Endocrinology Practice Questions

Q: All of the following are seen in Growth Hormone (GH) deficiency except?

Hyperglycemia. Growth Hormone (GH) is a potent **anabolic [1] and counter-regulatory hormone**. Its primary metabolic function is to antagonize the effects of insulin, thereby increasing blood glucose levels. **1. Why Hyperglycemia is the correct answer:** GH deficiency leads to a lack of insulin-antagonistic activity. Instead of hyperglycemia, patients typically present with **hypoglycemia** (especially fasting hypoglycemia in children). GH promotes gluconeogenesis and reduces peripheral glucose uptake; without it, blood sugar levels drop. Therefore, hyperglycemia is not a feature of GH deficiency. **2. Analysis of other options:** * **Stunting (B):** GH is essential for linear growth via the production of IGF-1. Deficiency results in proportionate short stature or stunting. * **Delayed bone age (C):** In GH deficiency, skeletal maturation is significantly slowed. The bone age is typically delayed compared to the chronological age. * **High-pitched voice (D):** This occurs due to the underdevelopment of the larynx and facial bones (midfacial hypoplasia), leading to a characteristic "doll-like" appearance and a high-pitched, squeaky voice. **Clinical Pearls for NEET-PG:** * **Laron Syndrome:** A condition of GH insensitivity (mutated GH receptor) characterized by **high GH levels but low IGF-1 levels**. * **Micropenis:** A classic sign of congenital GH deficiency in male neonates, often accompanied by hypoglycemia. * **Diagnosis:** The gold standard is a **GH stimulation test** (using insulin, glucagon, or arginine). A single random GH measurement is useless due to its pulsatile secretion. * **Treatment:** Recombinant Human GH (Somatropin).

Q: A 19-year-old female presents with neck pain for 5 days, making it difficult to wear a tie for her job. She reports a 10-day history of fatigue and lethargy, preceded by flu-like symptoms 20 days ago that resolved spontaneously. Her blood pressure is 110/80 mmHg, and her pulse is 48/min. Her extremities are cold and dry. The neck is very tender. An ECG is normal, TSH is elevated, and ESR is 30 mm/hr. What is the next appropriate step?

Aspirin. ### Explanation **Diagnosis: Subacute Granulomatous Thyroiditis (De Quervain’s Thyroiditis)** The clinical presentation of a young female with **severe neck tenderness**, a preceding **viral (flu-like) illness**, and an **elevated ESR** is classic for Subacute Thyroiditis. 1. **Why Aspirin is Correct:** Subacute thyroiditis is an inflammatory condition. The primary goal of treatment is pain relief and reducing inflammation. **NSAIDs (like Aspirin)** or Salicylates are the first-line treatment for mild-to-moderate cases. If the pain is severe or unresponsive to NSAIDs, corticosteroids (Prednisolone) are indicated. 2. **Why the other options are incorrect:** * **Atropine:** While the patient has bradycardia (48/min), it is a physiological consequence of her current hypothyroid state, not a primary cardiac conduction defect. Treating the underlying thyroid condition is the priority. * **Levothyroxine:** This patient is currently in the **hypothyroid phase** (elevated TSH, cold/dry skin, bradycardia) which follows the initial thyrotoxic phase. This phase is usually transient and self-limiting. Levothyroxine is only indicated if symptoms are severe or prolonged. * **Iodine intake:** Increasing iodine is used for nutritional deficiency goiters or to block thyroid hormone release (Wolff-Chaikoff effect) in Graves' disease, neither of which is relevant here. ### NEET-PG High-Yield Pearls * **Triphasic Course:** Hyperthyroid phase (due to release of stored hormone) → Hypothyroid phase → Euthyroid state. * **Key Diagnostic Marker:** Markedly elevated **ESR** (often >50 mm/hr) and low radioactive iodine uptake (**RAIU**) during the thyrotoxic phase. * **Pathology:** Histology shows **giant cells** and granulomatous inflammation. * **Management Rule:** Treat the symptoms (Pain = NSAIDs; Tachycardia = Beta-blockers). Anti-thyroid drugs (PTU/Methimazole) have **no role** because there is no excess synthesis of hormone.

Q: A 40-year-old man presents with gynecomastia. Ultrasound reveals a 1 cm solid mass within the body of the testis. Serum testosterone is 600 ng/dL, and estradiol is 35 pg/mL. What is the most likely diagnosis?

Leydig cell tumor. ***Correct: Leydig cell tumor*** - **Most common** sex cord-stromal tumor in adults, accounting for **1-3%** of all testicular tumors - Arises from interstitial cells that produce **testosterone and estradiol** through aromatization [2], [4] - Classic presentation: **Gynecomastia** (30-40% of cases) due to increased estrogen production or altered testosterone/estrogen ratio [1], [3] - Typically presents as a **small, benign solid mass** (90% are <5 cm and benign) [3] - Ultrasound shows **solid, well-circumscribed intratesticular mass** [3] - Laboratory findings: **Elevated estradiol**, testosterone may be normal or elevated [3] *Incorrect: Sertoli cell tumor* - Less common sex cord-stromal tumor (also can cause gynecomastia but **much rarer** than Leydig cell tumor) - Only **10-20%** present with endocrine manifestations - More likely to present with painless testicular mass without hormonal effects - When hormonal effects occur, usually **estrogen production** but less pronounced than Leydig cell tumor *Incorrect: Spermatocytic tumor* - Germ cell tumor that occurs in **older men** (mean age 50-55 years) - **Does NOT produce hormones** - no gynecomastia - Presents as painless testicular enlargement - Typically larger masses, good prognosis, virtually **never metastasizes** *Incorrect: Granulosa cell tumor* - **Extremely rare** in males (primarily an ovarian tumor) - When it occurs in males, can produce estrogen and cause gynecomastia - However, represents **<1%** of testicular tumors in males - Leydig cell tumor is far more common with this presentation

Q: A patient with hypertension is taking anti-hypertensive drugs but BP is not controlled even after adding diuretics in treatment. Patient's serum electrolyte shows hypokalemia. What is the next step in treatment of this patient?

Spironolactone. ***Spironolactone*** - The combination of **resistant hypertension** (uncontrolled BP despite standard therapy including a diuretic) and **hypokalemia** strongly suggests **Primary Aldosteronism**. - **Spironolactone** is an **aldosterone antagonist** (potassium-sparing diuretic) and is the drug of choice for treating hypertension secondary to hyperaldosteronism, as it corrects both the hypokalemia and the high blood pressure [1]. *KCL* - **Potassium chloride** (KCL) would correct the hypokalemia temporarily, but it does not address the underlying cause (aldosterone excess) or control the **resistant hypertension** [1]. - Supplementation alone is insufficient when the source of hypokalemia is excessive renal potassium loss driven by high aldosterone levels. *Torasemide* - **Torasemide** is a **loop diuretic**; adding it to the regimen will significantly increase potassium excretion, thereby **worsening the existing hypokalemia**. - Loop diuretics are potent potassium-wasting agents and are contraindicated when the suspicion is high for Primary Aldosteronism presenting with hypokalemia. *Hydrochlorothiazide* - **Hydrochlorothiazide** (HCTZ) is a **thiazide diuretic** (also a potassium-wasting drug). - Similar to Torasemide, adding HCTZ would exacerbate the **hypokalemia** and is not the appropriate therapy for hypertension suspected to be caused by mineralocorticoid excess.

Q: A patient presents with complaints of excessive thirst and increased urination of around 6–7 liters per day. He had a history of cerebral trauma one month ago. What is the most appropriate treatment?

Desmopressin. ***Desmopressin***- This clinical presentation of excessive thirst and massive polyuria (6–7 L/day) following **cerebral trauma** strongly suggests **Central Diabetes Insipidus (CDI)**, which results from inadequate production or release of **Antidiuretic Hormone (ADH)/Vasopressin** in the posterior pituitary or hypothalamus.- **Desmopressin** (DDAVP) is a synthetic ADH analog and acts as the highly effective hormone replacement therapy [1], directly addressing the underlying deficiency and drastically reducing urine output.- This causes water permeability of the collecting ducts to increase through binding of ADH to the V2 receptor, which enhances collecting duct water permeability through the insertion of aquaporin (AQP-2) channels into the luminal cell membrane [2].*Hydrochlorothiazide*- This medication is paradoxically used in the treatment of **Nephrogenic Diabetes Insipidus (NDI)**, where the renal tubules fail to respond to ADH [1].- It works by inducing mild volume depletion, which leads to increased proximal tubule reabsorption of solutes and water, thereby decreasing fluid delivery to the collecting duct.*Tolvaptan*- **Tolvaptan** is a **V2 vasopressin receptor antagonist** primarily used to promote water excretion in conditions like **SIADH** (Syndrome of Inappropriate ADH) to correct hyponatremia.- Administering an ADH antagonist in a state of ADH deficiency (Diabetes Insipidus) would be contraindicated, as it would worsen polyuria and potentially cause severe **hypernatremia**.*Insulin*- **Insulin** is the definitive treatment for **Diabetes Mellitus**, a condition characterized by high blood glucose levels and subsequent osmotic diuresis leading to polyuria.- While Diabetes Mellitus can cause polyuria, the history of recent **cerebral trauma** and the absence of expected accompanying symptoms like persistent hyperglycemia and glycosuria make CDI the far more likely diagnosis.

Q: A female presents with amenorrhea and galactorrhea. Serum prolactin is elevated. MRI shows pituitary adenoma. Best management for this patient?

Bromocriptine. ***Bromocriptine***- It is a **dopamine agonist** and represents the initial and standard treatment for **prolactinomas**, effectively reducing tumor size and lowering prolactin levels [1].- Dopamine agonists resolve symptoms such as **amenorrhea** and **galactorrhea** by inhibiting prolactin secretion from the pituitary [1]. *Letrozole*- This is an **aromatase inhibitor** primarily used in the management of hormone-sensitive breast cancer or for ovulation induction in conditions like PCOS. - Its mechanism is unrelated to suppressing prolactin secretion from the pituitary or shrinking a prolactinoma. *Tamoxifen*- This is a **Selective Estrogen Receptor Modulator (SERM)** most commonly used in the treatment and prevention of estrogen receptor-positive breast cancer. - It does not act on dopamine receptors and is ineffective in reversing elevated prolactin levels or associated symptoms. *Goserelin*- This agent is a **Gonadotropin-Releasing Hormone (GnRH) agonist** used primarily for conditions like endometriosis, uterine fibroids, or prostate cancer by initially stimulating then desensitizing the GnRH receptor. - While it suppresses LH and FSH [2], it is not the primary treatment for hyperprolactinemia caused by a pituitary adenoma.

Q: A 35-year-old male has had chronic hypercalcemia for the last 1.5 years, but PTH levels are normal. Which of the following is most likely the cause?

Sarcoidosis. ***Sarcoidosis*** - Causes hypercalcemia via ectopic synthesis of **1,25-dihydroxyvitamin D** (calcitriol) by activated macrophages in the granulomas, leading to increased intestinal calcium absorption [1]. - Although the resulting hypercalcemia usually suppresses PTH (making it low), in chronic, mild cases, the PTH level may appear in the lower end of the **normal reference range**, consistent with the clinical picture of a non-PTH-mediated cause [1]. *Malignancy* - Hypercalcemia related to solid tumors (Humoral Hypercalcemia of Malignancy) is typically mediated by **PTH-related peptide (PTHrP)**, resulting in high calcium. - This non-PTH mediated hypercalcemia leads to appropriate **suppression of the parathyroid glands**, meaning PTH levels would be significantly **low or undetectable**, not normal [1]. *Parathyroid hyperplasia* - This condition represents **primary hyperparathyroidism**, characterized by autonomous secretion of PTH [1]. - In primary hyperparathyroidism, PTH levels are typically inappropriately **elevated** (or grossly high-normal) despite the presence of hypercalcemia, which contradicts a normal PTH value [1]. *C.K.D* - Chronic kidney disease usually results in **hypocalcemia** due to impaired 1-alpha-hydroxylase function and resultant low 1,25(OH)₂D levels [2]. - If hypercalcemia were present (e.g., due to tertiary hyperparathyroidism), PTH levels would be markedly **elevated**, not normal, due to persistent glandular stimulation [2].

Question 1

All of the following are seen in Growth Hormone (GH) deficiency except?

Accepted Answer

Hyperglycemia

Answer

Stunting

Answer

Delayed bone age

Answer

High pitched voice

Question 2

A young lady presents with symptoms of hyperthyroidism, including elevated T4 and TSH levels. On examination, she is not experiencing tachycardia or excessive sweating. Further examination reveals bitemporal hemianopia. What is the next best step in management?

Accepted Answer

Start antithyroid drugs and perform urgent MRI.

Answer

Start beta-blockers immediately.

Answer

Conservative management is sufficient.

Answer

Start antithyroid drugs and wait for symptoms to resolve.

Question 3

A 19-year-old female presents with neck pain for 5 days, making it difficult to wear a tie for her job. She reports a 10-day history of fatigue and lethargy, preceded by flu-like symptoms 20 days ago that resolved spontaneously. Her blood pressure is 110/80 mmHg, and her pulse is 48/min. Her extremities are cold and dry. The neck is very tender. An ECG is normal, TSH is elevated, and ESR is 30 mm/hr. What is the next appropriate step?

Accepted Answer

Aspirin

Answer

Atropine injection

Answer

Levothyroxine administration

Answer

Increase iodine intake in food

Question 4

A patient with cushingoid features presents with hemoptysis. The patient shows no response to a dexamethasone suppression test. What is the most likely diagnosis?

Accepted Answer

Lung cancer with ectopic ACTH production

Answer

Adrenal hyperplasia

Answer

Adrenal adenoma

Answer

Pituitary microadenoma

Question 5

Which of the following statements are true or false? 1. Hirsutism, defined as androgen-dependent excessive male pattern hair growth, affects approximately 25% of women. 2. Virilization refers to a condition in which androgen levels are sufficiently high to cause additional signs and symptoms. 3. Patients with growth hormone excess (i.e., acromegaly) frequently present with hirsutism. 4. A simple and commonly used method to grade hair growth is the modified Ferriman-Gallwey scale. 5. Scores above 8 suggest excess androgen-mediated hair growth.

Accepted Answer

Statements 2, 4, and 5 are true; statements 1 and 3 are false.

Answer

Statements 1, 2, and 3 are true; statements 4 and 5 are false.

Answer

Statements 1, 3, and 5 are true; statements 2 and 4 are false.

Answer

Statements 1, 2, 3, and 4 are true; statement 5 is false.

Question 6

A 40-year-old man presents with gynecomastia. Ultrasound reveals a 1 cm solid mass within the body of the testis. Serum testosterone is 600 ng/dL, and estradiol is 35 pg/mL. What is the most likely diagnosis?

Accepted Answer

Leydig cell tumor

Answer

Sertoli cell tumor

Answer

Spermatocytic tumor

Answer

Granulosa cell tumor

Question 7

A patient with hypertension is taking anti-hypertensive drugs but BP is not controlled even after adding diuretics in treatment. Patient's serum electrolyte shows hypokalemia. What is the next step in treatment of this patient?

Accepted Answer

Spironolactone

Answer

KCL

Answer

Hydrochlorothiazide

Answer

Torasemide

Question 8

A patient presents with complaints of excessive thirst and increased urination of around 6–7 liters per day. He had a history of cerebral trauma one month ago. What is the most appropriate treatment?

Accepted Answer

Desmopressin

Answer

Hydrochlorothiazide

Answer

Tolvaptan

Answer

Insulin

Question 9

A female presents with amenorrhea and galactorrhea. Serum prolactin is elevated. MRI shows pituitary adenoma. Best management for this patient?

Accepted Answer

Bromocriptine

Answer

Tamoxifen

Answer

Goserelin

Answer

Letrozole

Question 10

A 35-year-old male has had chronic hypercalcemia for the last 1.5 years, but PTH levels are normal. Which of the following is most likely the cause?

Accepted Answer

Sarcoidosis

Answer

Malignancy

Answer

C.K.D

Answer

Parathyroid hyperplasia

Endocrinology — MCQs

Endocrinology — MCQs

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