Final answer:
DIC leads to tissue ischemia and hemolytic anemia as ATP deficiency in RBCs impairs the Na+/K+-ATPase, causing cell lysis and a rise in plasma bilirubin. The destruction of RBCs causes hemolytic anemia, and increased 2,3BPG levels lead to reduced tissue oxygenation.
Step-by-step explanation:
Mechanism of Tissue Ischemia and Hemolytic Anemia in DIC
Disseminated intravascular coagulation (DIC) is a complex condition that can lead to tissue ischemia and hemolytic anemia. In the context of RBCs, the deficiency in ATP due to impaired glycolysis leads to ineffective functioning of the Na+/K+-ATPase. This results in an accumulation of intracellular sodium, causing water to enter the cells, leading to their swelling and eventual lysis. The plasma bilirubin levels increase as RBCs are lysed, potentially resulting in jaundice. As the RBCs are destroyed, hemolytic anemia occurs. Moreover, an increase in 2,3-bisphosphoglycerate (2,3BPG) may occur, causing a 'right shift' in the hemoglobin oxygen saturation curve, which signifies a lower oxygen affinity and earlier oxygen release from hemoglobin, leading to impaired tissue oxygenation and causing ischemia.
Additionally, in cases like a hemolytic transfusion reaction, where transfused RBCs are destroyed due to the presence of incompatible antigens, there can be a rapid development of tissue ischemia and organ damage due to the obstruction of blood vessels by agglutinated RBCs and inflammatory responses triggered by the activation of the complement system.