Система Orphus

Symptoms of disease - violation of the circulatory system

The health of the human body as a whole depends on the state of the circulatory system.

Violation of blood supply to an organ leads to the fact that the tissues do not receive the necessary amount of nutrients and oxygen. As a result of this, the man slows down the metabolism and hypoxia.

Violation of blood supply to an organ leads to the fact that the tissues do not receive the required for the normal functioning of nutrients and oxygen, as a result of which a person hypoxia and slows down the metabolism. This may well lead to the development of various diseases. In other words, the condition of blood circulation system depends on the health of the organism as a whole.

Ensuring adequate blood flow is a complex process, which depends on the proper functioning of the heart, the integrity of the vascular system and the exact balance between the coagulation and anticoagulation systems of blood.

On the prevalence and localization of the process of disorders of blood circulation divided into General and local. General disorders occur in the whole body, the whole system of blood circulation and are associated with disorders of the heart or changes in the volume and physical and chemical properties of blood.

Local violations of lymph and blood circulation due to structural and functional damage the vascular bed on any of its sites - in one organ, part of an organ or body part.

Which diseases there is violation of the circulatory system

Division of circulatory disorders in the General and local is conditional and it should be understood in the aspect of the dialectical unity of the local and General. For example, reduction in blood pressure in the aorta in General acute anemia leads to a decrease in blood supply of the cortical substance of the kidneys, which will activate the renin-angiotensin system and in turn, causes an increase in pressure in the same aorta. In the majority of cases the local circulatory disorders are the result of common violations of the circulatory system. Thus, a total venous plethora often develop thrombosis of the veins of the lower extremities. In their turn, local blood circulation disturbance may be the cause of common violations. Myocardial infarction is the cause of heart failure, morphological substrate which represents the total venous hyperemia. Bleeding as a local process can be the cause of global acute anemia.

General disorders of blood circulation.
To the General violations of the circulatory system are:
- the total blood hyperemia;
- the total venous hyperemia;
- General lack of red blood cells is an acute and chronic;
- thickening of the blood;
- the dilution of the blood;
- shock;
- disseminated intravascular coagulation (DIC-syndrome).

General blood hyperemia (hyperaemia universalis arteriosa)
General blood hyperemia, or arterial hyperemia is the increase in the number of uniform elements of blood (red blood cells), sometimes combined with an increase in the volume of circulating blood. The process is relatively rare: at elevation (climbers), the residents of mountain places, in persons with pathology of the lung, as well as in newborns after ligation of the umbilical cord. Clinically marked redness of the skin and mucous membranes, increase in blood pressure. In practice, the greatest importance is the General blood hyperemia in case of Osier's disease (policitemia true) - a disease in which it is the place of true hyperproduction of erythrocytes.

Total venous hyperemia (hyperaemia universalis venosa)
Total venous hyperemia - one of the most frequent types of common violations of the circulatory system and is a clinical-morphological manifestations of cardiac or pulmonary-cardiac insufficiency.

Pathophysiological and pathological the essence of the total venous plethora of is in the redistribution of the volume of blood in the General range of diseases with the accumulation of it in a venous part of the big circulation (the hollow veins, and sometimes in the blood vessels of light) and a decrease in arterial part. murka

In the mechanism of development (i.e. in the pathogenesis of) total venous plethora of playing the role of the following three main factors:
1. Violation of the activity of the heart, determined as heart failure, the causes of which may be:
acquired and congenital heart defect;
- inflammatory diseases of the heart (pericarditis, myocarditis and endocarditis);
- cardiosclerosis of different etiology (atherosclerotic, postinfarction, etc.);
- myocardial infarction, etc.
2. Lung diseases accompanied by the decrease of the volume of vessels of the small circle of blood circulation:
- pulmonary emphysema;
- chronic nonspecific pneumonia;
- pneumosclerosis of different etiology;
- pneumoconiosis (dust lung disease), and others.
3. Injury of the thoracic cage, pleura, diaphragm, accompanied by violation of stick functions of the chest:
- pleuritis (including adhesive);
- pneumothorax;
- deformation of the chest and spine.

Total venous hyperemia may be on the clinical flow of the acute and chronic.

Acute General venous hyperemia is a manifestation of the syndrome of acute cardiac insufficiency and fetal hypoxia (asphyxia). The reason it can be:
- myocardial infarction;
acute myocarditis;
- acute exudative pleurisy with excessive accumulation of pleural effusion, compressing the lungs;
- high standing aperture (in peritonitis), restricting breathing;
- a pulmonary embolism;
- pneumothorax;
- all kinds of asphyxia.

As a result of hypoxia damaged histogematogenous barrier and dramatically increases the permeability of capillaries. In the tissues of the observed venous stagnation, plasmatic saturation (plasmorrhagia), swelling, stasis in capillaries and multiple diapedesic bleeding. In the parenchymal organs appear dystrophic and necrotic changes. The most characteristic morphological changes in acute General venous plethora develop in the lungs and the liver.
The cause of venous plethora of light is of left ventricular heart failure. Acute venous hyperemia causes expansion of the alveolar capillaries, which is accompanied by a clinically transudation fluid in the alveoli (pulmonary edema). There may also be intraalveolar bleeding. At autopsy from the surface of the incision light flows in a large number of pinkish-reddish, small - and large foamy liquid.

Right ventricular heart failure causes stagnation in the big circle of blood circulation. When the liver is observed expansion of the Central hepatic veins and the stagnation of the sinusoids in the Central part of hepatic lobules. These stagnant red Central areas alternate with normal more pale cloth in the peripheral areas and create a sort of figure, reminiscent of nutmeg (the so-called «Muscat liver»). In the liver, in connection with the peculiarities of architectonics of hepatic lobules and its blood circulation, in case of acute venous plethora appear centrilobular hemorrhage and necrosis.

General anaemia (anaemia universalis)
Depending on the etiology and pathogenesis are distinguished:
- General acute anemia;
- common chronic anemia.

General acute anaemia (anaemia universalis acuta)

This condition, developing at fast a large loss of blood, then there is a decrease in circulating blood volume (CBV) in General circle of blood circulation in a short period of time.

Causes of General acute anemia:
- a variety of injuries damage to organs, tissues and vessels (household, industrial, military, road accidents, etc.);
- spontaneous rupture of a large, pathologically modified vessel or heart (rupture of an aneurysm of the aorta and AIDS, atherosclerosis);
- the gap pathologically modified body (break the fallopian tube for ectopic pregnancy, the gap infectious diseases of the spleen with malaria, reflexive typhoid, massive blood loss tuberculosis of the lung, stomach ulcer, cancer of various localization).

Clinical manifestations of global acute anemia: paleness skin and mucous membranes, dizziness, often unconscious state or loss of consciousness, rapid weak pulse, low blood pressure. Patients often die from acute anemia. Why are dying patients? Due to hypovolemic shock.

Common chronic anaemia (anaemia universalis chronica)
Common chronic anemia, or anemia is a decrease in the number of red blood cells and/or hemoglobin content in the volume unit of blood. The total volume of circulating blood in the body is not changed.

In the pathogenesis of common chronic anemia have a value of two factors:
- violation of the functions of the blood;
- increased hemolysis of erythrocytes.

Causes of General chronic anemia:
- diseases of the blood-forming organs (hemoblastosis, anemia);
- chronic infectious diseases (tuberculosis, syphilis);
- chronic parasitic diseases (helminthic invasions);
- exogenous intoxication (poisoning by lead, arsenic and its preparations, benzene, carbon monoxide, etc.);
- endogenous intoxication (poisoning products of nitrogen metabolism - for diseases of the kidneys, bile acids in the mechanical jaundice, endogenous toxins in malignant tumors, etc.);
- fasting (full or partial), vitamin deficiency;
- small, but often repeated blood when ulcers stomach and duodenal ulcer, tuberculosis of the lung, uterine and hemorrhoidal bleeding).

Clinical manifestations common chronic anemia: pallor, easy fatigue, weakness, reduced efficiency, dizziness, fainting. In the analysis of blood - reduction in the number of red blood cells and decrease of hemoglobin.

Blood clots (anhydraemia, inspisatio sanguinis)
Thickening of the blood is the impoverishment of the blood of the liquid part of, a decrease of content in the peripheral blood of water and some electrolytes. As a result, the blood thickens, increases its viscosity, altered rheological properties of the blood, the number of cells per unit volume of about increases.
Blood clots develop in the loss of large amounts of fluid.

Causes thickening of the blood:
- persistent diarrhea and vomiting (cholera, heavy forms of dysentery, salmonellosis);
- common second degree burns, when the mass of the liquid goes in burn bubbles;
- poisoning chemical-warfare agents (beans) choking action, when the poisonous by gas develops heavy chemical burn of the lung and the lung tissue accumulates up to 10 liters of fluid - toxic pulmonary edema;
- iatrogenic pathology inadequately carried out by forced diuresis in case of poisoning for excretion with urine toxic products in the cases, when this therapy is carried out uncontrollably (without regard to the ratio of the volume of incoming and output of liquid).

The dilution of the blood (hydraemia)
The dilution of the blood, or hydraemia - increase the quantity of water in human peripheral blood. Is rarely seen at:
- diseases of the kidneys, when disturbed osmotic, oncotic pressure, protein-energy balance fluid is held in the blood;
- at a rapid descent, though, gipervolemia;
- on the compensation of volume of circulating blood plasma and blood substitutes after resuscitation;
- in some cases of resuscitation and intensive therapy, if the doctors with the aim of detoxification and/or restoration of hemodynamic injected a large amount of fluid intravenously. Comes gipergidratation (a lot of water) and gipervolemia, that is, of the BCC. One of the manifestations of it is the dilution of the blood.

The syndrome of disseminated intravascular coagulation (DIC-syndrome, thrombo haemorrhagic syndrome, consumption coagulopathy)
The syndrome of disseminated intravascular coagulation is characterized by the widespread formation of small blood clots (fibrin, erythrocytes, hyaline) in the microvasculature of the whole organism in conjunction with incoagulability blood, leading to multiple massive bleeding. This is a serious and often fatal complication of numerous diseases and requires early diagnosis and treatment. Its origins lie in the discoordination of the functions of coagulation and anticoagulation blood systems, responsible for hemostasis.

In many cases, the cause of disseminated intravascular coagulation is unknown. The most frequent causes of DIC-syndrome:
1. Infectious diseases:
Gram-negative and gram-positive bacteremia
- Meningococcal septicaemia
- Disseminated fungal infection
- Rickettsiosis
- Heavy viremia (e.g. haemorrhagic fever)
"Malaria, caused by Plasmodium falciparum
- Neonatal or intrauterine infection
2. Gynecological diseases:
- Amniotic fluid embolism
- Intrauterine foetal death
- Detachment of the placenta
3. Liver diseases:
- Extensive necrosis of the liver
- Cirrhosis of the liver
4. Malignant tumor
- Acute leukemia promyelocytic
- Metastatic cancer, the most often - adenocarcinoma
5. Other diseases
- Vasculitis of small vessels (for example, with the development of the hypersensitivity cytotoxic and immunocomplex (II and III) types)
- Massive trauma
- Fever
- Heat stroke
- Surgical operations with artificial blood circulation
- Snake bites
- A heavy shock
- Intravascular hemolysis

Numerous blood clots of blood vessels of microvasculature in DIC-syndrome lead to a violation of the perfusion of tissues to accumulation in them of lactic acid and the development of their ischemia, as well as to the formation of microinfarction in a large number of bodies. Blood clots are particularly common in microvessels of the lungs, kidneys, liver, adrenal, pituitary gland, brain, gastrointestinal tract, skin and combined with multiple hemorrhages, dystrophy and necrosis of organs and tissues (cortical necrosis of the kidney, necrosis and hemorrhage of the lungs, brain, etc.). You must know that, in some cases at autopsy due to the parallel and the prevailing action of fibrinolytic system microthrombs may not be detected (the so-called fibrinolysis).

The shock of clinical state, associated with the reduction of the effective cardiac output, violation of autoregulation microcirculatory system and characterized by generalized decrease in blood supply of tissues, which leads to destructive changes of internal organs.

On the basis of the peculiarities of the etiology and pathogenesis distinguish the following types of hypovolemic shock:, neurogenic, septic, cardiogenny and anaphylactic.

Local disorders of blood circulation

To local disturbances of blood circulation are:
- blood hyperemia;
- venous hyperemia;
- stasis blood;
- the bleeding and hemorrhage;
- embolism;
- ischemia (local anemia);
- heart attack.

Local blood hyperemia (hyperaemia arteriosa localis)
Local blood hyperemia (arterial hyperemia) - increase in the inflow of arterial blood to the organ or tissue.

Distinguish between physiological and pathological hyperemia.
An example of physiological arterial hyperemia can be flush of shame on his face, pink and red skin at the place of its thermal or mechanical irritation.

On the basis of the etiology and mechanisms of development distinguish the following types of abnormal arterial hyperemia:
Angioneurotic hyperemia was observed in vasomotor disorders, caused by the irritation of the vasodilatory nerves, or paralysis of vasoconstrictive nerves, irritation sympathetic gangliev. Examples of such disorders can serve as acute lupus erythematosus, in which on the face are areas hyperemia in the form of a symmetrical lying butterflies, or redness of the face and the conjunctiva of the eye with many acute infections. To angioneurotic hyperemia refers hyperemia of the extremities in the event of damage of the respective nerve plexuses, hyperemia half of the persons with neuralgia, connected with the stimulation of the trigeminal nerve, etc.

Angioneurotic hyperemia is characterized by the acceleration of blood flow not only in the generally functioning, but also in the opening reserve capillaries. The skin and mucous membranes become red, slightly swollen, at the touch of warm or hot. Usually this hyperemia passes quickly and leaves no traces.

Collateral congestion occurs in the conditions of the closing of the main artery, for example, atherosclerotic plaque. Affluent blood rushes to collaterals, which are expanding. Of great importance in the development of the collateral arterial hyperemia under equal other conditions, is the rate of closing the main vessel and the level of blood pressure. Stenoses and even the closure of large arteries, when they are developing for years, may not be accompanied by severe consequences. This is due to the fact that collaterals in the arterial system are developed in parallel with the growth of obstacles blood flow in the course of the main trunk. Sometimes, for example, in atherosclerosis, the closure of both the coronary arteries of the heart is not accompanied by pronounced phenomena of heart failure, as collateral blood circulation developed here due to the mediastinal, inter costal, pericardial and bronchial arteries. Knowledge of the anatomical opportunities of collateral circulation allows surgeons to conduct operations successfully by ligation of femoral, popliteal, carotid arteries without the development of severe complications in the form of necrosis of the relevant authorities.

Postanemic hyperemia (redness after anemia) develops in those cases, when the factor (for example, a tumor, a accumulation of fluid in the cavities), causing local anemia (ischemia), quickly removed. The vessels previously bled dry cloth sharply expand and fill with blood. The danger of such a arterial hyperemia lies in the fact that the overcrowded vessels, especially in the elderly, can rupture, leading to bleeding and hemorrhage. In addition, in connection with sharp redistribution of the blood may be a lack of red blood cells of other organs such as the brain, which in the clinic accompanied by the development of fainting. Therefore, such manipulation as the removal of fluid from the chest and abdominal cavities produce slowly.

Vakathypertrophie hyperemia (from the Latin vacuus - the-blank) develops in connection with reduction of barometric pressure. An example of such a plethora of a hyperemia of skin under the influence of medical cans.

Inflammatory hyperemia is one of the important clinical signs of any inflammation.

Hyperemia on the grounds of arteriovenous shunt arises in cases where the injury is formed anastomosis between the artery and vein and arterial blood rushes into a vein. The danger of this hyperemia is determined by possibility to divide the anastomosis and development of bleeding.

Local venous hyperemia (hyperaemia venosa localis)
Local venous hyperemia (venous hyperemia) develops when the violation of the outflow of venous blood from the body or parts of the body. Based on the etiology and mechanisms of development, there are:
- obstructive venous congestion, caused by a blockage of the lumen of the vein thrombus, embolus (obliterating thrombophlebitis of the hepatic veins - Chiari disease, in which as well as in General venous plethora will develop Muscat liver, and in case of chronic over - moschatus cirrhosis of the liver; cyanotic induration of the kidney under tromboze renal veins);
- the compressor venous hyperemia, observed in the compression of the veins from the outside inflammatory edema, swelling, ligature, and growing connective tissue;
- collateral venous hyperemia, which can be observed at the closing of a major trunk venous trunk, for example, portocaval anastomosis because of the difficulty of blood flow in the portal vein (thrombosis of the portal vein, hepatic cirrhosis).

Morphological restructuring of venous collaterals comes on the same principle that and arterial, with a view, however, the macroscopic difference that expanding venous vessels take serpentine and angular forms. Such changes are called varicose veins can be seen on the lower limbs, in seed cord (varicocele), in the broad ligaments of the uterus, in the field of the urethra, in the field of anal holes and the nearby part of the rectum - the so-called hemorrhoids. On the front abdominal wall crowded venous blood vessels are of the type, known in the literature the name of the “head of Medusa”, having in mind the hair of the Medusa Gorgon from Greek mythology. Overflowing with blood collateral veins expand dramatically, and the wall of their thins out. This may be the cause dangerous bleeding (for example, massive bleeding from bulge in the lumen of the rectum haemorrhoids, bleeding from the extended and thin veins of the esophagus with cirrhosis of the liver). Varicose veins of the lower extremities (mainly, v. saphena magna et parva and their collaterals, as well as small leg veins) are cyanosis, swelling, expressed atrophic processes: skin and subcutaneous tissue, especially the lower third of the Shin, very thinner, and arising then ulcers Shin be cured with great difficulty (“varicose ulcers Shin”).
Exodus. Local venous hyperemia - the process is reversible, if the reason for the timely corrected.

Stasis (from the Latin stasis - standing) is slowing down to a stop, the blood flow in the vessels of microvasculature, mainly in the capillaries.

Remained blood may be preceded by venous hyperemia (stagnant stasis) or ischemia (ischemic stasis). However, it can also occur without prior listed disorders of blood circulation, under the influence of endo - and exogenous causes, as a result of infections (e.g. malaria, typhus), various chemical and physical agents on the fabric (high temperature, cold), resulting in violation of innervation of microvasculature, with infectious-allergic and autoimmune (rheumatic disease) diseases, etc.

Stasis blood is characterized by stopping the blood in the capillaries and venules with the enlargement of the clearance and gluing of red blood cells in homogeneous posts - this is what distinguishes stasis of venous hyperemia. Hemolysis and blood clotting when this does not occur.

Stasis need to be differentiated from the “sludge-phenomenon”. Sludge is a phenomenon of gluing of erythrocytes not only in the capillaries, and in vessels of different calibres, including in the veins and arteries. This syndrome is also the name of intravascular aggregation of erythrocytes was observed in a variety of infections, intoxications in force increased bonding red blood cells, changes in their charge. In the clinic of sludge-phenomenon reflects the increase in the ESR. As a local (regional) sludge process is developing in the pulmonary veins, for example, in the so-called shock lung, or acute respiratory failure adults (respiratory distress syndrome).

When different origin hypoxia can be isolated spasm of the veins, the so-called “venous kriz” on Ricker. This may cause leukostasis accumulation of granulocytes inside the vascular bed: in venules and capillaries. Leukostasis often with shock and are accompanied by leuco diapedesis.

Exodus. Stasis - the phenomenon of reversible. Stasis is accompanied by degenerative changes in the organs, where it is observed. Irreversible stasis leads to necrosis.

The clinical significance of eyes is determined by the frequency of this phenomenon. Stasis and static limit conditions are observed in the angio neurotic krizah (hypertension, arteriosclerosis), the acute forms of inflammation, in shock, for viral diseases, such as influenza, measles. The most sensitive to disorders of blood circulation and hypoxia is the cerebral cortex. Stasis can lead to the development of the microinfarction. Extensive stasis in the nidus of inflammation bring with them the danger of the development of ossification tissue that at the root can change the course of the inflammatory process. For example, when an inflammation of the lungs that can lead to fester and development of gangrene, that is, death.

From the biological point of view stasis is a decompensation adaptive mechanisms underlying the regulation of the peripheral blood circulation and blood supply of organs.

Bleeding (haemorrhagia) - the output of blood from the lumen of the vessel or cavity of the heart. If the blood is poured into the environment, then we talk about the external bleeding, if in the cavity of the body of the organism - the internal bleeding. Examples of external bleeding can be hemoptysis (haemoptoe), nose bleeding (epistaxis), vomiting blood (haematomesis), the allocation of blood on the stool (melena), bleeding from the uterus (metrorrhagia). If internal bleeding blood can accumulate in the pericardium (haemopericardium), pleura (haemothorax), the abdominal cavity (haemoperitoneum).

The output of the blood outside of the vascular bed with a accumulation of it in a tissue called a hemorrhage. Haemorrhage - this is a special type of bleeding.
Causes of bleeding (hemorrhage) can be gap, ulcers and increased permeability of the walls of the vessel.

Bleeding due to the rupture of the walls of the vessel or heart - haemorrhagia per rhexin - occurs when necrosis, inflammation or sclerosis of the walls of a vessel or heart. This type of bleeding occurs, for example, when you break the heart as a result myomalacia in acute myocardial infarction (acute ischemic heart disease), a rupture of the aorta with necrosis of its medium shell (medionecrosis), with the inflammation of the middle of the shell of the aorta (mesaortitis) and AIDS. Often there are aneurysm rupture of the heart, the aorta and the arteries of the brain, the pulmonary artery in vasculitis of different etiology, hypertension, atherosclerosis, etc.

Bleeding as a result of corrosion vessel walls - haemorrhagia per diabrosin - or arrosion bleeding, occurs when corrosion vessel walls gastric juice in the bottom of ulcers, cheesy necrosis in the wall of the cavern for tuberculosis, cancer, purulent exudation when the abscess, phlegmon. Arrosion bleeding develops and for ectopic (tubal) pregnancy, when the NAPs villus sampling germinate and corrode the wall of the fallopian tube and its vessels.

Bleeding in connection with an increase in the permeability of the walls of a vessel (without any apparent violation of its integrity) - haemorrhagia per diapedesin - arises from the arterioles, capillaries and venules for many reasons. Diapedetic hemorrhage occur in the system vasculitis, infectious and infectious-allergic diseases, for diseases of the blood system (hemoblastosis and anemia), coagulopathies, beriberi, when some of intoxication, overdose anticoagulants, etc. When diapedetic hemorrhage take a systemic nature, they become the manifestation of the hemorrhagic syndrome.

Bleeding on macroscopic picture distinguish:
- point - petechiaea and ekhimozy;
- bruise - dimensional bleeding in the skin and mucous membranes;
- hematoma - accumulation of blood in the tissue with a violation of her integrity and the formation of the cavity;
- hemorrhagic infiltration - saturation of the blood tissue without compromising its integrity.

Exodus. Full absorption of blood is the most favorable outcome of bleeding, and bleeding.
Organization - replacement izlivsheysya blood connective tissue. Encapsulation is a growth around spout blood connective tissues with the formation of capsules. Petrification - precipitation of salts of Ca2+ in the blood. The accession of infection and suppuration - adverse outcome.

The value of bleeding and bleeding is determined by his appearance, that is how pours blood from the arteries, veins, capillaries; localization, which is where poured out the blood, the amount of lost blood, speed of blood loss, state of the organism. Rupture of the aorta, the aneurysm is leading to a rapid loss of large quantities of blood and in the vast majority of cases - to the death of General acute anemia. Long-term, recurrent bleeding (for example, with ulcers stomach and duodenal ulcers, hemorrhoids) can lead to chronic anemia. Especially dangerous, often fatal, a bleeding in the brain, for example, when the rupture of an aneurysm of the arteries of the brain, haemorrhagic stroke in hypertensive disease. Often fatal is bleeding in the lungs at arrosion vessels in the wall of the TB caverns or in decaying tumors. At the same time, massive bleeding in the subcutaneous adipose tissue, muscles may not represent any danger to the life.

Thrombosis (from Greek thrombosis) - lifetime clotting of blood in the lumen of the vessel, in the cavities of the heart or the loss of blood dense masses. Produced during this bundle of blood is called a thrombus.

Blood coagulation is observed in the vessels after the death of the (post-mortem blood clotting). And dropped out of the dense mass of blood is called the postmortem bundle of his blood.
In addition, blood clotting occurs in the tissues at bleeding from the damaged vessel and is a normal hemostatic mechanism, which aims at stopping the bleeding in the damaged vessel.

According to modern view, the process of blood clotting takes place in the form of a cascade reaction (“the theory of the cascade”) - serial activation of proteins predecessors, or clotting factor, present in the blood or tissues (for details, this theory was presented in the lectures of the Department of pathological physiology).

In addition to the coagulation system, and there is anticoagulant system, which provides regulation of hemostasis system - liquid state of the blood in sossoudistom in normal conditions. Proceeding from this, thrombosis is a manifestation of impaired regulation of hemostasis system.

Thrombosis is different from coagulation of the blood, however, this difference of a few conditionally, because in either case starts the chain reaction of blood clotting. The blood clot is always attached to a bullet and is made up of layers of interconnected platelets, fibrin threads and formed elements of the blood, and the blood package contains randomly oriented strands of fibrin located between them platelets and red blood cells.

Violations of hemostasis
Normal balance that exists between the formation of the convolution and fibrinolysis, ensures the formation of the convolution of the blood of optimal size, sufficient to stop the bleeding from the vessel. Fibrinolytic activity prevents excessive blood clot. Violation of this balance leads in some cases to over thrombus formation, in the other - to bleeding.

Excessive blood clot leads to narrowing of the lumen of the vessel or to the occlusion (full closing). This usually occurs as a result of the impact of local factors, which inhibit the activity of fibrinolytic system in norm preventing excessive blood clot.

On the contrary, decrease clotting of the blood leads to excessive bleeding and observed in the various violations entailing increased bleeding: a decrease in the number of platelets in the blood, the deficiency of coagulation factors and increased fibrinolytic activity.

Factors affecting blood clot:
- damage of vascular endothelium, which promotes and platelet adhesion and activation of the blood clotting cascade, is a dominant factor, causing blood clot in a blood channel. In the formation of a blood clot in the veins and in the microvasculature of endothelial damage plays a lesser role;
- changes the current of a blood, for example, slowing the blood flow and turbulent flow;
- changes in the physico-chemical properties of the blood (blood clots, increased blood viscosity, increased fibrinogen levels and the number of platelets) - more significant factors for venous thrombosis.

Causes of thrombosis:
1. Illnesses of the cardiovascular system
2. Malignant tumor
3. Infection
4. The post-operative period

In relation to the clearing of a vessel are distinguished:
- near the wall clot (much of the lumen of the free);
- occlusive or plugging a thrombus (lumen of the vessel almost fully closed).

Localization of blood clots

1. Arterial thrombosis: blood clots in the arteries much rarer than in the veins, and usually occur after endothelial damage and local changes of the blood flow (turbulent flow), for example, in atherosclerosis. Among the arteries of large and medium-caliber most often affects the aorta, carotid arteries, artery Willis circle, coronary heart arteries, the arteries of the intestines and extremities.
Rarely arterial thrombosis is a complication of arteritis, for example, when periarteritis nodosa, giant cell arteritis, obliterating thromboangiitis and Henoch Schonlein and other rheumatic diseases. In hypertensive disease most often affects the arteries of medium-and small-caliber.

2. Heart thrombosis: blood clots are formed within the chambers of the heart, in the following circumstances:
1. Inflammation of the heart valves leads to damage to the endothelium, the local turbulent blood flow and sedimentation of platelets and fibrin on valves. Small blood clots called warty (rheumatism), large - vegetations. The growing season can be very large and loose, crumbling (for example, with infectious endocarditis). Fragments clot often come off and carried by the blood stream in the form of emboli.
2. Damage to the parietal endocardium. Damage to the endocardium may occur in acute myocardial infarction and the formation of ventricular aneurysm. Blood clots forming on the walls of the chambers are often large and may also crumble with the formation of emboli.
3. Turbulent blood flow and stasis
 in the Atria. Blood clots are often formed in the cavity fibrillation in case of turbulent blood flow or eyes blood, for example, with mitral stenosis holes and atrial fibrillation. Blood clots can be so large (ball) that impede blood flow through cardioversion ventricular hole.

2. Venous thrombosis:
1. Thrombophlebitis. At a thrombophlebitis venous thrombosis occurs a second time, as a result of an acute inflammation of the veins. Throm - the frequent phenomenon of the infected wounds or ulcers; more often affected by the superficial veins of the extremities. Damaged Vienna has all the signs of acute inflammation (pain, redness, feeling of warmth, swelling). This type of blood clot has a tendency firmly attached to the vessel wall. From it rarely are formed emboli.
Sometimes thrombosis develops in numerous surface veins of the legs (migrating thrombophlebitis) in patients with malignant neoplasms, most often with cancer of the stomach and pancreas (a symptom of Troisier), as mucins and other substances, formed by the tumor cells, have thromboplastin activity.
2. Phlebothrombosis - this vein thrombosis, which occurs in the absence of obvious signs of inflammation. Phlebothrombosis is observed, mainly in the deep veins of the legs (deep vein thrombosis). Less affected by the Vienna pelvic venous plexus. Deep vein thrombosis is observed quite frequently and is of great medical importance, because the blood clots that form in the veins, rather loosely attached to the vessel wall and often easily torn. They migrate with blood flow to the heart and the light and close the gap of the pulmonary artery thromboembolism of the pulmonary trunk and its branches).

The reasons for phlebothrombosis: the factors causing phlebothrombosis of deep veins, are typical for thrombosis at all, but endothelial damage usually expressed little and it is difficult to determinability. The most important causal factor in the occurrence of phlebothrombosis - reducing blood flow. Venous plexus legs of the blood flow in the norm is supported by the reduction of muscles of the legs (the muscle pump). The development of the eyes of the blood and the development of thrombosis contributes to the prolonged immobilization in bed, heart failure. The second factor was the increased bonding and aggregational ability of platelets, as well as the acceleration of blood coagulation due to increased levels of certain coagulation factors (fibrinogen, factor VII and VIII) - takes place in the postoperative and post-Natal period, in the application of oral contraceptives, especially with high doses of estrogen, in cancer patients. Sometimes several factors may act together.

Clinical manifestations: thrombosis of deep veins of the legs may be mild or no symptoms. During the survey of the patient revealed moderate swelling of ankles and pain in the calf muscles in the plantar flexion of the foot (the symptom of Homan). The majority of patients with pulmonary embolism is the first clinical manifestation of phlebothrombosis. Deep vein thrombosis can be found at the phlebography, ultrasound, radiology methods, comparative measurement of the thighs centimeter tape.

The outcome of thrombosis
The formation of blood clots causes the body's response, which aims to remove a blood clot and restore blood circulation in the damaged blood vessel. For this there are several mechanisms:
1. Blood clot lysis (fibrinolysis), leading to a total disruption of the clot - ideal favorable outcome, but is very rare. Fibrin of a blood clot, is destroyed plasmin, which is activated factor gene is associated (factor IX) the activation of the internal cascade of blood clotting (that is fibrinolytic the system is activated at the same time with the system of coagulation; this mechanism prevents excessive thrombosis). Fibrinolysis ensures the prevention of the formation of excess fibrin and the disintegration of the small blood clots. Fibrinolysis is less effective in the destruction of large blood clots occur in the arteries, veins or the heart. Some substances, such as streptokinase and tissue activators plasminogen, which activate fibrinolytic system, are effective inhibitors of thrombosis when used immediately after thrombosis and cause lysis of the clot and restore blood flow. They are used successfully in the treatment of acute myocardial infarction, thrombosis deep.

Which doctor should I contact if there is a violation of the circulatory system

  • Cardiologist
  • Therapeutist
  • Family doctor
  • Neurologist
  • Vascular surgeon (angiosurgeon)
  • Resuscitator

Are you experiencing violation of the circulatory system? You want to know more detailed information, or you need an inspection? Please sign up on reception to the doctor! Doctors will examine you, examine the external signs and help to determine the disease the symptoms, they will consult you and provide the necessary assistance. You can also call the doctor on the house.

Do you feel disrupted circulatory system? You should be very careful approach to your health in general. People pay not enough attention to the symptoms of the disease and don't realize that these diseases can be critically dangerous. There are many diseases that in the beginning didn't manifest in our body, but in the end it turns out, unfortunately, it have already been treated too late. Every disease has its own specific features typical symptoms - called symptoms of the disease. Definition of symptoms is the first step in the diagnosis of diseases in general. You just need a few times a year to be screened by a doctor, not only to prevent a terrible disease, but also to maintain a healthy spirit in a body and the organism in general.

Disorders by category

Disorders by alphabet

Map of the symptoms and the types of disorders is intended solely for educational purposes. We strongly recommend do NOT self-medicate; on all matters relating to the definition of the disease and ways of its treatment, contact your doctor. Md-tips is not responsible for the consequences of use information posted on the site.