Endocrinology Practice Questions

Q: Gynaecomastia is seen in all of the following conditions except?

Prolactinoma. The correct answer is **A. Prolactinoma**. **1. Why Prolactinoma is the correct answer:** While hyperprolactinemia causes galactorrhea (milky nipple discharge), it does **not** directly cause gynecomastia (proliferation of glandular breast tissue) [1]. Prolactinoma leads to hypogonadotropic hypogonadism by inhibiting GnRH [2]. While the resulting low testosterone can theoretically alter the estrogen/androgen ratio, clinical gynecomastia is rarely seen in pure prolactinomas unless there is significant secondary estrogen elevation or co-secretion [1]. In the context of NEET-PG, prolactinoma is the classic "distractor" often tested against gynecomastia. **2. Analysis of Incorrect Options:** * **TSH secreting adenoma:** Hyperthyroidism increases the production of **Sex Hormone Binding Globulin (SHBG)**. SHBG binds testosterone more avidly than estrogen, leading to an increase in "free estrogen," which stimulates breast tissue. * **HCG secreting tumor:** (e.g., Choriocarcinoma, Germ cell tumors). HCG is structurally similar to LH and stimulates testicular **Leydig cells** to produce both testosterone and estrogen. However, the aromatization to estrogen is disproportionately high, leading to gynecomastia. * **Estrogen secreting tumor:** (e.g., Sertoli or Leydig cell tumors). These directly secrete excess estradiol, shifting the hormonal balance in favor of breast tissue proliferation [3]. **Clinical Pearls for NEET-PG:** * **Physiological Gynecomastia:** Seen in neonates, at puberty (most common), and in the elderly [1]. * **Drug-induced Gynecomastia (High Yield):** Remember the mnemonic **"DISCO"** – **D**igoxin, **I**soniazid, **S**pironolactone (most common drug cause), **C**imetidine, **O**estrogens/Ketoconazole. * **Key Distinction:** Gynecomastia is a proliferation of **glandular** tissue; "Pseudogynecomastia" refers to fat deposition (lipomastia) seen in obese individuals [1].

Q: A 33-year-old man presents with complaints of polydipsia and polyuria. Physical examination reveals a normal JVP at the sternal angle. Laboratory findings include serum sodium of 150 mEq/L, glucose of 120 mg/dL, and serum osmolality of 315 mOsm/kg. Urine studies show urine sodium of 20 mEq/L and urine osmolality of 260 mOsm/kg. Which of the following drugs is most likely to cause this clinical presentation?

lithium. **Explanation:** The patient presents with the classic triad of **Diabetes Insipidus (DI)**: polyuria, polydipsia, and hypernatremia (150 mEq/L) with high serum osmolality (315 mOsm/kg) and inappropriately dilute urine (260 mOsm/kg). The normal JVP indicates a state of euvolemic hypernatremia, typical of DI [1]. **Why Lithium is correct:** Lithium is the most common cause of **drug-induced Nephrogenic Diabetes Insipidus**. It enters the principal cells of the collecting duct through epithelial sodium channels (ENaC) and inhibits glycogen synthase kinase-3 ̧. This interferes with the action of ADH (Vasopressin) on V2 receptors, preventing the insertion of **Aquaporin-2 channels** into the apical membrane [2]. Consequently, the kidneys cannot concentrate urine despite high serum osmolality. **Why other options are incorrect:** * **Cyclophosphamide, Barbiturates, and Nicotine:** These drugs are associated with **SIADH** (Syndrome of Inappropriate Antidiuretic Hormone). SIADH presents with the exact opposite biochemical profile: hyponatremia, low serum osmolality, and inappropriately concentrated urine [3]. **NEET-PG High-Yield Pearls:** * **Diagnosis:** If urine osmolality remains low after Desmopressin administration, it confirms Nephrogenic DI. If it increases by >50%, it is Central DI [1]. * **Management of Lithium-induced DI:** The drug of choice is **Amiloride**, which blocks ENaC channels, preventing lithium from entering the collecting duct cells. * **Other causes of Nephrogenic DI:** Hypercalcemia, hypokalemia, and drugs like Demeclocycline or Amphotericin B [1].

Q: Conn's disease is characterized by an excess of which hormone?

Aldosterone. **Explanation:** **Conn’s Syndrome** (Primary Hyperaldosteronism) is caused by an aldosterone-secreting adenoma of the adrenal cortex (specifically the *zona glomerulosa*) [2]. **Why Aldosterone is Correct:** Aldosterone is a mineralocorticoid that acts on the distal convoluted tubules and collecting ducts of the kidney. It promotes **sodium and water reabsorption** in exchange for **potassium and hydrogen ion excretion** [1]. Consequently, an excess of aldosterone leads to the classic clinical triad of: 1. **Hypertension** (due to sodium/water retention) 2. **Hypokalemia** (due to potassium wasting) 3. **Metabolic Alkalosis** (due to hydrogen ion loss) **Why Other Options are Incorrect:** * **Adrenaline & Noradrenaline (Options A & D):** These are catecholamines secreted by the adrenal medulla [3]. Excess levels are characteristic of **Pheochromocytoma**, which presents with episodic hypertension, palpitations, and diaphoresis. * **Cortisol (Option B):** Excess cortisol leads to **Cushing’s Syndrome**. While it can cause hypertension, it is also associated with distinct features like truncal obesity, striae, and hyperglycemia [2]. **High-Yield NEET-PG Pearls:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A ratio **>20-30** is highly suggestive. * **Confirmatory Test:** Saline infusion test or Oral salt loading test (failure to suppress aldosterone). * **Gold Standard for Lateralization:** Adrenal Venous Sampling (AVS) to distinguish between a unilateral adenoma (Conn's) and bilateral adrenal hyperplasia [4]. * **Treatment:** Surgical excision for unilateral adenoma; **Spironolactone** (aldosterone antagonist) for bilateral hyperplasia.

Q: A man presents with gynecomastia and infertility. What is the most likely cause?

Cimetidine. The correct answer is **Cimetidine**. This is a classic high-yield topic in endocrinology and pharmacology for NEET-PG. **Why Cimetidine is Correct:** Cimetidine, an H2-receptor antagonist, is a notorious cause of drug-induced gynecomastia and infertility through three distinct mechanisms: 1. **Anti-androgenic effects:** It acts as a competitive antagonist at the androgen receptor, blocking testosterone action. 2. **Inhibition of Cytochrome P450:** It inhibits the metabolism of estradiol, leading to increased estrogen levels. 3. **Hyperprolactinemia:** It can stimulate prolactin release, which suppresses the hypothalamic-pituitary-gonadal (HPG) axis, leading to decreased LH/FSH and subsequent infertility. **Analysis of Incorrect Options:** * **B. Omeprazole:** While Proton Pump Inhibitors (PPIs) are used for similar indications as H2 blockers, they do not possess anti-androgenic properties and are not typically associated with gynecomastia. * **C. Erythromycin:** This is a macrolide antibiotic. While it is a potent CYP450 inhibitor, it does not affect sex steroid receptors or prolactin levels. * **D. Digitalis:** Digoxin *can* cause gynecomastia because its steroid nucleus mimics estrogen; however, it is not typically associated with infertility in the same clinical context as cimetidine. **Clinical Pearls for NEET-PG:** * **Mnemonic for Gynecomastia (DISCO):** **D**igoxin, **I**soniazid, **S**pironolactone (most common cause), **C**imetidine, **O**estrogens [1]. * **Ketoconazole** is another common culprit that inhibits steroid synthesis (17,20-desmolase). * When a patient presents with both gynecomastia and infertility, always look for drugs that interfere with the **Androgen:Estrogen ratio** [1].

Q: Which of the following conditions is associated with pretibial myxedema?

Thyrotoxicosis. **Explanation:** **Pretibial Myxedema** (also known as Thyroid Dermopathy) is a classic extrathyroidal manifestation of **Graves' Disease**, the most common cause of **Thyrotoxicosis** [1]. 1. **Why Thyrotoxicosis is Correct:** The underlying mechanism is autoimmune. In Graves' disease, Thyroid Stimulating Immunoglobulins (TSI) bind to TSH receptors located on fibroblasts in the pretibial dermis [1]. This stimulates the overproduction of glycosaminoglycans (primarily hyaluronic acid). The accumulation of these substances leads to non-pitting edema, skin thickening, and an "orange-peel" (peau d'orange) appearance [2]. It is almost exclusively seen in Graves' thyrotoxicosis and is often associated with Graves' ophthalmopathy [1], [3]. 2. **Why Other Options are Incorrect:** * **Hypothyroidism:** While hypothyroidism is associated with "Generalized Myxedema" (due to systemic deposition of mucopolysaccharides), it does **not** cause the localized, infiltrative dermopathy known as pretibial myxedema. * **Hyperparathyroidism:** This condition involves calcium metabolism (stones, bones, abdominal groans, and psychic moans) and has no pathophysiological link to dermal fibroblast stimulation or TSH-receptor antibodies. **High-Yield Clinical Pearls for NEET-PG:** * **The Graves' Triad:** Hyperthyroidism (Goiter), Ophthalmopathy (Exophthalmos), and Dermopathy (Pretibial Myxedema) [1], [3]. * **Location:** Despite the name, it can occasionally occur on the dorsum of the foot or shoulders, though the pretibial area is most common. * **Biopsy Finding:** Increased dermal hyaluronic acid and chondroitin sulfate. * **Management:** Topical glucocorticoids under occlusive dressings are the first-line treatment for symptomatic cases.

Q: Which of the following is contraindicated in diabetics with Congestive Heart Failure?

Pioglitazone. **Explanation:** The correct answer is **Pioglitazone**. **1. Why Pioglitazone is Contraindicated:** Pioglitazone belongs to the **Thiazolidinedione (TZD)** class. Its primary mechanism involves activating the PPAR-gamma receptor, which leads to increased sodium and water reabsorption in the renal collecting ducts. This results in **fluid retention, peripheral edema, and plasma volume expansion** [1]. In patients with pre-existing Congestive Heart Failure (CHF), this volume overload can precipitate acute decompensation. According to clinical guidelines (NYHA Class III or IV), TZDs are strictly contraindicated in symptomatic heart failure. **2. Analysis of Incorrect Options:** * **Empagliflozin (SGLT2 Inhibitor):** Far from being contraindicated, these are now a **gold standard** treatment for patients with both Diabetes and CHF (HFrEF and HFpEF). They promote osmotic diuresis and natriuresis, significantly reducing heart failure hospitalizations. * **Metformin (Biguanide):** Historically avoided in HF due to fears of lactic acidosis; however, current guidelines state it is safe in stable CHF if renal function is preserved (eGFR >30 mL/min) [2]. * **Linagliptin (DPP-4 Inhibitor):** Most DPP-4 inhibitors are safe in CHF [1]. While *Saxagliptin* is associated with increased HF hospitalizations, Linagliptin has shown cardiovascular safety (CARMELINA trial) and is safe to use. **Clinical Pearls for NEET-PG:** * **SGLT2 inhibitors** (Empagliflozin, Dapagliflozin) are the drugs of choice for Diabetics with HF. * **Saxagliptin** is the specific DPP-4 inhibitor to avoid in HF (mnemonic: "S" for Saxagliptin, "S" for Stay away in HF). * **TZDs** (Pioglitazone) also increase the risk of **osteoporotic fractures** and are associated with a potential risk of **bladder cancer**.

Question 1

Increased serum calcium is seen in all of the following except?

Accepted Answer

Primary hyperparathyroidism

Answer

Myxedema

Answer

Sarcoidosis

Answer

Familial hypocalciuric hypercalcemia

Question 2

Gynaecomastia is seen in all of the following conditions except?

Accepted Answer

Prolactinoma

Answer

TSH secreting adenoma

Answer

HCG secreting tumor

Answer

Estrogen secreting tumor

Question 3

Cardiovascular manifestations are more dominant in which of the following conditions?

Accepted Answer

Secondary thyrotoxicosis

Answer

Primary thyrotoxicosis

Answer

Simple goitre

Answer

All of the above

Question 4

A 33-year-old man presents with complaints of polydipsia and polyuria. Physical examination reveals a normal JVP at the sternal angle. Laboratory findings include serum sodium of 150 mEq/L, glucose of 120 mg/dL, and serum osmolality of 315 mOsm/kg. Urine studies show urine sodium of 20 mEq/L and urine osmolality of 260 mOsm/kg. Which of the following drugs is most likely to cause this clinical presentation?

Accepted Answer

lithium

Answer

cyclophosphamide

Answer

barbiturates

Answer

nicotine

Question 5

Conn's disease is characterized by an excess of which hormone?

Accepted Answer

Aldosterone

Answer

Adrenaline

Answer

Cortisol

Answer

Noradrenaline

Question 6

Ketoacidosis without glycosuria is seen in which of the following conditions?

Accepted Answer

Prolonged starvation

Answer

Aspirin poisoning

Answer

Renal tubular acidosis

Answer

Paracetamol poisoning

Question 7

A man presents with gynecomastia and infertility. What is the most likely cause?

Accepted Answer

Cimetidine

Answer

Omeprazole

Answer

Erythromycin

Answer

Digitalis

Question 8

A 40-year-old female with a known history of ischemic heart disease (IHD) is diagnosed with hypothyroidism. Which of the following would be the most appropriate line of management for her?

Accepted Answer

Start levothyroxine at a low dose

Answer

Do not start levothyroxine

Answer

Use levothyroxine

Answer

Thyroid extract is a better option

Question 9

Which of the following conditions is associated with pretibial myxedema?

Accepted Answer

Thyrotoxicosis

Answer

Hypothyroidism

Answer

Hyperparathyroidism

Answer

All of the above

Question 10

Which of the following is contraindicated in diabetics with Congestive Heart Failure?

Accepted Answer

Pioglitazone

Answer

Empagliflozin

Answer

Metformin

Answer

Linagliptin

Endocrinology — MCQs

Endocrinology — MCQs

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