The liver produces the majority of the proteins that function as clotting factors and as anticoagulants. These cells release proteins involved in clotting and platelet aggregation. Some of their unique structural elements include plasma membrane, open canalicular system, spectrin and actin cytoskeleton, microtubules, mitochondria, lysosomes, granules, and peroxisomes. These are non-nucleated disc-like cells created from megakaryocytes that arise from the bone marrow. Factor III, IV, and VIII all undergo K dependent gamma-carboxylation of their glutamic acid residues, which allows for binding with calcium and other ions while in the coagulation pathway. Most notably are those processes associated with the endothelium, platelets, and hepatocytes.Įndothelium. Clotting factors III and VIII originate from the endothelial cells while the clotting factor IV comes from the plasma. There are various cellular components in the process of coagulation. However, it can lead to bleeding/thrombosis in cases of inappropriate dosage, non-compliance, medication interactions, and result in significant morbidity and mortality. The way these medications affect the functionality of the various components of clotting cascade can help patients with their clinical conditions. Medicine is currently in the era of widespread use of antiplatelet agents like aspirin, clopidogrel, ticagrelor and anticoagulants like warfarin, heparin, low molecular weight heparin, rivaroxaban, apixaban, dabigatran, fondaparinux amongst others for various commonly encountered clinical conditions like cardiac stenting/ percutaneous coronary intervention, atrial fibrillation, deep venous thrombosis, pulmonary embolism, and many more. Some of the examples include Von Willebrand disease, hemophilia, disseminated intravascular coagulation, deficiency of the clotting factors, platelet disorders, collagen vascular disorders, etc. When there is any defect in the functionality of any component of this hemostatic cascade, it can lead to ineffective hemostasis and inability to control hemorrhage this can lead to severe blood loss, hemorrhage and also complications that can hence ensue due to the inhibited blood supply to vital organs. Some of the examples include Antiphospholipid antibody syndrome, Factor 5 Leiden mutation, Protein C deficiency, protein S deficiency, Prothrombin gene mutation, etc. In this way, a physiologic process becomes a pathologic process leading to morbidity and/or mortality. This situation leads to a pathologic phenomenon of thrombosis, which can have catastrophic complications by obstructing blood flow leading to ischemia and even infarction of the tissues supplied by the occluded blood vessels. At times, this process is triggered inadvertently while the blood is within the lumen of the blood vessel and without any bleeding. The hemostatic cascade is meant to control hemorrhage and be a protective mechanism. Once the injury starts to heal, the plug slowly remodels, and it dissolves with the restoration of normal tissue at the site of the damage. This clot seals the injured area, controls and prevents further bleeding while the tissue regeneration process takes place. Purpose. Hemostasis facilitates a series of enzymatic activations that lead to the formation of a clot with platelets and fibrin polymer. 4) Formation of “fibrin plug” or the final clot. 2) Formation of a temporary “platelet plug." 3) Activation of the coagulation cascade. The mechanism of hemostasis can divide into four stages. 1) Constriction of the blood vessel. It begins with trauma to the lining of the blood vessel. This cascade culminates into the formation of a “plug” that closes up the damaged site of the blood vessel controlling the bleeding. It is a process that involves multiple interlinked steps. Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |