Pre-auditory self-work materials.
3.1.Basic knowledge, skills, experiences, necessary for study the topic:
| Subject | To know | To be able to |
| Biology and Medical Genetics | Inheritance main ways | Analyze primary thrombocytopathies, vasculopathies and coagulopathies inheritance ways |
| Pathophysiology | Vascular-platelet hemostasis, coagulation reasons, classification, blood analysis changes and developmental mechanisms; DIC-syndrome ethiology, pathogenesis, clinics, diagnostics, therapy and prevention principles; about hemorrhagies main types | Interpret data received about primary and secondary hemostasis and coagulogram of DIC-syndrome (at different stages) as well; say about primary and secondary hemostasis disorders differential-diagnostical signs |
| Pediatry with Neonatology | Vascular-platelet, coagulative hemostasis peculiarities in children of different age; DIC-syndrome in different-aged children | Treat and prevent primary and secondary hemostasis disturbances and DIC-syndrome in children as well |
| Internal Diseases | Vascular-platelet, coagulative hemostasis peculiarities as well as DIC-syndrome in the adult | Treat and prevent primary and secondary hemostasis disturbances and DIC-syndrome in the adult in general medicine clinics |
| Surgery | Vascular-platelet, coagulative hemostasis peculiarities as well as DIC-syndrome development and expression in patients with surgical pathology | Treat and prevent primary and secondary hemostasis disturbances and DIC-syndrome in the adult in surgical clinics |
| Dentistry | Coagulogram changes at typical pathological processes in maxillar-facial area; DIC-syndrome peculiarities in oral cavity | To prevent and to liquidate DIC-syndrome in stomatological patients |
Topic content
DIC-syndrome is the most dangerous and widely-spread hemostasis pathology type. Lethality comprises 30-60% in the adults and 70-90% in the new-borned. It is developed rather more often than it is considered to be present. It is always secondary as for one or another disease. In turn, DIC can be the reason of many symptoms and syndromes development. And DIC determines clinical picture of main pathological process.
DIC-syndrome represents hemostasis system reaction to various pathological agents influencings. That is why it is not occasional that it has different names in different countries in part:
· DIC-syndrome;
· “defibrination syndrome”;
· “coagulopathy of consumption”;
· “thrombo-hemorrhagic syndrome”;
|
|
|
· “defibrinative-occlusive syndrome” et al.
But the most suitable is the term “DIC-syndrome”.
Its basis is disseminated blood coagulation in circulation with many microclots and blood cells aggregates formation. They inhibit circulation in organs and tissues and cause deep dystrophic changes in them. Hypocoagulation, thrombocytopeny and hemorrhagy come after intensive coagulation.
This syndrome is universal, non-specific. It is so because it is observed at different diseases and means catastrophy, accident, similarly to shock. It is accompanied by blood liquid features loosing and its circulation disturbance in capillaries. Normal vital activity is impossible under such conditions. Gravity, distribution and velocity of DIC development vary greatly: from lightened, very rapid, in seconds with lethal result till latent and durable, chronic; from general blood coagulation till regional and organic thrombohemorrhagies.
This process can be triggered both with external and internal factors. External ones: bacterias, viruses, rickettsias, medicines, hypoxy, tissular acidosis and others. Internal ones: tissues decomposition products, thromboplastin appearance in blood, vascular endothelium injure et al.
Main pathological processes and influences accompanied by DIC-syndrome development (DIC ethiology)
1. Generalized infections and septic states (bacteriemy, viremy) in part:
· at abortions;
· in deliveries;
· at vessels catheterization;
· at septic shock;
· at infections in the new-borned.
2. All shock types:
· traumatic;
· hemorrhagic;
· burning;
· anaphylactic;
· cardiogenic;
· septic et al.
DIC-syndrome is obligatory and constant shock component that correlates to its gravity.
3. Traumatic surgical interventions (bleedings, collapse, blood massive transfusions make DIC-syndrome more frequent).
4. Terminal states:
· predagony;
· agony.
5. Acute intravascular hemolysis and cytolysis (it occurs frequently at hemotransfusions especially of incompatible blood).
6. Obstetric pathology:
· placenta preliminary self-taking away;
|
|
|
· placenta manual taking away;
· embolism with near-fetal waters;
· fetus intraembryonal death;
· late pregnancy toxicosis;
· Cesar's section;
· abundant hypotonic bleedings;
· womb intensive massage;
· sometimes at physiological delivery.
7. Tumorogenic processes:
· leucosis;
· lungs cancer;
· liver cancer;
· pancreas cancer and the one in other organs.
8. Destructive processes in liver, kidney, pancreas and other organs.
9. Thermal and chemical burnings, esophagus and stomach burnings.
10. Immune and immune complexes diseases:
· systemic red lupus;
· rheumatism;
· rheumatoid arthritis with visceral injuries;
· glomerulonephritis;
· hemorrhagic vasculitis et al.
11. Hemolythic-uremic syndrome.
12. Allergic reactions of medical and other genesis.
13. Abundant bleedings.
14. Thrombocytic thrombocytopenic purpura.
15. Intoxications with snake venoms.
16. Massive hemotransfusions and hemoreinfusions, injections of medicines containing activated blood coagulation factors.
17. Therapy with medicines causing platelets aggregation, hypercoagulation, hypofibrinolysis:
· alpha-adrenostimulators;
· synthetic progestins (contraceptive agents!!!!!); that is why oral contraception is forbidden to women who are predisposed to thrombophyly and moreover possess varicous disease and thromboses, especially in lower extremities; also women with the II-nd and the IV-th blood groups are tended to have hypercoagulation as it has been mentioned below;
· fibrinolysis inhibitors;
18. Wrong applying fibrinolytics and anticoagulants in dosages causing antithrombin III and fibrinolysis exhaustion.
19. Therapy with defibrinating medicines such as:
· arvin;
· ancrod;
· defibrase;
· reptilase et al.
20. Multiplied and giant angiomes.
Central pathogenesis link – thrombinemia and exhaustion of mechanisms preventing platelets aggregation and blood coagulation. Thromboplastin is blood coagulation process trigger. This substance comes into blood stream from damaged tissues during traumas, operations, necroses, destructions and others as well as with near-embryonal liquid. Tissular thromboplastin (salivary particularly) plays dominant role in DIC syndrome development in oral cavity. Thromboplastin can be produced by damaged endothelium with platelets participation during immune, immune-complex damages as well as endothelium damage with toxins, hemolysis products et al. Tissular thromboplastin is synthesized by macrophages (monocytes) and it plays essential role in DIC-syndrome pathogenesis at bacteriemies, endotoxinemy as well as at immune and immune complexes diseases. DIC-syndrome at malignant tumors deals with blood coagulation activating with proteases associated with tumorogenic cells as well as tissular thromboplastin major mass. Cancerogenic thromboplastin belongs to the strongest among all known thromboplastins. Also monocytes can be thromboplastin source at many cancer types.
|
|
|
Very important DIC distinguishing feature is other protheolytic systems activation – fibrinolytic, kallikrein-kinin and complement (so-called “protheolytic burst”). Antithrombin III (main anticoagulant) level in plasma is diminished during DIC-syndrome. Similarly, fibrinolytic system components and its activators are consumped.
Thrombinemy leads to blood intravascular coagulation not at once. First, part of fibrin-monomers appearing under thrombin influence forms soluble complexes (fibrin-monomeric) or soluble fibrin. This limits blood intravascular coagulation, provides complexes fibrinolysis. Coagulation appears after 20-24% of fibrinogen coming in soluble complexes. Thus, fibrinogen is transformed into 2 fibrin types – soluble and coagulative one. Their correlation determines microcirculation blockage expression as well as dystrophic changes gravity in kidney, lungs and other organs. That is why soluble fibrin tests expression (so-called paracoagulation tests) are used for thrombinemy criterium diagnostics.
Bleedings are determined by disorder both of blood coagulation (anticoagulant action of fibrin and fibrinogen degrading products, coagulation factors consumption) as well as vascular-platelet hemostasis – protheolysis products toxic influence on vascular wall, platelets aggregation and coming out of the blood stream. Both thrombocytopeny and thrombocytopathy represent hemorrhagies essential factor at DIC-syndrome.
|
|
|
The syndrome pathogenesis and gravity depend on organs microcirculative disturbances as well as their dysfunction degree. Complications and death reasons are as follows as:
· shocked lung;
· acute kidney insufficiency;
· acute circulative insufficiency;
· acute respiratory insufficiency;
· more seldom – liver diseases with parenchymatous jaundice development.
Hemostasis disorders have 4 main stages at DIC-syndrome:
· hypercoagulation;
· different-directed changes (one indexes group testifies to hypercoagulation, another one - to hypocoagulation);
· hypocoagulation;
· ending (recovery or death).
DIC types:
· lightning;
· acute;
· subacute;
· chronic.
As both hypercoagulation and hypocoagulation are observed, main treatment measurements comprise:
· fresh-frozen plasma – procoagulants source;
· heparin – anticoagulant.
Preventive physiologic methods: healthy life style:
· constant (regular) physical training (in trained organism anticoagulants and fibrinolysis activators content is always bigger);
· individual restricted feeding: animal products especially rich in fats will enforce blood coagulation reactions, plant food – will weaken it;
· not to smoke.
Дата добавления: 2018-09-22; просмотров: 450; Мы поможем в написании вашей работы! |
Мы поможем в написании ваших работ!