NCLEX Practice Exam for Endocrine Disorders 2

EXPLANATION

✔ Correct answer:

Blood glucose levels. Cushing’s syndrome is characterized by prolonged exposure to high cortisol levels, which contribute to hyperglycemia (elevated blood glucose levels). Cortisol increases blood glucose by stimulating gluconeogenesis (glucose production in the liver) and reducing insulin sensitivity, leading to insulin resistance. As the condition is successfully treated, cortisol levels decrease, allowing for improved insulin sensitivity and lower blood glucose levels.

Cortisol, a glucocorticoid hormone produced by the adrenal glands, plays a crucial role in metabolism, stress response, and immune function. Excessive cortisol disrupts normal glucose homeostasis, promoting persistent hyperglycemia, which can lead to secondary diabetes. Once Cushing’s syndrome is treated—whether through medication, surgery, or tapering corticosteroid use—blood glucose levels typically decline toward normal levels.

Imagine a car with a stuck accelerator, constantly increasing speed (glucose production). When the issue is fixed, the car (blood sugar) naturally slows down and returns to normal speed. Similarly, reducing excess cortisol helps restore normal glucose regulation.

Successful treatment of Cushing’s syndrome requires ongoing monitoring and patient education to prevent complications related to hormonal adjustments.

• Monitor blood glucose levels closely, as patients previously experiencing hyperglycemia may need adjustments in their diabetes management plan.
• Educate patients on signs of hypoglycemia if their body is adjusting to lower cortisol levels.
• Encourage a balanced diet and regular physical activity to maintain glucose stability and overall health.
• Support the patient through changes in energy levels, weight, and mood, as cortisol reduction affects metabolism and mental well-being.
• Schedule regular follow-ups to assess adrenal function and potential recurrence of symptoms.

✘ Incorrect answer options:

Hair thinning or loss. Hair thinning, known as telogen effluvium, can be caused by excess cortisol, but it does not necessarily decrease immediately with treatment. Hair regrowth is a slower process and depends on multiple factors, including nutrition, stress levels, and underlying health conditions.

Bone mineral density. Cushing’s syndrome leads to osteoporosis due to cortisol-induced bone resorption and reduced calcium absorption. However, bone mineral density does not immediately decrease with successful treatment; instead, it gradually improves over time.

Menstrual cycle regularity. Women with Cushing’s syndrome often experience irregular or absent menstrual cycles due to cortisol’s suppression of gonadotropin-releasing hormone (GnRH), which affects estrogen and progesterone levels. As treatment progresses, menstrual cycles are expected to become more regular, not decrease.

EXPLANATION

✔Correct answer:

Distended neck veins.  The syndrome of inappropriate antidiuretic hormone (SIADH) is characterized by excessive secretion of antidiuretic hormone (ADH), leading to water retention, dilutional hyponatremia, and increased extracellular fluid volume. Distended neck veins are a clinical sign of fluid overload, which can occur as a complication of SIADH due to the kidneys’ inability to excrete excess water. This reflects a physiological imbalance in fluid and electrolyte homeostasis, potentially progressing to pulmonary edema or cerebral edema if untreated. The presence of distended neck veins indicates increased central venous pressure, a serious complication requiring urgent intervention.

In SIADH, elevated ADH levels cause the kidneys to reabsorb water, decreasing serum osmolality and sodium concentration. This expands plasma volume, elevating venous pressure and manifesting as distended neck veins. Severe hyponatremia can also lead to neurological symptoms (e.g., confusion, seizures) due to cerebral swelling.

Picture the body as a sponge. In SIADH, too much water (ADH effect) soaks into the sponge, making it swell (fluid overload), and you can see the pressure build up in the tubes (veins) trying to hold it all.

Nurses must vigilantly monitor and manage SIADH complications to prevent further deterioration. Key actions include:

• Assess for additional signs of fluid overload, such as crackles in the lungs, edema, or shortness of breath.
• Monitor serum sodium levels and osmolality frequently, reporting critical values (e.g., sodium <120 mEq/L) promptly.
• Restrict fluid intake as prescribed to reduce water retention and correct hyponatremia gradually.
• Administer hypertonic saline or demeclocycline if ordered, while observing for rapid sodium correction risks (e.g., osmotic demyelination).
• Provide psychological support for confusion or anxiety caused by neurological effects of hyponatremia.

✘Incorrect answer options:

Muscle spasms and tetanic contractions. This is incorrect because muscle spasms and tetany are associated with hypocalcemia, not SIADH. SIADH causes hyponatremia, which may lead to neurological symptoms like seizures, but not calcium-related neuromuscular irritability. Tetany would be more relevant to parathyroid dysfunction.

Unintentional weight loss. Unintentional weight loss is not a complication of SIADH. Instead, patients typically gain weight due to water retention. Weight loss might suggest hyperthyroidism or malignancy-related SIADH etiology, but it is not a direct complication of the condition itself.

Increased urine output. Increased urine output contradicts SIADH pathophysiology, where ADH excess reduces urine production, concentrating the urine and retaining water. Polyuria would be more indicative of diabetes insipidus, a condition with insufficient ADH, not SIADH.

EXPLANATION

✔ Correct answer:

Phentolamine. Pheochromocytoma is a rare adrenal gland tumor that causes excessive secretion of catecholamines (epinephrine and norepinephrine), leading to severe hypertension, tachycardia, sweating, and headaches. An acute hypertensive crisis in pheochromocytoma can be life-threatening and requires immediate intervention.

Phentolamine, a nonselective alpha-adrenergic blocker, is the drug of choice for rapidly lowering blood pressure in patients with pheochromocytoma. It works by blocking alpha-1 adrenergic receptors, leading to vasodilation and a rapid decrease in blood pressure. Phentolamine is administered intravenously (IV) during a hypertensive crisis for immediate effect.

In pheochromocytoma, excessive catecholamines cause persistent activation of alpha-adrenergic receptors, leading to vasoconstriction and severe hypertension. By blocking these receptors, phentolamine prevents catecholamine-induced vasoconstriction, allowing blood vessels to relax and blood pressure to decrease.

Imagine a water hose with extreme pressure due to a tightly closed nozzle. The more it stays closed, the higher the pressure inside. Phentolamine acts like loosening the nozzle, allowing water (blood) to flow freely and reducing pressure.

Managing a hypertensive crisis in pheochromocytoma requires close monitoring and careful medication administration.

• Monitor blood pressure and heart rate continuously during and after phentolamine administration.
• Be prepared for hypotension, which can occur due to excessive vasodilation.
• Administer intravenous fluids cautiously if hypotension develops.
• Educate the patient about pheochromocytoma management, including preoperative alpha-blockade before surgery (if applicable).
• Collaborate with the healthcare team for potential beta-blocker therapy (e.g., propranolol) after alpha-blockade to control tachycardia.

✘ Incorrect answer options:

Methyldopa. This centrally acting alpha-2 agonist is used for chronic hypertension and gestational hypertension. However, it is not appropriate for hypertensive crises in pheochromocytoma as it does not rapidly counteract catecholamine effects.

Mannitol. Mannitol is an osmotic diuretic used to reduce intracranial pressure and treat acute kidney injury. It does not have a role in hypertensive crisis management.

Felodipine. Felodipine is a calcium channel blocker used for long-term hypertension management. While calcium channel blockers may help control blood pressure, they do not act quickly enough for a hypertensive emergency and do not directly counteract catecholamine-induced vasoconstriction.

EXPLANATION

✔ Correct answer:

"Take glipizide 30 minutes before meals for the best effect." Glipizide is a second-generation sulfonylurea used to treat type 2 diabetes mellitus (T2DM) by stimulating the pancreas to release insulin. It works by binding to pancreatic beta-cell receptors, triggering insulin secretion in response to meals.

For optimal effectiveness, glipizide should be taken 30 minutes before meals to allow time for insulin release before food intake, preventing post-meal hyperglycemia. Taking it after a meal can reduce its effectiveness because it may not coincide with glucose absorption.

Glipizide lowers blood glucose by increasing insulin secretion from the pancreas. It relies on functional beta cells and is not effective for type 1 diabetes or for patients with severe beta-cell dysfunction. The timing of administration is crucial to ensure insulin release aligns with carbohydrate absorption.

Think of glipizide as an alarm that reminds the pancreas to release insulin. Taking it before a meal is like setting an alarm to wake up before work starts—ensuring insulin is ready when glucose enters the bloodstream. Taking it after a meal is like waking up after work has already begun, making insulin response delayed and less effective.

Since glipizide increases insulin secretion, hypoglycemia is a major risk, especially if meals are skipped or delayed.

• Educate the patient to take glipizide 30 minutes before meals for maximum effect.
• Monitor for signs of hypoglycemia (sweating, dizziness, tachycardia, confusion) and instruct the patient to carry glucose tablets or a snack.
• Avoid alcohol, as it can cause a disulfiram-like reaction (flushing, nausea, vomiting, palpitations) and worsen hypoglycemia.
• Emphasize regular blood glucose monitoring, as sulfonylureas can cause variable glucose responses.
• Assess renal and liver function, as glipizide is metabolized by the liver and excreted through the kidneys. Impaired function increases the risk of drug accumulation and hypoglycemia.

✘ Incorrect answer options:

"This medication may lower your sodium levels, so you'll need monthly sodium checks." Glipizide does not significantly affect sodium levels. Instead, it primarily lowers blood glucose by increasing insulin secretion. Monthly sodium monitoring is unnecessary.

"Once you start taking glipizide, you won’t need to monitor your blood glucose." This is incorrect because blood glucose monitoring remains essential to assess medication effectiveness and prevent hypoglycemia. Glipizide can cause fluctuations in blood sugar levels, requiring dose adjustments based on glucose readings.

"To prevent heartburn, take glipizide after a meal." Taking glipizide after a meal delays its onset and reduces its effectiveness in controlling post-meal blood sugar. Heartburn is not a common side effect of glipizide.

EXPLANATION

✔ Correct answer:

Depression. Cushing’s syndrome is caused by prolonged exposure to high levels of cortisol, which affects multiple body systems, including the central nervous system. Many patients with Cushing’s syndrome experience psychological and cognitive disturbances, including agitation, irritability, mood swings, anxiety, poor concentration, memory deficits, and depression. The patient’s symptoms—agitation, irritability, poor memory, decreased appetite, and an unkempt appearance—are consistent with depression, a common psychiatric complication of Cushing’s syndrome.

Excess cortisol alters neurotransmitter activity, particularly serotonin and dopamine, which play crucial roles in mood regulation. Chronic exposure to high cortisol levels leads to neuronal atrophy in the hippocampus, a brain region involved in memory and emotion. These changes contribute to mood disorders such as depression, anxiety, and cognitive impairment.

Imagine cortisol as a stress amplifier. When it's chronically elevated, it overwhelms the brain, making it harder to regulate emotions and memory—similar to how excessive noise in a room makes it difficult to concentrate or have a conversation.

Nurses play a key role in recognizing and managing the psychological effects of Cushing’s syndrome.

• Assess the patient for signs of depression, including changes in mood, sleep patterns, appetite, and social withdrawal.
• Encourage open communication about feelings and provide emotional support.
• Collaborate with mental health professionals if depressive symptoms worsen or suicidal ideation is present.
• Educate the patient on the impact of cortisol on mood and the potential improvement of symptoms with successful treatment.
• Promote a healthy routine with a balanced diet, light physical activity, and stress-reduction techniques.

✘ Incorrect answer options:

Neuropathy. While Cushing’s syndrome can contribute to peripheral neuropathy due to prolonged hypercortisolism and possible diabetes, neuropathy primarily presents with symptoms such as numbness, tingling, and burning pain, rather than mood disturbances and cognitive issues.

Low blood sugar levels. Hypoglycemia typically causes confusion, dizziness, sweating, palpitations, and shakiness, rather than persistent depression and cognitive impairment. In contrast, Cushing’s syndrome is associated with high blood glucose levels (hyperglycemia), not hypoglycemia.

Overactive thyroid function. Hyperthyroidism can cause agitation and irritability, but it is also associated with weight loss, heat intolerance, and increased appetite—which contradicts the decreased appetite seen in this patient. Additionally, hyperthyroidism does not typically lead to poor memory and unkempt appearance as seen in depression.

EXPLANATION

✔Correct answer:

Primary hypothyroidism.  Levothyroxine, a synthetic form of thyroxine (T4), is the standard treatment for primary hypothyroidism, a condition where the thyroid gland fails to produce sufficient thyroid hormones. Following a subtotal thyroidectomy, removal of part of the thyroid gland can impair its ability to synthesize and secrete adequate levels of T4 and triiodothyronine (T3), leading to hypothyroidism. This is classified as primary hypothyroidism because the dysfunction originates in the thyroid gland itself, as opposed to secondary causes (e.g., pituitary failure). The patient’s prescription of levothyroxine 25 mcg daily aims to replace the deficient thyroid hormone, restoring metabolic balance. This aligns with the endocrine nursing focus on hormone replacement therapy to manage glandular insufficiency.

Thyroid hormones regulate metabolism, growth, and development. In primary hypothyroidism, low T4 and T3 levels result in symptoms such as fatigue, weight gain, cold intolerance, and bradycardia. The hypothalamic-pituitary-thyroid axis compensates by increasing thyroid-stimulating hormone (TSH) production, a hallmark of primary hypothyroidism detectable in lab results.

Think of the thyroid as a furnace heating a house (your body). If the furnace breaks down (thyroid gland removal), there’s not enough heat (thyroid hormone). Levothyroxine is like adding fuel to keep the house warm (restore hormone levels).

Nurses are pivotal in managing hypothyroidism treatment and patient education to ensure therapeutic efficacy and safety. Key actions include:

• Educate the patient on taking levothyroxine on an empty stomach, ideally 30-60 minutes before breakfast, to optimize absorption.
• Monitor for signs of under- or over-replacement (e.g., fatigue vs. palpitations) and assess TSH levels periodically as ordered.
• Advise the patient to report symptoms like chest pain or rapid heartbeat, which could indicate excessive dosing.
• Encourage adherence to the medication regimen, explaining its lifelong necessity post-thyroidectomy.
• Provide psychological support for body image changes or fatigue, connecting the patient to community resources if needed.

✘Incorrect answer options:

Graves’ disease. This is incorrect because Graves’ disease is an autoimmune condition causing hyperthyroidism, not hypothyroidism. Treatment typically involves antithyroid drugs (e.g., methimazole), radioactive iodine, or surgery—not levothyroxine, which would worsen the excess thyroid hormone state.

Thyrotoxicosis. Thyrotoxicosis refers to a state of excess thyroid hormone from any cause (e.g., Graves’ disease, toxic nodules). Levothyroxine is contraindicated as it would exacerbate hyperthyroidism symptoms like tachycardia and weight loss, rather than treat the underlying issue.

Euthyroidism. Euthyroidism indicates a normal thyroid function state with balanced hormone levels. Levothyroxine is not prescribed for euthyroid patients, as they do not require hormone replacement. It is used to correct a deficiency, as seen in hypothyroidism, not to maintain a normal state.

EXPLANATION

✔ Correct answer:

"Aid in wound debridement and facilitate healing by secondary intention." A wet-to-dry dressing is a type of mechanical debridement used to remove necrotic tissue, debris, and infected material from a wound. It is commonly used for chronic wounds, diabetic foot ulcers, and pressure injuries where necrotic tissue impairs healing.

In this technique:

1. Moist gauze (wet with saline or an antiseptic solution) is applied to the wound.
2. As the dressing dries, it adheres to necrotic tissue and debris.
3. When the dressing is removed, it pulls away dead tissue, promoting wound debridement and healing by secondary intention (where the wound heals from the inside out, rather than being closed surgically).

Diabetic foot ulcers occur due to neuropathy, poor circulation, and impaired immune response, leading to chronic wounds that are slow to heal. Removing necrotic or infected tissue is critical for promoting granulation tissue formation and reducing the risk of worsening infection. Secondary intention healing allows the body to fill in the wound gradually with new tissue.

Think of wet-to-dry dressings like removing a scab with dirt underneath—when you pull it off, it removes the dirt and dead skin, allowing fresh, healthy skin to form underneath.

Since wet-to-dry dressings can be painful and delay healing if misused, proper wound care is essential.

• Assess the wound for signs of infection, such as redness, swelling, foul odor, or increased drainage.
• Ensure adequate pain management before dressing changes, as removal can be uncomfortable.
• Monitor blood glucose levels, as hyperglycemia impairs wound healing and increases infection risk.
• Educate the patient on foot care and pressure offloading to prevent further ulcers.
• Collaborate with the wound care team for alternative debridement options, such as enzymatic or autolytic debridement, if needed.

✘ Incorrect answer options:

"Absorb exudate while maintaining a moist wound environment." While moist dressings promote healing, wet-to-dry dressings are primarily used for debridement, not moisture retention. Other dressings, such as hydrocolloids or alginates, are better for maintaining a moist wound environment.

"Shield the wound from trauma and support the healing process." While wet-to-dry dressings do provide some protection, their main function is debridement. Other dressings, like transparent films or foam dressings, are better suited for protecting fragile wounds.

"Block microorganisms from entering and reduce discomfort at the wound site." Wet-to-dry dressings do not act as a microbial barrier—in fact, once dry, they can increase infection risk if not changed regularly. Additionally, they can be painful, rather than reducing discomfort. Antimicrobial dressings (e.g., silver-impregnated dressings) are better suited for infection prevention.

EXPLANATION

✔ Correct answer:

Provide 15 to 20 grams of a fast-acting carbohydrate, such as orange juice. Ms. Lopez is exhibiting classic symptoms of mild to moderate hypoglycemia, including confusion, light-headedness, and unusual behavior. Since she is still conscious and able to swallow, the preferred first-line treatment is oral administration of a fast-acting carbohydrate to quickly raise her blood glucose levels.

The "15-15 Rule" is commonly used for treating hypoglycemia:

1. Give 15-20 grams of fast-acting carbohydrates, such as:
   • 4 oz (½ cup) of fruit juice (e.g., orange juice)
   • 4 oz (½ cup) of regular soda (not diet)
   • 1 tablespoon of honey or sugar
   • Glucose tablets (per package instructions)
2. Wait 15 minutes, then recheck blood glucose.
3. If blood glucose remains low (<70 mg/dL), repeat the process.

Oral carbohydrates are preferred when the patient is conscious because they are quickly absorbed and effective at resolving hypoglycemic symptoms.

Imagine your body is like a car running low on fuel. Giving a fast-acting carbohydrate is like adding enough gas to keep the car running immediately, preventing it from stalling (losing consciousness).

In cases of hypoglycemia, nurses should take prompt action to prevent complications.

• Monitor the patient's blood glucose level before and after administering carbohydrates.
• Assess the patient's level of consciousness to ensure they can safely swallow.
• Educate the patient on recognizing early symptoms of hypoglycemia to prevent severe episodes.
• Encourage patients to carry glucose tablets or a carbohydrate source if prone to hypoglycemia.
• Adjust insulin or meal schedules if recurrent hypoglycemia is an issue.

✘ Incorrect answer options:

Administer glucagon via intramuscular or subcutaneous injection. Glucagon is used only when the patient is unconscious, unable to swallow, or experiencing severe hypoglycemia (e.g., seizures). Since Ms. Lopez is still conscious, oral carbohydrates should be used first.

Give an intravenous bolus of dextrose 50%. Dextrose 50% (D50) IV is reserved for severe hypoglycemia in unconscious or nonresponsive patients. Since Ms. Lopez can take oral carbohydrates, this intervention is unnecessary at this stage.

Administer 10 units of fast-acting insulin. Giving insulin would worsen hypoglycemia by further lowering blood glucose, potentially leading to unconsciousness or seizures. Insulin is used for hyperglycemia, not hypoglycemia.

EXPLANATION

✔ Correct answer:

The adrenal cortex. Primary hyperaldosteronism, also known as Conn’s syndrome, is a condition caused by excessive secretion of aldosterone from the adrenal cortex. Aldosterone is a mineralocorticoid hormone produced by the adrenal cortex that regulates sodium and potassium balance. Excess aldosterone leads to sodium retention, potassium excretion, and water retention, resulting in hypertension and hypokalemia (low potassium levels).

The adrenal cortex consists of three layers, each producing different hormones:

• Zona glomerulosa → Aldosterone (mineralocorticoids)
• Zona fasciculata → Cortisol (glucocorticoids)
• Zona reticularis → Androgens (sex hormones)

In primary hyperaldosteronism, excessive aldosterone from the zona glomerulosa leads to increased renal sodium reabsorption and potassium excretion, causing hypertension and metabolic alkalosis due to the loss of hydrogen ions.

Imagine the adrenal cortex as a thermostat controlling sodium and water levels in the body. If it malfunctions and produces too much aldosterone, it acts like a broken thermostat that keeps adding heat (sodium and water retention), leading to high blood pressure and low potassium levels.

Since primary hyperaldosteronism affects blood pressure and electrolyte balance, nursing care focuses on managing hypertension and correcting potassium levels.

• Monitor blood pressure and potassium levels closely.
• Assess for signs of hypokalemia, such as muscle weakness, arrhythmias, and fatigue.
• Administer potassium-sparing diuretics (e.g., spironolactone) as prescribed to counteract aldosterone effects.
• Educate the patient on a low-sodium, potassium-rich diet to balance electrolytes.
• Prepare the patient for adrenalectomy (surgical removal of the affected adrenal gland) if indicated.

✘ Incorrect answer options:

The pancreas. The pancreas produces insulin and glucagon, which regulate blood glucose levels. It is not involved in aldosterone secretion or blood pressure regulation related to hyperaldosteronism.

The adrenal medulla. The adrenal medulla secretes catecholamines (epinephrine and norepinephrine), which are responsible for fight-or-flight responses. Excess catecholamine secretion (as in pheochromocytoma) can cause hypertension, but this is different from primary hyperaldosteronism, which specifically involves the adrenal cortex.

The parathyroid gland. The parathyroid gland regulates calcium levels through parathyroid hormone (PTH). It does not produce aldosterone or regulate blood pressure and sodium balance.

EXPLANATION

✔Correct answer:

Tetany.  Tetany is a condition characterized by involuntary muscle contractions, twitching, and sensory disturbances such as tingling and numbness, often due to hypocalcemia. Following a thyroidectomy, accidental removal or damage to the parathyroid glands—which regulate calcium levels—can lead to decreased parathyroid hormone (PTH) secretion. This disrupts calcium homeostasis, causing hypocalcemia, which manifests as muscle twitching, paresthesia (tingling and numbness) in the extremities and perioral area, and potentially more severe signs like carpopedal spasms or laryngospasm. These symptoms align with the patient’s presentation and are a known postoperative complication of thyroid surgery, reflecting a physiological disruption in endocrine function.

Calcium ions stabilize nerve and muscle cell membranes. Hypocalcemia increases membrane excitability, leading to spontaneous nerve firing and muscle contractions. The Chvostek’s sign (facial twitching upon tapping the facial nerve) and Trousseau’s sign (carpal spasm with blood pressure cuff inflation) are clinical indicators of tetany, often assessed in suspected cases.

Imagine calcium as the brakes on a car (nerves and muscles). If the brakes fail (low calcium), the car starts moving uncontrollably (twitching and spasms), even when you don’t want it to.

Nurses must promptly recognize and manage tetany to prevent progression to life-threatening complications like laryngospasm or seizures. Key actions include:

• Monitor serum calcium levels and report abnormalities to the healthcare provider immediately.
• Assess for additional signs of hypocalcemia, such as Chvostek’s or Trousseau’s signs, to confirm the diagnosis.
• Administer calcium supplements (e.g., calcium gluconate) as prescribed, often intravenously in acute cases, to restore levels.
• Educate the patient about symptoms of hypocalcemia and the importance of follow-up care for parathyroid function.
• Provide psychological support, as sensory disturbances and muscle twitching can cause anxiety.

✘Incorrect answer options:

Hemorrhage. This is incorrect because hemorrhage post-thyroidectomy typically presents with signs of bleeding, such as neck swelling, bruising, difficulty breathing due to hematoma compression, or hypovolemic shock (e.g., tachycardia, hypotension). Muscle twitching, tingling, and numbness are not associated with hemorrhage, which is a vascular rather than neuromuscular complication.

Thyroid storm. Thyroid storm, an acute hyperthyroid crisis, is unlikely following thyroidectomy since the thyroid gland has been removed, reducing thyroid hormone production. It presents with hypermetabolic symptoms like fever, tachycardia, agitation, and sweating—not neuromuscular symptoms like twitching or tingling. This option does not fit the clinical picture.

Laryngeal nerve damage. Damage to the recurrent laryngeal nerve during thyroidectomy can cause hoarseness, voice changes, or respiratory distress due to vocal cord paralysis. However, it does not produce systemic neuromuscular symptoms like twitching or paresthesia, which are tied to calcium imbalance rather than nerve injury localized to the larynx.

EXPLANATION

✔ Correct answer:

Hypocalcemia. After a thyroidectomy, there is a risk of hypocalcemia due to unintentional damage or removal of the parathyroid glands, which regulate calcium homeostasis by producing parathyroid hormone (PTH). A drop in PTH leads to decreased calcium levels, which can result in neuromuscular excitability and tetany.

Chvostek’s sign and Trousseau’s sign are classic indicators of hypocalcemia:

• Chvostek’s sign: Facial twitching occurs when the facial nerve is tapped near the cheek.
• Trousseau’s sign: A carpal spasm occurs when a blood pressure cuff is inflated above systolic pressure for 3 minutes.

These signs result from increased neuromuscular excitability due to low calcium levels affecting nerve conduction.

Think of calcium as a stabilizer for electrical signals in the body. When calcium is low, nerves and muscles become overly sensitive, like an overcharged battery causing unpredictable sparks (muscle spasms and twitching).

Since post-thyroidectomy hypocalcemia can lead to serious complications like laryngospasm and seizures, early recognition and intervention are critical.

• Monitor serum calcium levels regularly (normal range: 8.5–10.5 mg/dL).
• Assess for Chvostek’s and Trousseau’s signs in high-risk patients.
• Keep IV calcium gluconate readily available for severe hypocalcemia.
• Educate the patient about symptoms of low calcium, such as tingling, muscle cramps, and spasms.
• Encourage consumption of calcium-rich foods or supplements if prescribed.

✘ Incorrect answer options:

Hypercalcemia: High calcium levels typically reduce neuromuscular excitability, causing muscle weakness, lethargy, and constipation, not the twitching and spasms seen in hypocalcemia.

Hypokalemia: Low potassium primarily affects cardiac and skeletal muscle function, leading to weakness, arrhythmias, and cramps, but does not cause Chvostek’s or Trousseau’s signs.

Hyperkalemia: High potassium affects cardiac conduction, leading to irregular heart rhythms (dysrhythmias), but does not present with Chvostek’s or Trousseau’s signs.

EXPLANATION

✔ Correct answer:

"You’ll require less insulin when you exercise or eat less food." In type 1 diabetes mellitus (T1DM), the body does not produce insulin, so individuals must take exogenous insulin to regulate blood glucose levels. The amount of insulin needed depends on food intake and physical activity levels:

• Exercise lowers blood glucose levels because muscles use glucose for energy. This means less insulin is needed to prevent hypoglycemia.
• Eating less food means less glucose enters the bloodstream, so less insulin is required to balance blood sugar levels.
• Conversely, eating more food or having higher carbohydrate intake increases blood glucose, requiring more insulin.

Insulin helps move glucose from the bloodstream into cells for energy. Without proper insulin dosing adjustments:

• Too much insulin can cause hypoglycemia (low blood sugar).
• Too little insulin can cause hyperglycemia (high blood sugar) and diabetic ketoacidosis (DKA).

Exercise is particularly important because it enhances glucose uptake by muscles even in the absence of insulin, reducing the amount of insulin required to maintain normal blood sugar levels.

Imagine insulin as the key that unlocks the door to let glucose into the cells.

• When you eat more, more glucose enters the bloodstream, requiring more insulin keys to unlock the doors.
• When you exercise, muscles use glucose directly, so fewer insulin keys are needed to regulate blood sugar.

Nurse Rachel should educate Mr. Daniels on balancing insulin, diet, and exercise to maintain stable blood glucose levels.

• Adjust insulin doses before exercise to prevent hypoglycemia, especially if exercising for a prolonged period.
• Monitor blood glucose before, during, and after exercise to ensure safe levels.
• Consume a snack with carbohydrates before or after exercise if glucose levels drop.
• Maintain a consistent meal schedule to match insulin action and avoid blood sugar fluctuations.
• Recognize signs of hypoglycemia (shakiness, sweating, dizziness) and always carry a fast-acting carbohydrate source (e.g., glucose tablets, juice) for emergencies.

✘ Incorrect answer options:

"You’ll require more insulin when you exercise or eat more food."

• Exercise lowers blood glucose, so less insulin is needed, not more.
• Eating more food does require more insulin, but the first part of the statement makes it incorrect.

"You’ll require less insulin when you eat more food."

• Eating more food increases blood glucose, so more insulin is needed, not less.

"You’ll require more insulin when you exercise or eat less food."

• Exercise lowers blood sugar, so less insulin is needed, making this statement incorrect.
• Eating less food also reduces glucose levels, further decreasing insulin requirements.

EXPLANATION

✔ Correct answer:

Increased susceptibility to infection. Addison’s disease, or primary adrenal insufficiency, is a condition in which the adrenal cortex fails to produce adequate cortisol and aldosterone. Cortisol plays a crucial role in immune function, stress response, metabolism, and inflammation regulation. When cortisol levels are deficient, the immune system becomes weakened, making the patient more vulnerable to infections.

• Cortisol deficiency impairs the normal immune response by reducing the body's ability to control inflammation and fight off infections.
• Aldosterone deficiency leads to sodium loss, water loss, and potassium retention, causing dehydration and hypotension rather than fluid excess.
• Patients with Addison’s disease are at risk of an Addisonian crisis, a life-threatening emergency characterized by severe hypotension, electrolyte imbalances, and shock.

Think of cortisol as the body's "security guard" that keeps harmful invaders (infections) under control. When there’s not enough cortisol, the guard is missing, making it easier for infections to take over.

Since infection risk is a major concern for Addison’s disease patients, nurses should implement strategies to prevent complications.

• Monitor for signs of infection such as fever, fatigue, and elevated white blood cell count.
• Educate the patient on infection prevention, including good hygiene and avoiding sick contacts.
• Ensure corticosteroid replacement therapy (hydrocortisone) is properly managed, as abrupt discontinuation can worsen symptoms.
• Monitor for signs of an Addisonian crisis (severe fatigue, hypotension, shock) and prepare emergency glucocorticoid administration if needed.
• Encourage a well-balanced diet with adequate sodium intake, especially during stress or illness, to compensate for aldosterone deficiency.

✘ Incorrect answer options:

Excess fluid volume. Addison’s disease causes fluid loss, not excess, due to aldosterone deficiency, which leads to sodium and water depletion. Patients are more prone to dehydration and hypotension, rather than fluid overload.

Difficulty with urine elimination. Addison’s disease does not directly affect bladder function or urinary elimination. However, polyuria (increased urination) may occur due to sodium and water loss.

Lower-than-normal body temperature. While Addison’s disease can cause fatigue and general weakness, it does not typically lead to hypothermia. Instead, symptoms include weight loss, hyperpigmentation, and low blood pressure.

EXPLANATION

✔ Correct answer:

It binds to plasma membrane receptors, stimulating enzymatic processes that influence protein, fat, and carbohydrate metabolism. Corticotropin, also known as adrenocorticotropic hormone (ACTH), is a hormone secreted by the anterior pituitary gland that stimulates the adrenal cortex to release glucocorticoids (such as cortisol), mineralocorticoids, and androgens. When administered as a medication, corticotropin mimics the function of endogenous ACTH by binding to specific receptors on the adrenal cortex. This receptor interaction activates enzymatic pathways, leading to increased steroidogenesis—specifically the production of cortisol and other adrenal hormones. These hormones play crucial roles in metabolism, stress response, immune function, and electrolyte balance.

Corticotropin works by binding to melanocortin 2 receptors (MC2R) on adrenal cortical cells, which activates adenylate cyclase and increases cyclic adenosine monophosphate (cAMP) levels. The rise in cAMP triggers a cascade of enzymatic reactions necessary for the synthesis of steroid hormones. These hormones regulate glucose metabolism (gluconeogenesis), protein catabolism, and fat mobilization, helping the body respond to physiological stressors.

Think of ACTH (corticotropin) as a manager in a factory (adrenal cortex). When it arrives, it activates workers (enzymes) to start production (steroid hormone synthesis). Without this manager, the factory would not operate efficiently, leading to hormone deficiencies.

Since corticotropin therapy influences adrenal function, nurses must monitor for side effects and ensure proper patient education.

• Monitor blood glucose levels, as increased cortisol can lead to hyperglycemia.
• Assess for signs of Cushingoid effects (e.g., moon face, weight gain, fluid retention) due to excess corticosteroid production.
• Educate the patient on the importance of adherence to medication therapy to prevent adrenal insufficiency.
• Monitor electrolyte levels, particularly sodium and potassium, as mineralocorticoid effects can impact fluid balance.
• Encourage stress management techniques, as stress increases the body's demand for cortisol.

✘ Incorrect answer options:

It reduces cyclic adenosine monophosphate (cAMP) production, altering the metabolic rate of target organs. This is incorrect because corticotropin actually increases cAMP levels, not reduces them. The rise in cAMP is essential for activating enzymes that stimulate steroid hormone production in the adrenal cortex.

It binds to plasma membrane receptors to block enzymatic activity. Rather than blocking enzymatic activity, corticotropin stimulates it. The enzymatic processes activated by corticotropin are crucial for the synthesis and release of adrenal hormones.

It controls the kidney’s threshold for water reabsorption. This statement describes the action of antidiuretic hormone (ADH), not corticotropin. ADH, or vasopressin, regulates water reabsorption in the kidneys, whereas corticotropin primarily affects adrenal steroid hormone production.

EXPLANATION

✔ Correct answer:

"Imbalanced nutrition: Less than body requirements due to thyroid hormone excess." Hyperthyroidism is a condition in which the thyroid gland produces excess thyroid hormones (T3 and T4), leading to an accelerated metabolic rate. One of the hallmark effects of hyperthyroidism is increased energy expenditure and unintentional weight loss, despite normal or increased appetite. This can lead to nutritional deficiencies and muscle wasting, making imbalanced nutrition: less than body requirements the highest priority nursing diagnosis.

Thyroid hormones (T3 and T4) regulate metabolism by increasing oxygen consumption, heat production, and energy expenditure. In hyperthyroidism:

• The body burns calories too quickly, leading to weight loss and malnutrition.
• Protein and fat stores break down rapidly, causing muscle wasting and weakness.
• Increased gut motility can lead to diarrhea and malabsorption, further contributing to nutritional deficiencies.

Imagine your body's metabolism as a car engine running at high speed all the time. The faster it runs, the more fuel (calories) it burns. In hyperthyroidism, the body burns energy too quickly, leading to unintentional weight loss and malnutrition despite normal eating.

To prevent severe weight loss and malnutrition, Nurse Emma should implement nutritional support strategies and monitor for complications of hyperthyroidism.

• Encourage a high-calorie, high-protein diet to compensate for increased metabolism.
• Monitor weight trends regularly to assess nutritional status.
• Assess for signs of malnutrition, such as muscle wasting, fatigue, and electrolyte imbalances.
• Monitor for thyroid storm, a life-threatening condition characterized by severe hyperthyroidism, fever, tachycardia, and delirium.
• Encourage small, frequent meals to maintain energy levels and prevent further weight loss.

✘ Incorrect answer options:

"Risk for imbalanced nutrition: More than body requirements due to thyroid hormone excess." This is incorrect because hyperthyroidism causes weight loss, not weight gain. Hypothyroidism, not hyperthyroidism, is associated with weight gain and decreased metabolism.

"Risk for impaired skin integrity related to edema, skin fragility, and poor wound healing." While hyperthyroidism may cause skin changes, it does not typically lead to skin fragility and poor wound healing. Hypothyroidism, especially severe cases like myxedema, is more likely to cause edema and skin fragility.

"Body image disturbance related to weight gain and edema." This is incorrect because hyperthyroidism causes weight loss, not weight gain. While patients may experience anxiety or concern about physical changes, weight gain and edema are more common in hypothyroidism, not hyperthyroidism.

EXPLANATION

✔ Correct answer:

"Checking serum osmolarity." Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) is a life-threatening complication of type 2 diabetes mellitus characterized by extreme hyperglycemia, severe dehydration, and high serum osmolarity without significant ketoacidosis. The hallmark laboratory finding in HHNS is an elevated serum osmolarity (>320 mOsm/kg), which confirms the diagnosis.

HHNS occurs due to insufficient insulin to facilitate glucose uptake into cells, leading to severe hyperglycemia (usually >600 mg/dL). This draws water out of cells into the bloodstream, causing profound dehydration and hyperosmolarity. Unlike diabetic ketoacidosis (DKA), HHNS does not produce significant ketones because some insulin is still present, preventing excessive lipolysis and ketone formation.

Imagine sugar (glucose) as a sponge soaking up water in your blood vessels. The more sugar present, the more water is pulled from your cells into your bloodstream, making the blood thicker and increasing osmolarity. This leads to severe dehydration, confusion, and even coma.

Since severe dehydration and electrolyte imbalances are critical concerns in HHNS, Nurse Brian should prioritize fluid replacement and electrolyte monitoring.

• Monitor serum osmolarity to assess dehydration severity and treatment response.
• Administer IV fluids (0.9% or 0.45% saline) to restore hydration.
• Monitor blood glucose levels, as levels can exceed 600 mg/dL.
• Assess for neurological changes, such as confusion or seizures, due to hyperosmolarity.
• Correct electrolyte imbalances, particularly potassium, sodium, and phosphorus.

✘ Incorrect answer options:

"Measuring serum potassium levels." While potassium levels are important in diabetes-related emergencies, they do not confirm HHNS. Potassium may be normal, low, or high, depending on hydration status and insulin therapy.

"Evaluating serum sodium levels." HHNS often causes altered sodium levels, but serum sodium alone does not confirm the diagnosis. High glucose levels can cause false low sodium readings (dilutional hyponatremia).

"Assessing arterial blood gas (ABG) values." ABGs are crucial for diagnosing diabetic ketoacidosis (DKA), which involves metabolic acidosis (low pH, low bicarbonate). However, HHNS does not cause significant acidosis because ketone production is minimal or absent.

EXPLANATION

✔ Correct answer:

"Always follow the same sequence when drawing different types of insulin into the syringe." When mixing two types of insulin in a single syringe (e.g., rapid- or short-acting insulin with intermediate-acting insulin such as NPH), it is crucial to follow the correct sequence to prevent contamination and ensure accurate dosing.

The correct sequence is:

1. Inject air into the NPH (cloudy) vial first, then into the regular (clear) vial.
2. Withdraw the clear (short-acting) insulin first.
3. Withdraw the cloudy (intermediate-acting) insulin next.

This order is important because:

• Drawing the clear insulin first prevents contamination of the short-acting insulin with the intermediate-acting insulin.
• NPH insulin contains added proteins to prolong its action, and mixing it into the regular insulin vial could alter the effectiveness of the rapid-acting insulin.

Imagine you have a clean glass of water (clear insulin) and a glass of milk (cloudy insulin). If you dip a spoon into the milk first and then into the water, you will contaminate the water. But if you dip into the water first, the milk remains unchanged. The same principle applies when drawing insulin.

Nurses educating patients on insulin administration should ensure they understand the correct technique and storage guidelines.

• Teach the correct sequence when mixing insulin: "Clear before cloudy."
• Advise patients to gently roll NPH insulin between their hands instead of shaking it.
• Ensure patients store insulin properly—refrigerate unopened vials and store opened vials at room temperature.
• Assess the patient’s understanding with a return demonstration.
• Emphasize the importance of rotating injection sites to prevent lipodystrophy.

✘ Incorrect answer options:

"Shake the insulin vials before drawing up the dose." Shaking insulin can cause air bubbles and disrupt the protein structure of intermediate- and long-acting insulins, potentially affecting their effectiveness. Instead, patients should gently roll vials between their hands to mix the suspension evenly.

"Store unopened insulin vials in the freezer at subzero temperatures." Insulin should be stored in the refrigerator (36°F–46°F or 2°C–8°C), not in the freezer. Freezing insulin damages its structure, making it ineffective. Opened vials can be stored at room temperature for up to 28 days.

"Throw away intermediate-acting insulin if it looks cloudy." Intermediate-acting insulin (NPH) is naturally cloudy due to the added proteins that extend its duration. However, if there are clumps or crystals that do not dissolve when the vial is rolled, it should be discarded.

EXPLANATION

✔ Correct answer:

Onset at 2:30 p.m., peak at 4 p.m. Regular insulin is a short-acting insulin that is commonly used for managing hyperglycemia, including in conditions such as diabetic ketoacidosis (DKA). It has a well-defined onset, peak, and duration:

• Onset: 30 to 60 minutes
• Peak: 2 to 4 hours
• Duration: 6 to 8 hours

Given that the patient receives regular insulin at 2 p.m., its onset of action will occur approximately 30 minutes later (2:30 p.m.), and the peak effect (when insulin activity is strongest) will be expected around 4 p.m.

Insulin is essential for glucose uptake by cells and helps lower blood glucose by promoting cellular glucose utilization and glycogen storage. In DKA, a life-threatening condition caused by insulin deficiency, insulin therapy is critical to reversing hyperglycemia and stopping ketone production. Regular insulin is often used intravenously in DKA treatment due to its predictability and relatively rapid onset. However, when given subcutaneously (as in this scenario), its onset is slower than rapid-acting insulins like lispro or aspart.

Imagine insulin as a train departing from a station (injection site). A regular insulin train takes about 30 minutes to start moving (onset) and reaches peak speed in 2 to 4 hours. By contrast, a rapid-acting insulin train like lispro starts moving almost immediately (5–15 minutes) and reaches peak speed much faster.

When administering regular insulin, nurses must carefully monitor the patient’s response to prevent hypoglycemia and ensure effective glucose control.

• Monitor blood glucose levels closely, particularly around peak insulin activity (e.g., 4 p.m.).
• Assess for signs of hypoglycemia, including sweating, confusion, tremors, and tachycardia.
• Ensure the patient has access to a carbohydrate source in case of hypoglycemia.
• Educate the patient on insulin timing in relation to meals, as regular insulin is typically administered 30 minutes before eating.
• Coordinate with the healthcare provider regarding insulin adjustments if the patient’s blood glucose trends too high or too low.

✘ Incorrect answer options:

Onset at 2 p.m., peak at 3 p.m. This is incorrect because regular insulin does not act immediately after injection. It takes about 30 to 60 minutes to start working, so an onset at 2 p.m. is too early.

Onset at 2:15 p.m., peak at 3 p.m. While slightly closer, this still underestimates the onset time of regular insulin, which typically takes 30 minutes or more to begin working.

Onset at 4 p.m., peak at 6 p.m. This overestimates the onset time, as regular insulin begins acting within 30 to 60 minutes after administration, not 2 hours later. Additionally, the peak is expected within 2 to 4 hours, not after 4 hours.

EXPLANATION

✔ Correct answer:

Beta-blockers. Glucagon is a hormone used to raise blood glucose levels in cases of severe hypoglycemia. It works by stimulating glycogenolysis (the breakdown of glycogen into glucose) and gluconeogenesis (the production of new glucose) in the liver. However, glucagon can interact negatively with beta-blockers, which are commonly prescribed for hypertension, arrhythmias, and heart disease.

Mechanism of Interaction:  

Beta-blockers, such as propranolol and metoprolol, reduce sympathetic nervous system activity and lower heart rate and blood pressure. When given with glucagon, they can lead to exaggerated cardiovascular effects, including:

• Increased risk of tachycardia – Glucagon stimulates cardiac contractility, which may counteract the beta-blocker’s effects and cause a sudden spike in heart rate.
• Potential hypertensive crisis – In patients on non-selective beta-blockers, glucagon can cause excessive catecholamine release, leading to dangerous increases in blood pressure.
• Altered glucose regulation – Beta-blockers can mask symptoms of hypoglycemia, making it harder to detect and treat appropriately.

Imagine glucagon as a "gas pedal" that speeds up the heart and increases glucose, while beta-blockers act as a "brake" to slow everything down. When used together, the conflicting signals can cause the heart to behave unpredictably, leading to sudden surges in heart rate or blood pressure.

When administering glucagon to a patient on beta-blockers, nurses should take precautions to monitor for adverse reactions.

• Monitor vital signs, particularly heart rate and blood pressure, for signs of excessive cardiovascular stimulation.
• Assess blood glucose levels frequently, as beta-blockers can mask hypoglycemic symptoms.
• Be prepared to manage potential tachycardia or hypertension with appropriate interventions.
• Educate the patient and caregivers on recognizing hypoglycemia despite masked symptoms.
• Coordinate with the healthcare provider to adjust medications if needed.

✘ Incorrect answer options:

Antacids: Antacids primarily affect gastric acid levels and do not have a significant interaction with glucagon. Their main concern is interfering with the absorption of other oral medications, but this does not apply to glucagon, which is typically administered via injection.

Antibiotics: There is no known significant interaction between glucagon and antibiotics. While some antibiotics can impact glucose metabolism, they do not directly affect glucagon’s mechanism of action.

Antihistamines: Antihistamines primarily act on histamine receptors and do not interfere with glucagon's effects on blood glucose or the cardiovascular system. They are not a major concern in this scenario.

EXPLANATION

✔ Correct answer:

"You should avoid coughing, sneezing, and blowing your nose." A transsphenoidal hypophysectomy is a surgical procedure in which a pituitary tumor is removed through the sphenoid sinus, which is accessed via the nose. Since the procedure involves the nasal cavity, any activity that increases intracranial pressure (ICP) or disrupts the surgical site can lead to serious complications, such as cerebrospinal fluid (CSF) leakage, infection, and delayed healing.

Coughing, sneezing, and blowing the nose create significant pressure in the surgical area, increasing the risk of CSF leaks and surgical site disruption. Patients must be instructed to avoid these actions and use measures like open-mouth sneezing or gentle tissue dabbing if necessary.

During a transsphenoidal hypophysectomy, the surgeon removes the pituitary tumor via the nasal passage, creating a potential pathway between the brain and nasal cavity. If this delicate barrier is disrupted, CSF leakage (rhinorrhea) can occur, increasing the risk of meningitis and delayed healing.

Imagine a newly patched hole in a wall. If you press or knock on it before it’s fully dry, the patch can break open. Similarly, after pituitary surgery, excessive pressure from sneezing or nose blowing can disrupt the healing process and cause CSF leakage.

Postoperative care focuses on preventing complications such as CSF leaks, infection, and increased ICP.

• Instruct the patient to avoid activities that increase intracranial pressure, such as coughing, sneezing, straining, or vigorous nose-blowing.
• Monitor for CSF leakage, indicated by clear drainage from the nose, a persistent headache, or a halo sign (yellow ring around drainage on a gauze pad).
• Encourage head-of-bed elevation (30–45 degrees) to reduce ICP and promote drainage.
• Assess for neurological changes, as pituitary surgery can affect hormone levels and cranial nerves.
• Monitor urine output closely for signs of diabetes insipidus (excessive urination and thirst), a potential complication due to pituitary disruption.

✘ Incorrect answer options:

"You need to remain lying flat for the first 24 hours after surgery." This is incorrect because patients should have their head elevated (30–45 degrees) to reduce ICP and minimize swelling. Lying flat can increase intracranial pressure and worsen CSF leakage.

"You must strictly limit your fluid intake." While fluid balance should be monitored, strict limitation is not recommended unless diabetes insipidus (DI) develops. Some patients may actually require increased fluids if DI occurs due to pituitary disruption.

"You should report any ringing in your ears immediately." While neurological symptoms should always be reported, ringing in the ears (tinnitus) is not a primary concern after transsphenoidal surgery. Instead, the patient should report clear nasal drainage, severe headaches, or vision changes, which may indicate a CSF leak or other complications.

EXPLANATION

✔ Correct answer:

"Increasing fluid intake." Hyperparathyroidism is a condition characterized by excess secretion of parathyroid hormone (PTH), which leads to increased calcium levels (hypercalcemia) in the blood. One of the major complications of hypercalcemia is kidney stone formation due to excessive calcium excretion in the urine. Increasing fluid intake is essential to promote calcium excretion through the kidneys and prevent stone formation.

PTH regulates calcium and phosphorus balance by:

• Increasing calcium resorption from bones, weakening bone density (risk for osteoporosis).
• Enhancing calcium reabsorption in the kidneys, raising blood calcium levels.
• Stimulating vitamin D activation, which increases calcium absorption from the intestines.

As a result, hyperparathyroidism leads to hypercalcemia and hypophosphatemia, increasing the risk of nephrolithiasis (kidney stones). Adequate hydration helps flush out excess calcium, reducing the likelihood of stone formation.

Imagine calcium as sugar in a glass of water. If too much sugar (calcium) is added and there’s not enough water (fluid intake), the sugar crystallizes at the bottom, similar to kidney stones forming in the kidneys. By increasing fluid intake, the calcium stays dissolved and is easily excreted.

To reduce complications from hyperparathyroidism, Nurse Olivia should educate the patient on proper dietary and lifestyle modifications.

• Encourage increased fluid intake (at least 2–3 liters/day) to prevent kidney stones.
• Promote a moderate calcium intake, as excessive dietary calcium is not recommended.
• Encourage weight-bearing exercises to help maintain bone strength and reduce bone loss.
• Monitor for signs of hypercalcemia (e.g., fatigue, muscle weakness, constipation, confusion).
• Assess renal function regularly to detect any stone formation or kidney impairment.

✘ Incorrect answer options:

"Limiting fluid intake." This is incorrect because reducing fluid intake would increase the risk of kidney stone formation due to the high calcium levels in the urine.

"Reducing sodium consumption." While excessive sodium intake can contribute to calcium loss through the urine, the primary concern in hyperparathyroidism is promoting calcium excretion, which is best achieved through increased fluid intake rather than sodium restriction alone.

"Cutting back on potassium-rich foods." Hyperparathyroidism does not directly affect potassium levels, so there is no need to restrict potassium-rich foods. The main concerns are calcium balance and kidney health.

EXPLANATION

✔ Correct answer:

Fat accumulation in the trunk and upper back. Cushing’s syndrome results from prolonged exposure to excessive glucocorticoids, often due to corticosteroid medication use or endogenous overproduction by the adrenal glands. One of the hallmark physical manifestations of Cushing’s syndrome is the redistribution of fat, leading to truncal obesity and dorsocervical fat deposition, commonly known as a "buffalo hump." Patients may also develop a rounded, moon-like facial appearance ("moon face").

Glucocorticoids, particularly cortisol, play a major role in metabolism, promoting lipogenesis (fat formation) in certain areas of the body while contributing to lipolysis (fat breakdown) in others. In Cushing’s syndrome, cortisol excess shifts fat deposition predominantly to the trunk, upper back, and face while causing muscle wasting and thinning in the extremities.

Imagine a person wearing a backpack on their front and back, but with very little weight in their arms and legs. The backpack represents fat accumulation in the trunk and upper back, while the arms and legs remain relatively thin.

Since Cushing’s syndrome affects multiple body systems, nursing care focuses on managing symptoms, preventing complications, and providing patient education.

• Monitor blood glucose levels, as hyperglycemia is common due to cortisol’s effect on insulin resistance.
• Assess for signs of infection, as excess cortisol suppresses the immune response.
• Encourage a diet rich in protein and potassium while limiting sodium intake to prevent fluid retention and muscle wasting.
• Provide emotional support, as changes in appearance and mood disturbances (e.g., depression) are common in Cushing’s syndrome.
• Educate the patient on medication adherence if corticosteroids are the cause, including tapering doses gradually under medical supervision.

✘ Incorrect answer options:

Low blood pressure readings. Cushing’s syndrome typically leads to hypertension due to increased cortisol levels, which enhance the effects of catecholamines and promote sodium and water retention. Hypotension is more characteristic of adrenal insufficiency (Addison’s disease).

Thickened and coarse skin texture. Patients with Cushing’s syndrome often experience thinning of the skin rather than thickening. This can lead to easy bruising, purple striae (stretch marks), and poor wound healing due to impaired collagen synthesis.

Increased fat deposits in the arms and legs. The opposite occurs in Cushing’s syndrome—patients typically have muscle wasting and thinning in the arms and legs due to catabolic effects on muscle proteins. Fat accumulation is centralized in the trunk, face, and upper back.

EXPLANATION

✔Correct answer:

Hypocalcemia. A positive Chvostek’s sign—facial muscle twitching elicited by tapping the facial nerve (cranial nerve VII)—is a hallmark of hypocalcemia (low serum calcium). Calcium ions stabilize nerve membranes and regulate neuromuscular excitability. In hypocalcemia, reduced extracellular calcium increases neuronal membrane permeability to sodium, leading to hyperexcitability. This manifests as spontaneous muscle contractions (e.g., Chvostek’s and Trousseau’s signs). Hypocalcemia may result from hypoparathyroidism, vitamin D deficiency, or renal dysfunction.

Calcium deficiency disrupts the normal depolarization-repolarization cycle of nerves, lowering the threshold for action potentials. This results in exaggerated responses to mechanical stimuli (like tapping the facial nerve) and spontaneous muscle twitching.

Imagine a car alarm (nerve) set to trigger at the slightest vibration (stimulus). If the alarm system is overly sensitive (hypocalcemia), even a gentle tap (Chvostek’s test) sets it off (muscle twitch). Calcium acts as the "sensitivity adjuster" for nerves.

Nurses should prioritize interventions to address hypocalcemia and prevent complications:

• Monitor for laryngospasm or seizures (life-threatening complications of severe hypocalcemia).
• Administer IV calcium gluconate (if severe) or oral calcium/vitamin D supplements as prescribed.
• Educate patients on calcium-rich diets (e.g., dairy, leafy greens) and sunlight exposure for vitamin D synthesis.
• Assess for Trousseau’s sign (carpal spasm with blood pressure cuff inflation) to confirm hypocalcemia.
• Avoid medications that lower calcium (e.g., loop diuretics) unless indicated.

✘Incorrect answer options:

Hyponatremia: Low sodium primarily causes neurological symptoms (e.g., confusion, seizures) due to cellular swelling, not neuromuscular irritability. Chvostek’s sign is not associated with sodium imbalances.

Hypokalemia: Low potassium leads to muscle weakness, cramps, and cardiac arrhythmias due to impaired muscle cell depolarization. It does not cause hyperexcitable nerves or Chvostek’s sign.

Hypermagnesemia: High magnesium levels depress neuromuscular activity, causing hyporeflexia and respiratory depression—not twitching. This is the opposite of hypocalcemia’s effects.

EXPLANATION

✔ Correct answer:

"If you have nasal congestion or blockage, you may not be able to use desmopressin nasally." Desmopressin (DDAVP) is a synthetic analog of antidiuretic hormone (ADH) used to treat diabetes insipidus (DI), a condition characterized by excessive urination and intense thirst due to ADH deficiency. Desmopressin is available in various forms, including intranasal spray, oral tablets, and injections. The intranasal form is commonly prescribed, but its effectiveness can be compromised if the nasal passages are congested or blocked. This is because proper absorption requires an intact nasal mucosa. If the patient experiences congestion, an alternative route (oral or injection) may be necessary.

In diabetes insipidus, the kidneys fail to concentrate urine due to a lack of ADH, leading to excessive urine output (polyuria) and extreme thirst (polydipsia). Desmopressin mimics ADH, reducing urine output and preventing dehydration. However, its effectiveness depends on proper administration, and nasal congestion can interfere with the absorption of the intranasal formulation.

Imagine using a nasal spray when you have a severely stuffy nose—it won't be absorbed properly, and its intended effect will be reduced. Similarly, desmopressin nasal spray won't work well if the nasal passages are blocked.

Nurse Lina should educate the patient on proper medication administration and the importance of monitoring fluid balance.

• Instruct the patient to assess nasal patency before using the nasal spray and report any persistent congestion.
• Encourage regular monitoring of fluid intake and urine output to prevent dehydration or water intoxication.
• Advise the patient to wear a medical alert bracelet to inform healthcare providers about their condition in case of emergencies.
• Educate the patient on recognizing symptoms of overcorrection, such as fluid retention, weight gain, or hyponatremia (headache, confusion, seizures).
• Reinforce the need for follow-up visits to adjust medication dosage as needed.

✘ Incorrect answer options:

"Make sure to administer desmopressin while it is still cold." Desmopressin should be stored properly, but it does not need to be administered cold. The nasal spray should be at room temperature before use, as cold medication can cause discomfort or reduced absorption.

"Since your condition is not long-term, wearing a medical ID bracelet isn't necessary." Diabetes insipidus is a chronic condition, and patients should wear a medical ID bracelet to alert healthcare providers in case of an emergency, especially since dehydration or electrolyte imbalances can be life-threatening.

"Once you start taking desmopressin, monitoring your fluid intake and output won’t be necessary." Fluid balance monitoring is crucial for patients on desmopressin. Overuse of desmopressin can lead to water retention and hyponatremia, while underuse can cause dehydration. Patients should continue tracking urine output and fluid intake to adjust dosage appropriately.

EXPLANATION

✔ Correct answer:

"If I experience low blood sugar, I'll drink orange juice to raise it quickly." Acarbose is an alpha-glucosidase inhibitor that delays carbohydrate digestion and absorption in the small intestine, helping to prevent post-meal spikes in blood glucose levels. However, because it works by blocking the breakdown of complex carbohydrates into simple sugars, the usual treatments for hypoglycemia, such as fruit juice or table sugar (sucrose), are less effective. Instead, patients must use glucose (dextrose) tablets or gel to quickly raise blood sugar levels if they experience hypoglycemia.

Acarbose inhibits alpha-glucosidase enzymes in the intestines, which are responsible for breaking down complex carbohydrates (such as starches and sucrose) into absorbable simple sugars (like glucose and fructose). Because acarbose prevents the digestion of sucrose, sources of sucrose like orange juice, table sugar, and candy are not effective for treating low blood sugar. Instead, pure glucose (dextrose) must be used since it does not require enzymatic breakdown.

Imagine your intestines as a locked door, and the enzyme alpha-glucosidase as the key that unlocks carbohydrates so they can enter your bloodstream. Acarbose removes the key, meaning complex carbs and sucrose cannot be broken down. Only glucose (dextrose), which doesn’t need a key, can pass through immediately.

Patients taking acarbose should be educated on proper hypoglycemia management and medication usage.

• Instruct the patient to take acarbose with the first bite of each main meal, as it works in the intestines during digestion.
• Emphasize that if hypoglycemia occurs, glucose (dextrose) tablets or gel should be used instead of sucrose-containing foods like orange juice or candy.
• Monitor for gastrointestinal side effects such as bloating, flatulence, and diarrhea, which result from undigested carbohydrates fermenting in the colon.
• Encourage a balanced diet with consistent carbohydrate intake to prevent extreme blood sugar fluctuations.
• Assess liver function regularly, as acarbose has been associated with elevated liver enzymes in long-term use.

✘ Incorrect answer options:

"I should take this medication with the first bite of each main meal." This statement is correct. Acarbose must be taken at the beginning of a meal to effectively block carbohydrate digestion in the small intestine.

"This medication helps slow carbohydrate absorption in my intestines." This statement is also correct. Acarbose delays the breakdown and absorption of carbohydrates, leading to a gradual rise in blood sugar rather than a sharp spike.

"I may experience bloating or gas as a side effect of this medication." This statement is correct. Since acarbose prevents carbohydrate digestion in the small intestine, the undigested carbohydrates reach the colon, where gut bacteria ferment them, leading to bloating, flatulence, and diarrhea.