Endocrine System NCLEX Practice Questions

A blood glucose below 70 mg/dL with adrenergic symptoms (shakiness, diaphoresis, anxiety, hunger, palpitations) indicates hypoglycemia. Because this client is alert and can swallow, the first action is the Rule of 15: give 15 g of fast-acting simple carbohydrate — 4 oz of regular juice, 3-4 glucose tablets, or 1 tbsp honey — then recheck the glucose in 15 minutes and repeat if it is still below 70 mg/dL. Once the glucose normalizes, a complex-carbohydrate-plus-protein snack helps prevent recurrence.

(B) is wrong because glucagon is reserved for hypoglycemia when the client is unconscious or unable to swallow safely; giving it to an alert client who can take oral carbohydrate is unnecessary and commonly causes nausea/vomiting. (C) is wrong because the fat and protein in cheese and the fiber in whole-grain crackers slow gastric emptying and glucose absorption, so they do not raise blood glucose fast enough for acute hypoglycemia (a protein snack is appropriate only AFTER the glucose has normalized). (D) is dangerous — giving insulin drives glucose intracellularly and would deepen the hypoglycemia, risking seizures, coma, and death.

Clinical pearl: ‘Rule of 15 — 15 g carb, wait 15 minutes, recheck.’ Fast-acting carbohydrate first; glucagon only when the client cannot safely swallow.

Levothyroxine absorption is significantly reduced by food, so it should be taken on an empty stomach with water 30-60 minutes before breakfast (bedtime dosing at least 3-4 hours after the last meal is an acceptable alternative). Consistent timing keeps thyroid hormone levels stable, and the client must understand that hypothyroidism requires lifelong replacement.

(A) is wrong because taking it with breakfast lowers bioavailability substantially — food, especially fiber and soy, binds the drug in the GI tract. (C) is wrong because calcium and iron (and antacids and PPIs) chelate levothyroxine and markedly decrease absorption; these should be separated by at least 4 hours. (D) is wrong because levothyroxine is replacement therapy for a gland that no longer makes enough hormone; stopping it when the client feels well causes symptoms to return and can precipitate severe hypothyroidism. Feeling better is a sign the dose is working, not a reason to stop.

Clinical pearl: ‘Levothyroxine — empty stomach, water only, wait 30-60 minutes, and keep 4 hours away from calcium/iron/antacids.’ Signs of over-replacement (palpitations, tremor, weight loss, insomnia) should be reported.

Pituitary surgery is a classic trigger for central diabetes insipidus (DI) from disrupted ADH release. The picture is textbook: massive dilute urine output (350 mL/hr, specific gravity 1.002) with rising serum sodium (152 mEq/L; normal 135-145). Desmopressin (DDAVP) is synthetic ADH that binds V2 receptors in the renal collecting ducts, restores water reabsorption, reduces urine output, and corrects the hypernatremia.

(A) is wrong and dangerous — the client is already losing large volumes of water; restricting fluids would accelerate dehydration, worsen hypernatremia, and risk hypovolemic shock and seizures. (C) is wrong because a loop diuretic increases urine output and free-water loss, worsening both the polyuria and the hypernatremia. (D) is wrong because serum sodium is already dangerously high; adding sodium would worsen hypernatremia and neurologic risk.

Clinical pearl: DI = ‘dry inside’ — dilute urine, high serum sodium; treat with DDAVP and free-water replacement. (Contrast with SIADH, which is the opposite: concentrated urine, low serum sodium, treated with fluid restriction.)

Hyperosmolar hyperglycemic state (HHS) occurs mainly in older adults with type 2 diabetes and is defined by extreme hyperglycemia (usually greater than 600 mg/dL), high serum osmolality (greater than 320 mOsm/kg), profound dehydration, and the ABSENCE of significant ketosis or acidosis. This client’s glucose of 940 mg/dL, osmolality of 335 mOsm/kg, normal pH, and ketone-negative status fit HHS precisely. Enough endogenous insulin remains to suppress ketogenesis but not to control glucose, so no ketoacidosis develops.

(A) is wrong because diabetic ketoacidosis is defined by ketones and metabolic acidosis (low pH, low bicarbonate) — both absent here. (C) is wrong because hypoglycemia is a LOW glucose, the opposite of this presentation. (D) is wrong because SIADH is a water-retention disorder producing dilutional hyponatremia and concentrated urine, not severe hyperglycemia.

Clinical pearl: HHS is ‘high and dry’ — the highest glucose values you’ll see, severe dehydration, but no ketones. Management mirrors DKA: aggressive isotonic fluid resuscitation first, then IV insulin, with close potassium monitoring.

Thyroid storm (thyrotoxic crisis) is a life-threatening exacerbation of hyperthyroidism marked by hyperthermia (often greater than 104°F), extreme tachycardia/tachyarrhythmias, hypertension with a widened pulse pressure, and CNS changes (agitation, delirium). It is typically precipitated by a stressor such as infection, surgery, trauma, or abrupt withdrawal of antithyroid medication — here, pneumonia in a client with untreated Graves disease. This is a medical emergency.

(A) is wrong because myxedema coma is the opposite (severe hypothyroidism): hypothermia, bradycardia, hypotension, and decreased level of consciousness. (C) is wrong because Addisonian crisis presents with HYPOtension, hyponatremia, hyperkalemia, and hypoglycemia — not the hypertension and hyperthermia seen here. (D) is wrong because DKA presents with hyperglycemia, Kussmaul respirations, fruity breath, and ketoacidosis, none of which are described.

Clinical pearl: Thyroid storm = ‘everything sped up and on fire’ — fever + extreme tachycardia + agitation after a stressor. Treatment targets the metabolic surge: a beta-blocker (e.g., propranolol) for the cardiac effects, an antithyroid drug (PTU or methimazole), and glucocorticoids, plus active cooling and supportive care.

NPH is an intermediate-acting insulin with an onset of about 1-2 hours, a peak of roughly 4-12 hours, and a duration of roughly 12-18 hours (up to about 24 hours in some references). The risk of hypoglycemia is greatest at the peak, so a client dosing at 0700 is most vulnerable in the late-morning through late-afternoon window and should be sure to eat lunch and monitor glucose during that time.

(A) is wrong because NPH has not yet begun to act within 30 minutes; onset is 1-2 hours. (B) matches onset, not peak — glucose-lowering is only beginning to ramp up at 1-2 hours. (D) is wrong because 18-24 hours is well past the 4-12 hour peak of NPH; by then its glucose-lowering effect has largely waned, so this is not the window of greatest hypoglycemia risk.

Clinical pearl: Match meals and snacks to insulin peaks. Rapid-acting (lispro/aspart) peaks in ~1-2 hours (give within 15 minutes of eating); regular peaks in ~2-4 hours; NPH peaks in ~4-12 hours; long-acting glargine and degludec are essentially peakless. Knowing the peak tells you when hypoglycemia is most likely.

Addison disease is primary adrenal insufficiency with deficiency of both aldosterone and cortisol. Loss of aldosterone causes the kidneys to waste sodium and retain potassium, producing hyponatremia and hyperkalemia. Loss of cortisol impairs gluconeogenesis, producing hypoglycemia (especially under the stress of a crisis). The sodium and water loss also explains the hypovolemia, hypotension, and tachycardia seen here.

(B) is wrong because it describes the OPPOSITE electrolyte pattern (seen with mineralocorticoid EXCESS, such as Cushing or hyperaldosteronism), not deficiency. (C) is wrong because Addison causes hypoglycemia, not hyperglycemia, and does not typically alter calcium (hypercalcemia points to hyperparathyroidism or malignancy). (D) is wrong on both counts — sodium is low and glucose is low in Addison, not high.

Clinical pearl: Addison = you ‘add’ potassium and ‘lose’ sodium and sugar — hyperkalemia, hyponatremia, hypoglycemia, hypotension. Adrenal crisis is treated urgently with IV hydrocortisone and IV normal saline (often with dextrose).

In SIADH, excess antidiuretic hormone causes the kidneys to retain water, producing dilutional hyponatremia and concentrated urine. Management targets the water excess and protects the brain from hyponatremic cerebral edema. (B) Fluid restriction is the cornerstone treatment because the problem is retained water. (C) For severe, symptomatic hyponatremia (sodium of 119 with confusion), a small volume of 3% hypertonic saline is given to cautiously raise serum sodium; correction must be slow to avoid osmotic demyelination. (D) Seizure precautions are appropriate because a sodium this low predisposes to cerebral edema and seizures. (F) Frequent sodium monitoring is essential to guide therapy and ensure correction is gradual.

(A) is wrong because encouraging free water would further dilute the serum sodium and worsen the hyponatremia — the opposite of what is needed. (E) is wrong because desmopressin is synthetic ADH used to TREAT diabetes insipidus; giving it in SIADH would add to the already-excessive ADH effect and deepen the hyponatremia.

Clinical pearl: SIADH = ‘Soaked Inside’ — too much water, low sodium; restrict fluids. DI is the mirror image (dry inside, high sodium) and is the disorder that actually gets DDAVP.

DKA management follows a clear priority sequence. (A) Isotonic IV fluid (0.9% normal saline) is started FIRST to restore the profound volume deficit from osmotic diuresis and to improve perfusion before insulin shifts fluid and electrolytes intracellularly. (C) A continuous IV regular insulin infusion (about 0.1 unit/kg/hr) stops ketogenesis and lowers glucose; it is safe to start here because potassium is above 3.3-3.5 mEq/L. (D) Dextrose is added to the IV fluids once glucose falls to roughly 200-250 mg/dL so the insulin infusion can continue to clear ketones without causing hypoglycemia. (F) Potassium must be watched closely because insulin and correction of acidosis drive potassium into cells; the initially ‘high-normal’ 5.4 will fall, and replacement is started as it drops (typically once it is below about 5.0 mEq/L).

(B) is wrong because bicarbonate is NOT given routinely; it is reserved for severe acidosis (pH below about 7.0) and can cause paradoxical CNS acidosis and worsen hypokalemia — this client’s pH of 7.20 corrects with fluids and insulin. (E) is wrong because subcutaneous NPH (intermediate-acting) is unreliable in a dehydrated, poorly perfused client and is not used for acute DKA; IV regular insulin is required.

Clinical pearl: DKA priority order is Fluids, then Insulin, then Potassium (and dextrose once glucose hits ~200). Never push insulin before checking potassium.

Cushing syndrome results from chronic cortisol EXCESS, and its manifestations reflect cortisol’s metabolic effects. (B) Cortisol redistributes fat centrally, causing truncal obesity, a supraclavicular ‘buffalo hump,’ and thin extremities from muscle-protein catabolism. (D) The characteristic rounded ‘moon’ face is from the same fat redistribution. (E) Cortisol promotes gluconeogenesis and insulin resistance, producing hyperglycemia. (F) Protein catabolism thins the skin and weakens capillary and connective-tissue support, causing easy bruising and purple/violaceous striae.

(A) is wrong because hypotension and salt craving are hallmarks of adrenal INSUFFICIENCY (Addison disease); cortisol excess instead causes sodium and water retention with HYPERtension. (C) is wrong because bronze hyperpigmentation is seen in primary adrenal insufficiency (Addison), where elevated ACTH stimulates melanocytes — it is not a feature of cortisol excess.

Clinical pearl: Cushing is ‘too much cortisol’ — think of an over-stressed body: high sugar, high blood pressure, central fat, thin fragile skin, and muscle wasting. Addison is the mirror image (low sodium/BP, high potassium, hyperpigmentation, salt craving).