Is heparin intrinsic or extrinsic? Warfarin acts on the extrinsic pathway, whilst heparin acts on the intrinsic pathway. Thus, warfarin efficacy is monitored using the INR — which utilises the prothrombin time. This is because warfarin acts on the extrinsic pathway — and the PT is a measure of the extrinsic pathway.
Quinti Ziat Explainer. What causes coagulation? The mechanism of coagulation involves activation, adhesion and aggregation of platelets, as well as deposition and maturation of fibrin. Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the blood vessel. Lhassane Madrigal Pundit. Is PTT intrinsic or extrinsic? Two laboratory tests are used commonly to evaluate coagulation disorders: Prothrombin Time PT which measures the integrity of the extrinsic system as well as factors common to both systems and Partial Thromboplastin Time PTT , which measures the integrity of the intrinsic system and the common components.
Lesia Planells Pundit. What do you mean by coagulation? Coagulation is the process by which blood forms clots. Coagulation may also refer to: Coagulation water treatment , in colloid chemistry, a process in which dispersed colloidal particles agglomerate. Coagulation milk , the coagulation of milk into curd by rennet or acid. Felisbela Bossmanns Pundit.
What is intrinsic pathway of coagulation? Intrinsic pathway of blood coagulation. As such, the proteins required for such clotting to take place are part of the intrinsic pathway of blood coagulation. This pathway involves a series of proteins, protein cofactors, and enzymes, which interact in reactions that take place on membrane surfaces.
Iru Mazzeo Pundit. Where do the intrinsic and extrinsic pathways converge? Activated factor Xa is the site at which the intrinsic and extrinsic coagulation cascades converge.
The extrinsic pathway is initiated at the site of injury in response to the release of tissue factor factor III and thus, is also known as the tissue factor pathway. A nick in a blood vessel results in exposure of what we call "the wetable surface. The "platelet reaction" really consists of platelets sticking to the wetable surface, swelling and attracting other platelets. When punctures in the blood vessels are small enough, platelet plugs will stop the blood flow and no blood clot is required.
Remember, "like" charges repel one another, so platelets don't want to stick to the healthy endothelium that lines the blood vessels. However, the damaged tissue that is exposed when the lining of a blood vessel is damaged is positively charged! This positively charged, wetable surface will attract and hold the negatively charged platelet membranes When platelets contact damaged tissue inside a blood vessel wall, the damaged tissue triggers a response from the platelets called the "platelet reaction.
The platelets begin to release a bunch of arachidonic acid metabolites arachidonic is a fatty acid! Among the arachadonic acid metabolites released by platelets are thromboxanes TX's and prostaglandins PG's. Activated platelets also release serotonin 5-HT and thrombopoietin! But what do all of these factors released by platelets actually do, you ask??? Perhaps most importantly, these factors i attract more platelets into the region of the damaged tissue, ii cause vasoconstriction, and iii increase the production rate of new platelets.
The reasons that we want to do all this may seem self-evident, but let's go into a bit more detail on these factors released by platelets. These arachidonic acid metabolites also induce vascular spasm! This ADH-like peptide, released by the platelets, causes the platelets, themselves, to send out pseudopod-like processes to grab fibrin "threads. Platelets actually have specific fibrin binding sites and they grab fibrin to anchor blood clots together more on this below!
You can read more about vascular spasm below! People develop small tears in hundreds of vessels every day, but the holes are small and are routinely plugged by platelets. In thrombocytopenia, these routine vascular tears are not repaired and petechial hemmorhages will be seen under the skin, in addition to internal hemorrhages which cannot be seen. The platelet mechanism does not interfere with vessel function, whereas full coagulation sometimes does; that is, blood clots may actually block blood flow by blocking the lumen of some small blood vessels.
Part 3 of Hemostasis Blood coagulation clotting : One way to think of a clot is as follows: the platelet reaction gets going and a network of fibrin molecules are added to link the platelets together and make a stronger patchwork over a traumatized area.
In fact, platelets appear to have specific binding sites for attachment to fibrin. Fibrin "threads" are strong protein filaments! As the "patchwork" or "clot" is formed, a bunch of blood cells get trapped in the middle of the "net. Remember, the RBC's are not really part of the clotting mechanism, they simply get caught up in the fibrin network and end up being used as "building blocks" in the plug that stops the bleeding!
We have a fairly simple construct outline of the factors involved in the clotting mechanisms pathways. Note that, as there are over 40 known endogenous pro-coagulants and anticoagulants, all known factors and cofactors in the pathways are not shown in this construct!
Under normal circumstances, anti coagulant activity outweighs pro- coagulant activity in the bloodstream and the blood keeps flowing.
When tissues are traumatized, pro-coagulant activity outweighs anticoagulant activity in the area of trauma in order to stop the bleeding. The terms Extrinsic and Intrinsic can be more than a little bit confusing! Extrinsic means "from outside the blood. In the extrinsic clotting pathway, Factor III released by the traumatized tissue the wetable surface activates a simple series of biochemical reactions involving factors produced by platelets.
Note that activation of the extrinsic pathway leads to the conversion of prothrombin to thrombin. This is an important step! Subsequent steps in the pathway will lead to the formation of a blood clot within seconds in severe trauma and within minutes with minor trauma.
For this reason, the extrinsic clotting pathway is often called the "fast pathway. We used to remember that the extrinsic pathway was the fast pathway by saying, "the ex trinsic pathway is ex tra fast!
In the intrinsic pathway, prothrombin activation begins within the blood; that is, in this pathway, prothrombin activation is driven by platelets, which are formed elements of the blood! The term "intrinsic pathway" refers to a series of biochemical reactions that lead to clotting, where the process is driven by factors within the blood Notice that the factor that keeps the pathway going is factor XII from platelets.
The clotting cascade occurs through two separate pathways that interact, the intrinsic and the extrinsic pathway. Extrinsic Pathway The extrinsic pathway is activated by external trauma that causes blood to escape from the vascular system. This pathway is quicker than the intrinsic pathway. It involves factor VII. Intrinsic Pathway The intrinsic pathway is activated by trauma inside the vascular system, and is activated by platelets, exposed endothelium, chemicals, or collagen.
This pathway is slower than the extrinsic pathway, but more important. Common Pathway Both pathways meet and finish the pathway of clot production in what is known as the common pathway. Instructor's Note: A diagram may be found in your text illustrating the clotting cascade. The student does not need to be concerned about learning the details of these pathways.
The liver requires the fat-soluble vitamin K to produce many of them. Vitamin K along with biotin and folate is somewhat unusual among vitamins in that it is not only consumed in the diet but is also synthesized by bacteria residing in the large intestine. The calcium ion, considered factor IV, is derived from the diet and from the breakdown of bone. Some recent evidence indicates that activation of various clotting factors occurs on specific receptor sites on the surfaces of platelets.
Factor VI was once believed to be a distinct clotting factor, but is now thought to be identical to factor V. Rather than renumber the other factors, factor VI was allowed to remain as a placeholder and also a reminder that knowledge changes over time. The quicker responding and more direct extrinsic pathway also known as the tissue factor pathway begins when damage occurs to the surrounding tissues, such as in a traumatic injury.
Upon contact with blood plasma, the damaged extravascular cells, which are extrinsic to the bloodstream, release factor III thromboplastin. This enzyme complex leads to activation of factor X Stuart—Prower factor , which activates the common pathway discussed below.
The events in the extrinsic pathway are completed in a matter of seconds. The intrinsic pathway also known as the contact activation pathway is longer and more complex. In this case, the factors involved are intrinsic to present within the bloodstream. The pathway can be prompted by damage to the tissues, resulting from internal factors such as arterial disease; however, it is most often initiated when factor XII Hageman factor comes into contact with foreign materials, such as when a blood sample is put into a glass test tube.
Within the body, factor XII is typically activated when it encounters negatively charged molecules, such as inorganic polymers and phosphate produced earlier in the series of intrinsic pathway reactions. Factor XII sets off a series of reactions that in turn activates factor XI antihemolytic factor C or plasma thromboplastin antecedent then factor IX antihemolytic factor B or plasma thromboplasmin.
In the meantime, chemicals released by the platelets increase the rate of these activation reactions. Finally, factor VIII antihemolytic factor A from the platelets and endothelial cells combines with factor IX antihemolytic factor B or plasma thromboplasmin to form an enzyme complex that activates factor X Stuart—Prower factor or thrombokinase , leading to the common pathway.
The events in the intrinsic pathway are completed in a few minutes. Both the intrinsic and extrinsic pathways lead to the common pathway , in which fibrin is produced to seal off the vessel. Once factor X has been activated by either the intrinsic or extrinsic pathway, the enzyme prothrombinase converts factor II, the inactive enzyme prothrombin, into the active enzyme thrombin.
Note that if the enzyme thrombin were not normally in an inactive form, clots would form spontaneously, a condition not consistent with life. Then, thrombin converts factor I, the insoluble fibrinogen, into the soluble fibrin protein strands. Factor XIII then stabilizes the fibrin clot. The stabilized clot is acted upon by contractile proteins within the platelets. As these proteins contract, they pull on the fibrin threads, bringing the edges of the clot more tightly together, somewhat as we do when tightening loose shoelaces see Figure 1a.
This process also wrings out of the clot a small amount of fluid called serum , which is blood plasma without its clotting factors. To restore normal blood flow as the vessel heals, the clot must eventually be removed. Fibrinolysis is the gradual degradation of the clot. Again, there is a fairly complicated series of reactions that involves factor XII and protein-catabolizing enzymes. During this process, the inactive protein plasminogen is converted into the active plasmin , which gradually breaks down the fibrin of the clot.
Additionally, bradykinin, a vasodilator, is released, reversing the effects of the serotonin and prostaglandins from the platelets. This allows the smooth muscle in the walls of the vessels to relax and helps to restore the circulation.
An anticoagulant is any substance that opposes coagulation. Several circulating plasma anticoagulants play a role in limiting the coagulation process to the region of injury and restoring a normal, clot-free condition of blood. For instance, a cluster of proteins collectively referred to as the protein C system inactivates clotting factors involved in the intrinsic pathway. TFPI tissue factor pathway inhibitor inhibits the conversion of the inactive factor VII to the active form in the extrinsic pathway.
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