Nursing practice questions with comprehensive rationales
NurseDive Free Nursing Practice Question
What is the physiologic mechanism behind the development of pyrexia?
A. Release of pyrogens resetting the hypothalamic thermostat
Pyrexia (fever) occurs when pyrogens, like cytokines (IL-1, IL-6), released during infection or inflammation, act on the hypothalamus to raise the body’s temperature set point. This triggers heat production via shivering and vasoconstriction, conserving heat to create a fever, enhancing immune response. This statement accurately describes the primary mechanism of pyrexia.
B. Increased peripheral vasoconstriction reducing heat loss
Peripheral vasoconstriction occurs during fever to conserve heat but is a response, not the cause, of pyrexia. It results from hypothalamic signaling after pyrogens reset the thermostat. This statement is inaccurate, as vasoconstriction is a secondary effect, not the initiating physiologic mechanism of fever development.
C. Decreased metabolic rate increasing heat production
Fever increases, not decreases, metabolic rate to generate heat via thermogenesis. Pyrogens elevate the hypothalamic set point, prompting energy expenditure through shivering and muscle activity. This statement is inaccurate, as reduced metabolism would lower body temperature, counteracting the fever response triggered by infection or inflammation.
D. Inhibition of prostaglandin synthesis in the hypothalamus
Prostaglandin synthesis, particularly PGE2, in the hypothalamus is stimulated by pyrogens, raising the temperature set point to cause fever. Inhibiting prostaglandin synthesis (e.g., by NSAIDs) reduces fever, not causes it. This statement is inaccurate, as prostaglandin inhibition opposes the physiologic mechanism of pyrexia.
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Full Explanation
Choice A reason: Pyrexia (fever) occurs when pyrogens, like cytokines (IL-1, IL-6), released during infection or inflammation, act on the hypothalamus to raise the body’s temperature set point. This triggers heat production via shivering and vasoconstriction, conserving heat to create a fever, enhancing immune response. This statement accurately describes the primary mechanism of pyrexia.
Choice B reason: Peripheral vasoconstriction occurs during fever to conserve heat but is a response, not the cause, of pyrexia. It results from hypothalamic signaling after pyrogens reset the thermostat. This statement is inaccurate, as vasoconstriction is a secondary effect, not the initiating physiologic mechanism of fever development.
Choice C reason: Fever increases, not decreases, metabolic rate to generate heat via thermogenesis. Pyrogens elevate the hypothalamic set point, prompting energy expenditure through shivering and muscle activity. This statement is inaccurate, as reduced metabolism would lower body temperature, counteracting the fever response triggered by infection or inflammation.
Choice D reason: Prostaglandin synthesis, particularly PGE2, in the hypothalamus is stimulated by pyrogens, raising the temperature set point to cause fever. Inhibiting prostaglandin synthesis (e.g., by NSAIDs) reduces fever, not causes it. This statement is inaccurate, as prostaglandin inhibition opposes the physiologic mechanism of pyrexia.
Similar Questions
A client is diagnosed with cholelithiasis. Which condition is least likely to lead to this disorder?
A. Too much absorption of bile acids
Excessive bile acid absorption, often due to ileal dysfunction, reduces bile acid availability in the gallbladder, promoting cholesterol supersaturation and gallstone formation. This contributes to cholelithiasis, particularly cholesterol gallstones, by altering bile composition, making this condition a significant risk factor, not the least likely.
B. History of elevated serum calcium
Elevated serum calcium (hypercalcemia) is not directly linked to cholelithiasis. While hypercalcemia can cause kidney stones, gallstone formation is driven by bile composition changes, like cholesterol or bile acid imbalances, not serum calcium levels. This makes it the least likely contributor to gallstone development.
C. History of elevated cholesterol in the diet
Elevated dietary cholesterol increases hepatic cholesterol secretion into bile, leading to supersaturation and cholesterol gallstone formation. This is a well-established risk factor for cholelithiasis, as excess cholesterol overwhelms bile acid and phospholipid solubilization, promoting crystal formation, making it a significant contributor, not the least likely.
D. Inflammation of epithelial tissue
Inflammation of epithelial tissue, such as in chronic cholecystitis, promotes gallstone formation by altering gallbladder motility and bile stasis. Inflammatory changes disrupt bile acid metabolism and increase mucin production, facilitating stone nucleation. This condition is a known risk factor for cholelithiasis, not the least likely contributor.
Full Explanation
Choice A reason: Excessive bile acid absorption, often due to ileal dysfunction, reduces bile acid availability in the gallbladder, promoting cholesterol supersaturation and gallstone formation. This contributes to cholelithiasis, particularly cholesterol gallstones, by altering bile composition, making this condition a significant risk factor, not the least likely.
Choice B reason: Elevated serum calcium (hypercalcemia) is not directly linked to cholelithiasis. While hypercalcemia can cause kidney stones, gallstone formation is driven by bile composition changes, like cholesterol or bile acid imbalances, not serum calcium levels. This makes it the least likely contributor to gallstone development.
Choice C reason: Elevated dietary cholesterol increases hepatic cholesterol secretion into bile, leading to supersaturation and cholesterol gallstone formation. This is a well-established risk factor for cholelithiasis, as excess cholesterol overwhelms bile acid and phospholipid solubilization, promoting crystal formation, making it a significant contributor, not the least likely.
Choice D reason: Inflammation of epithelial tissue, such as in chronic cholecystitis, promotes gallstone formation by altering gallbladder motility and bile stasis. Inflammatory changes disrupt bile acid metabolism and increase mucin production, facilitating stone nucleation. This condition is a known risk factor for cholelithiasis, not the least likely contributor.
The client’s blood sugar this morning is 50 mg/dL. The client states they are cold, sweating, and clammy. Which nursing intervention is most appropriate?
A. The blood sugar is normal, the client needs to drink water
A blood sugar of 50 mg/dL indicates hypoglycemia, not normal glucose levels (70-110 mg/dL). Symptoms like sweating and clamminess confirm this. Drinking water does not address hypoglycemia, as it lacks glucose to raise blood sugar, making this intervention inappropriate and potentially harmful.
B. Give the client fruit juice with additional sugar
Hypoglycemia (50 mg/dL) with symptoms like sweating requires rapid glucose correction. Fruit juice with added sugar provides fast-acting carbohydrates (15-20g), raising blood sugar within minutes by stimulating glycogenolysis and glucose absorption. This is the most appropriate intervention to reverse hypoglycemia safely and effectively.
C. Give 5 units of insulin
Administering insulin during hypoglycemia (50 mg/dL) would further lower blood sugar, worsening symptoms and risking seizures or coma. Insulin drives glucose into cells, exacerbating the glucose deficit. This intervention is contraindicated and dangerous in the context of low blood sugar and neuroglycopenic symptoms.
D. Call the healthcare provider immediately
While consulting a healthcare provider may be needed for recurrent hypoglycemia, the immediate priority is correcting low blood sugar (50 mg/dL) with fast-acting carbohydrates. Delaying treatment by calling first risks prolonged hypoglycemia, potentially causing neurological damage, making this less appropriate than direct intervention.
Full Explanation
Choice A reason: A blood sugar of 50 mg/dL indicates hypoglycemia, not normal glucose levels (70-110 mg/dL). Symptoms like sweating and clamminess confirm this. Drinking water does not address hypoglycemia, as it lacks glucose to raise blood sugar, making this intervention inappropriate and potentially harmful.
Choice B reason: Hypoglycemia (50 mg/dL) with symptoms like sweating requires rapid glucose correction. Fruit juice with added sugar provides fast-acting carbohydrates (15-20g), raising blood sugar within minutes by stimulating glycogenolysis and glucose absorption. This is the most appropriate intervention to reverse hypoglycemia safely and effectively.
Choice C reason: Administering insulin during hypoglycemia (50 mg/dL) would further lower blood sugar, worsening symptoms and risking seizures or coma. Insulin drives glucose into cells, exacerbating the glucose deficit. This intervention is contraindicated and dangerous in the context of low blood sugar and neuroglycopenic symptoms.
Choice D reason: While consulting a healthcare provider may be needed for recurrent hypoglycemia, the immediate priority is correcting low blood sugar (50 mg/dL) with fast-acting carbohydrates. Delaying treatment by calling first risks prolonged hypoglycemia, potentially causing neurological damage, making this less appropriate than direct intervention.
Prednisone is an oral corticosteroid that has less mineralocorticoid activity than other oral steroids. What does the nurse expect when giving this medication?
A. It will cause less extreme hyperglycemia
Prednisone causes hyperglycemia by increasing gluconeogenesis and insulin resistance, similar to other corticosteroids. Its lower mineralocorticoid activity does not significantly reduce this effect compared to other steroids. This statement is inaccurate, as prednisone’s glycemic impact is comparable, not less extreme, than other corticosteroids.
B. It will cause less sodium and water retention
Prednisone has minimal mineralocorticoid activity compared to steroids like hydrocortisone, resulting in less sodium and water retention. Mineralocorticoids promote renal sodium reabsorption, causing fluid retention. Prednisone’s glucocorticoid dominance reduces these effects, making this statement accurate for expected nursing observations during administration.
C. It will cause more sodium retention and less water retention
Prednisone’s low mineralocorticoid activity leads to less, not more, sodium retention. It does not disproportionately affect water retention independently of sodium. This statement is inaccurate, as prednisone’s profile minimizes both sodium and water retention compared to steroids with higher mineralocorticoid effects.
D. It will cause more extreme hyperglycemia
Prednisone causes hyperglycemia, but its effect is not more extreme than other corticosteroids like dexamethasone. Its glucocorticoid activity drives gluconeogenesis similarly across the class. This statement is inaccurate, as prednisone’s hyperglycemic effects are standard, not uniquely severe, among oral corticosteroids.
Full Explanation
Choice A reason: Prednisone causes hyperglycemia by increasing gluconeogenesis and insulin resistance, similar to other corticosteroids. Its lower mineralocorticoid activity does not significantly reduce this effect compared to other steroids. This statement is inaccurate, as prednisone’s glycemic impact is comparable, not less extreme, than other corticosteroids.
Choice B reason: Prednisone has minimal mineralocorticoid activity compared to steroids like hydrocortisone, resulting in less sodium and water retention. Mineralocorticoids promote renal sodium reabsorption, causing fluid retention. Prednisone’s glucocorticoid dominance reduces these effects, making this statement accurate for expected nursing observations during administration.
Choice C reason: Prednisone’s low mineralocorticoid activity leads to less, not more, sodium retention. It does not disproportionately affect water retention independently of sodium. This statement is inaccurate, as prednisone’s profile minimizes both sodium and water retention compared to steroids with higher mineralocorticoid effects.
Choice D reason: Prednisone causes hyperglycemia, but its effect is not more extreme than other corticosteroids like dexamethasone. Its glucocorticoid activity drives gluconeogenesis similarly across the class. This statement is inaccurate, as prednisone’s hyperglycemic effects are standard, not uniquely severe, among oral corticosteroids.