This is a real-world medical entrance exam question, please give the true answer based on the question and selection. Topic name: None, Subject name: Pathology
[{'content': 'In myocardial, the Reperfusion injury maximum effect is caused due to - \nSelect and explain. \nA. Neutrophil, B. Monocytes, C. Free radicals, D. Eosinophils', 'role': 'user'}, {'content': 'Answer: C \nExplanation: Reperfusion injury refers to myocardial vascular or electrophysiological dysfunction that is induced by the\xa0restoration of blood flow to previously ischemic tissue.\no Manifestation includes:\n\nReperfusion arrhythmias.\nEndothelial cell damage leading to microvascular dysfunction,\nMyocardial stunning.\nMyocyte death and infarction.\n\nPATHOPHYSIOLOGY-\nWhen blood flow to cardiac myocytes is disrupted by occlusion of a coronary artery, a series of events is set in\xa0motion that results in cellular injury and death. These processes are largely related to energy production and\xa0utilization and include the following :\n\nReduced energy production with a fall in intracellular ATP levels,\nA transition from aerobic to anaerobic energy utilization,\nAn accumulation of the products of anaerobic metabolism,\nReduced intracellular pH.\n\nFactors that contribute to reperfusion injury include the following :\n\nDamage to cellular and organelle membranes, including mitochondria,\nMyocyte hypercontracture.\nFree radical formation.\nAggregation of leukocytes and inflammatory mediators,\nPlatelet activation.\nComplement activation.\nActivation of the pro-apoptotic signalling cascade.\nEndothelium damage and vasoconstriction.\n\nOxygen and other free radicals -\n\nFree radicals are produced within a minute of reperfusion and continue to be generated for hours after the\xa0restoration of blood flow to ischemic tissue.\nSuperoxide anion (O2)\nHydrogen peroxide (H2O2)\nHypochlorous acid (HClO)\nNitric oxide-derived peroxynitrite.\nHydroxyl radical (OH)\nSeveral mechanisms have been proposed for the development of these free radicals including xanthine oxidase, activated neutrophils, electron leakage from ischemic mitochondrion, catecholamine oxidation, as well as\xa0cyclooxygenase and lipoxygenase enzymes.\nThe relative importance of each of these pathways is not clear, but they are probably interrelated and may\xa0potentiate one another.\nFree radicals damage myocytes directly by altering membrane proteins and phospholipids. Because these\xa0membrane constituents play crucial roles as receptors, enzymes, and ion channels, free radical injury can\xa0lead to fatal metabolic and structure derangements. As an example, oxygen radicals inure the\xa0sarcolemma and may impair the contractile function of the myocyte on this basis. The role for free radicals\xa0as a source of significant myocardial damage is further supported by studies showing that free radical\xa0scavengers, such as superoxide dismutase, administered during thrombolytic therapy help preserve\xa0myocardial function. Finally, reactive oxygen species stimulate leukocyte activation, chemotaxis, and\xa0leukocyte-endothelial adherence.', 'role': 'assistant'}]