Endocrinology Practice Questions

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: Which of the following are monogenic and autosomal dominant causes of hypertension?

Familial Conn's syndrome and Glucocorticoid-remediable hyperaldosteronism. The correct answer is **A**. This question tests your knowledge of **Monogenic Hypertension**, a group of rare disorders caused by single-gene mutations, typically inherited in an **Autosomal Dominant (AD)** fashion, leading to mineralocorticoid excess. 1. **Why Option A is correct:** * **Glucocorticoid-remediable hyperaldosteronism (GRA/Familial Hyperaldosteronism Type I):** Caused by a chimeric gene crossover between *CYP11B1* and *CYP11B2*. It is AD and results in ACTH-dependent aldosterone secretion. * **Familial Conn’s Syndrome (Familial Hyperaldosteronism Type II/III):** These are AD conditions (e.g., *KCNJ5* mutations) causing autonomous aldosterone production. Both conditions present with hypertension, hypokalemia, and low renin. 2. **Why other options are incorrect:** * **Pregnancy-induced hypertension (Option B):** This is a complex, polygenic, and multifactorial condition, not a monogenic AD disorder. * **17-α hydroxylase deficiency (Options C & D):** While this causes mineralocorticoid-induced hypertension, it is inherited in an **Autosomal Recessive (AR)** pattern. It also presents with delayed puberty/hypogonadism due to impaired sex steroid synthesis. **Clinical Pearls for NEET-PG:** * **Liddle Syndrome:** Another high-yield AD cause of monogenic hypertension. It involves a "gain-of-function" mutation in the ENaC channel. Note: Aldosterone levels are **low** in Liddle syndrome, unlike GRA. * **GRA Diagnosis:** Suspect GRA if hypertension is early-onset and family history is strong. It is uniquely treated with low-dose **Dexamethasone** (which suppresses ACTH). * **Key Differentiator:** In monogenic hypertension, the **Plasma Renin Activity (PRA)** is almost always **suppressed**.

Q: A 53-year-old woman with a past medical history of chronic kidney disease due to diabetic nephropathy is noted to have hyperphosphatemia and hypocalcemia on routine electrolyte measurement. The disturbance is likely a result of metabolic bone disease seen in patients with chronic kidney disease. Which of the following findings is most likely associated with this electrolyte disturbance?

Neuromuscular irritability. The patient presents with **hypocalcemia** and **hyperphosphatemia** secondary to Chronic Kidney Disease (CKD), a condition known as **CKD-Mineral and Bone Disorder (CKD-MBD)**. In CKD, the kidneys fail to excrete phosphate and cannot adequately convert 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D (calcitriol) [3], [4]. This leads to decreased intestinal calcium absorption and reciprocal hypocalcemia. **1. Why Neuromuscular Irritability is Correct:** Low extracellular calcium levels decrease the threshold for depolarization of excitable membranes. This increases the permeability of neuronal membranes to sodium ions, leading to spontaneous action potentials. Clinically, this manifests as **neuromuscular irritability**, which includes: * **Paresthesias** (perioral and fingertips) [1]. * **Tetany** (involuntary muscle contractions). * **Chvostek sign** (facial twitching on tapping the facial nerve). * **Trousseau sign** (carpopedal spasm induced by BP cuff inflation). **2. Why the other options are incorrect:** * **Lethargy and Anorexia:** These are classic symptoms of **hypercalcemia**, not hypocalcemia [2]. Hypercalcemia "moans" include CNS depression and GI upset. * **Tachyarrhythmias:** Hypocalcemia typically causes **QT interval prolongation**, which can lead to Torsades de Pointes (a form of ventricular tachycardia), but it is more classically associated with bradycardia or heart block rather than simple tachyarrhythmias. **High-Yield Clinical Pearls for NEET-PG:** * **CKD-MBD Triad:** Hyperphosphatemia, Hypocalcemia, and Secondary Hyperparathyroidism [3]. * **ECG in Hypocalcemia:** Prolonged QT interval (specifically the ST segment). * **Phosphate Binders:** Used in CKD to manage hyperphosphatemia (e.g., Sevelamer, Calcium acetate). * **Hungry Bone Syndrome:** Severe hypocalcemia seen post-parathyroidectomy in patients with long-standing hyperparathyroidism.

Q: What is the treatment for neurogenic diabetes insipidus?

Desmopressin. **Explanation:** **Neurogenic (Central) Diabetes Insipidus (DI)** is characterized by a deficiency in the synthesis or release of Antidiuretic Hormone (ADH) from the posterior pituitary [1]. This leads to the inability to concentrate urine, resulting in polyuria and polydipsia. **Why Desmopressin is the Correct Answer:** **Desmopressin (dDAVP)** is a synthetic analogue of vasopressin and is the **drug of choice** for Central DI [1]. It is highly selective for **V2 receptors** located in the renal collecting ducts, which mediate the antidiuretic effect [2]. Unlike natural vasopressin, it has minimal activity at V1 receptors (vasoconstrictor receptors), meaning it does not cause significant hypertension or cramping [2]. It also has a longer half-life, allowing for twice-daily dosing via nasal spray, oral, or parenteral routes. **Analysis of Incorrect Options:** * **Vasopressin (A):** While it works, it is non-selective (stimulates both V1 and V2) and has a very short half-life (minutes), making it impractical for long-term maintenance compared to Desmopressin. * **Terlipressin (C):** This is a prodrug of lysine vasopressin with high affinity for **V1 receptors** [2]. It is primarily used in the management of esophageal variceal bleeding and Hepatorenal Syndrome, not DI. * **Amiodarone (D):** This is a Class III antiarrhythmic drug. It is not used to treat DI; in fact, it is more commonly associated with thyroid dysfunction. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The **Water Deprivation Test** is used to diagnose DI [1]. In Central DI, the administration of exogenous Desmopressin will result in a significant increase in urine osmolality (>50%), whereas Nephrogenic DI shows little to no response. * **Nephrogenic DI Treatment:** The drug of choice is **Thiazide diuretics** (paradoxical effect) or Amiloride (especially if lithium-induced). * **Pregnancy:** Desmopressin is safe to use for DI during pregnancy.

Q: All of the following are features of pheochromocytoma except?

Wheezing. **Explanation:** Pheochromocytoma is a catecholamine-secreting tumor arising from the chromaffin cells of the adrenal medulla. The clinical presentation is primarily driven by the excessive release of epinephrine and norepinephrine. **Why Wheezing is the Correct Answer:** Wheezing is not a feature of pheochromocytoma. In fact, catecholamines (especially epinephrine) act on **$\beta_2$-adrenergic receptors** in the bronchioles to cause **bronchodilation**. Therefore, pheochromocytoma would physiologically oppose wheezing rather than cause it. Wheezing is more characteristic of **Carcinoid Syndrome**, which is a common differential diagnosis. **Analysis of Incorrect Options:** * **Hypertensive Paroxysm:** This is the hallmark of the disease. Sudden bursts of catecholamines cause severe vasoconstriction ($\alpha_1$ effect), leading to episodic, life-threatening hypertension. * **Headache:** This is the most common symptom during a paroxysm (seen in >90% of symptomatic patients) due to the sudden increase in cerebral blood pressure. * **Orthostatic Hypotension:** Though counterintuitive, this is a classic feature. It occurs due to **decreased intravascular volume** (chronic vasoconstriction leads to pressure natriuresis) and impaired autonomic reflexes. **High-Yield Clinical Pearls for NEET-PG:** * **The Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paragangliomas), and 10% familial. * **The Classic Triad:** Episodic headache, sweating (diaphoresis), and tachycardia. * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** or plasma free metanephrines. * **Management:** Always give **$\alpha$-blockers first** (e.g., Phenoxybenzamine) before $\beta$-blockers to avoid an unopposed $\alpha$-mediated hypertensive crisis.

Q: Hypogonadotropic hypogonadism with diabetes mellitus is seen in which of the following conditions?

Prader-Willi Syndrome. **Explanation:** **Prader-Willi Syndrome (PWS)** is the correct answer because it is a complex multisystem genetic disorder (deletion of the paternal copy of chromosome 15q11-q13) characterized by hypothalamic dysfunction [1]. This dysfunction leads to **Hypogonadotropic Hypogonadism** (due to GnRH deficiency) and **Hyperphagia**, which results in morbid obesity [1]. The severe obesity and associated insulin resistance frequently lead to the development of **Type 2 Diabetes Mellitus** in these patients. **Analysis of Incorrect Options:** * **Kallman Syndrome:** Characterized by hypogonadotropic hypogonadism and anosmia due to failure of GnRH neuron migration. While it causes infertility, it is not classically associated with obesity or diabetes mellitus. * **Hypothalamic Hamartoma:** These are benign tumors typically presenting with **Precocious Puberty** (due to ectopic GnRH secretion) and gelastic seizures, rather than hypogonadism. * **Granulomatous Hypophysitis:** An inflammatory condition of the pituitary (often associated with Sarcoidosis or TB). While it can cause panhypopituitarism (including hypogonadism), it does not have a primary association with diabetes mellitus; in fact, pituitary failure often *increases* insulin sensitivity. **High-Yield Clinical Pearls for NEET-PG:** * **PWS Triad:** Hypotonia (infancy), Hyperphagia/Obesity (childhood), and Hypogonadism. * **Genetics:** Paternal deletion of 15q11-q13 or Maternal Uniparental Disomy (UPD). * **Hand/Foot findings:** Small hands and feet (acromicria) are characteristic. * **Contrast:** **Angelman Syndrome** involves the same locus but results from *maternal* deletion ("Happy Puppet" syndrome).

Question 1

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 2

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 3

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 4

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 5

Which of the following are monogenic and autosomal dominant causes of hypertension?

Accepted Answer

Familial Conn's syndrome and Glucocorticoid-remediable hyperaldosteronism

Answer

Pregnancy-induced hypertension and Familial Conn's syndrome

Answer

Familial Conn's syndrome and 17-α hydroxylase deficiency

Answer

Glucocorticoid-remediable hyperaldosteronism and 17-α hydroxylase deficiency

Question 6

Calcification in basal ganglia is seen in which of the following conditions?

Accepted Answer

Hypoparathyroidism

Answer

Hypothyroidism

Answer

Hypopituitarism

Answer

Hypoaldosteronism

Question 7

A 53-year-old woman with a past medical history of chronic kidney disease due to diabetic nephropathy is noted to have hyperphosphatemia and hypocalcemia on routine electrolyte measurement. The disturbance is likely a result of metabolic bone disease seen in patients with chronic kidney disease. Which of the following findings is most likely associated with this electrolyte disturbance?

Accepted Answer

Neuromuscular irritability

Answer

Lethargy

Answer

Anorexia

Answer

Tachyarrhythmias

Question 8

What is the treatment for neurogenic diabetes insipidus?

Accepted Answer

Desmopressin

Answer

Vasopressin

Answer

Terlipressin

Answer

Amiodarone

Question 9

All of the following are features of pheochromocytoma except?

Accepted Answer

Wheezing

Answer

Hypertensive paroxysm

Answer

Headache

Answer

Orthostatic hypotension

Question 10

Hypogonadotropic hypogonadism with diabetes mellitus is seen in which of the following conditions?

Accepted Answer

Prader-Willi Syndrome

Answer

Kallman Syndrome

Answer

Hypothalamic hamartoma

Answer

Granulomatous hypophysitis

Endocrinology — MCQs

Endocrinology — MCQs

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