Injured cells suffer secondary injury from two main causes. What are they?

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Multiple Choice

Injured cells suffer secondary injury from two main causes. What are they?

Explanation:
When tissue is injured, the damage doesn’t stop with the initial hit; the cells face ongoing stress from factors that worsen their function. The two main drivers of this secondary injury are lack of oxygen delivery (hypoxia) and the resulting decreased blood flow to the area. Without enough oxygen, cells can’t produce ATP efficiently, so the ion pumps fail, leading to ions and water flooding into cells, swelling, and disruption of membranes. At the same time, reduced blood flow means fewer nutrients reach the tissue and waste products aren’t cleared, which promotes acidosis and activates enzymes and inflammatory processes that further damage cell structures. Together, these mechanisms push cells over the edge, increasing injury beyond the original event. Other factors like infection, dehydration, excessive warmth, or friction can worsen outcomes, but hypoxia and decreased perfusion are the primary culprits driving secondary cellular injury.

When tissue is injured, the damage doesn’t stop with the initial hit; the cells face ongoing stress from factors that worsen their function. The two main drivers of this secondary injury are lack of oxygen delivery (hypoxia) and the resulting decreased blood flow to the area. Without enough oxygen, cells can’t produce ATP efficiently, so the ion pumps fail, leading to ions and water flooding into cells, swelling, and disruption of membranes. At the same time, reduced blood flow means fewer nutrients reach the tissue and waste products aren’t cleared, which promotes acidosis and activates enzymes and inflammatory processes that further damage cell structures. Together, these mechanisms push cells over the edge, increasing injury beyond the original event. Other factors like infection, dehydration, excessive warmth, or friction can worsen outcomes, but hypoxia and decreased perfusion are the primary culprits driving secondary cellular injury.

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