Just a Little Thick Blooded, but It Matches my THICK HEAD, Doc!
		This is merely a description of my medical stats and info for those who are curious or concerned...      I did not realize this until June of 1999 but as a kindergarten dummy of blood situations and clots, I had received a B+ by a very good friend and doctor of mine that I knew at the time and I wasn't in medical school ever, really!!!:)LOL... on this paper I wrote..."Coagulation and Fibrinolysis", an attempt at a simplified understanding of the bloods system" by djd_201, 1999    When I went into the hospital in April of 1998, they found a pretty big blood clot in the inner thigh of my left leg. After starting the treatment for the clot, they did some blood workups on me and found a thick blood condition. This is merely a hereditary problem in that my blood is prone to clot, requiring me to stay on "blood thinners" from now on. The part that isn't so simple, is understanding what happened all of the sudden to make me have the clot in the first place. So the following is just a little bit complicated, but it tells you what is going on inside me, the bloods status and it's failure to be able to stay thin enough. In trying to understand the bloods clotting system, I was fortunate enough to have a very caring Phlebotomist. She gave me a chapter from a book by Dr Larry Miller MD, which discusses Fibrinolysis (the dissolving of a clot) and Coagulation (developing the clot).    Here, I am merely attempting to put it into simpler terms, in that I had to read it several times before even understanding as little as I do. The following is the result of my endeavors, to the best of my ability and limited knowledge of and on the issue. I have here within the following pages, included the paper which I good naturedly "bragged" about, but I also fully accept any corrections offered and ask forgiveness for any mistakes found. So, here we go:   "COAGULATION"   Simply to define and explain it, coagulation is the the arrest of bleeding from the body's cardiovascular system, and depends primarily upon "platelet plug formation", along and in conjunction with the extremely complicated formation of a "stable fibrin clot". This involves a sophisticated interaction of "plasma proteins", in a highly ordered sequence. It also includes a wide variety of other interactions of specific elements and factors that make up the body's cardivascular functions, in addition to other "materials" released by the body's tissues themselves which are called lipoproteins, in a complex chain of events. I've found the easiest way to comprehend this order is to merely realize that I won't understand EVERY tid bit of information, then again, just to read it slowly and let it soak in. I accept it and absorb it far easier than trying to understand it all from the start.   These essential proteins and elements are listed in the following chart, which helped to familiarize me with the terminology, jargon, and issues involved:    Fibrinogen:Factor I...origin: liver...function: a clot structual protein  Prothrombin:Factor II...origin: liver...function: serine protease Proaccelerin: Factor V: liver: cofactor Proconvertin: Factor VII: liver: serine protease Factor VIII C: Antihemophilic: liver: cofactor Factor VIII R: factor von Willebrand: endothelium: cofactor for platelets Factor IX: Christmas factor: liver: serine protease Factor X: Stuart-Prower factor: liver: serine protease Factor XI: Plasma Thromboplastin antecedent: liver: serine protease Factor XII: Hageman factor: liver?: serine protease Factor XIII: fibrin stabilizing factor: liver: Transamidase Prekillikrein: Fletcher factor: liver?: serine protease HMW kininogen: Fitzgerald factor: liver?: cofactor ______ (data compiled from Wintrobe [1981] & Thompson [1983] plus)_______    The above information is basically the "ingredients" of the "recipe" for correct blood function in this episode.     "CLOT FORMATION"   Thrombin formation is an essential factor to the clotting process. It "cleaves", or "separates to join", fragments to create what are called "fibrin monomers" that systematically form into a highly ordered "polymeric fibrin clot". Thrombin also functions as an extremely potent stimulus to platelet activation in the clot formation. In this stage, Thrombin produces activated forms of "factors V and VII" (thus becoming factor Va and factor VIIa) providing a base for an "amplified" activation of factor X (into factor Xa) and also of prothrombin. Formation of a "fibrin polymer" is almost the completion of the clotting process, although this formation of the clot is rather "loose" or in that it is "electro-statically" bound together by interacting with the "fibrin monomers" (as when metal particles become attracted to a magnet). Therefore it is necessary for the clot to become more stable through the activation of factor XIII into factor XIIIa. Factor XIIIa additionally "cross links" to the fibrin clot, making it less capable to dissolve. The coagulation system is also initiated by the activation of factor XII (the Haegman factor) and/or factor VII. Once formed and activated, factor XIIa participates in what is called a "positive feedback loop" interacting with "Prekellerin" and HMWK (high molecular weight kininogen) which in turn promotes an even greater generation of factor XIIa. Surface contact along with the presence of HMWK also accelerates the activation of factor XI by factor XIIa (producing factor XIa). Without the presence of HMWK, however, the process becomes greatly slowed and lethargic. In the presence of what are known as "lipoproteins" (the tissue elements), ionized calcium and factor VIIa promote the activation of factor IX and factor X. Factor IX is also activated in combination with factor XIa. In a "resting" or "non-activated state", the platelets remain in a normal stasis. Yet, in an "activated state", during the clotting process, there is a "flip flop" affect which causes the surface of the platelet to reverse it's outer and inner layers to create an "optimal surface" for adhesion during these reactions.   "INHIBITORS OF COAGULATION"   The regulation or adjustment of the coagulative reactions is just as extremely complex, inconsideration of the fact that multiple factors and co-factors are involved in these chains of events. Antithrombin is one of the most important "inhibitors" or "fighters" against clot formation. It is the primary inhibitor of Thrombin and also in the activation of factor X. It additionally inhibits the activation of factors XII, XI and IX. In the presence of Heparin, the anti-coagulation action of anti-thrombin III is so greatly enhanced that it literally increases anticoagulation 2000 times its normal capability, as with the presence of LMWH (low molecular weight heparin). 75% of Thrombin actually becomes inactivated by anti-thrombin III in the bloods coagulation processes.     FIBRINOLYSIS"   Clot formation serves to interrupt blood loss from the cardiovascular system, but eventually theclot must also be removed if normal blood flow is to be restored to the area. This is achieved by the blood's dissolving capability known as "Fibrinolysis". This system uses an enzyme [plasmin] which cleaves a series of bonds in Fibrin, releasing "FDPs" or "fibrin degredating products", which causes the clot to be dissolved slowly from the inside out, an action known as clot "lysis". Elements of "plasminogin" and "amino-terminal glumatic acid" (glu-plasminogen) cleave sites, creating a lysis or seperation of the plasminogins. "Urokanaise" and Streptokinase" are plasminogen activators. Plasmin, once formed, is capable of degrading not only the clot but also fibrinogen as well. By rendering fibrinogen unclottable and dissolving fibrin clots, plasmins directly counterbalance the blood's tendency towards clotting. It additionally exerts attacks against activated forms of factor VIII:C and factor Va, hastening their deactivation. Finally "FDPs" produced in the fibrin stage; possess anti-coagulation effects, inhibiting polymerization and thrombin activation. Since these processes rely heavily on multiple, systematically accurate activations, cleavages and reactions, each component is required to function in its respective order in the chain of events. Although certain elements "can" fail in their function and the process still be successful (due to the backup qualities of various other elements), certain factors are singularly responsible for their duties and have no backup programs to help them, thus the process fails if they do not function properly.   "PROTEIN C AND IT'S FUNCTIONS" Protein C is a natural inhibitor of the coagulation process in the blood system. Its synthesis is primarily dependant on the presence of vitamin K in the body and blood. Protein C circulates freely in the blood in its normal state, until activation by thrombin. It then cleaves the clotting process created by factor VIIIa and V, bringing about their inactivation. It "has" been found in cases, that there is a presence of a "natural inactivator" of protein C though, and that the absence of such an inactivator has been found to cause the rare combined deficiencies of factors V and VIII. Additionally, in hereditary cases of thrombotic disease and in some patients with cardiovascular disorders, decreased levels of protein C (protein C deficiencies or PCD) have been found.   "SUMMARY" October 2000   This pretty much explains the systems functions and requirements, and I hope it has made it a "little" easier to understand. If so, then you can see where, as in my case, having an "ActivatedProtein C Resistance" and a "Protein C Deficiency" would create a "dual" role in the proneness to clot. With the clot in my left leg, found April of '98, they admitted me straight from the emergency room. They automatically started treatment for an "Acute Deep Venous Thrombosis" (DVT) of the "Superficial Femoral Vein". Subsequent blood work found the Activated Protein C Resistance and a Protein C Deficiency. Without the body's capability to produce adequate amounts of Protein C to deactivate the clot formation and with a gene mutation of factor V Leiden causing the "resistance" to the activated protein C in the blood's haemostatic pathway, I have fun trying to keep my INRs in the proper range. I have "just now" arrived at the point where, even @ 10 mgs of Coumadin per day alternating with 12.5mgs the next (very high, for 5mgs to 7.5mgs daily is a normal dosage) my INRs are stable @ 2.0 for the first time in 11 months. By getting on Medicaid I receive more convenient care with the disorder and its symptoms, but in the failure of the Department of Family Services to notify me until 8/99 that I had been on it since 2/99, I had medical care only through the gracious generous help of Dr. Vinson of the Boone County/Columbia, MO health center there and am now presently getting care from Capitol Region Medical Clinic in California, MO after relocating here. I am endeavoring to return to school for "computer informational technologies" fields. Taking our life vitamins as I call them and then just plain attitude are the best medicines, and though hard to adjust at times, its more important to keep a constant determination at progressing, I know I have to keep trying ... its just in me. Take care and good health ya all!