This first figure is a cascade model of coagulation. The “intrinsic” and “extrinsic” pathways appear to be redundant and converge at the FXa/FVa complex. It seems reasonable that adding excess FVIIa would give more FX activation via FVIIa/TF and make up for the lack of the FIXa/FVIIIa complex in hemophilia. PL/Ca indicates the requirement for a negatively charged phospholipid surface and calcium ions. HMK indicates high molecular weight kininogen; and PK, pre-kallekrein. Professional illustration by Debra Tyler Dartez.

This first figure is a cascade model of coagulation. The “intrinsic” and “extrinsic” pathways appear to be redundant and converge at the FXa/FVa complex. It seems reasonable that adding excess FVIIa would give more FX activation via FVIIa/TF and make up for the lack of the FIXa/FVIIIa complex in hemophilia. PL/Ca indicates the requirement for a negatively charged phospholipid surface and calcium ions. HMK indicates high molecular weight kininogen; and PK, pre-kallekrein. Professional illustration by Debra Tyler Dartez.

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