The secondary injury model encompasses three factors. Which set correctly lists them?

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Multiple Choice

The secondary injury model encompasses three factors. Which set correctly lists them?

Explanation:
Secondary injury after the initial trauma is driven by conditions that undermine cellular survival: limited oxygen, reduced delivery of energy to cells, and poor removal of metabolic wastes. Hypoxia means cells don’t get enough oxygen to support normal aerobic metabolism, so ATP production drops and results in failure of ion pumps, cellular swelling, and potential cell death. Inadequate fuel delivery reflects reduced blood flow carrying glucose and other nutrients needed for energy production, compounding the energy crisis inside cells. Inadequate waste removal allows metabolic byproducts and edema to accumulate, causing acidosis and further cellular stress that accelerates injury. Together, these factors create a environment where cells continue to deteriorate long after the initial insult. The other options describe responses or signs rather than the driving factors of secondary injury. Inflammation, infection, and necrosis are processes that can follow injury but aren’t the trio that explains the secondary injury mechanism. Pain, swelling, and redness are signs of inflammation, not the core metabolic drivers. Bleeding, bruising, and scarring relate to initial damage or later healing changes, not the primary secondary-injury triad.

Secondary injury after the initial trauma is driven by conditions that undermine cellular survival: limited oxygen, reduced delivery of energy to cells, and poor removal of metabolic wastes. Hypoxia means cells don’t get enough oxygen to support normal aerobic metabolism, so ATP production drops and results in failure of ion pumps, cellular swelling, and potential cell death. Inadequate fuel delivery reflects reduced blood flow carrying glucose and other nutrients needed for energy production, compounding the energy crisis inside cells. Inadequate waste removal allows metabolic byproducts and edema to accumulate, causing acidosis and further cellular stress that accelerates injury. Together, these factors create a environment where cells continue to deteriorate long after the initial insult.

The other options describe responses or signs rather than the driving factors of secondary injury. Inflammation, infection, and necrosis are processes that can follow injury but aren’t the trio that explains the secondary injury mechanism. Pain, swelling, and redness are signs of inflammation, not the core metabolic drivers. Bleeding, bruising, and scarring relate to initial damage or later healing changes, not the primary secondary-injury triad.

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