Calling all nursing students! Sharpen your skills with our Endocrine Disorders NCLEX Quiz: Free Practice to Ace It! Dive into essential endocrine disorders NCLEX questions with targeted scenarios on Cushing's syndrome NCLEX quiz challenges, diabetes insipidus NCLEX practice drills, and broader endocrine system NCLEX questions - all designed to simulate the real exam. Whether you're reviewing for success or testing your knowledge, this NCLEX endocrine disorder practice is your go-to resource. Ready to boost your confidence and conquer exam day? Jump in now for endocrine disorders NCLEX questions or explore our NCLEX endocrine disorders practice test and start acing it today!
What is the primary cause of Cushing's syndrome?
Overproduction of aldosterone by the adrenal cortex.
Chronic use of exogenous glucocorticoid medications.
Chronic hypersecretion of thyroid hormones.
Excess secretion of growth hormone by the pituitary.
Cushing's syndrome results from prolonged exposure to high cortisol levels, most commonly due to exogenous glucocorticoid therapy. Endogenous causes such as pituitary or adrenal tumors are less frequent. Recognizing medication history is crucial for diagnosis and treatment. For more details, see Mayo Clinic.
Which physical feature is characteristic of Cushing's syndrome?
Decreased blood pressure
Cold intolerance and weight gain
Moon-shaped face
Increased muscle bulk in the extremities
Fat redistribution in Cushing's syndrome leads to the classic 'moon face' appearance. Other features include truncal obesity, buffalo hump, and muscle weakness. Recognizing these signs helps in early diagnosis and management. For more information, see Endocrine Society.
Which electrolyte imbalance is most commonly associated with Cushing's syndrome?
Hyponatremia
Hypermagnesemia
Hypokalemia
Hypercalcemia
Excess cortisol has mineralocorticoid effects leading to increased renal potassium excretion and resultant hypokalemia. Sodium retention may also occur but hypokalemia is more pronounced clinically. Monitoring electrolytes is essential in managing these patients. Learn more at NCBI.
What is the hallmark clinical feature of diabetes insipidus?
Oliguria and concentrated urine
Bradycardia and hypotension
Persistent hypoglycemia
Excessive dilute urine output
Diabetes insipidus is characterized by the inability to concentrate urine, leading to large volumes of dilute urine. This causes polydipsia and risk of dehydration if fluid intake is inadequate. Distinguishing from other causes of polyuria is key for correct treatment. See Mayo Clinic for more.
Central diabetes insipidus results from a deficiency of which hormone?
Antidiuretic hormone (ADH)
Aldosterone
Thyroid-stimulating hormone (TSH)
Prolactin
Central diabetes insipidus is caused by impaired synthesis or release of antidiuretic hormone (ADH) from the posterior pituitary. Without ADH, the kidneys cannot concentrate urine, leading to polyuria. Differentiating central from nephrogenic DI guides appropriate therapy. For details visit NCBI.
A laboratory finding in nephrogenic diabetes insipidus is:
High urine specific gravity
Low urine specific gravity
Hyperglycemia
Hyponatremia
Nephrogenic diabetes insipidus involves renal insensitivity to ADH, resulting in excretion of large volumes of dilute urine with low specific gravity. Serum sodium may be elevated, but urine specific gravity remains low. Differentiation from central DI is confirmed by response to desmopressin. More info at Endocrine Society.
Which symptom is most indicative of hypothyroidism?
Weight loss
Tachycardia
Heat intolerance
Cold intolerance
Hypothyroidism slows metabolic processes, resulting in cold intolerance, weight gain, bradycardia, and fatigue. Cold intolerance is a hallmark symptom distinguishing it from hyperthyroidism. Early detection and thyroid hormone replacement mitigate complications. Read more at Mayo Clinic.
Primary hyperthyroidism is characterized by which set of lab values?
Elevated T3 and T4 with elevated TSH
Low T3 and T4 with decreased TSH
Elevated T3 and T4 with decreased TSH
Low T3 and T4 with elevated TSH
In primary hyperthyroidism, the thyroid gland overproduces T3 and T4, which exerts negative feedback on the pituitary, leading to suppressed TSH. This lab pattern confirms the diagnosis and distinguishes it from secondary causes. Accurate interpretation guides appropriate treatment. More at NCBI.
Addison's disease is defined by:
Thyroid hormone deficiency
Primary adrenal insufficiency
Excess cortisol production
Secondary hyperaldosteronism
Addison's disease involves destruction or dysfunction of the adrenal cortex, leading to deficient cortisol and aldosterone production. It is termed primary adrenal insufficiency and presents with hypotension, hyperpigmentation, and electrolyte imbalances. Differentiating primary from secondary causes affects management. Learn more at Mayo Clinic.
A patient with Cushing's syndrome is at highest risk for which metabolic complication?
Hyperglycemia
Hypokalemia
Hypoglycemia
Hypernatremia
Excess cortisol increases gluconeogenesis and insulin resistance, predisposing patients to hyperglycemia and diabetes mellitus. This metabolic alteration is a common complication of Cushing's syndrome. Monitoring blood glucose levels is vital in management. More details at NCBI.
What is the first-line pharmacological treatment for central diabetes insipidus?
Desmopressin acetate
Spironolactone
Hydrochlorothiazide
Levothyroxine
Desmopressin acetate, a synthetic analog of ADH, is the treatment of choice for central diabetes insipidus as it replaces deficient hormone. Thiazide diuretics like hydrochlorothiazide are used in nephrogenic DI, not central. Proper dosing reduces polyuria and polydipsia. See Endocrine Society.
A patient with SIADH will demonstrate which serum finding?
Decreased serum sodium
Increased serum osmolality
Elevated serum calcium
Increased serum potassium
SIADH causes water retention without sodium retention, diluting serum sodium and resulting in hyponatremia. Serum osmolality is also low in this condition. Recognizing these lab values is key to diagnosis and management. Learn more at Mayo Clinic.
What is the underlying mechanism of Graves' disease?
Autoimmune production of thyroid-stimulating immunoglobulins
Thyroid carcinoma
Iodine deficiency
Pituitary TSH-secreting adenoma
Graves' disease is an autoimmune disorder in which thyroid-stimulating immunoglobulins bind to the TSH receptor, causing unregulated thyroid hormone production. This mechanism distinguishes it from other hyperthyroid etiologies like adenomas or carcinomas. Understanding this guides immunomodulatory treatment approaches. More at NCBI.
A key nursing intervention for a patient after thyroidectomy is:
Encourage increased iodine intake
Monitor for signs of hypocalcemia such as tingling and muscle twitching
Maintain the patient in Trendelenburg position
Administer lithium to reduce hormone release
Thyroidectomy can inadvertently damage or remove the parathyroid glands, leading to hypocalcemia. Signs include perioral numbness, tingling, and positive Chvostek's sign. Early detection allows prompt calcium replacement. For more, see NCBI.
Which therapy is indicated for myxedema coma?
Beta blockers
Radioactive iodine
Intravenous levothyroxine
Oral propylthiouracil
Myxedema coma is a life-threatening severe hypothyroid state requiring immediate intravenous levothyroxine to restore thyroid hormone levels. Oral therapy is unreliable due to ileus and poor absorption. Supportive measures and glucocorticoids may also be needed. See Medscape.
What is the mechanism of action of propylthiouracil in hyperthyroidism?
Inhibition of thyroid peroxidase and peripheral T4 to T3 conversion
Stimulation of iodide uptake
Increased clearance of thyroid hormones
Blockade of TSH receptors
Propylthiouracil inhibits thyroid peroxidase, blocking iodination of tyrosine residues in thyroglobulin, and also inhibits peripheral conversion of T4 to the more active T3. This dual action makes it effective in reducing thyroid hormone levels. Monitor for liver toxicity. More info at NCBI.
A characteristic clinical feature of pheochromocytoma is:
Episodic hypertension and tachycardia
Chronic hypotension
Hyperkalemia
Persistent hypoglycemia
Pheochromocytomas are catecholamine-secreting tumors causing episodic hypertension, tachycardia, headache, and sweating. These paroxysmal episodes differentiate them from other causes of hypertension. Diagnosis involves measuring metanephrines and imaging. Visit Mayo Clinic.
Which diet is most appropriate for a patient with hyperthyroidism?
Low-carbohydrate diet
Low-fat diet
High-calorie, high-protein diet
High-iodine diet
Hyperthyroidism increases metabolic rate, leading to weight loss and muscle wasting. A high-calorie, high-protein diet helps meet increased energy needs and maintain nutritional status. Sodium and fluids are also important to replace insensible losses. More dietary guidance at Endocrine Society.
In the water deprivation test, what response to desmopressin indicates central diabetes insipidus?
Marked increase in serum ADH with no urine change
No change in urine osmolality
Significant increase in urine osmolality
Immediate decrease in urine output before desmopressin
In central DI, exogenous desmopressin replaces deficient ADH and leads to increased urine osmolality. In nephrogenic DI, renal insensitivity means desmopressin has little effect. This response distinguishes the two conditions. See NCBI.
Ketoconazole is used in Cushing's syndrome to control cortisol levels by:
Inhibiting adrenal steroid synthesis
Enhancing hepatic cortisol metabolism
Stimulating pituitary ACTH production
Blocking cortisol receptors
Ketoconazole inhibits cytochrome P450 enzymes involved in cortisol biosynthesis in the adrenal cortex. This off-label use helps reduce cortisol levels in patients with Cushing's syndrome who are not surgical candidates. Liver function monitoring is required. More at Endocrine Society.
During an Addisonian crisis, the nurse's highest priority is to:
Restore vascular volume with intravenous fluids
Administer oral glucocorticoids
Give IV insulin
Provide oxygen therapy only
Addisonian crisis leads to severe hypotension and shock; urgent IV fluid resuscitation with isotonic saline is critical to restore vascular volume and perfusion. Glucocorticoids should follow after initial stabilization. Delaying fluids increases mortality risk. Guidelines at Mayo Clinic.
Ectopic ACTH production, as seen in small cell lung carcinoma, results in:
Syndrome of inappropriate ADH secretion
Secondary hypothyroidism
Primary adrenal insufficiency
Paraneoplastic Cushing's syndrome
Small cell lung carcinoma can produce ACTH, leading to paraneoplastic Cushing's syndrome with hypercortisolism. This ectopic secretion bypasses pituitary regulation. Identifying the source is essential for targeted therapy. Read more at NCBI.
What is the primary purpose of radioactive iodine therapy in hyperthyroidism?
Block iodine uptake
Destroy thyroid tissue to reduce hormone production
Increase thyroid hormone release
Stimulate TSH release
Radioactive iodine is selectively taken up by thyroid follicles and emits beta particles that destroy thyroid tissue, reducing hormone synthesis. It is a definitive treatment for Graves' disease and toxic nodular goiter. Patients often require lifelong thyroid hormone replacement afterward. For details see Endocrine Society.
The primary concern during thyroid storm is:
Hyperthermia and cardiovascular collapse
Hyponatremia
Hypotension without fever
Hypoglycemia
Thyroid storm is a life-threatening hypermetabolic state with fever, tachycardia, and risk of arrhythmias and cardiovascular collapse. Immediate treatment includes antithyroid medications, beta-blockers, cooling, and supportive care. Early recognition reduces mortality. See NCBI.
Which laboratory findings distinguish secondary adrenal insufficiency?
Low ACTH and high cortisol
High ACTH and low cortisol
High ACTH and high cortisol
Low ACTH and low cortisol
Secondary adrenal insufficiency results from pituitary dysfunction leading to decreased ACTH and subsequent low cortisol production. Aldosterone is usually normal because it is regulated by the renin-angiotensin system. Distinguishing primary from secondary guides treatment. More at Mayo Clinic.
What perioperative glucocorticoid management is appropriate for adrenalectomy?
Switch to fludrocortisone monotherapy
Maintain only the patient's usual oral dose
Administer stress-dose hydrocortisone perioperatively
Discontinue glucocorticoids 48 hours before surgery
Patients undergoing adrenalectomy require stress-dose glucocorticoids to prevent acute adrenal insufficiency due to loss of cortisol production. Hydrocortisone is typically given before, during, and after surgery and tapered gradually. Failure to provide adequate steroids risks hypotension and shock. Guidelines at NCBI.
Which laboratory findings confirm SIADH?
High serum sodium and high serum osmolality
High serum osmolality and low urine osmolality
High urine osmolality and low serum osmolality
Low urine osmolality and low serum osmolality
SIADH is characterized by inappropriate ADH secretion causing water reabsorption, which concentrates urine (high urine osmolality) while diluting serum (low serum osmolality and hyponatremia). These lab results are diagnostic when other causes are excluded. Treatment focuses on fluid restriction and addressing the underlying cause. More at Endocrine Society.
Which dexamethasone suppression test result differentiates Cushing's disease from ectopic ACTH production?
Suppression with low-dose dexamethasone only
No suppression with either low or high-dose dexamethasone
Suppression of cortisol with high-dose but not low-dose dexamethasone
Suppression with both low and high-dose dexamethasone
In Cushing's disease (pituitary adenoma), the pituitary retains partial feedback sensitivity, so cortisol suppresses with high-dose dexamethasone but not with low-dose. Ectopic ACTH-producing tumors lack this feedback and show no suppression. This test helps localize the source of ACTH. See NCBI.
A mutation in the thyroid peroxidase gene leads to congenital hypothyroidism by:
Impaired iodide oxidation and coupling of iodotyrosines
Reduced TSH receptor binding
Overproduction of anti-thyroid antibodies
Excessive thyroid hormone degradation
Thyroid peroxidase catalyzes iodide oxidation and coupling of iodotyrosines on thyroglobulin. Mutations in this enzyme prevent thyroid hormone synthesis, leading to congenital hypothyroidism. Early detection and levothyroxine replacement prevent developmental delays. More at NCBI.
Tolvaptan is used in SIADH management primarily through:
Increased ADH release
Enhanced ADH degradation
Antagonism of renal V2 receptors
Inhibition of aquaporin channel synthesis
Tolvaptan is a selective V2 receptor antagonist that blocks ADH action in the renal collecting ducts, promoting free water excretion (aquaresis) and correcting hyponatremia. It is indicated for euvolemic and hypervolemic hyponatremia such as SIADH. Liver function monitoring is necessary. See Endocrine Society.
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Study Outcomes
Identify Pathophysiological Mechanisms -
Describe the hormonal imbalances and underlying causes of Cushing's syndrome, diabetes insipidus, and thyroid disorders to strengthen your foundational knowledge.
Differentiate Clinical Manifestations -
Distinguish the signs, symptoms, and lab findings of hyper- versus hypothyroidism and other endocrine imbalances for accurate assessment.
Interpret Diagnostic Lab Values -
Analyze cortisol, ADH, TSH, T3, and T4 results to inform clinical decision-making in endocrine system NCLEX questions.
Apply Evidence-Based Nursing Interventions -
Outline priority actions and patient education strategies for managing endocrine disorders in a simulated NCLEX quiz format.
Evaluate Clinical Scenarios -
Solve case-based questions to test your mastery of endocrine disorders NCLEX questions and refine your critical-thinking skills.
Develop Test-Taking Strategies -
Employ proven techniques to approach NCLEX endocrine disorder practice items with confidence and accuracy.
Cheat Sheet
Cushing's Syndrome Pathophysiology -
Excess cortisol from a pituitary adenoma or long-term glucocorticoid therapy disrupts the HPA axis, causing hyperglycemia, hypertension, and the classic "moon face" and "buffalo hump." Use the "CUSHING" mnemonic (Central obesity, Urinary cortisol ↑, Skin thinning, Hypertension, Infection risk ↑, Neoplasia risk, Glucose ↑) to lock in clinical signs. Labs show ↑ serum cortisol with low ACTH in adrenal causes and ↑ ACTH in pituitary adenomas (Endocrine Society).
Diabetes Insipidus vs. SIADH -
In diabetes insipidus (DI), ADH deficiency leads to polyuria, polydipsia, and very low urine specific gravity (<1.005), whereas SIADH causes water retention and concentrated urine (>1.030). Remember "DI = Dry Inside" to differentiate high serum sodium in DI from dilutional hyponatremia in SIADH. This distinction is tested frequently in NCLEX endocrine disorder practice questions, so watch fluid balance and lab values carefully (Mayo Clinic).
Thyroid Imbalance Labs -
Hyperthyroidism shows ↑ T3/T4 and ↓ TSH, while hypothyroidism flips the pattern with low T3/T4 and high TSH. A handy tip: "T3 and T4 have 3 - 4 letters, so they come from the Thyroid; TSH has 3 letters but comes from the pituitary" to avoid confusion. Always correlate lab trends with symptoms like weight changes, heart rate, and temperature for endocrine system NCLEX questions (American Thyroid Association).
Addison's Disease Essentials -
Primary adrenal insufficiency causes ↓ cortisol and aldosterone, leading to hyperkalemia, hyponatremia, hypotension, and hyperpigmentation. Use the phrase "Addison's Add Salt" to recall aldosterone deficiency and salt wasting. Diagnostic tests will show low cortisol levels that fail to rise after an ACTH stimulation test (NIH).
Nursing Interventions & Prioritization -
When tackling endocrine disorders NCLEX questions, prioritize fluid and electrolyte monitoring, daily weights, and strict I&O to detect shifts early. Administer hormone replacements - desmopressin for DI, levothyroxine for hypothyroidism, or hydrocortisone for adrenal insufficiency - per protocol and educate the patient on dose timing and side effects. Always assess vital signs and neurologic status first to ensure stability in any NCLEX endocrine disorder practice scenario.
