In ITP, blood platelets (which cause blood clotting) are destroyed. Potassium leaks out of platelets after clotting has occurred. The thrombosis is directed in concordance of platelets, neutrophils and monocytes. It is absent from erythrocytes, platelets, and neutrophils. Endothelial prostacyclin binds to prostanoid receptors on the surface of resting platelets. Here all erythrocytes, platelets, and most leukocytes form in adults. Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. Eventually thrombocytopenia, a decrease of blood platelets develops. Fibrin forms long strands of tough insoluble protein that are bound to the platelets. Thromboxanes are responsible for the aggregation of platelets that form blood clots. Platelets and white blood cells are also components. A decrease in blood platelets (thrombocytopenia) also may occur. Another adverse effect is inhibition of platelets (thrombocytopenia). When the endothelial layer is disrupted, collagen and VWF anchor platelets to the subendothelium. Glycosylation restores survival of chilled blood platelets.