Introduction to Hemostasis is a course focusing on the three hemostatic components, the concepts of hypocoagulation and hypercoagulation, and the overview of the hemostatic mechanism.
The extrinsic pathway of coagulation is activated when there is vascular endothelial injury which causes the exposure of the tissue factor (TF).
The binding of tissue factor (TF) and plasma factor VII will lead to a series of enzymatic reactions that causes the activation of the common pathway.
Fibrinolysis is the system whereby a temporary fibrin clot is systematically and gradually dissolved as the blood vessel heals.
Fibrinolysis is a mechanism simultaneously activated with coagulation when there is vessel injury in order to restore normal blood flow.
Damaged tissues release tissue plasminogen activator (tPA), which activates the inert substance, plasminogen to its active form, plasmin.
The common pathway begins with the activation of factor X to its active form, either through the ex- or intrinsic pathway.
The ultimate goal of common pathway activation is the formation and stabilization of a platelet-fibrin clot.
Plasmin is capable of degrading the fibrin clot formed.
Tissue factor (TF) is a receptor protein on cells that underlie the endothelium.
The extrinsic pathway of coagulation is now thought to be the primary mechanism which coagulation is initiated.
Prefixes in medical terms include a-/an-, aniso-, cyt-, dys-, erythro-, ferr-, hemo-, hypo-, hyper-, macro-, mega-, meta-, micro-, myel(o)-, pan-, phleb-, phago-, poikilo-, poly-, schis-, scler-, splen-, thromb(o)-, xanth-.
Suffixes in medical terms include -cyte, -emia, -itis, -lysis, -oma, -opathy, -osis, -penia, -phil(ic), -plasia (plastic), -poiesis, -poietin.
Derive a definition based on the prefix, root word, and suffix.
Hematopoiesis refers to the production, formation, and development of blood.
Macrocytosis is a condition in which there would be large cells.
Aplasia is a condition of absence of cell production.
Endothelial cells have antiplatelet activity.
Hemolysis is the destruction of blood.
The anti-thrombotic lining of BVs provides a smooth, non-reactive surface that facilitates blood flow and reduces turbulence which can promote thrombosis.
In the undisturbed state of blood vessels (BVs), the BVs maintain blood in the liquid state because the intact endothelial lining of BVs is anti-thrombotic.
Endothelial cells are capable of producing the enzyme, nitric oxide synthase, responsible for the production of NO, which comes from substrate L-arginine, and is responsible for vasodilation.
The anti-thrombotic properties of BVs are due to the absence of turbulence, the tunic intima of BVs, which is comprised of the endothelial lining, individually comprised of endothelial cells that have (-) charge which will repel the plts.
The anti-thrombotic lining of BVs does not activate platelets or promote coagulation.
The substances listed in Table 8 are released from the endothelial cells and sub-endothelial smooth muscles contribute to normal blood flow and prevent abnormal formation of clots in BVs.
Coagulopathy is a disease of clotting.
Splenomegaly is a condition of having a large or giant spleen.
Pancytopenia is a condition of decrease in all cell type.
Agranulocytopenia is a condition of decrease in granulocytes.
Intravascular refers to inside blood vessels.
VWF assists platelet adhesion to the sub-endothelium to provide a coagulation surface.
Fibrinogen is converted to fibrin for clot formation.
Platelet Factor 4 promotes platelet aggregation and inhibits heparin.
Calcium promotes platelet aggregation.
Alpha-2 Antiplasmin is a plasmin inhibitor and inhibits clot lysis.
Serotonin promotes vasoconstriction at the injury site.
Factor V is a co-factor in fibrin clot formation.
Plasminogen is a precursor to plasmin, which includes clot lysis.
Neurosinin II inhibits Factor X Ia and thus factor IX activation.
Platelet-derived Growth Factor promotes smooth muscle growth for vessel repair.