Q:

Which of the following statement(s) is/are correct concerning the pathophysiology of frostbite?

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Which of the following statement(s) is/are correct concerning the pathophysiology of frostbite?


  1. Frostbite injury may have two components: initial freeze injury and a reperfusion injury that follows during rewarming
  2. The formation of extracellular ice crystals in the tissue begins to occur at -10°C
  3. The release of oxygen free radicals and arachidonic acid metabolites aggravates vasoconstriction and platelet and leukocyte aggregation
  4. Experimental evidence suggests that a substantial component of severe cold injury may be mediated due to platelet aggregation

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a. Frostbite injury may have two components: initial freeze injury and a reperfusion injury that follows during rewarming

c. The release of oxygen free radicals and arachidonic acid metabolites aggravates vasoconstriction and platelet and leukocyte aggregation

Recent evidence suggests that frostbite injury may have two components: the initial freeze injury, and a reperfusion injury that occurs during rewarming. The initial response to tissue cooling is vasoconstriction and arterio-venous shunting, intermittently relieved by vasodilatation. With prolonged exposure, this response fails, and the temperature of the freezing tissues will approximate ambient temperature until -2°C. At this point, extracellular ice crystals form, and as these crystals enlarge, the osmotic pressure of the interstitium increases resulting in movement of intracellular water into the interstitium. Cells begin to shrink and become hyperosmolar, disrupting cellular enzyme function. During rewarming, red cell, platelet and leukocyte aggregation is known to occur and results in patchy thrombosis of the microcirculation. These accumulated blood elements are thought to release, among other products, the toxic oxygenfree radicals and the arachidonic acid metabolites which further aggravate vasoconstriction and platelet and leukocyte aggregation. Recent experimental evidence suggests that a substantial component of severe cold injury may be neutrophil-mediated in that a monoclonal antibody to neutrophil-endothelial and neutrophil-neutrophil adherence can markedly ameliorate the pathology of severe injury

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