Система Orphus

Symptoms of disease - violation of hemostasis

The key concepts of violation of hemostasis:

1. Violation of hemostasis, coagulopathy (coagulopathia, coagulation - + Greek patos - suffering, illness) is a violation of the coagulation and anticoagulation blood systems.
2. Hyper coagulation-thrombotic condition - the condition, accompanied by a pathological process of strengthening of blood coagulation due to excessive platelet aggregation and activation of plasma and tissue factors of blood coagulation with the formation of a platelet and fibrin clots.
3. Hypocoagulation-hemorrhagic condition - the condition, accompanied by a pathological process of reduction of blood coagulation due to a decrease in platelet aggregation, inactivation of plasma and tissue factors of blood coagulation with the occurrence of bleeding and bleeding.
4. DIC-syndrome (thrombotic-hemorrhagic state) - the syndrome of disseminated intravascular coagulation - the typical pathological process of hemostasis disturbance as a result of consistently proceeding of the reactions of blood coagulation: hypercoagulable (education disseminated blood clots in the microcirculatory vascular network) and of hypocoagulation (depletion of thrombogenic factors and the strengthening of fibrinolysis), accompanied by massive bleeding, severe hemo-coagulation shock and acute dystrophy of the internal organs.

Which diseases there is violation of hemostasis

Hemostasis is a complex process, which prevents or stops the flow of blood from the lumen of the vessel, provides the occurrence of the convolution of fibrin, required to restore the integrity of the tissue, and, finally, removes the fibrin, when the need for it falls. In this process involves four basic physiological mechanism.

With the help of system of a hemostasis blood performs its most important function is the maintenance of a liquid state of the blood flow in the blood vessels, and blood clotting in violation of the integrity of the vascular wall and, thus, the termination of the bleeding and the preservation of the volume and composition of the blood. System of a hemostasis multicomponent. In the participation of platelets and other blood cells, vascular wall, extravascular fabric, biologically active substances (thrombocyte-vascular hemostasis), plasma, tissue factors such as blood clotting (coagulation hemostasis), located in close cooperation with anticoagulation, fibrinolytic and kallikrein-kinin systems. Violation of any of these components leads to hemostasis pathology.

Classification of disorders of hemostasis. Pathology of hemostasis is classified by dominating the defeat of its various components on the violations of the thrombocyte-vascular hemostasis and coagulation hemostasis. On the etiology of these violations may be acquired or inherited, and on the direction of change should be developed on the lowering of blood clotting (hypocoagulation) and increase of blood clotting (hypercoagulability), which can be local (thrombosis) and generalized (DIC-syndrome).

Lowering of blood clotting
Lowering of blood clotting is manifested high krovotochivostyu (hemorrhagic syndrome) - repeated bleeding, bleeding disorders, arising as spontaneously, and with minor injuries.
Thrombocyte-vascular hemostasis broken when the quantitative and qualitative changes of platelets (thrombocytopenia and thrombocytopathies), as well as lesions of the vascular wall.
A low platelet count is called a decrease in the content of platelets in the blood is lower than normal (180-320 G/l or 180-320x109/l). However, spontaneous bleeding occur only when a decrease in their number is less than 30 G/l. Under thrombocytopathies understand the qualitative inferiority and platelet dysfunction in normal or reduced their content.

Causes of low blood clotting. The reason of occurrence of thrombocytopenia are often immune reactions when you change the antigenic structure of platelets under the influence of viruses, medicines, production of antiplatelet antibodies (with chronic limfoleikoze, idiopathic thrombocytopenia), the incompatibility of platelet-derived antigens mother and fetus. In addition, thrombocytopenia develops due to the destruction megakaryocyte sliver of bone marrow of ionizing radiation, chemical substances or wipe his tumor metastases, leukemic infiltrates. Reduction of thrombocytopoiesis may be caused by the deficit of cyanocobalamin, folic acid, a hereditary defect of platelets (including the deficit of platelet poetinov). Thrombocytopenia occurs as a result of mechanical damage of platelets in of splenomegaly, artificial heart valves, as well as an increased consumption of platelets in the local and generalized intravascular blood clotting.
The etiological factors causing thrombocytopathies include the action of toxic substances and drugs (alcohol, acetylsalicylic acid), ionizing radiation, endogenous metabolites (with uremia, cirrhosis of the liver); lack cyanocobalamin, hormonal disorders (hypothyroidism). There are genetic defects of the structure of the membrane and biochemical composition of platelets (deficit trombostenina, factor of 3, ATP, ADP, G-6-FDG, membrane receptors for the factors V, VIII, XI, etc.).

When hemorrhagic angiopathy defeat of the vascular wall, leading to the destruction of thrombocyte-vascular hemostasis and bleeding, occurs due to the increase in permeability of the walls of the blood vessels and its destruction in violation of the synthesis of collagen (the oral deficiency of ascorbic acid, inherited defect in the synthesis of collagen), under the action of biologically active substances (Allergy), radiotoxins (radiation sickness), immune hemorrhagic vasculitis, reducing angio trophic the function of platelets in thrombocytopenia and thrombocytopathies, the destruction of the vascular wall leukemic infiltrates. One of the causes of bleeding is the decrease of endothelium vascular wall von Willebrand factor - macromolecular component of the coagulation factor VIII-the-blood (a hereditary disease Villebranda). This factor is accumulated in platelets and relieved at their degranulation.

It is necessary for the normal platelet adhesion to collagen wall, and without it, there is no platelet thrombus. Haemorrhagic syndrome is observed and with the strengthening of peroxidation of membrane phospholipids, as a result of which in the endothelium is synthesized and secreted by the amount of the excess powerful inhibitors of platelet aggregation - prostacyclines. In addition, to reduce the thrombocyte-vascular hemostasis result of violation of neurogenic and humoral regulation of vascular tone, lowering of which leads to the impossibility of blockage of small vessels platelet a blood clot.

The pathogenesis of low blood clotting. There are four basic mechanism of the thrombocytopenia: reduction of production, increased destruction, increased consumption (blood clot), the redistribution of the platelets.

Violation of hemostasis and the development of bleeding when thrombocytopenia caused by the following mechanisms:
- increase of permeability of vessels for red blood cells and other components of the blood (diapedetic haemorrhage) and fragility of blood vessels from dystrophy wall when you turn off the angio trophic platelet function;
- reduction of adhesively-aggregational platelet function;
- violation of the reaction of the liberation of the platelet-derived clotting factors, ADP, serotonin, adrenaline, anti heparin factor, the result of which is the lack of formation of platelet thrombus, the absence of a spasm of the blood vessels and the deceleration of coagulation;
- the decrease of the retraction of the clot as a result of the decreased activity of the contractile protein platelet - trombostenina (factor 8 platelets).

In the pathogenesis of thrombocytopathy is possible to allocate two basic mechanisms of their origin - products of pathological platelets in the bone marrow and the destruction of platelets in all departments of the blood system. The pathogenesis of violations of thrombocyte-vascular hemostasis in thrombocytopathy the same as when thrombocytopenia, as it is related to off platelet function.

Violation of coagulation hemostasis, which leads to the development of the bleeding may be caused by the following factors:
- acquired and hereditary or decreasing perversion synthesis of plasma and platelet-derived clotting factors and components of kallikrein-kinin system;
- inhibition or higher consumption of these factors;
- increase in endogenous anticoagulants;
- activation of the fibrinolytic system;
- overdose anticoagulants, fibrinolytic and defibrin drugs. All of this lies at the basis of a violation by one of the three phases of blood clotting and the retraction of the clot, or combined their changes.

The reasons for violations of the first phase of clotting - education thromboplastin - is the reduction of production factors (IX, X) in the pathology of the liver, the formation of antibodies to certain factors (VIII, IX) in case of diseases in the pathogenesis of which has an autoimmune component (leukemia, connective tissues), or overdose of such a universal anticoagulant, as heparin. Known genetic defects synthesis VIII, IX and XI of factors, the deficit of which lies in the basis of development of hemophilia (respectively sequence of these factors - hemophilia A, b and C).

Violation of the second phase of clotting of blood - the formation of thrombin - arises not only in diseases of the liver, but also in Hypo - and beriberi To, when also decreases the synthesis in the liver of factors II, V, VII, participating in this phase (with mechanical jaundice, enteritis, extensive resection of the small intestine, medicinal dysbacteriosis. It is possible appearance of immune inhibitors of factors V, VII (for example, in the treatment of streptomycin sulfate), increased their excretion kidneys, a hereditary deficiency (factor V when parahemophilia) or inactivation of the components of anticoagulation system - antithrombin, geparinom (if anaphylactic shock, overdose of heparin).

Diates bloody, associated with the violation of the third phase of clotting - phase formation of fibrin arises when reducing the synthesis of prothrombin in the affected pathological process of the liver, lung, or as a result of hereditary hypo-afibrinogenemia and deficit fibrin stabilizing factor (factor XIII). However, much more often violation of the third phase is a consequence of the strengthening of fibrinolysis in injury (operations) of the lung, cervix, pancreas; burns, shock. This is due to the increased inflows in the blood of activators plasminogen - tissue, microbial fibrinogen, leiko - and erythrocytes activators, the components of the kallikrein-kinin system and complement system complexes of heparin with fibrinogen, plasminogen and epinephrine (these complexes provide non-enzymatic fibrinolysis, B. A. At).

Pathogenesis. The main links in the pathogenesis of hemorrhagic diathesis, developed by the violation of any of the phases of blood clotting, are chronic blood loss and its consequences, as well as structural and functional changes in the location of the bleeding (in the joints, internal organs, skin and other tissues).

Increased coagulation of blood
Increased coagulation of blood is evident local (thrombosis) or generalized intravascular blood coagulation, in the base of which is the violation of thrombocyte-vascular and coagulation hemostasis.

Hypercoagulation can be caused by:
- increase of functional activity of blood coagulation system at the cost of increased - - revenues in the blood of procoagulants and activators of blood coagulation;
- the increase of the blood content of platelets;
- reduction of antithrombotic properties of the vascular wall;
- the decrease of the activity anticoagulation of the blood system;
- the weakening of fibrinolysis.

Generalized (disseminated) intravascular coagulation (DIC-syndrome) is a severe violation of hemostasis, which occurs when the excessive enrolment in the blood procoagulants and activators of blood coagulation, leading to the formation of multiple microthrombi in the vessels of microvasculature, and then development of hypocoagulation, thrombocytopenia and haemorrhage as a result of "consumption" of the factors of coagulation system and increase of functional activity of the system of anti clotting and fibrinolysis blood with the subsequent depletion of all three systems. murka games

Etiology. Universality and nonspecificity DIC-syndrome are caused by the variety of causal factors of its occurrence. They include first of all generalized infection and septic condition, all kinds of shock, traumatic surgery, obstetrics complications (placental, manual removal of placenta), acute intravascular hemolysis, uremia in renal failure, all the terminal condition.

Pathogenesis. The main link in the pathogenesis of generalized hypercoagulable is the violation of the balance between the kallikrein-kinin, blood clotting, anticoagulation and fibrinolytic systems of the blood upon admission to the vascular system of a large number of procoagulants and their activators. This leads to a violation of this important function of the blood, as the preservation of the normal state of aggregation, with the result that in the phase of hypercoagulable blood in the vessels of the coils and terminated its circulation with the development of severe degenerative and functional disorders in organs and tissues, often incompatible with life. In the subsequent phase of hypocoagulation the dilution of the blood and the loss of the ability to clot and aggregation of platelets cause bleeding, which is difficult to therapeutic correction. With a favorable outcome, there comes a third - recovery phase, when a normalization of hemostasis.

Which doctor should I contact if there is a violation of hemostasis

  • Resuscitator
  • Anesthesiologist

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