There are three types of fluid in the organs of human internal environment. They are blood, lymph, tissue fluid. Metabolism in these fluids, their qualitative and quantitative changes are closely connected with each other and are regulated by complicated neurohumoral mechanisms. The factors which cause the failure in these mechanisms as well as the disturbances of blood and lymph circulation and those appearance in the tissue are numerous.

All the disturbances of blood circulation can be divided into three groups: 1) disturbances of blood filling or disturbances in the volume of the circulating blood (hyperemia and anemia), 2) disturbances of blood vessel wall permeability (hemorrhage, plasmor-rhagia), 3) disturbances of blood rheology (stasis, sludge, thrombosis, embolism).

Disturbance of blood circulation is the cause of such phenomena as disseminated intravascular coagulation (DIC), thromboembolic syndrome, shock, acute or chronic cardiac insufficiency.

Hyperemia (plethora)can be arterial and venous.

Arterial hyperemia is increased blood filling of the organ or tissue due to increased flow of the arterial

blood. It may be general or local. General arterial hyperemia develops at increase of circulating blood volume or at increase of erythrocyte amount. Clinically, general arterial hyperemia manifests by elevation of arterial pressure and skin reddening. Local arterial hyperemia occurs more often and can be physiological and pathological. Physiological arterial hyperemia is due to increase in the organ function or as a result of shame and rage. Pathological arterial hyperemia may be: 1) angioneurotic, 2) collateral, 3) postanemic (hyperemia after anemia), 4) vacant, 5) inflammatory, 6) caused by arteriovenous fistula.

Angioneurotic hyperemia is caused by irritation of vasodilatory nerves or by paralysis of vaso-constric-tory nerves.

Collateral hyperemia is caused by obstruction to the blood flow in the main arterial trunk (thrombosis, embolism). In this case the blood gains entry to the collateral vessels and they dilate.

Postanemic hyperemia is observed when the factor causing anemia (tumor, fluid in the cavity) is eliminated. The vessels of anemic tissue are overfilled which may cause their rupture and hemorrhage as well as anemia in the brain. That is why manipulations aimed at removal of a tumor, fluid or ligature should be performed slowly.

Vacant hyperemia is observed at reduction of barometric pressure. It may be general (in divers) or local (on the place of cups).

Inflammatory hyperemia is caused by inflammation.

Hyperemia caused by arteriovenous fistula is observed at injury, when anastomosis between an artery and vein is formed and the arterial blood enters the vein.

The significance of arterial hyperemia is different. In some cases it is a protective or adaptive reaction but vacant hyperemia is an important factor in caisson disease morphogenesis, postanemic hyperemia may cause death.

Venous hyperemia is increased filling with blood of the organ or tissue due to difficulties with blood outflow when blood supply is not changed or decreased. It may be general or local. General venous hyperemia develops in acute or chronic cardiovascular insufficiency. Local venous hyperemia develops when there are difficulties with venous blood outflow from the organ or a part of the body (tumor, thrombus, embolus). Morphogenesis of the both types of venous hyperemia is similar, the only difference is the range of the lesion. In general venous hyperemia a number of organs are damaged, in local only one organ.

General venous hyperemia may be acute or chronic.

Acute venous hyperemia is a manifestation of a syndrome of acute cardiac insufficiency (e.g. in myocardial infarction) and is characterized by edematous plasmorrhagia, hemorrhage and degeneration.

Chronic venous hyperemia develops in chronic cardiovascular insufficiency. It is accompanied by tissue hypoxia development which increases vascular permeability, which in turn results in development of edema, plasmorrhagia, diapedesis of erythrocytes, degeneration in surrounding parenchymatous cells, with outcomes like necrosis and sclerosis. Sclerosis results in congestive induration of the organ. One of the final links in chronic venous hyperemia morphogenesis is formation of capillary parenchymatous block due to thickening of basement endothelial and epithelial membranes because of increase in collagen fibroblast production. It's known that collagen fibroblast production increases due to hypoxia.

The most prominent changes develop in parenchymatous organs.

The liver is called «nutmeg» liver, it is enlarged, dense, its borders are rounded, it has «nutmeg» appearance at incision. In this case you can see gray-yellow and dark-red areas. Microscopically, the veins and sinusoids are plethoric, diapedesis of erythrocytes and fat degeneration of hepatocytes in the peripheral regions are observed. Morphogenesis of «nutmeg» liver at first congestion of the venous blood develops, it is accompanied by tissue hypoxia development which increases vascular permeability, as a result diapedesis of erythrocytes and fat degeneration in hepatocytes are observed. Due to hypoxia sclerosis and pathologic regeneration develop.

In «brown induration» of the lungs. The organs are dense, brown with multiple hemorrhages, besides sclerosis is observed.

In the kidneys and spleen cyanotic induration is observed. Morphogenesis of cyanotic induration in the kidney and spleen is similar to liver one.

Ischemia(originates from Greek ischo — delay) is decreased filling with blood of the tissue, organ, part of the body due to insufficient blood flow.

Depending on the cause and conditions ischemia can be classified into:

1) angiospastic caused by arterial spasm because of irritation, e.g. pain;

2) obturation, i.e. due to closure of the artery lumen with a thrombus or embolus or growth of connective tissue in inflammation, arteriosclerosis;

3) compression, i.e. squeezing of the artery with a tumor, fluid, tourniquet, etc.;

4) ischemia as a result of blood redistribution in case of postanemic hyperemia.

If the duration of ischemia is short, the structure and the function of tissue may be restored. When the lesion is continuous, infarct, atrophy or sclerosis may develop.

Hemorrhageis exit of the blood from the lumen of the vessel or from the heart cavity. This may be external (to the environment) such as from the nose (epistaxis), vomiting of blood (hemotenesis) and other or internal (in the body cavity) such as hemoperi-cardium, hemothorax, hemoperitoneum.

Hemorrhage is also defined as accumulation of blood in the tissues.

Hematomais accumulation of clotted blood in the tissues with disturbance of their entity. Large extravasations of blood into the skin and mucous membranes are called ecchymoses.

Hemorrhagic saturationis accumulation of the blood in the tissue when its entity is preserved.

According to the mechanism, bleeding can result from: 1) rupture of the vessel (per rhexin); 2) corrosion of the vessel (per diabrosin);3) diapedesis (per diapedesin).

The hemorrhage can be caused by:

1. Trauma to the vessel wall, e.g. penetrating wound in the heart or great vessels.

2. Spontaneous hemorrhage, e.g. rupture of an aneurysm, septicemia, acute leukemias, pernicious anemia.

3. Inflammatory lesions of the vessel wall, e.g. bleeding from chronic peptic ulcer from tuberculous cavity in the lungs.

4. Neoplastic invasion e.g., hemorrhage following vascular invasion in cancer.

5. Vascular diseases, e.g., atherosclerosis.

6. Elevated pressure within the vessels, e.g. cerebral hemorrhage in systemic hypertension.

Outcomes: blood resorption, cyst formation (brain), encapsulation, organization, suppuration.

Plasmorrhagiais exit of plasma from the circulatory system. This can be caused by vascular spasm, tissue hypoxia, immune pathology. As a result, vascular permeability increases, plasma saturates the vessel and the surrounding tissues, plasma saturation occurs resulting in fibrous edema, fibrous necrosis and sclerosis. Plasmorrhagia is significant in morphogenesis of hypertension, infectious and allergic diseases, autoimmune diseases.

Stasis(stasis — stop) is arrest of blood flow in the vessels of microcirculatory system (capillaries). It is preceded by slowing the blood flow which is called prestasis. Sludge syndrome (phenomenon) is regarded as a type of stasis. It is characterized by sticking of erythrocytes, leukocytes and thrombocytes to each other, which is accompanied by blood viscosity increase. Stasis may be discirculatory as a result of venous hyperemia or ischemia. It develops due to:

1) physical factors (temperature elevation, cold);

2) chemical factors; 3) infection; 4) infectious-allergic factors; 5) autoimmune factors.

Hemostasisis a striking example of circulation adaptation failure. Short stasis is reversible, long one causes hyaline thrombi formation, vascular permeability increase, edema, bleeding.

Isolated vein spasm may cause leukostasis, accumulation of erythrocytes within venules (small veins) and capillaries. It is observed in hypoxia.

In shock, leukostasis may be generalized, but as a rule it is localized in the venules. Microcirculation disturbances. There are four links in microcirculation:

1) the link of inflow and distribution of the blood (arterioles and precapillaries);

2) intermediate (exchange) link (capillaries);

3) depot link (postcapillaries and venules);

4) drainage link (lymphatic capillaries and postcapillaries).

The function of microcirculation is exchange between the blood and tissue. Pathology of microcircu-latory system is formed of vascular, intravascular and extravascular changes.

Vascular changes are those in the thickness and shape of the vessels, angiopathies with disturbance of vascular permeability as a result of hypoxia.

Intravascular changes manifest as different disturbances of blood rheology (sludge, prestasis, stasis). They are observed in shock of different origin.

Extravascular changes are perivascular edema, hemorrhage, lyphostasis on the lymph vessels.

Thrombosis(originates from Greek thrombus — blood clot) is a pathologic manifestation of homeostasis, i.e. intravital coagulation of blood with formation of a blood clot called thrombus in the lumen of the vessel. The thrombus may partially or completely close the lumen and cause serious disturbances of blood circulation. At the same time

homeostasis is a protective mechanism and it becomes active at the vessel rupture. The mechanism of thrombus formation includes four consequent stages: thrombocytes agglutination, fibrinogen coagulation and fibrin formation, erythrocyte agglutination and plasma protein precipitation. Thrombosis pathogenesis includes local and general factors which cause thrombus formation. Local factors are changes in the vascular wall, slowing the blood flow and disturbance of turbulent motion. General factors include disturbances of regulation of coagulation and anticoagulation systems and changes in the blood composition.

Morphology. The thrombus is attached to the vascular wall, it is dense, with corrugated surface. It is composed of branching bars of stuck thrombocytes and bands of fibrin with erythrocytes and leukocytes located between them.

Thrombi may be white, red, mixed and hyaline. Hyaline thrombus consists of precipitating plasma proteins, destructed erythrocytes, leukocytes and thrombocytes. They do not contain fibrin. They resemble hyaline and are located in the microcircu-latory bed.

According to the degree of the lumen obliteration, thrombi may be parietal or obstructive. Parietal thrombi develop in large arteries and heart cavities. Obstructive thrombi most commonly develop in small arteries and veins.

The thrombus enlarges with adding new masses to the primary one. It may grow both with the blood flow and against it.

If the thrombus which appeared in the veins (e.g. leg) enlarges with the flow and reaches the collecting veins (e.g. inferior vena cava), thrombosis is called progressive. The thrombus in the aneurysm is called dilatation. Thrombi in the veins can be revealed in 31.0 — 22.0% of autopsies, those in the heart in 45.8%.

Thrombosis is the main factor in morphogenesis of disseminated intravascular coagulation (DIC) syndrome and is the basis of thromboembolic syndrome.

The outcome of thrombosis may be favorable: aseptic thrombus autolysis or growth of connective tissue from vascular intima with formation of clefts and channels, covered with endothelium, so called thrombus canalization. Then these canals turn into vessels with restored blood flow, it is so called vascularization of the thrombus. Calcification of thrombus with stones (phlebolith) formation is possible.

Unfavorable outcome: thromboembolism, septic thrombus autolysis, thrombobacterial vascular embolism in sepsis.

Embolism(originates from Greek emballein — to cast into) circulation in the blood or lymph of particles which do not normally occur and obstruction of the vessels with them. These particles are called emboli.

Depending of the way of their movement embolism may be:

1) orthograde (with the flow):

• from the veins of general circulation to the vessels of pulmonary circulation,

• from the left part of the heart, aorta, large arteries to the arteries of the heart, brain, kidneys, spleen, etc.,

• from the veins of the portal system to the portal vein of the liver;

2) retrograde embolism, movement of embolus against the flow with his own weight (e.g. through inferior vena cava to femur vein);

3) paradoxical embolism, in defect of atrial or ventricular septum when the embolus enters the arteries from the general circulation.

According to the type of embolus the following types of embolism are distinguished:

1) thromboembolism, the most frequent form occurring when a thrombus or its part separate. It may be either venous or arterial;

2) air embolism is caused by the air entering the venous system in injuries of the veins located near the heart. Air embolism may be caused by injection of air to the uterine cavity at criminal abortion, at intravenous injections if the air has not been evacuated from the syringe.

Diagnosis: at autopsy, the right heart is punctured without taking it out. The cavity of the cardiac sac

should be preliminary filled with water. Air discharge and foamy blood are observed;

3) gas embolism occurs as a result of exudation of bubbles of the gas dissolved in the blood, e.g. at rapid transition from high atmospheric pressure to normal in caisson disease, gas gangrene, in pilots;

4) fat embolism occurs in bone injuries when the fat is crushed and turned into emulsion;

5) tissue embolism occurs in the fetus during delivery if amniotic fluid and chorion enter the veins of the uterus. The other examples are tumor cells and septic thrombus;

6) foreign bodies (fragments of shells, bullets), embolism with lime, cholesterol crystals.

Thromboembolic syndromeis separation of a thrombus or a part of it and circulation of these particles in the blood of general system with obstruction of lumina of different arteries accompanied by multiple infractions. Infarct is vascular necrosis. Most frequently it is caused by thrombi in aortic or mitral valves, intratrabecular thrombi of the left ventricle and auricle of the left atrium, the thrombi of aorta and large arteries which turn into thromboemboli. All these develops in rheumatic and bacterial endocarditis, atherosclerosis, cardiac aneurysm, heart defects.

In thromboembolic syndrome, infarcts frequently develop in the kidneys (white with hemorrhagic rim), spleen (white), brain (white and red), heart (white with hemorrhagic rim), intestine (red), gangrene of

extremities. A variety of thromboembolic syndrome is pulmonary thromboembolism. Thromboemboli formed in the veins of the general system and in the right heart and enter the pulmonary artery. They may enter small branches of the pulmonary artery causing hemorrhagic lung infarction. If the embolus enters a large branch of the artery, the patients die suddenly because of pulmonocoronary reflex. This condition is characterized by spasm of bronchial tree, branches of pulmonary artery and coronary arteries.

Thromboembolic syndrome may complicate infectious, cardiovascular, and oncological diseases, it may occur after different operations.

Disseminated intravascular coagulation(consumption coagulopathy, defibrination, throm-bohemorrhagic syndrome or phenomenon) is pathological syndrome which is characterized by formation of disseminated blood clots in the micro-circulatory bed (often in combination with simultaneous reduction of blood coagulability) causing hemorrhages. It often develops in complicated pregnancy, profuse uterine bleedings, Cesarean section, large injuries, anemias, thrombocytopenias, leukosis, in 36—50% of cases of asphyxia in premature children.

The causes of its development are numerous, the mechanisms of development are different.

The most important are:

1. Massive formation of thromboplastin or its activators. It may be thromboplastin of erythrocytes

in intravascular hemolysis (hemolytic disease of newborn, massive blood transfusions, poisoning, infections) or thromboplastin of amniotic fluid at massive aspiration of amniotic fluid by the fetus, tissue thromboplastin in injury (especially that of brain and lungs).

2. Generalized disturbance of microcirculation accompanied by changes in blood rheology and its clotting which is observed in hypoxia and shock of different origin. Bacterial toxins and immune complexes act similarly. They activate factor XII which plays the most important role both in blood coagulation and anticoagulation activation. The same mechanism regulates disseminated intravascular coagulation syndrome in thrombosis of large arteries or at severe loss of fibrinogen at formation of hyaline membranes in the lungs of newborns.

3. Reduction of the number of thrombocytes (consumption thrombocytopenia in Kasabach-Merritt syndrome).

4. Generalized angiopathy in infectious diseases and hemolytic disease of newborn also causes disseminated intravascular coagulation syndrome. At the first stage it is characterized by generalized increase of blood coagulation in the microvessels. Large number of fibrin clots are formed. They close the vessel (fibrinoembolism).

At the second stage the amount of thrombocytes, fibrinogen, protrombin in the blood decreases sharply

because they have already been used at the first stage with the resultant consumption coagulopathy. Thus, hemorrhagic syndrome develops.

At the third stage fibrinolysis activation takes place in response to generalized increase of coagulation occurring at the first stage which makes hemorrhagic syndrome more severe.

In severe cases the three stages develop simultaneously. Disturbance in blood clotting is accompanied by stasis, opening of arteriovenous shunts, capillary paralysis, decrease in arterial pressure. Degenerative and necrotic changes develop in parenchymatous organs.

Morphological changes in disseminated intravascular coagulation (DIC) syndrome:

1) large amount of fibrin thrombi and emboli in the small vessels of the liver, red pulp of spleen, adrenals, brain, lungs, kidneys, placenta, thymus,

2) mucoid swelling, fibrinous swelling and fibrinous necrosis with endothelium desquamation in the walls of small arteries,

3) thromboses of large vessels are possible. Often the thrombi occur in the sinuses of the dura mater, hepatic veins, aorta,

4) in thrombosis of microcirculatory bed, vital processes of blood-tissue metabolism stop. Under these conditions organ pathology is not distinct, general changes (like toxicosis or shock) develop,

5) in thrombosis of larger arteries, organ pathology prevails, i.e. acute renal or hepatic insufficiency, shock lung, brain edema, myocardial infarction,

6) DIC (disseminated intravascular coagulation) results in hemorrhages in different organs, those in the capsule are most frequent.


According to N. A. Kraievsky, «shock is a special reaction of the organism to a stimulus. It is fulfilled with nervous mechanisms and characterized by peculiar «shock» disturbance of circulation)) (1944). But one of the founders of shock theory, W. Connon (1943) believed that the role of nervous reaction in shock development is not significant. According to him, main feature of shock is peculiar disturbance in blood circulation due to exit of the blood from the circulation but not from the body. Later it was called «hemorrhage into the vessels» or «blood depot». Recently this point of view became predominant owing to the achievements in microcirculation study. Shock is nonspecific clinical syndrome caused by reduction in tissue perfusion with blood. Shock believed to be based not so much on the primary disturbance of central neuro-regulatory mechanisms as disturbance of autoregulation in microcirculatory system due to the release of abundant biologically active substances.

In contemporary textbooks the following definition can be found: «Shock is acute pathologic process due to development of extrapowerful stimuli and characterized by disturbances in CNS function, metabolism and microcirculatory system autoregulation resulting in destructive changes in the organs and tissues».

According to etiology and pathogenesis shock is classified as:

1. Hypovolemic (blood loss, trauma, peritonitis, cholera).

2. Cardiogenic (caused by the reduction in cardiac output in myocardial infarction, vascular insufficiency).

3. Bacterial (caused by endotoxins).

4. Anaphylactic (immediate reaction of hypersensitivity).

5. Neurogenic (in intoxication with hypnotic preparations, ganglioblockers, narcotics).

6. Shock developing as a result of obstruction to the blood flow (pulmonary thromboembolism).

7. Shock developing in hormonal insufficiency (thyrotoxic shock, myxedema, adrenal insufficiency).

Shock morphology

Three main pathological processes are observed in shock: DIC (disseminated intravascular coagulation) syndrome, hemorrhagic diathesis, liquid cadaver blood.

Microscopically it is characterized by generalized spasms of the vessels, microthrombosis, signs of increased vascular permeability in microcirculatory system, hemorrhages, degenerations, necroses connected with hypoxia and damaging effect of endotoxins.

Some examples of changes in the different organs in shock are:

• shock kidney, degeneration and necrosis in proximal canals with development of necrotic nephrosis (or symmetrical cortical necroses are possible) which results in acute renal insufficiency,

• shock liver, glycogen amount in the hepatocytes decreases, hydropic degeneration and centrolobular necroses resulting in acute hepatic insufficiency develop. Combination of renal and hepatic insufficiency is called hepatorenal syndrome,

• shock lung, atelectasis foci, serous-hemor-rhagic edema, stases and thromboses in the microcirculatory bed resulting in acute respiratory insufficiency,

• shock heart, degeneration and necrosis in cardiomyocytes, reduction in glycogen amount, fat degeneration, necrosis foci.

Similar changes occur in gastrointestinal tract, nervous, endocrine systems, immune organs.

Shock morphology depends not only on the cause of the shock but also on its stage. At the early stage, disturbances of hemodynamics and DIC (disseminated intravascular coagulation) syndrome are noted. At the last stages degenerative and necrotic process occur.

Intensive transfusion therapy of shock masks clinico-morphological picture. But the constant features are liquid cadaver blood irrespective of the compo-sition of transfused fluids. Blood clots in the cardiac cavities and vessels are characteristic for terminal states of nonshock origin. So blood composition is a criterion for differential diagnosis.

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