NCLEX-RN Med-Surg: Endocrine Practice Questions

230 Med-Surg: Endocrine questions written for the NCLEX-RN, each with a rationale explaining why the correct answer is correct and why the others are not. Free, no account required. 10 examples are shown below.

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Topics covered

Adrenal Disorders (50)
Parathyroid & Calcium Disorders (40)
Thyroid Disorders (38)
Diabetic Ketoacidosis & HHS (20)
Type 1 & Type 2 Diabetes (20)
Hypoglycemia & Hyperglycemia (20)
Pituitary Disorders (19)
Metabolic Disorders (19)
Diabetic Ketoacidosis (1)
HHNS (1)
Adrenal Crisis (1)
Thyroid Storm (1)

Example questions with rationales

Answers are shown so you can read these as worked examples. To answer them yourself and track what you get wrong, start a practice set.

1Diabetic Ketoacidosis
Based on the clinical presentation and diagnostic findings, what is the most likely primary problem requiring immediate intervention?
- Diabetic ketoacidosis (DKA) - Uncontrolled Type 1 Diabetes with metabolic acidosis — correct
- Acute pancreatitis secondary to diabetic ketoacidosis
- Sepsis from influenza infection causing hyperglycemia
- Diabetic hyperosmolar hyperglycemic state (HHS)
Rationale
The answer: A — Diabetic ketoacidosis (DKA) — Uncontrolled Type 1 Diabetes with metabolic acidosis Think of it this way: In Type 1 diabetes, the pancreas makes NO insulin at all. Insulin is the key that opens body cells to glucose. Without it, the cells are starving even though blood sugar is sky-high. The body's backup plan: break down fat for energy, but fat breakdown produces ketone bodies (acidic byproducts). As ketones accumulate, the blood becomes acidic — a dangerous state called ketoacidosis. DKA is the classic, life-threatening emergency of Type 1 diabetes, and the clinical picture of hyperglycemia + ketones + metabolic acidosis points directly to it. Why A is right: DKA is the hallmark emergency of Type 1 diabetes mellitus (T1DM). Without insulin, glucose cannot enter cells → cells shift to fat catabolism (beta-oxidation) → acetyl-CoA excess → ketone body production (acetoacetate, beta-hydroxybutyrate, acetone) → metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L) + hyperglycemia (usually >250 mg/dL) + ketonemia (high ketones in blood) + ketonuria (ketones in urine). The classic presentation: polyuria (frequent urination), polydipsia (excessive thirst), Kussmaul respirations (deep, rapid breathing as the body tries to blow off CO2 to compensate for metabolic acidosis), fruity breath odor (from acetone), nausea/vomiting, and altered mental status in severe cases. Why the others are wrong: - B: Acute pancreatitis secondary to DKA — pancreatitis can COMPLICATE DKA (the clinical picture may overlap with abdominal pain and elevated lipase), but it is not the PRIMARY presenting problem. DKA is the main diagnosis driving the clinical picture. - C: Sepsis from influenza infection causing hyperglycemia — influenza infection can trigger DKA (infection is a common precipitant of DKA by increasing stress hormones that oppose insulin), but 'stress hyperglycemia from sepsis' would not typically produce the profound ketoacidosis (ketonemia, very low pH, high ketones) seen in T1DM. The metabolic acidosis with ketones points to DKA, not simple infection-induced hyperglycemia. - D: Diabetic hyperosmolar hyperglycemic state (HHS) — HHS (formerly called HONK — hyperosmolar non-ketotic coma) occurs primarily in Type 2 diabetes. Unlike DKA, HHS has VERY HIGH glucose (often >600 mg/dL), profound dehydration, minimal to no ketones (because residual insulin in T2DM prevents significant ketogenesis), and no significant metabolic acidosis. HHS does NOT occur in classic T1DM with no insulin production. Remember: DKA diagnosis requires the 'DKA triad': (1) Hyperglycemia (usually >250 mg/dL), (2) Metabolic acidosis (pH <7.3, bicarb <18), (3) Ketosis (ketones in blood and urine). Management: IV fluids + insulin infusion + electrolyte replacement (especially potassium — insulin drives K+ into cells, causing dangerous hypokalemia during treatment). Monitor glucose hourly and electrolytes every 1-2 hours. Technical note: DKA precipitants (the 'I's): Infection (most common), Insufficient insulin (missed doses, new diagnosis), Ischemia/Infarction (MI, stroke), Intoxication (alcohol), Inflammation (pancreatitis). Insulin must NOT be started until potassium is ≥3.5 mEq/L — insulin drives K+ into cells and can cause fatal hypokalemia if started in a patient with already-low K+. Close monitoring: pH, glucose, K+, phosphate, anion gap (AG = Na - [Cl + bicarb]; normal AG = 8-12, elevated in DKA). DKA is resolved when: glucose <200 mg/dL + pH >7.3 + bicarb >15 + AG normalized — NOT when glucose alone normalizes.
2Type 1 & Type 2 Diabetes
A client newly diagnosed with Type 1 diabetes mellitus asks the nurse what caused the disease. Which response by the nurse is most accurate?
- Your pancreas no longer produces insulin because the immune system destroyed the insulin-producing cells — correct
- Your body does not use insulin properly due to excess weight and poor diet
- Your pancreas produces too much insulin, causing the body to become resistant
- Your diabetes is caused by stress and emotional factors affecting hormone levels
Rationale
Type 1 diabetes is an autoimmune disorder where the immune system destroys the beta cells in the pancreas, resulting in absolute insulin deficiency. Type 2 diabetes involves insulin resistance and relative insulin deficiency, often associated with obesity and lifestyle factors.
3Hypoglycemia & Hyperglycemia
A client with diabetes is experiencing hypoglycemia and is alert and able to swallow. Which intervention should the nurse implement first?
- Administer glucagon subcutaneously
- Give 15-20 grams of fast-acting carbohydrates — correct
- Call the healthcare provider immediately
- Place the client in the prone position
Rationale
For a conscious client with hypoglycemia, the first intervention is to administer 15-20 grams of fast-acting carbohydrates, such as 4-6 oz of juice, 3-4 glucose tablets, or 1 tablespoon of sugar. This is the rule of 15: wait 15 minutes, recheck glucose, and repeat if needed.
4Thyroid Disorders
A client is scheduled for a thyroidectomy. Which preoperative instruction is most important for the nurse to provide?
- Demonstrate how to support the neck when coughing — correct
- Practice deep breathing exercises
- Explain that the voice will be unaffected after surgery
- Describe the procedure for radioactive iodine therapy
Rationale
After thyroidectomy, clients must support their neck when coughing, turning, or sitting up to prevent strain on the surgical incision and promote healing. Voice changes can occur due to laryngeal nerve damage, so the nurse should NOT guarantee an unaffected voice. Deep breathing is important but supporting the neck is more specific to thyroid surgery.
5Thyroid Disorders
A client with hyperthyroidism is prescribed propranolol. The nurse understands that this medication is given primarily to:
- Treat the underlying cause of hyperthyroidism
- Block the conversion of T4 to T3
- Control cardiovascular symptoms such as tachycardia and anxiety — correct
- Prevent thyroid storm during surgery
Rationale
Propranolol is a beta-blocker used in hyperthyroidism to control sympathetic nervous system symptoms including tachycardia, palpitations, anxiety, tremor, and heat intolerance. It does not treat the underlying cause or block hormone synthesis. PTU and methimazole block hormone synthesis and T4-T3 conversion. Beta-blockers may be used preoperatively but are primarily for symptom control.
6Adrenal Disorders
A client with Addison's disease is being discharged. Which dietary instruction is most appropriate?
- Limit sodium intake to 2 grams daily
- Increase potassium-rich foods
- Add extra salt to meals and carry salt packets — correct
- Follow a low-protein diet
Rationale
Clients with Addison's disease have mineralocorticoid deficiency leading to sodium loss and hyponatremia. They are instructed to liberalize salt intake—adding extra salt to meals and carrying salt packets for stress or illness—to prevent hyponatremia and volume depletion. Limiting sodium would be contraindicated.
7Parathyroid & Calcium Disorders
A client with hypercalcemia is receiving IV normal saline and furosemide. The nurse understands that the purpose of furosemide in this treatment is to:
- Correct fluid overload caused by aggressive hydration
- Promote calcium excretion by inhibiting calcium reabsorption in the loop of Henle — correct
- Prevent potassium loss during calcium-wasting diuresis
- Reduce calcium absorption from the gastrointestinal tract
Rationale
Loop diuretics like furosemide inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, which also blocks calcium reabsorption. This promotes calcium excretion in the urine, helping to lower serum calcium levels. This is used after adequate hydration in the treatment of hypercalcemia.
8Adrenal Disorders
A client with Cushing's syndrome develops a wound infection. Which nursing intervention is the priority?
- Monitor for signs of infection and notify the provider immediately — correct
- Apply warm compresses to the wound
- Encourage high-protein diet
- Schedule wound care for once daily
Rationale
Clients with Cushing's syndrome have impaired immune function due to cortisol's immunosuppressive effects, making them susceptible to infections. Infection can also worsen cortisol excess. The priority is close monitoring for infection signs (fever, increased WBC, wound changes) and prompt provider notification for early intervention.
9Diabetic Ketoacidosis & HHS
Select all that apply: When caring for a client with DKA receiving an insulin drip, the nurse monitors for and reports which of the following ECG changes that may indicate hypokalemia:
- Flattened T waves — correct
- U waves — correct
- Peaked T waves
- Prolonged QT interval — correct
Rationale
Hypokalemia causes characteristic ECG changes including flattened T waves, U waves, ST segment depression, and prolonged QT interval. Peaked T waves and narrowed QRS complexes are seen with hyperkalemia. The nurse must monitor for these changes because insulin therapy drives potassium intracellularly, potentially causing dangerous hypokalemia during DKA treatment.
10Parathyroid & Calcium Disorders
Select all potential complications of untreated chronic hypoparathyroidism: (SATA)
- Renal calculi
- Cataracts — correct
- Osteitis fibrosa cystica
- Cardiac arrhythmias — correct
Rationale
Chronic hypoparathyroidism can lead to: cataracts (due to calcium deposition in the lens), cardiac arrhythmias (due to altered cardiac conduction), and neuropsychiatric changes. Osteitis fibrosa cystica is a complication of hyperparathyroidism (excess PTH), not hypoparathyroidism. Renal calculi are associated with hypercalcemia/hyperparathyroidism.

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Example questions with rationales

Answers are shown so you can read these as worked examples. To answer them yourself and track what you get wrong, start a practice set.

1Diabetic Ketoacidosis

Based on the clinical presentation and diagnostic findings, what is the most likely primary problem requiring immediate intervention?

Diabetic ketoacidosis (DKA) - Uncontrolled Type 1 Diabetes with metabolic acidosis — correct
Acute pancreatitis secondary to diabetic ketoacidosis
Sepsis from influenza infection causing hyperglycemia
Diabetic hyperosmolar hyperglycemic state (HHS)

Rationale

The answer: A — Diabetic ketoacidosis (DKA) — Uncontrolled Type 1 Diabetes with metabolic acidosis Think of it this way: In Type 1 diabetes, the pancreas makes NO insulin at all. Insulin is the key that opens body cells to glucose. Without it, the cells are starving even though blood sugar is sky-high. The body's backup plan: break down fat for energy, but fat breakdown produces ketone bodies (acidic byproducts). As ketones accumulate, the blood becomes acidic — a dangerous state called ketoacidosis. DKA is the classic, life-threatening emergency of Type 1 diabetes, and the clinical picture of hyperglycemia + ketones + metabolic acidosis points directly to it. Why A is right: DKA is the hallmark emergency of Type 1 diabetes mellitus (T1DM). Without insulin, glucose cannot enter cells → cells shift to fat catabolism (beta-oxidation) → acetyl-CoA excess → ketone body production (acetoacetate, beta-hydroxybutyrate, acetone) → metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L) + hyperglycemia (usually >250 mg/dL) + ketonemia (high ketones in blood) + ketonuria (ketones in urine). The classic presentation: polyuria (frequent urination), polydipsia (excessive thirst), Kussmaul respirations (deep, rapid breathing as the body tries to blow off CO2 to compensate for metabolic acidosis), fruity breath odor (from acetone), nausea/vomiting, and altered mental status in severe cases. Why the others are wrong: - B: Acute pancreatitis secondary to DKA — pancreatitis can COMPLICATE DKA (the clinical picture may overlap with abdominal pain and elevated lipase), but it is not the PRIMARY presenting problem. DKA is the main diagnosis driving the clinical picture. - C: Sepsis from influenza infection causing hyperglycemia — influenza infection can trigger DKA (infection is a common precipitant of DKA by increasing stress hormones that oppose insulin), but 'stress hyperglycemia from sepsis' would not typically produce the profound ketoacidosis (ketonemia, very low pH, high ketones) seen in T1DM. The metabolic acidosis with ketones points to DKA, not simple infection-induced hyperglycemia. - D: Diabetic hyperosmolar hyperglycemic state (HHS) — HHS (formerly called HONK — hyperosmolar non-ketotic coma) occurs primarily in Type 2 diabetes. Unlike DKA, HHS has VERY HIGH glucose (often >600 mg/dL), profound dehydration, minimal to no ketones (because residual insulin in T2DM prevents significant ketogenesis), and no significant metabolic acidosis. HHS does NOT occur in classic T1DM with no insulin production. Remember: DKA diagnosis requires the 'DKA triad': (1) Hyperglycemia (usually >250 mg/dL), (2) Metabolic acidosis (pH <7.3, bicarb <18), (3) Ketosis (ketones in blood and urine). Management: IV fluids + insulin infusion + electrolyte replacement (especially potassium — insulin drives K+ into cells, causing dangerous hypokalemia during treatment). Monitor glucose hourly and electrolytes every 1-2 hours. Technical note: DKA precipitants (the 'I's): Infection (most common), Insufficient insulin (missed doses, new diagnosis), Ischemia/Infarction (MI, stroke), Intoxication (alcohol), Inflammation (pancreatitis). Insulin must NOT be started until potassium is ≥3.5 mEq/L — insulin drives K+ into cells and can cause fatal hypokalemia if started in a patient with already-low K+. Close monitoring: pH, glucose, K+, phosphate, anion gap (AG = Na - [Cl + bicarb]; normal AG = 8-12, elevated in DKA). DKA is resolved when: glucose <200 mg/dL + pH >7.3 + bicarb >15 + AG normalized — NOT when glucose alone normalizes.

2Type 1 & Type 2 Diabetes

A client newly diagnosed with Type 1 diabetes mellitus asks the nurse what caused the disease. Which response by the nurse is most accurate?

Your pancreas no longer produces insulin because the immune system destroyed the insulin-producing cells — correct
Your body does not use insulin properly due to excess weight and poor diet
Your pancreas produces too much insulin, causing the body to become resistant
Your diabetes is caused by stress and emotional factors affecting hormone levels

Rationale

Type 1 diabetes is an autoimmune disorder where the immune system destroys the beta cells in the pancreas, resulting in absolute insulin deficiency. Type 2 diabetes involves insulin resistance and relative insulin deficiency, often associated with obesity and lifestyle factors.

3Hypoglycemia & Hyperglycemia

A client with diabetes is experiencing hypoglycemia and is alert and able to swallow. Which intervention should the nurse implement first?

Administer glucagon subcutaneously
Give 15-20 grams of fast-acting carbohydrates — correct
Call the healthcare provider immediately
Place the client in the prone position

Rationale

For a conscious client with hypoglycemia, the first intervention is to administer 15-20 grams of fast-acting carbohydrates, such as 4-6 oz of juice, 3-4 glucose tablets, or 1 tablespoon of sugar. This is the rule of 15: wait 15 minutes, recheck glucose, and repeat if needed.

4Thyroid Disorders

A client is scheduled for a thyroidectomy. Which preoperative instruction is most important for the nurse to provide?

Demonstrate how to support the neck when coughing — correct
Practice deep breathing exercises
Explain that the voice will be unaffected after surgery
Describe the procedure for radioactive iodine therapy

Rationale

After thyroidectomy, clients must support their neck when coughing, turning, or sitting up to prevent strain on the surgical incision and promote healing. Voice changes can occur due to laryngeal nerve damage, so the nurse should NOT guarantee an unaffected voice. Deep breathing is important but supporting the neck is more specific to thyroid surgery.

5Thyroid Disorders

A client with hyperthyroidism is prescribed propranolol. The nurse understands that this medication is given primarily to:

Treat the underlying cause of hyperthyroidism
Block the conversion of T4 to T3
Control cardiovascular symptoms such as tachycardia and anxiety — correct
Prevent thyroid storm during surgery

Rationale

Propranolol is a beta-blocker used in hyperthyroidism to control sympathetic nervous system symptoms including tachycardia, palpitations, anxiety, tremor, and heat intolerance. It does not treat the underlying cause or block hormone synthesis. PTU and methimazole block hormone synthesis and T4-T3 conversion. Beta-blockers may be used preoperatively but are primarily for symptom control.

6Adrenal Disorders

A client with Addison's disease is being discharged. Which dietary instruction is most appropriate?

Limit sodium intake to 2 grams daily
Increase potassium-rich foods
Add extra salt to meals and carry salt packets — correct
Follow a low-protein diet

Rationale

Clients with Addison's disease have mineralocorticoid deficiency leading to sodium loss and hyponatremia. They are instructed to liberalize salt intake—adding extra salt to meals and carrying salt packets for stress or illness—to prevent hyponatremia and volume depletion. Limiting sodium would be contraindicated.

7Parathyroid & Calcium Disorders

A client with hypercalcemia is receiving IV normal saline and furosemide. The nurse understands that the purpose of furosemide in this treatment is to:

Correct fluid overload caused by aggressive hydration
Promote calcium excretion by inhibiting calcium reabsorption in the loop of Henle — correct
Prevent potassium loss during calcium-wasting diuresis
Reduce calcium absorption from the gastrointestinal tract

Rationale

Loop diuretics like furosemide inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, which also blocks calcium reabsorption. This promotes calcium excretion in the urine, helping to lower serum calcium levels. This is used after adequate hydration in the treatment of hypercalcemia.

8Adrenal Disorders

A client with Cushing's syndrome develops a wound infection. Which nursing intervention is the priority?

Monitor for signs of infection and notify the provider immediately — correct
Apply warm compresses to the wound
Encourage high-protein diet
Schedule wound care for once daily

Rationale

Clients with Cushing's syndrome have impaired immune function due to cortisol's immunosuppressive effects, making them susceptible to infections. Infection can also worsen cortisol excess. The priority is close monitoring for infection signs (fever, increased WBC, wound changes) and prompt provider notification for early intervention.

9Diabetic Ketoacidosis & HHS

Select all that apply: When caring for a client with DKA receiving an insulin drip, the nurse monitors for and reports which of the following ECG changes that may indicate hypokalemia:

Flattened T waves — correct
U waves — correct
Peaked T waves
Prolonged QT interval — correct

Rationale

Hypokalemia causes characteristic ECG changes including flattened T waves, U waves, ST segment depression, and prolonged QT interval. Peaked T waves and narrowed QRS complexes are seen with hyperkalemia. The nurse must monitor for these changes because insulin therapy drives potassium intracellularly, potentially causing dangerous hypokalemia during DKA treatment.

10Parathyroid & Calcium Disorders

Select all potential complications of untreated chronic hypoparathyroidism: (SATA)

Renal calculi
Cataracts — correct
Osteitis fibrosa cystica
Cardiac arrhythmias — correct

Rationale

Chronic hypoparathyroidism can lead to: cataracts (due to calcium deposition in the lens), cardiac arrhythmias (due to altered cardiac conduction), and neuropsychiatric changes. Osteitis fibrosa cystica is a complication of hyperparathyroidism (excess PTH), not hypoparathyroidism. Renal calculi are associated with hypercalcemia/hyperparathyroidism.