Prednisone is an oral corticosteroid that has less mineralocorticoid activity than other oral steroids. What does the nurse expect when giving this medication?
It will cause less extreme hyperglycemia
It will cause less sodium and water retention
It will cause more sodium retention and less water retention
It will cause more extreme hyperglycemia
The Correct Answer is B
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
Choice A reason: Bladder cancer primarily affects the bladder, causing hematuria or obstruction, leading to post-renal injury, not intra-renal. Intra-renal damage involves nephron injury, which is less likely with bladder cancer unless advanced metastasis affects kidneys, making this patient less at risk than one on nephrotoxic chemotherapy.
Choice B reason: Benign prostatic hyperplasia causes urinary obstruction, leading to post-renal kidney injury from backpressure, not intra-renal damage. The kidneys’ nephrons are not directly harmed by BPH, making this 65-year-old male less at risk for intra-renal injury compared to a patient receiving nephrotoxic drugs.
Choice C reason: Chemotherapy, especially agents like cisplatin, is nephrotoxic, causing intra-renal acute kidney injury by damaging renal tubules. This 25-year-old female faces high risk due to direct tubular toxicity, leading to acute tubular necrosis, making her the most likely to develop intra-renal injury among the options.
Choice D reason: Renal artery stenosis causes pre-renal kidney injury by reducing renal perfusion, not intra-renal damage. The nephrons remain intact unless chronic ischemia leads to secondary damage. This 36-year-old female has a lower risk of intra-renal injury compared to the chemotherapy patient’s direct nephrotoxic exposure.
Correct Answer is A
Explanation
Choice A reason: SGLT-2 inhibitors, like empagliflozin, block sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption. This increases urinary glucose excretion, lowering blood sugar in type 2 diabetes. The mechanism is insulin-independent, reducing hyperglycemia and promoting weight loss, making this statement accurate for their primary action.
Choice B reason: SGLT-2 inhibitors do not interact with transcription factors to improve insulin sensitivity. This describes metformin’s action via AMPK activation in liver and muscle. SGLT-2 inhibitors act renally, not on transcription factors, making this statement inaccurate as it misattributes their mechanism to a different drug class.
Choice C reason: Inhibiting hepatic glucose production and increasing insulin sensitivity is metformin’s mechanism, not SGLT-2 inhibitors. SGLT-2 inhibitors work renally to excrete glucose, not by altering hepatic gluconeogenesis or peripheral insulin sensitivity. This statement is inaccurate, as it describes a different antidiabetic drug’s action.
Choice D reason: Blocking ATP-sensitive K+ channels is the mechanism of sulfonylureas, like glipizide, which stimulate insulin secretion from beta cells. SGLT-2 inhibitors act on renal glucose reabsorption, not beta cell channels. This statement is inaccurate, as it incorrectly assigns a sulfonylurea mechanism to SGLT-2 inhibitors.
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