Prepare for the Tissue Injury, Healing, and Pain Test. Utilize flashcards and multiple-choice questions with hints and explanations. Ensure you're ready for the exam!

Multiple Choice

Ischemia-reperfusion injury occurs due to what mechanism?

Ischemia-reperfusion injury happens when blood supply is restored after a period of ischemia, and the injury is driven by a burst of reactive oxygen species (ROS) and an inflammatory response. During ischemia, cells switch to anaerobic metabolism, ATP stores fall, and ion pumps fail, leading to cellular edema and accumulation of metabolites. When reperfusion occurs, the sudden influx of oxygen leads to excessive ROS production from mitochondria, xanthine oxidase, and activated neutrophils. These ROS damage cell membranes, proteins, and DNA, causing lipid peroxidation and mitochondrial dysfunction. At the same time, endothelial cells become activated and inflammatory mediators recruit neutrophils, whose degranulation and additional ROS release amplify tissue injury. Calcium overload and mitochondrial permeability transition also contribute to cell death. Thus, the tissue injury results from oxidative stress plus inflammation triggered by reperfusion, not from ischemia alone, and it is not limited to the brain.

Ischemia-reperfusion injury happens when blood supply is restored after a period of ischemia, and the injury is driven by a burst of reactive oxygen species (ROS) and an inflammatory response. During ischemia, cells switch to anaerobic metabolism, ATP stores fall, and ion pumps fail, leading to cellular edema and accumulation of metabolites. When reperfusion occurs, the sudden influx of oxygen leads to excessive ROS production from mitochondria, xanthine oxidase, and activated neutrophils. These ROS damage cell membranes, proteins, and DNA, causing lipid peroxidation and mitochondrial dysfunction. At the same time, endothelial cells become activated and inflammatory mediators recruit neutrophils, whose degranulation and additional ROS release amplify tissue injury. Calcium overload and mitochondrial permeability transition also contribute to cell death. Thus, the tissue injury results from oxidative stress plus inflammation triggered by reperfusion, not from ischemia alone, and it is not limited to the brain.