Endocrinology Practice Questions

Q: All of the following are seen in Addison's disease EXCEPT?

Metabolic alkalosis. **Explanation:** Addison’s disease (Primary Adrenocortical Insufficiency) is characterized by the destruction of the adrenal cortex, leading to a deficiency of both **cortisol** and **aldosterone** [1]. **Why Metabolic Alkalosis is the Correct Answer:** Aldosterone normally acts on the distal convoluted tubules and collecting ducts to reabsorb sodium and water in exchange for secreting potassium ($K^+$) and hydrogen ions ($H^+$) [2]. In Addison’s disease, the **absence of aldosterone** leads to the retention of $H^+$ ions. This results in **Hyperchloremic Metabolic Acidosis**, not alkalosis [3]. Metabolic alkalosis is instead a hallmark of mineralocorticoid excess, such as in Conn’s syndrome or Cushing’s syndrome [3]. **Analysis of Incorrect Options:** * **Hyponatremia (A):** Lack of aldosterone causes "salt wasting" (loss of $Na^+$ in urine). Additionally, cortisol deficiency leads to increased ADH secretion, causing water retention and dilutional hyponatremia [4]. * **Hyperkalemia (B):** Without aldosterone, the kidney cannot effectively excrete potassium, leading to its accumulation in the serum [2]. * **Hypotension (C):** Chronic volume depletion (due to $Na^+$ loss) and the loss of cortisol’s permissive effect on catecholamines (which maintain vascular tone) result in orthostatic or persistent hypotension [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Hyperpigmentation:** Seen only in *Primary* insufficiency due to increased ACTH/POMC levels (stimulating melanocytes). It is absent in secondary (pituitary) insufficiency [1]. * **The "Addisonian Triad":** Hyponatremia, Hyperkalemia, and Azotemia. * **Gold Standard Test:** ACTH Stimulation Test (Cosyntropin test) [4]. * **ECG Changes:** Look for tall peaked T-waves due to hyperkalemia.

Q: What is the immediate effect of rapid intravenous insulin administration in a patient with diabetic ketoacidosis?

Hypokalemia. The correct answer is **Hypokalemia (Option A)**. **Mechanism:** Insulin acts as a potent stimulator of the **Na+/K+-ATPase pump** located on cell membranes. When rapid intravenous insulin is administered, it drives potassium from the extracellular fluid (ECF) into the intracellular fluid (ICF) compartment [2]. In Diabetic Ketoacidosis (DKA), patients often have a total body potassium deficit due to osmotic diuresis, despite having normal or high serum potassium levels initially (due to acidosis-induced shift) [1][2]. Rapid insulin administration causes a swift drop in serum potassium, which can lead to life-threatening arrhythmias [4]. **Analysis of Incorrect Options:** * **B. Hypernatremia:** Insulin does not directly cause hypernatremia. In DKA, sodium levels are often low (pseudohyponatremia) due to hyperglycemia; as glucose falls, sodium levels typically normalize or rise slightly, but this is not the "immediate" effect of insulin itself [2]. * **C. Hyperkalemia:** This is the opposite of the physiological effect. While acidosis causes hyperkalemia, insulin therapy is a standard treatment to *lower* potassium [2]. * **D. Hypocalcemia:** Insulin does not have a significant immediate effect on serum calcium levels. **High-Yield Clinical Pearls for NEET-PG:** * **The "Potassium Rule" in DKA:** Never start insulin if the serum potassium is **<3.3 mEq/L**. Always replace potassium first to prevent cardiac arrest [3]. * **The Shift:** For every 0.1 unit decrease in arterial pH, serum potassium increases by approximately 0.6 mEq/L. * **Management Goal:** In DKA, the goal of insulin is to close the anion gap and stop ketogenesis, but monitoring electrolytes (especially K+) is the priority during the first few hours of replacement [3].

Q: Which of the following is NOT a feature of MEN2B syndrome?

Meningioma. **Explanation:** Multiple Endocrine Neoplasia type 2B (MEN2B) is an autosomal dominant syndrome caused by a specific germline mutation in the **RET proto-oncogene** (typically codon 918). It is characterized by a distinct constellation of endocrine and physical findings. **Why Meningioma is the correct answer:** Meningiomas are not associated with MEN2B. They are classically seen in **Neurofibromatosis Type 2 (NF2)**, which is characterized by the mnemonic "MISME" (Multiple Inherited Schwannomas, Meningiomas, and Ependymomas). [1] **Analysis of Incorrect Options:** * **Mucosal Neuromas:** These are the most specific clinical sign of MEN2B, typically appearing as painless, fleshy bumps on the tongue, lips, and eyelids. * **Marfanoid Habitus:** Patients often exhibit a tall, slender build with long extremities and joint laxity, mimicking Marfan syndrome, though they lack the ectopia lentis and aortic root dilation seen in true Marfan syndrome. * **Medullated Corneal Nerve Fibers:** Thickened, visible corneal nerves are a highly characteristic ophthalmologic finding in MEN2B, detectable via slit-lamp examination. **High-Yield Clinical Pearls for NEET-PG:** 1. **Components of MEN2B:** Medullary Thyroid Carcinoma (MTC) - 100%, Pheochromocytoma - 50%, Mucosal Neuromas, and Marfanoid habitus. 2. **MEN2A vs. MEN2B:** MEN2A includes Parathyroid hyperplasia; MEN2B does **not** have parathyroid involvement but includes neuromas and marfanoid features. 3. **MTC Prophylaxis:** In MEN2B, MTC is highly aggressive and occurs early; prophylactic thyroidectomy is recommended in **infancy (before age 1)**. 4. **GI Involvement:** Intestinal ganglioneuromatosis is common, often presenting as chronic constipation or megacolon.

Q: Fasting hyperglycemia is almost always seen in which of the following conditions?

Pheochromocytoma. **Explanation:** **Pheochromocytoma** is a catecholamine-secreting tumor (usually of the adrenal medulla) that leads to fasting hyperglycemia through several synergistic mechanisms [1]. High levels of circulating epinephrine and norepinephrine stimulate **alpha-2 adrenergic receptors** on pancreatic beta cells, which directly inhibits insulin secretion. Simultaneously, catecholamines promote **glycogenolysis** and **gluconeogenesis** in the liver and induce peripheral insulin resistance [1], [2]. This combination of "insulin deficiency" and "glucose overproduction" makes hyperglycemia a classic feature of the condition. **Analysis of Incorrect Options:** * **Gastric Carcinoma:** This is more commonly associated with **hypoglycemia** (if it causes paraneoplastic syndromes or malnutrition) or "dumping syndrome" post-surgery, rather than fasting hyperglycemia. * **Adrenal Tumor:** While a cortisol-secreting adrenal adenoma (Cushing’s Syndrome) can cause hyperglycemia, the term "Adrenal tumor" is non-specific. Pheochromocytoma is the more "classic" and potent driver of acute fasting glucose elevation in this context. * **Carcinoid Tumor:** These tumors primarily secrete serotonin and kallikrein. They are associated with flushing and diarrhea (Carcinoid syndrome) but do not typically present with fasting hyperglycemia. **NEET-PG High-Yield Pearls:** * **Rule of 10s:** Pheochromocytoma is 10% bilateral, 10% malignant, 10% extra-adrenal, and 10% familial. * **Clinical Triad:** Episodic headache, sweating, and tachycardia. * **Diagnosis:** Best initial screening test is **urinary or plasma metanephrines**. * **Management:** Always give **Alpha-blockers (e.g., Phenoxybenzamine) BEFORE Beta-blockers** to avoid a hypertensive crisis from unopposed alpha-stimulation.

Q: All of the following are causes of hypertension with hypokalemia except?

End-stage renal disease. ### Explanation The combination of **hypertension and hypokalemia** is a classic clinical triad suggesting an overactive mineralocorticoid effect, either due to primary excess or secondary activation of the Renin-Angiotensin-Aldosterone System (RAAS) [1]. **Why End-Stage Renal Disease (ESRD) is the correct answer:** In ESRD, the kidneys lose their ability to excrete potassium effectively. As the Glomerular Filtration Rate (GFR) falls below 15-20 mL/min, patients typically develop **hyperkalemia**, not hypokalemia. While hypertension is common in ESRD (due to fluid overload and RAAS activation), the electrolyte profile is characterized by potassium retention. **Analysis of Incorrect Options:** * **Bilateral Renal Artery Stenosis:** This causes decreased renal perfusion, triggering the RAAS. High levels of Renin lead to high Aldosterone (Secondary Hyperaldosteronism), which causes sodium retention (hypertension) and potassium wasting (hypokalemia). * **Primary Hyperaldosteronism (Conn’s Syndrome):** An adrenal adenoma or hyperplasia secretes aldosterone autonomously [2]. This leads to suppressed renin but high aldosterone, causing classic hypertension with hypokalemia. * **Cushing’s Disease:** Excess cortisol can saturate the 11β-HSD2 enzyme in the kidneys. Once saturated, cortisol acts on mineralocorticoid receptors, mimicking aldosterone action and leading to hypertension and hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** 1. **Liddle’s Syndrome:** A rare genetic cause of hypertension + hypokalemia that mimics hyperaldosteronism but presents with **low renin and low aldosterone**. 2. **Screening:** The best initial test for primary hyperaldosteronism is the **Aldosterone-to-Renin Ratio (ARR)**. 3. **Diuretics:** Always rule out diuretic use (Thiazides/Loop) as the most common "extrinsic" cause of hypertension with hypokalemia before pursuing endocrine workups.

Q: A patient presents with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Which of the following medications is the most appropriate treatment?

Antidiuretic hormone antagonists. **Explanation:** **SIADH (Syndrome of Inappropriate Antidiuretic Hormone)** is characterized by the excessive release of ADH (Vasopressin) from the posterior pituitary or ectopic sources [1]. This leads to water retention, dilutional hyponatremia [2], and concentrated urine, despite normal intravascular volume (euvolemic hyponatremia) [2]. 1. **Why Option A is Correct:** **Antidiuretic hormone antagonists** (Vaptans, such as **Tolvaptan** and **Conivaptan**) are the most appropriate pharmacological treatment. They work by selectively blocking V2 receptors in the renal collecting ducts [1], promoting "aquaresis" (excretion of free water without loss of electrolytes). This directly addresses the underlying pathophysiology of ADH excess. 2. **Why Other Options are Incorrect:** * **B. Thiazide Diuretics:** These are contraindicated in SIADH as they inhibit sodium reabsorption in the distal convoluted tubule, which can worsen hyponatremia [2]. * **C. Loop Diuretics:** While sometimes used with saline in severe cases to induce water loss, they are not the primary "most appropriate" medication compared to specific ADH antagonists. * **D. Insulin:** Insulin has no role in the management of SIADH; it is used for glycemic control or hyperkalemia. **NEET-PG High-Yield Pearls:** * **First-line management:** Fluid restriction (<800ml/day) is the initial step for mild-to-moderate SIADH. * **Demeclocycline:** An antibiotic (Tetracycline) used in chronic SIADH because it induces a reversible state of nephrogenic diabetes insipidus. * **Correction Rate:** Avoid rapid correction of hyponatremia to prevent **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)**. Aim for <8-10 mEq/L in 24 hours. * **Common Causes:** Small cell carcinoma of the lung (ectopic ADH), CNS disorders, and drugs (SSRIs, Carbamazepine, Cyclophosphamide).

Q: Which of the following is NOT true about Hashimoto's thyroiditis?

Presence of antithyroid nuclear antibodies. Hashimoto’s Thyroiditis (Chronic Lymphocytic Thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient regions. It is an autoimmune disorder characterized by the destruction of thyroid follicles by T-cells and autoantibodies. **Why Option B is the correct answer:** **Antithyroid nuclear antibodies** are not a feature of Hashimoto’s thyroiditis. While Antinuclear Antibodies (ANA) are markers for systemic autoimmune diseases like SLE, they are not specific to or diagnostic of Hashimoto’s. The primary antibodies involved in Hashimoto's target thyroid-specific antigens, not nuclear components. **Analysis of other options:** * **Option A (Antithyroid microsomal antibodies):** These are now commonly known as **Anti-TPO (Thyroid Peroxidase) antibodies**. They are present in >95% of patients and are the hallmark of the disease. * **Option C (Anti-TSH receptor antibodies):** While typically associated with Graves’ disease (stimulating type), **TSH-receptor blocking antibodies** can occur in Hashimoto’s, contributing to thyroid atrophy and hypothyroidism [1]. * **Option D (Increased levels of thyroid hormones):** Although Hashimoto’s typically causes hypothyroidism, patients can experience a transient thyrotoxic phase called **"Hashitoxicosis"** due to the leakage of preformed hormones from damaged follicles [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for **Hurthle cells** (Askanazy cells)—large eosinophilic follicular cells—and dense lymphocytic infiltrates with **germinal centers**. * **Risk Factor:** Strongly associated with **HLA-DR3 and HLA-DR5**. * **Complication:** Patients have an increased risk of developing **Primary Thyroid B-cell Lymphoma** (MALToma). * **Physical Exam:** Typically presents as a firm, painless, diffuse goiter.

Question 1

All of the following are seen in Addison's disease EXCEPT?

Accepted Answer

Metabolic alkalosis

Answer

Hyponatremia

Answer

Hyperkalemia

Answer

Hypotension

Question 2

What is the immediate effect of rapid intravenous insulin administration in a patient with diabetic ketoacidosis?

Accepted Answer

Hypokalemia

Answer

Hypernatremia

Answer

Hyperkalemia

Answer

Hypocalcemia

Question 3

Which of the following is NOT a feature of MEN2B syndrome?

Accepted Answer

Meningioma

Answer

Mucosal neuroma

Answer

Marfanoid habitus

Answer

Medullated corneal nerve fibers

Question 4

Fasting hyperglycemia is almost always seen in which of the following conditions?

Accepted Answer

Pheochromocytoma

Answer

Gastric carcinoma

Answer

Adrenal tumor

Answer

Carcinoid tumor

Question 5

All of the following are causes of hypertension with hypokalemia except?

Accepted Answer

End-stage renal disease

Answer

Bilateral renal artery stenosis

Answer

Primary hyperaldosteronism

Answer

Cushing's disease

Question 6

A patient presents with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Which of the following medications is the most appropriate treatment?

Accepted Answer

Antidiuretic hormone antagonists

Answer

Thiazide diuretics

Answer

Loop diuretics

Answer

Insulin

Question 7

A 41-year-old woman with a history of multiple endocrine neoplasia syndrome presents with severe diarrhea associated with low gastric acid secretion and a normal gastrin level. Her family history includes parathyroid, pancreatic, and/or pituitary adenomas. Which of the following serum assays would be best to evaluate the possible cause of the diarrhea?

Accepted Answer

Vasoactive intestinal peptide (VIP)

Answer

Glucagon

Answer

Cholecystokinin

Answer

Serotonin

Question 8

Tertiary hyperparathyroidism is defined as:

Accepted Answer

An autonomous state due to monoclonal outgrowth of previously hyperplastic parathyroid glands

Answer

Increased sensitivity to serum calcium

Answer

A condition seen in patients with parathyroid adenoma

Answer

A state dependent on hypothalamic stimulus

Question 9

A female patient presents with anorexia, weight loss, hyperpigmentation, bowel changes, and lightheadedness on standing. The cosyntropin stimulation test shows a random serum cortisol of 11 mcg/dL (normal is greater than or equal to 20 mcg/dL). Serum cortisol 1 hour after 0.25 mg cosyntropin IM is 14 mcg/dL (the rise in cortisol is expected to be > 7 mcg/dL). Aldosterone level is 10 ng/dL. Which of the following is an appropriate treatment for this patient?

Accepted Answer

Hydrocortisone 15 mg and fludrocortisone 0.1 mg daily for life

Answer

Hydrocortisone 15 mg daily for life

Answer

Prednisone 5 mg daily for life

Answer

Prednisone 60 mg daily tapering to 10 mg a day and fludrocortisone 0.1 mg daily for life

Question 10

Which of the following is NOT true about Hashimoto's thyroiditis?

Accepted Answer

Presence of antithyroid nuclear antibodies

Answer

Presence of antithyroid microsomal antibodies

Answer

Presence of anti-TSH receptor antibodies

Answer

Increased levels of thyroid hormones

Endocrinology — MCQs

Endocrinology — MCQs

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