NURS 6501: MIDTERM EXAM: Please contact Assignment Samurai for help with NURS 6501: Midterm Exam or any other assignment. Email: assignmentsamurai@gmail.com Why is an increased influx of calcium into an injured cell problematic in ischemia-reperfusion injury? Group of answer choices

• It prevents the recruitment of inflammatory cells.
• It causes excessive muscle contractions.
• It enhances the efficiency of ATP production in mitochondria.
• It triggers cell death.

  The correct answer is: It triggers cell death.   Explanation: In ischemia-reperfusion injury, when blood flow is restored to tissues after a period of ischemia (lack of oxygen), the sudden increase in blood supply can lead to a cascade of harmful events. One of the key contributors to the damage is the influx of calcium ions into the injured cells.

• During ischemia, ATP levels drop, and the function of calcium pumps in the cell membrane and mitochondria is impaired. This leads to an accumulation of calcium within the cell.
• When reperfusion occurs, the sudden return of oxygen can exacerbate this calcium influx, because the mechanisms for calcium removal are overwhelmed or dysfunctional.

The excessive calcium influx triggers several harmful processes, including:

• Activation of enzymes such as phospholipases, proteases, and endonucleases, which damage cell membranes, proteins, and DNA.
• Initiation of apoptotic pathways and cell death through the activation of calcium-dependent signaling pathways.

Why the other options are incorrect:

• It prevents the recruitment of inflammatory cells: Calcium influx does not prevent the recruitment of inflammatory cells; rather, it promotes the release of pro-inflammatory signals and cytokines, which leads to further tissue damage and inflammation.
• It causes excessive muscle contractions: While excessive calcium can lead to muscle contraction (e.g., in heart muscle during reperfusion injury), this is a secondary effect. The primary issue in ischemia-reperfusion injury is the cellular damage and eventual cell death.
• It enhances the efficiency of ATP production in mitochondria: In fact, the influx of calcium impairs mitochondrial function, rather than enhancing it. Calcium overload can lead to mitochondrial dysfunction, which further reduces ATP production and exacerbates the injury.

Conclusion: The influx of calcium during ischemia-reperfusion injury primarily triggers cell death by activating destructive enzymes and signaling pathways that cause damage to cellular structures.