From Big Robbins:
ISCHEMIC AND HYPOXIC INJURYThis is the most common type of cell injury in clinical medicine and has been studied extensively in humans, in experimental animals, and in culture systems. Hypoxia, referring to reduced oxygen availability, may occur in a variety of clinical settings, described earlier. In ischemia, on the other hand, the supply of oxygen and nutrients is decreased most often because of reduced blood flow as a consequence of a mechanical obstruction in the arterial system. It can also be caused by reduced venous drainage. In contrast to hypoxia, during which energy production by anaerobic glycolysis can continue, ischemia compromises the delivery of substrates for glycolysis. Thus, in ischemic tissues, not only is aerobic metabolism compromised but anaerobic energy generation also stops after glycolytic substrates are exhausted, or glycolysis is inhibited by the accumulation of metabolites that would have been removed otherwise by blood flow. For this reason,
ischemia tends to cause more rapid and severe cell and tissue injury than does hypoxia in the absence of ischemia.
If ischemia persists, irreversible injury and necrosis ensue. Irreversible injury is associated morphologically with severe swelling of mitochondria, extensive damage to plasma membranes (giving rise to myelin figures) and swelling of lysosomes (see
Fig. 1-10C ). Large, flocculent, amorphous densities develop in the mitochondrial matrix. In the myocardium, these are indications of irreversible injury and can be seen as early as 30 to 40 minutes after ischemia. Massive influx of calcium into the cell then occurs, particularly if the ischemic zone is reperfused. Death is mainly by necrosis, but apoptosis also contributes; the apoptotic pathway is probably activated by release of pro-apoptotic molecules from leaky mitochondria. The cell's components are progressively degraded, and there is widespread leakage of cellular enzymes into the extracellular space and, conversely, entry of extracellular macromolecules from the interstitial space into the dying cells. Finally, the dead cells may become replaced by large masses composed of phospholipids in the form of myelin figures. These are then either phagocytosed by leukocytes or degraded further into fatty acids.
Calcification of such fatty acid residues may occur, with the formation of calcium soaps.
I believe it's an ischemia vs hypoxia issue that causes the difference you're looking for. Hope this helps.
