terine Fibroids (Leiomyoma) [1]. * **Differential Diagnosis:** To distinguish secondary polycythemia (due to tumors) from **Polycythemia Vera**, check the serum EPO level. In Polycythemia Vera, EPO is **low**; in tumor-induced erythrocytosis, EPO is **high**. * **VHL Syndrome:** Always screen for RCC and Pheochromocytoma if a patient presents with a Cerebellar Hemangioblastoma.

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