FIBRINOLYSIS AND ANTICOAGULANTS. BLOOD COAGULATION AND FIBRINOLYSIS REGULATION
1.The topic studied actuality. Anticoagulants and fibrinolysis represents powerful system in any organism that provides blood support in a liquid state. As it was mentioned above, oral cavity produces substances influencing on fibrinolysis. Maximal fibrinolytic activity has mixed saliva, less one – sublingual, minimal – parotid. There are plasminogen, its pro- and activators as well as inhibitors. There exists point of view that plasminogen activators role in saliva is in salivary ducts conductance preservation.
Any inflammation in its second phase is accompanied by fibrinolytic system activation.
2. Study aims:
To know: fibrinolysis process algorhythm and the process regulation, main primary and secondary anticoagulants; blood coagulation and fibrinolysis main regulative mechanisms.
To be able to: determine blood fibrinolytic activity.
Pre-auditory self-work materials.
Basic knowledge, skills, experiences, necessary for study the topic:
| Subject | To know | To be able to |
| Pathophysiology | Main anticoagulants, their action mechanisms; fibrinolysis system work | Explain main pathophysiological mechanisms of anticoagulative and fibrinolytic systems disturbances |
| Pediatry with Neonatology | Anticoagulative and fibrinolytic systems peculiarities in different-aged children; mentioned systems disturbances ethiology, pathogenesis, diagnostics, clinics, therapy and prophylaxy principles | Treat and prevent anticoagulative and fibrinolytic systems disorders in different-aged children |
| Internal Diseases | Main anticoagulants, their action mechanisms; fibrinolysis system work; mentioned systems disturbances ethiology, pathogenesis, diagnostics, clinics, therapy and prophylaxy principles | Treat and prevent anticoagulative and fibrinolytic systems disorders in internal diseases clinics |
| Surgery | Main anticoagulants, their action mechanisms; fibrinolysis system work; mentioned systems disturbances ethiology, pathogenesis, diagnostics, clinics, therapy and prophylaxy principles in surgery | Treat and prevent anticoagulative and fibrinolytic systems disorders in the adult in surgical clinics |
| Dentistry | Coagulogram changes at typical pathological processes in maxillar-facial area; maxillar-facial area role in anticoagulation and fibrinolysis | To prevent and to liquidate anticoagulative and fibrinolytic systems disorders in stomatological patients |
Topic content
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Inspite of circulation there are all necessary factors for the clot forming. Under physiological conditions in presence of uninjured vessels a blood remains fluid. It’s determined by the presence of components, preventing the blood coagulation (anticoagulants) in the circulation. Besides, a blood is kept fluid because of the haemostatic system fibrinolytic components in it.
But it’s necessary to underline that blood doesn’t coagulate in vessels due to others reasons too. Factors providing this feature are:
· blood stream velocity: it is well-known that where circulation velocity is the less, the more threat to intravascular blood coagulation (for example, blood is more often condensed in veins comparatively to arteries and phlebothrombosis, thrombophebitis is occured); it also observed in blood circulation regions where circulation is changed, for instance at bifurcations places;
· similar charge (negative) of vascular vessels internal layer;
· formed elements negative charge;
· most coagulational factors negative charge: charge similarity of blood vessels internal layer and blood coagulation factors creates forces for pushing away; at vascular walls injuries vascular wall charge is decreased or even is changed onto positive that creates additional conditions for intravascular coagulation initiating;
· blood coagulation factors are inactive in blood; blood coagulation are not triggered until factors are under unactive state;
· there are inhibitors to active blood coagulation factors (VIIIa, IXa, Xa, XIIa): even in a case of any factors activation further process development is not obligatory.
Probably, you paid your attention that blood coagulation is origined from the XIIth factor activation. It is activated by side surface or hyperadrenalinemia and it becomes XIIa only after this. Reaction cascade (chain) is begun directed to other blood coagulation factors activation. Moreover, this reaction is not spontaneous, it looks like stairs (fall) when one factor activates other one in definite order, in definite sequence.
But anticoagulants are essential factors preventing possible blood coagulation activating.
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The natural anticoagulants are divided into primary and secondary ones. The primary anticoagulants are such substances that are constantly present in the circulation. They may be of three groups: antithromboplastines, antithrombines and fibrin forming inhibitors. Otherwise, all these anticoagulants are the substances that act depending on the blood coagulation process stage.
The substances preventing the prothrombinase forming are the antithromboplasties(they are secreted by the vessel wall endothelium, their content in veins is larger than in arteries), vitamin K-dependent protein C (inhibits the factors V, VIII), protein S, the endothelium protein – thrombomodulin, the placenta anticoagulant protein and others.
The substances inhibiting thrombin action are antithrombines.They are of different groups but the most important of them are: antithrombin III and heparin. Antithrombin III – is a prothein of a globulin origin that is formed in liver, kidneys, spleen, lungs and blood vessels as well. Its content reduces with the age, its concentration is less in women as compared with men (NB! Women have the thrombophlebitis and phlebothromboses more often than men), its content in the pregnant gets smaller. Its content is smaller in human beings with the II(A) blood group and the people eating fat food (particularly of animal origin). Its activity decreases at the diseases of those organs where it is formed. Antithrombin III is a heparin co-factor. Besides, it inhibits up to 70 per cent of thrombin occuring in blood as well as the factors IXa, Xa, XIa, XIIa. There are cases of its hereditary insufficiency.
Heparin – is also an antithrombin.It is a polysaccharide transforming antithrombin III in anticoagulant of immediate action thus increasing its activity. In absence of antithrombin III heparin possesses a weak anticoagulant activity. Moreover, heparin without antithrombin III doesn’t prevent the external prothrombinase forming way. So, heparin efffect may be very weak as a result of antithrombin level decreasing in patients’ blood that it’s necessary to take into account at its administration. Heparin also forms the complex combinations with thrombogenic protheins and hormones which finally possess anticoagulant and fibrinolytic features. Heparin influences the thrombocyte aggregation, has antiviral action and antiinflammatory properties as well. In blood heparin can be found in basophiles, in vessels – in mast cells. It is degenerated by the heparinase enzyme in liver.
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Secondary anticoagulants – are the “worked-off” blood coagulation factors (that participated in blood coagulation process) and degradation fibrin and fibrinogen products or derivates (PDF) having antiaggregative and anticoagulative action. The secondary anticoagulants role comes to limiting of intravascular blood coagulation and thrombus dissemination via vessels.
At various diseases there may appear the pathological anticoagulants dealing with different immunoglobuline classes and inactivating separate blood coagulation factors.
These and some other data are collected in the table.
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