A nurse is caring for a client who sustained significant crush injuries and is being treated for acute renal injury. What is the pathophysiology behind the development of this renal injury?
High levels of myoglobin obstructed the tubules and caused intra-renal damage
Large amounts of IV fluids overloaded the kidneys and caused pre-renal damage
Pain medications for the injuries were nephrotoxic and caused pre-renal damage
Significant blood loss impaired renal perfusion and caused post-renal damage
The Correct Answer is A
Choice A reason: Crush injuries release myoglobin from damaged muscles, causing rhabdomyolysis. Myoglobin precipitates in renal tubules, obstructing them and leading to acute tubular necrosis, an intra-renal acute kidney injury. This toxic effect, combined with oxidative stress, impairs filtration, making this statement accurate for the pathophysiology of renal injury.
Choice B reason: Large IV fluid volumes are used to prevent renal injury in rhabdomyolysis by diluting myoglobin and maintaining perfusion. Fluid overload may cause pulmonary edema but does not typically cause pre-renal damage, which results from hypoperfusion. This statement is inaccurate, as fluids are protective, not harmful.
Choice C reason: Pain medications like NSAIDs can be nephrotoxic, causing intra-renal damage by reducing renal blood flow or causing interstitial nephritis. However, pre-renal damage results from hypoperfusion, not direct toxicity. In crush injuries, myoglobin is the primary cause, making this statement less accurate than myoglobin-related tubular damage.
Choice D reason: Significant blood loss causes pre-renal injury by reducing renal perfusion, not post-renal damage, which involves urinary obstruction. Crush injuries primarily cause intra-renal damage via myoglobin. This statement is inaccurate, as it misattributes the mechanism and type of renal injury in this context.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Reasoning:
Choice A reason: Levothyroxine (T4) replacement requires TSH monitoring to ensure adequate dosing, as TSH reflects thyroid function. T3 replacement also requires monitoring, but T3 is less commonly used due to its short half-life. This statement is inaccurate, as TSH monitoring is essential for T4 therapy.
Choice B reason: The body converts levothyroxine (T4) to triiodothyronine (T3) via deiodinase enzymes in peripheral tissues, restoring both hormone levels. T3 replacement is unnecessary, as T4 provides a stable precursor for T3 production, making this statement accurate for explaining hypothyroidism treatment rationale.
Choice C reason: T3 and T4 can be administered together in specific cases (e.g., combination therapy) without becoming inactive. However, T4 alone is standard due to its longer half-life and conversion to T3. This statement is inaccurate, as it falsely claims biochemical incompatibility between the hormones.
Choice D reason: T3 is the active thyroid hormone, not an inactive precursor to T4. T4 is converted to T3, which binds receptors to regulate metabolism. This statement is inaccurate, as it reverses the roles of T3 and T4 in thyroid hormone physiology and therapy.
Correct Answer is D
Explanation
Choice A reason: Prednisone reduces pain by inhibiting prostaglandin synthesis via phospholipase A2 suppression, not increasing it. Discontinuing prednisone may worsen autoimmune joint pain. This statement is inaccurate, as prednisone’s anti-inflammatory action is beneficial, and the issue lies in its combination with NSAIDs.
Choice B reason: Alternate-day prednisone dosing reduces side effects but may not adequately control chronic autoimmune joint pain, as consistent suppression of inflammation is needed. This statement is less appropriate, as it does not address the primary concern of gastrointestinal risk from combining prednisone with ibuprofen.
Choice C reason: Ibuprofen is a potent NSAID, but its strength is not the issue. Combining it with prednisone increases gastrointestinal bleeding risk due to additive mucosal damage. Suggesting stronger ibuprofen is inappropriate and ignores the ulcer risk, making this statement inaccurate for safe pain management.
Choice D reason: Prednisone and NSAIDs like ibuprofen increase gastric ulcer risk by suppressing mucosal protective prostaglandins and increasing acid production. This combination can lead to bleeding or perforation, especially in autoimmune patients on chronic steroids. This statement is accurate, as it prioritizes discussing safer pain management alternatives.
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