Endocrinology Practice Questions

Q: Which of the following drugs does NOT cause nephrogenic diabetes insipidus?

Acyclovir. **Explanation:** Nephrogenic Diabetes Insipidus (NDI) occurs when the renal tubules are resistant to the action of Antidiuretic Hormone (ADH/Vasopressin), leading to the inability to concentrate urine. **Why Acyclovir is the correct answer:** Acyclovir is primarily associated with **obstructive acute kidney injury (crystal-induced nephropathy)**. When administered intravenously, especially without adequate hydration, acyclovir crystals precipitate in the renal tubules, causing direct damage and obstruction. It does not typically interfere with ADH signaling or the aquaporin-2 channels required to cause NDI. **Why the other options are incorrect:** * **Lithium (Option A):** The most common cause of drug-induced NDI. It enters the principal cells of the collecting duct via ENaC channels and inhibits glycogen synthase kinase-3β, leading to the downregulation of Aquaporin-2 channels. * **Demeclocycline (Option B):** A tetracycline derivative that inhibits the action of ADH. It is actually used therapeutically to treat SIADH because it reliably induces a state of NDI. * **Amphotericin B (Option D):** This antifungal is notorious for nephrotoxicity. It increases the permeability of the tubular membrane, causing a "washout" of the medullary concentration gradient and interfering with ADH responsiveness, leading to NDI and distal Renal Tubular Acidosis (Type 1). **High-Yield Clinical Pearls for NEET-PG:** * **Most common electrolyte cause of NDI:** Hypercalcemia and Hypokalemia. * **Drug of choice for Lithium-induced NDI:** Amiloride (it blocks ENaC channels, preventing Lithium entry into principal cells). * **Management of NDI:** Thiazide diuretics, NSAIDs (Indomethacin), and salt restriction. * **Distinguishing NDI from Central DI:** In NDI, there is **no increase** in urine osmolality following the administration of exogenous Desmopressin (Water Deprivation Test).

Q: An elderly diabetic woman with chronic steroid-dependent bronchospasm has an ileocolectomy for a perforated cecum. She is taken to the ICU intubated and is maintained on broad-spectrum antibiotics, renal dose dopamine, and a rapid steroid taper. On postoperative day 2, she develops a fever of 39.2°C, hypotension, lethargy, and laboratory values remarkable for hypoglycemia and hyperkalemia. Which of the following is the most likely explanation for her deterioration?

Adrenal insufficiency. ### Explanation The correct answer is **Adrenal Insufficiency (Addisonian Crisis)**. **Why it is correct:** The patient has several risk factors for **Secondary Adrenal Insufficiency**: chronic steroid use (causing HPA axis suppression) and a "rapid steroid taper" during a period of extreme physiological stress (major surgery and sepsis). When a steroid-dependent patient faces stress, their body cannot mount the necessary cortisol response. The clinical triad of **refractory hypotension, fever, and altered mental status (lethargy)**, combined with classic biochemical markers—**hypoglycemia** (due to loss of cortisol's gluconeogenic effect) and **hyperkalemia**—strongly points to an adrenal crisis. **Why the other options are incorrect:** * **Sepsis:** While fever and hypotension are seen in sepsis, sepsis typically causes *hyperglycemia* (stress response) rather than hypoglycemia. Furthermore, the electrolyte pattern (hyperkalemia) is more specific to adrenal dysfunction in this context. * **Hypovolemia:** This would explain hypotension and lethargy but does not typically cause high-grade fever, hypoglycemia, or hyperkalemia. * **Acute Tubular Necrosis (ATN):** While ATN can cause hyperkalemia and follows hypotension, it does not explain the fever or the acute hypoglycemia. **NEET-PG High-Yield Pearls:** * **The "Rule of 2s" for HPA suppression:** Suspect suppression if a patient has taken **20 mg** of Prednisone (or equivalent) for **>2 weeks** in the last year. * **Electrolytes:** In *Primary* AI (Addison’s), you see hyperkalemia and hyponatremia (due to mineralocorticoid deficiency). In *Secondary* AI (Steroid withdrawal), mineralocorticoids are often spared by the RAAS, but hyperkalemia can still occur in acute crises due to severe metabolic shifts. * **Management:** Do not wait for ACTH stimulation test results. Treat immediately with **IV Hydrocortisone (100mg bolus)** and aggressive fluid resuscitation.

Q: Hypokalemia with hypertension is seen in which condition?

Primary hyperaldosteronism. **Explanation:** The combination of **hypertension and hypokalemia** is a classic clinical marker for states of mineralocorticoid excess. **1. Why Primary Hyperaldosteronism is correct:** In Primary Hyperaldosteronism (Conn’s Syndrome), autonomous secretion of aldosterone from the adrenal cortex leads to excessive stimulation of the ENaC channels in the renal distal tubule and collecting duct. This results in: * **Sodium retention and water reabsorption:** Leading to volume expansion and **hypertension**. * **Potassium excretion:** Leading to **hypokalemia**. * **Hydrogen ion excretion:** Leading to metabolic alkalosis. Notably, because of the volume expansion, plasma renin activity is suppressed. **2. Why the other options are incorrect:** * **Bartter Syndrome:** This is a "salt-wasting" tubulopathy (defect in the thick ascending limb). While it causes hypokalemia and metabolic alkalosis, it is characterized by **normotension or hypotension** due to chronic volume depletion and activated renin-angiotensin system. * **Primary Hyperparathyroidism:** This condition is characterized by hypercalcemia and hypophosphatemia. It is not typically associated with hypokalemia. * **Diuretic Therapy:** While loop and thiazide diuretics commonly cause **hypokalemia**, they are used to treat hypertension and generally result in **lower blood pressure**, not hypertension (unless the patient has underlying poorly controlled HTN). **NEET-PG High-Yield Pearls:** * **Screening Test:** Aldosterone-to-Renin Ratio (ARR). A high ratio (>20-30) suggests primary hyperaldosteronism. * **Liddle Syndrome:** A rare genetic cause of hypertension + hypokalemia that mimics hyperaldosteronism but presents with **low aldosterone** levels (Pseudohyperaldosteronism). * **Licorice Ingestion:** Can cause hypertension and hypokalemia by inhibiting the enzyme 11β-HSD2, allowing cortisol to act on mineralocorticoid receptors.

Q: Which of the following is not a feature of pseudohypoparathyroidism?

Hypoparathyroidism. Explanation: Pseudohypoparathyroidism (PHP) is a genetic disorder characterized by target organ resistance to Parathyroid Hormone (PTH) [1]. The primary defect lies in the Gsα subunit of the G protein-coupled receptor [3], which prevents PTH from activating its downstream signaling pathway. 1. Why "Hypoparathyroidism" is the correct answer: In PHP, the parathyroid glands are functioning normally, but the body cannot respond to the hormone. Because the kidneys and bones are "deaf" to PTH, the body perceives a deficiency. In response, the parathyroid glands undergo hyperplasia and secrete excessive PTH to compensate. Therefore, patients have Hyperparathyroidism (biochemically), not Hypoparathyroidism [1]. 2. Analysis of Incorrect Options: * Hypocalcemia (B): Since the kidneys cannot respond to PTH, there is decreased calcium reabsorption and impaired Vitamin D activation, leading to low serum calcium [1]. * Hyperphosphatemia (D): PTH normally promotes phosphate excretion (phosphaturia) [2]. Resistance to PTH leads to phosphate retention, resulting in high serum phosphate [1]. * Hyperparathyroidism (A): As explained above, low calcium levels trigger a feedback loop that causes a secondary rise in PTH levels [2]. NEET-PG High-Yield Pearls: * Albright’s Hereditary Osteodystrophy (AHO): A phenotypic presentation of PHP Type 1a featuring short stature, round face, obesity, and shortened 4th and 5th metacarpals [1]. * Pseudopseudohypoparathyroidism (PPHP): Patients have the AHO phenotype but normal biochemical levels (Calcium, Phosphate, and PTH are all normal) because the defect is inherited paternally [1]. * Biochemical Hallmark: High PTH + Low Calcium + High Phosphate.

Q: In thyrotoxicosis, which of the following is commonly seen?

All of the above. In thyrotoxicosis, particularly when caused by Graves' disease, multisystem involvement leads to a variety of clinical manifestations. [2] **Explanation of Options:** * **Pretibial Myxedema (Thyroid Dermopathy):** This is a specific autoimmune manifestation of Graves' disease. It occurs due to the accumulation of glycosaminoglycans (hyaluronic acid) in the dermis, triggered by TSH-receptor antibodies. [2] While it occurs in only 1–5% of patients, it is a classic finding associated with thyrotoxicosis. [1] * **Glycosuria:** Thyrotoxicosis is a "diabetogenic" state. Excess thyroid hormone increases glucose absorption from the gut, accelerates glycogenolysis, and enhances gluconeogenesis. [4] This often leads to postprandial hyperglycemia that exceeds the renal threshold, resulting in glucose in the urine. * **Unilateral Exophthalmos:** While Graves' ophthalmopathy is typically bilateral, it is frequently **asymmetric**. In fact, Graves' disease is the **most common cause of both bilateral and unilateral exophthalmos** in adults. **Why "All of the above" is correct:** Thyrotoxicosis encompasses both the metabolic effects of excess T4/T3 (leading to glycosuria) and the autoimmune associations of Graves' disease (dermopathy and ophthalmopathy). [4] Since all three features can be clinical components of the syndrome, Option D is the most accurate. **High-Yield NEET-PG Pearls:** * **Most common cause of thyrotoxicosis:** Graves' Disease. [4] * **Thyroid Acropachy:** A rare triad of clubbing, periosteal proliferation, and soft tissue swelling seen in severe Graves' disease. * **Cardiac sign:** High-output heart failure and atrial fibrillation are common in elderly patients (Apathetic Hyperthyroidism). [3] * **Stellwag’s sign:** Infrequent or incomplete blinking seen in thyrotoxicosis.

Question 1

Which of the following drugs does NOT cause nephrogenic diabetes insipidus?

Accepted Answer

Acyclovir

Answer

Lithium

Answer

Demeclocycline

Answer

Amphotericin B

Question 2

A 35-year-old emaciated male with a history of disseminated tuberculosis presents with the following features: BP = 85/60 mmHg, low volume pulse of 100 BPM, diffuse hyperpigmentation involving hand creases, serum Na+ = 120 meq/L, and serum K+ = 6.6 meq/L. What is your most immediate response?

Accepted Answer

Suspect adrenocortical insufficiency and start IV steroids.

Answer

Suspect secondary hyperaldosteronism and start IV steroids.

Answer

Suspect gram-negative sepsis and start IV antibiotics.

Answer

Suspect massive pulmonary thromboembolism and start IV Heparin.

Question 3

A patient presented with the following serum parameters: Normal serum ALP, normal PTH level, and increased Ca+ and PO4. What is the most likely cause?

Accepted Answer

Vitamin D intoxication

Answer

Hyperparathyroidism

Answer

Osteoporosis

Answer

Osteomalacia

Question 4

An elderly diabetic woman with chronic steroid-dependent bronchospasm has an ileocolectomy for a perforated cecum. She is taken to the ICU intubated and is maintained on broad-spectrum antibiotics, renal dose dopamine, and a rapid steroid taper. On postoperative day 2, she develops a fever of 39.2°C, hypotension, lethargy, and laboratory values remarkable for hypoglycemia and hyperkalemia. Which of the following is the most likely explanation for her deterioration?

Accepted Answer

Adrenal insufficiency

Answer

Sepsis

Answer

Hypovolemia

Answer

Acute tubular necrosis

Question 5

A 35-year-old woman, on hemodialysis for chronic renal disease, complains of pain in the hands. On examination, the joints are normal with no inflammation or tenderness on palpation. Lab values reveal a low calcium, high phosphate, and high PTH level. What is the most likely diagnosis?

Accepted Answer

Secondary hyperparathyroidism

Answer

Scleroderma

Answer

Gout

Answer

Pseudogout

Question 6

A 53-year-old female patient with a known history of osteoarthritis and diabetes, treated with metformin 500mg, sitagliptin, and glimepiride 1mg for 10 years, was recently diagnosed with chronic kidney disease (CKD) due to NSAID usage. What is the next step in her management regarding her diabetes and pain control?

Accepted Answer

All of the above.

Answer

Stop sitagliptin and start linagliptin.

Answer

Stop metformin and change her to subcutaneous insulin.

Answer

Stop NSAIDs and use opioids for arthritis pain.

Question 7

A 50-year-old lady with a history of carcinoid syndrome complains of flushing and diarrhea. Which of the following statements is not true regarding this syndrome?

Accepted Answer

Bright-red patchy flushing is typically seen with ileal carcinoids.

Answer

Carcinoid crisis occurs in <10% of patients with carcinoid tumors.

Answer

Octreotide injection is used to reduce symptoms of flushing and diarrhea.

Answer

Attacks can be precipitated by stress, alcohol, and large meals.

Question 8

Hypokalemia with hypertension is seen in which condition?

Accepted Answer

Primary hyperaldosteronism

Answer

Bartter syndrome

Answer

Primary hyperparathyroidism

Answer

Diuretic therapy

Question 9

Which of the following is not a feature of pseudohypoparathyroidism?

Accepted Answer

Hypoparathyroidism

Answer

Hyperparathyroidism

Answer

Hypocalcemia

Answer

Hyperphosphatemia

Question 10

In thyrotoxicosis, which of the following is commonly seen?

Accepted Answer

All of the above

Answer

Pretibial myxedema

Answer

Glycosuria

Answer

Unilateral exophthalmos

Endocrinology — MCQs

Endocrinology — MCQs

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