This has alot of the information that your were looking for.
Pharmacological Intervention in Bleeding
Coumarin drugs, such as warfarin as well as the glycosaminoglycans, heparin and heparan sulfate, are useful as anticoagulants. Heparin is useful as an anticoagulant because it binds to, and activates, antithrombin III which then inhibits the serine proteases of the coagulation cascade. Heparin is abundant in grnaules of the mast cells that line the vasculature. In response to injury, the heparin is released and inhibits coagulation. The coumarin drugs inhibit coagulation by inhibiting the vitamin K-dependent g-carboxylation reactions necessary to the function of thrombin, and factors VII, IX, and X as well as proteins C and S. These drugs act by inhibiting the reduction of the quinone derivatives of vitamin K to their active hydroquinone forms. Because of the mode of action of coumarin drugs, it takes several days for their maximum effect to be realized. For this reason, heparin is normally administered first followed by warfarin or warfarin-related drugs. The plasminogen activators also are useful for controlling coagulation. Because tPA is highly selective for the degradation of fibrin in clots, it is extremely useful in restoring the patency of the coronary arteries following thrombosis, in particular during the short period following myocardial infarct. Streptokinase (an enzyme from the Streptococci bacterium) is another plasminogen activator useful from a therapeutic standpoint. However, it is less selective than tPA, being able to activate circulating plasminogen as well as that bound to a fibrin clot. Aspirin is an important inhibitor of platelet activation. By virtue of inhibiting the activity of cyclooxygenase, aspirin reduces the production of TXA2. Aspirin also reduces endothelial cell production of prostacyclin (PGI2), an inhibitor of platelet aggregation and a vasodilator. Localized to the site of coagulation is a balance between the levels of platelet derived TXA2 and endothelial cell derived PGI2. This allows for platelet aggregation and clot formation but preventing excessive accumulation of the clot, thus maintaining blood flow around the site of the clot. Endothelial cells regenerate active cyclooxygenase faster than platelets because mature platelets cannot synthesize the enzyme, requiring new platelets to enter the circulation (platelet half-life is approximately 4 days). Therefore, PGI2 synthesis is greater than that of TXA2. The net effect of aspirin is more in favor of endothelial cell-mediated inhibition of the coagulation cascade. This reflects the cardiovascular benefits to low dose administration of aspirin.
Newer classes of anticoagulation drugs are being developed that function by inhibiting the activation of platelets and their subsequent aggregation. The drug clopidogrel: Plavix® (Bristol-Myers Squibb) is an irreversible inhibitor of the ADP receptor on platelet membranes. When ADP binds to platelets they are activated and aggregate leading to amplification of the coagulation response, thus Plavix interferes with this process. Plavix is prescribed for the treatment of peripheral vascular and cerebrovascular disease as well as coronary artery disease to prevent the formation of thrombotic plaques. http://www.med.unibs.it/~marchesi/blood.html
>Even this simplified version seems quite complicated for many of us.<
It is a complicated system and this is a necessary design feature for survival. The complexity is what assures that routine localized bleeds are stopped and do not result in systemic coagulation (DIC).
Let’s look at the diagram again paying attention to the color coding:
The clotting cascade begins with an injury and it has two branches as depicted. Items shown in blue are inactivated clotting factors; they are constantly circulating throughout the body but have no effect on clotting until they are activated. By being in constant circulation, they are able to respond to an injury in the body at any time, wherever it may occur.
An inactivated clotting factor in blue is converted to an activated clotting factor, shown in orange, via a reaction with either a prior activated factor in the cascade or a cofactor, shown in green. Thus, the clotting cascade is a tightly controlled sequence of biochemical reactions; if even one element in the cascade is missing, the system may fail to produce a clot. Under normal circumstances, this assures that clotting is restricted to the site of the injury.
>It would be helpful for some of us who are not well versed in this field if you could identify the places where the various agents work in this cascade, such as Plavix (if it can have a role in this cascade whatsoever), Aspirin, ATryn, Coumadin, and heparin<
Plavix and aspirin are antiplatelet drugs rather than anticoagulants (#msg-26739622, #msg-18197555); they work on a separate system from the one depicted in the clotting-cascade diagram in the prior post.
Coumadin (warfarin) inhibits Vitamin K, which is needed for the synthesis of various inactivated clotting factors (the blue items in the diagram). It thereby down-regulates the clotting cascade at various places in a dose-dependent (but highly unpredictable) manner.
Unfractionated heparin inhibits FIIa (thrombin) and FXa. Low-molecular-weight heparins (LMWH) such as Lovenox inhibit FIIa and FXa, but the inhibition of FIIa is less effective than it is for unfractionated heparin (#msg-26898084).
Antithrombin (a.k.a. ATIII) inhibits the clotting cascade at several places; it must be bound to heparin or LMWH for those substances to inhibit FIIa and FXa effectively (#msg-26898084).
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