Antiplatelet vs Anticoagulant
Blood clotting is an extremely complex process involving platelets, clotting factors, and endothelial cells lining the blood vessels. It is an important protective mechanism that limits blood loss after trauma. It also is a critical step in wound healing because the fiber framework formed in clotting acts as the foundation onto which multiplying cells migrate. Damage to blood vessels brings blood cells and the highly reactive extracellular matrix into contact. Blood cells latch on to binding sites in the extracellular material. Platelet activation and aggregation are the immediate result of this binding. Inflammatory mediators secreted by damaged platelets and endothelial cells activate blood cells to produce various potent chemicals. More platelets activate due to these chemicals and a platelet plug forms over the gap in the endothelium. Number and function of platelets directly correlate to the success of the process. Thrombocytopenia means low platelet number, and thrombasthenia means poor platelet function. Bleeding time is the test which assesses the integrity of the platelet plug formation. Intrinsic and the extrinsic pathway are the two routes along which clotting progresses from here.
Liver produces clotting factors. Liver diseases and genetic abnormalities lead to poor production of various clotting factors. Hemophilia is such a situation. Extrinsic pathway, also known as the tissue factor pathway involves factors VII and X while the intrinsic pathway involves factors XII, XI, IX, VIII and X. Both extrinsic and intrinsic pathways lead to the common pathway which starts with the activation of factor X. Fibrin meshwork forms as a result of the common pathway and provides the aforementioned foundation for other cellular processes.
Antiplatelet are drugs which interfere with platelet plug formation. In essence, these drugs interfere with platelet activation and aggregation. These drugs may be used as prophylaxis for clot formation, to treat acute thrombotic events and as anti-inflammatory drugs. Cyclooxygenase inhibitors, ADP receptor inhibitors, phosphodiesterase inhibitors, glycoprotein IIB/IIA inhibitors, thromboxane inhibitors and adenosine reuptake inhibitors are a few known drugs classes. Gastrointestinal bleeding is the commonest side effect of these drugs.
Anticoagulants are drugs that interfere with the coagulation cascade. Heparin and warfarin are the two most well-known anticoagulants. These drugs may be used as prophylaxis to prevent deep vein thrombosis, embolism, and also to treat thromboembolism, myocardial infarctions, and peripheral vascular diseases. These drugs act by inhibiting vitamin K dependent clotting factors and by activating anti-thrombin III. Heparin is not available as a tablet while warfarin is. Heparin and warfarin should be started together because warfarin increases blood coagulability for about three days and heparin provides the necessary protection against thromboembolic events. Warfarin increases INR and, therefore, INR is used as a method to monitor treatment. After atrial fibrillation INR should be kept between 2.5 to 3.5. Therefore, regular follow-up is essential.
Antiplatelet vs Anticoagulant
• Antiplatelet drugs block platelet plug formation while anticoagulants interfere with the extrinsic and intrinsic pathways.
• Anti-platelets usually may cause gastrointestinal bleeding due to increased acid secretion while anticoagulants may cause bleeding due to thrombocytopenia.
• Antiplatelet may be given while pregnant while warfarin should not be.