Endocrinology Practice Questions

Q: A patient presents with thin limbs, central obesity, fat cheeks, a ruddy complexion, and an elevated blood glucose level. What is the most likely diagnosis?

Cushing syndrome due to an adrenal tumor.. ### Explanation **Correct Answer: D. Cushing syndrome due to an adrenal tumor.** The clinical presentation described—**central obesity, thin limbs** (due to muscle wasting), **fat cheeks** (moon facies), and a **ruddy complexion** (plethora)—is classic for **Cushing Syndrome** [1]. These features result from chronic hypercortisolism. Cortisol promotes gluconeogenesis and insulin resistance, leading to the **elevated blood glucose levels** (secondary diabetes) seen in this patient. An adrenal tumor is a primary cause of ACTH-independent Cushing syndrome [2]. **Why other options are incorrect:** * **Option A:** Renal artery stenosis leads to secondary hyperaldosteronism. While it causes hypertension and hypokalemia, it does not cause the fat redistribution or hyperglycemia characteristic of cortisol excess. * **Option B:** Hyperprolactinemia typically presents with galactorrhea, amenorrhea, or infertility. It does not cause central obesity or the specific physical signs mentioned. * **Option C:** Acromegaly presents with enlargement of hands/feet, frontal bossing, and prognathism. While it can cause hyperglycemia (GH is counter-regulatory), it does not cause the "moon facies" or "thin limbs" pattern of Cushing syndrome. **NEET-PG High-Yield Pearls:** * **Screening Tests for Cushing:** 24-hour urinary free cortisol, Low-Dose Dexamethasone Suppression Test (LDDST), or late-night salivary cortisol [3]. * **Muscle Wasting:** Cortisol causes protein catabolism, specifically affecting proximal muscles (leading to thin limbs) [1]. * **Striae:** Look for "purple/violaceous striae" (>1 cm wide) in exam vignettes; these are pathognomonic for Cushing syndrome. * **Hypertension:** Cortisol has weak mineralocorticoid activity and increases sensitivity to catecholamines, leading to high BP.

Q: Signs and symptoms of uncomplicated pituitary diabetes insipidus can be controlled using?

Desmopressin. **Explanation:** **Pituitary Diabetes Insipidus (Central DI)** is characterized by a deficiency in the synthesis or release of **Arginine Vasopressin (AVP/ADH)** from the posterior pituitary. This leads to the inability of the kidneys to concentrate urine, resulting in polyuria and compensatory polydipsia. **Why Desmopressin is the Correct Answer:** **Desmopressin (dDAVP)** is a synthetic analogue of ADH. It is the treatment of choice for Central DI because it is a selective **V2 receptor agonist** [3, 5]. By binding to V2 receptors in the renal collecting ducts, it increases water reabsorption via aquaporin-2 channels [2]. Unlike natural ADH, dDAVP has minimal V1 activity (vasoconstriction), making it safer and more potent for long-term fluid management [1]. It can be administered intranasally, orally, or parenterally. **Analysis of Incorrect Options:** * **Mannitol (A):** An osmotic diuretic used to reduce intracranial pressure. It would worsen DI by increasing urinary water loss. * **Glycerol (B):** An osmotic agent sometimes used to reduce intraocular pressure; it has no role in ADH replacement. * **Ethylene Glycol (D):** A toxic alcohol found in antifreeze; ingestion leads to metabolic acidosis and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The **Water Deprivation Test** is used to diagnose DI [1]. In Central DI, urine osmolality increases by >50% after administering exogenous desmopressin. In Nephrogenic DI, there is little to no response. * **Drug of Choice for Nephrogenic DI:** Thiazide diuretics (paradoxical effect), Amiloride (especially for Lithium-induced DI), or NSAIDs. * **Emergency Management:** For acute Central DI (e.g., post-neurosurgery), aqueous vasopressin or IV desmopressin is used.

Q: A 39-year-old woman presents with weight gain, abnormal menstrual cycles, depression, and weakness. Physical examination reveals multiple purplish striae on the abdomen and bruises over the lower extremities. Laboratory studies show normal thyroid-stimulating hormone and thyroid hormone levels, along with elevated cortisol secretion. If the patient has adrenal hyperfunction, which of the following findings may also be present?

Hirsutism. **Explanation:** The clinical presentation of weight gain, purple striae, bruising, and weakness, combined with elevated cortisol, is diagnostic of **Cushing’s Syndrome** [1]. **1. Why Hirsutism is Correct:** In cases of adrenal hyperfunction (specifically ACTH-dependent Cushing’s disease or adrenal carcinomas), there is a simultaneous overproduction of **adrenal androgens** (such as DHEA-S) along with cortisol. These androgens lead to virilization signs, including **hirsutism** (excessive male-pattern hair growth), acne, and menstrual irregularities [1]. Even in ACTH-independent cases like adrenal adenomas, the high levels of cortisol can sometimes cross-react with androgen receptors or be associated with mild androgen excess. **2. Why the Other Options are Incorrect:** * **Enhanced glucose uptake (A) & Hypoglycemia (D):** Cortisol is a "stress hormone" that antagonizes insulin. It stimulates gluconeogenesis and inhibits peripheral glucose uptake, leading to **hyperglycemia** and secondary diabetes mellitus, not hypoglycemia. * **Hypocalciuria (C):** Glucocorticoids inhibit calcium reabsorption in the renal tubules and decrease intestinal calcium absorption. This leads to **hypercalciuria**, which increases the risk of nephrolithiasis (kidney stones). **Clinical Pearls for NEET-PG:** * **Proximal Myopathy:** The "weakness" in Cushing’s is due to cortisol-induced muscle catabolism, typically affecting the proximal limbs [1]. * **Screening Tests:** The best initial tests are the 24-hour urinary free cortisol, late-night salivary cortisol, or the Low-Dose Dexamethasone Suppression Test (LDDST) [2]. * **Hypokalemia:** Severe hypercortisolism (often from ectopic ACTH) can cause mineralocorticoid effects, leading to hypokalemic metabolic alkalosis.

Q: A 50-year-old patient presents with a history of jaw expansion and enlargement of the maxilla. What is the most likely diagnosis?

Paget's disease. **Explanation:** The clinical presentation of jaw expansion and maxillary enlargement in a 50-year-old is a classic hallmark of **Paget’s Disease of Bone (Osteitis Deformans)**. 1. **Why Paget's Disease is Correct:** This condition involves disordered bone remodeling characterized by excessive bone resorption followed by disorganized, exuberant bone formation [1]. While the skull and pelvis are commonly involved, when it affects the facial bones, the **maxilla** is involved much more frequently than the mandible. This leads to widening of the alveolar ridges, spreading of teeth, and a characteristic "lion-like" facies (leontiasis ossea). In older patients, a classic board-style clue is a patient complaining that their "hat no longer fits" or their "dentures have become too tight." 2. **Why the Other Options are Incorrect:** * **Acromegaly:** While it causes bone overgrowth, it characteristically affects the **mandible** (prognathism) rather than the maxilla, leading to an underbite. * **Fibrous Dysplasia:** This typically presents in younger patients (children/adolescents). While it can cause facial asymmetry (especially the monostotic form), the age of 50 makes Paget’s more likely. * **Hyperparathyroidism:** This leads to generalized bone resorption (osteitis fibrosa cystica) and "brown tumors," but it does not typically cause the massive, diffuse expansion of the maxilla seen in Paget’s. **High-Yield Clinical Pearls for NEET-PG:** * **Biochemical Marker:** Isolated elevation of **Alkaline Phosphatase (ALP)** with normal Calcium, Phosphate, and PTH. * **Radiology:** "Cotton wool" appearance of the skull [1]. * **Complications:** High-output heart failure (due to increased vascularity) [1] and Osteosarcoma (rare but serious) [2]. * **Treatment of Choice:** Bisphosphonates (Zoledronic acid).

Q: A patient's lab investigation shows low T3, low T4, and elevated TSH. This pattern is indicative of which of the following conditions?

Primary hypothyroidism. ### Explanation **Correct Option: A. Primary Hypothyroidism** In **Primary Hypothyroidism**, the pathology lies within the thyroid gland itself (e.g., Hashimoto’s thyroiditis) [1][2]. The gland is unable to produce sufficient thyroid hormones, leading to **low T3 and T4** levels [1]. Due to the loss of negative feedback on the Hypothalamic-Pituitary-Thyroid (HPT) axis, the anterior pituitary compensates by increasing the secretion of **Thyroid Stimulating Hormone (TSH)** [1]. Therefore, an elevated TSH in the presence of low T4 is the biochemical hallmark of primary thyroid failure [1]. **Incorrect Options:** * **B. Panhypopituitarism:** This is a form of **Secondary (Central) Hypothyroidism**. Here, the pituitary gland fails to produce TSH [2]. The lab pattern would show low T3/T4 with a **low or inappropriately normal TSH**. * **C. Liver Disease:** Liver dysfunction can lead to **Euthyroid Sick Syndrome**. While total T3 may be low due to decreased peripheral conversion of T4 and reduced Thyroid Binding Globulin (TBG), the TSH is typically normal or slightly low, not elevated. **NEET-PG High-Yield Pearls:** * **TSH is the most sensitive screening test** for thyroid dysfunction. * **Subclinical Hypothyroidism:** Characterized by **Elevated TSH** but **Normal T4** levels. * **Secondary Hypothyroidism:** Always suspect this if T4 is low but TSH is not elevated; it requires further imaging (MRI) of the pituitary [2]. * **Wolff-Chaikoff Effect:** Autoregulation where a large load of iodine inhibits thyroid hormone synthesis, potentially leading to primary hypothyroidism.

Q: In a patient, there are elevated plasma cortisol levels. Dexamethasone fails to suppress cortisol secretion. What is the next step in management?

Serum ACTH. This question tests the diagnostic algorithm for **Cushing’s Syndrome**. Once hypercortisolism is confirmed (via 24-hour urinary free cortisol, late-night salivary cortisol, or a low-dose dexamethasone suppression test), the next priority is to determine the **etiology** [1]. ### Why Serum ACTH is the Correct Answer The fundamental step in differentiating the causes of Cushing’s syndrome is determining if the condition is **ACTH-dependent** or **ACTH-independent** [1]. * **Low ACTH ( 15-20 pg/mL):** Suggests an ACTH-dependent cause, such as a pituitary adenoma (Cushing’s Disease) or ectopic ACTH production (e.g., Small Cell Lung Cancer) [1]. Since the patient has failed dexamethasone suppression (confirming hypercortisolism), measuring **Serum ACTH** is the mandatory next step to localize the pathology. ### Why Other Options are Incorrect * **Options B & C (Urinary Metanephrines/VMA):** These are screening tests for **Pheochromocytoma**, not Cushing’s syndrome. While both involve the adrenal gland, they assess the medulla (catecholamines), not the cortex (cortisol). * **Option D (Serum DHEAS):** While DHEAS may be elevated in adrenal carcinomas, it is not a primary step in the diagnostic algorithm for hypercortisolism. ### Clinical Pearls for NEET-PG * **Screening Test:** Overnight Low-Dose Dexamethasone Suppression Test (LDDST). * **Confirmatory Test:** 24-hour Urinary Free Cortisol (UFC). * **Localization Step 1:** Plasma ACTH levels [1]. * **Localization Step 2 (if ACTH is high):** High-Dose Dexamethasone Suppression Test (HDDST) or IPSS (Inferior Petrosal Sinus Sampling) to differentiate Pituitary vs. Ectopic sources. * **Most common cause of Cushing’s Syndrome:** Exogenous steroid use. * **Most common endogenous cause:** Cushing’s Disease (Pituitary adenoma).

Question 1

A patient presents with thin limbs, central obesity, fat cheeks, a ruddy complexion, and an elevated blood glucose level. What is the most likely diagnosis?

Accepted Answer

Cushing syndrome due to an adrenal tumor.

Answer

Elevated blood levels of aldosterone and renin resulting from an atherosclerotic plaque in a renal artery.

Answer

Hyperprolactinemia due to a pituitary tumor.

Answer

Acromegaly due to a GH-producing tumor that developed in adulthood.

Question 2

Signs and symptoms of uncomplicated pituitary diabetes insipidus can be controlled using?

Accepted Answer

Desmopressin

Answer

Mannitol

Answer

Glycerol

Answer

Ethyleneglycol

Question 3

A 39-year-old woman presents with weight gain, abnormal menstrual cycles, depression, and weakness. Physical examination reveals multiple purplish striae on the abdomen and bruises over the lower extremities. Laboratory studies show normal thyroid-stimulating hormone and thyroid hormone levels, along with elevated cortisol secretion. If the patient has adrenal hyperfunction, which of the following findings may also be present?

Accepted Answer

Hirsutism

Answer

Enhanced glucose uptake

Answer

Hypocalciuria

Answer

Hypoglycemia

Question 4

Hyperaldosteronism is characterized by the following, except?

Accepted Answer

Metabolic acidosis

Answer

Hypernatremia

Answer

Hypokalemia

Answer

Low plasma renin levels

Question 5

A man was diagnosed with myositis ossificans progressiva at the age of 20 years and died five years later. What is the most probable cause of his death?

Accepted Answer

Starvation and chest infection

Answer

Myocarditis

Answer

Hypercalcemia

Answer

Hyperphosphatemia

Question 6

A 22-year-old student is scheduled to undergo parathyroidectomy for hyperparathyroidism associated with familial multiglandular syndrome. His sister developed peptic ulcer disease secondary to a Zollinger-Ellison tumor of the pancreas. On examination, a swelling was noted over the posterior aspect of the patient's fifth rib. What is the most likely finding?

Accepted Answer

Osteitis fibrosa cystica (brown tumor) and subperiosteal resorption of the phalanges

Answer

Metastasis from a parathyroid carcinoma

Answer

Dermoid cyst

Answer

Eosinophilic granuloma

Question 7

A 50-year-old patient presents with a history of jaw expansion and enlargement of the maxilla. What is the most likely diagnosis?

Accepted Answer

Paget's disease

Answer

Acromegaly

Answer

Fibrous dysplasia

Answer

Hyperparathyroidism

Question 8

Adult Leydig cells are originated from which of the following?

Accepted Answer

Undifferentiated progenitor cells which appear in the testis after birth

Answer

Fetal Leydig cells

Answer

Undifferentiated progenitor cells which appear in the testis before birth

Answer

All of the above

Question 9

A patient's lab investigation shows low T3, low T4, and elevated TSH. This pattern is indicative of which of the following conditions?

Accepted Answer

Primary hypothyroidism

Answer

Panhypopituitarism

Answer

Liver disease

Answer

None of the above

Question 10

In a patient, there are elevated plasma cortisol levels. Dexamethasone fails to suppress cortisol secretion. What is the next step in management?

Accepted Answer

Serum ACTH

Answer

24-hour urinary metanephrines

Answer

24-hour urinary VMA

Answer

Serum DHEAS

Endocrinology — MCQs

Endocrinology — MCQs

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