Factors contributing to the onset of renal edema are
Edema is called a pathological congestionfluid in tissues and interstitial spaces due to the violation of water exchange between blood and tissues. Edema is a typical pathological process that occurs in many diseases.
The edema fluid contains water (97%), electrolytes(about 0.7%), a small amount (up to 3%) of the bleeding protein and is called the transudate. Its composition depends on the causes of origin, localization, species of animals.
Pathological accumulation of fluid in serouscavities of the body is called dropsy. Depending on the place of localization, there are abdominal edema - ascites of the pleural cavity - hydrothorax, cardiac shroud - hydropericardium, ventricles of the brain - hydrocephalus, articular bag - hydroartrosis.
The development of edema is due to many factors, butfrom them it is necessary to distinguish the leading ones, among which the change in the hydrodynamic, osmotic and oncotic pressures and the change in the permeability of the capillary wall.
Under normal physiological conditionsThe hydrodynamic pressure in the arterial part of the capillary is 35-40 mm Hg, it is higher than the oncotic (25 mm Hg). The buoyancy force is greater than the restraining force and blood plasma is directed through the histohematological barrier into the tissues. In the venous part of the capillary, the oncotic pressure remains the same (25 mm Hg), and the hydrodynamic pressure is reduced to 10-15 mm Hg. Art. The hydrodynamic factor promotes the development of edema, when the blood pressure in the venous part of the capillary exceeds the oncotic. At the same time, blood plasma enters the tissues from the arterial part of the microcirculatory bed, and reabsorption becomes difficult or impossible. There is swelling. liquid tissue body edema hydrops
Oncotic pressure promotes the development ofedema due to either a decrease in the oncotic blood pressure, or increase it in the intercellular fluid. Hypononkia of blood is most often due to a decrease in protein levels and mainly albumins. Hypoproteinemia can result from: insufficient intake of protein into the body, impaired albumin synthesis, liver disease, excessive loss of plasma proteins in the urine with certain kidney diseases, through damaged skin in case of extensive burns. Hypononkia of blood can be caused by disproteinemia, which is based on a violation of the normal ratio of albumins and globulins (normal 2: 1). Replacing the deficiency of albumins with other proteins (in the course of the infectious process, allergic reactions) does not prevent the hypone- nia of the blood.
The heteronuclear intercellular fluid can ariseas a result of the transfer of some of the plasma proteins into tissues with a pathological increase in the permeability of the vascular wall, the release of proteins from the cells upon their alteration, the increase in the hydrophilicity of proteins in the intercellular cell under the influence of excess ions of hydrogen, sodium, histamine, serotonin, or thyroxine deficiency.
The osmotic factor of edema development canarise when the osmotic pressure of the blood decreases or increases in the intercellular fluid. The osmotic pressure of the blood plasma is more than 90% determined by the sodium cation. Reduction of its content in the blood (alimentary failure, excessive loss) may occur, but rapidly developing severe disorders do not allow the development of edema of pronounced form. Tissue hyperosmia develops more often. Its causes can be: sodium retention in the intercellular space with excessive allocation of aldosterone, cell damage with the release of electrolytes, acidosis, hypoxia and others.
Increase in permeability of the capillary walloccurs as a result of stretching the walls of capillaries (for example, with arterial hyperemia), with excess histamine, serotonin in tissues, damage to endothelial cells (hypoxia, acidosis, toxins), violation of the structure of basal membranes (when enzymes are activated, inflammation). Infringement of permeability of vascular walls at an inflammation is connected with accumulation of mediators of damage, and also with frustration of nervous regulation of a tone of vessels. The permeability of the vascular wall can increase with the action of certain chemicals (chlorine, phosgene, diphosgene, lewisite, mustard and others), bacterial toxins (anthrax, diphtheria), and poisons of various insects and reptiles (mosquitoes, bees, hornets, snakes, scorpions and others).
Most often in the mechanism of development of edema, take all 4 factors. Hydrodynamic, oncotic, osmotic and membrane. However, in each specific case it is necessary to single out the main, main factor.
In the mechanism of development of edema and edema followstake into account the functional state of the nervous system. If braking processes predominate. That edema either does not develop or develop to a lesser degree. This phenomenon is used with a curative and preventive purpose.
In addition to the above factors in the developmentedema and dropsy an important role belongs to lymph circulation. The difficulty of transporting fluid and proteins through the lymphatic system from the interstitial space to the total blood flow creates favorable conditions for water retention in tissues and the development of edema. With heart failure, impaired lymph circulation is one of the important mechanisms of edema development. At nephroses, the protein content in the blood decreases significantly, the linear and volume velocity of the lymph flow increases several times. However, despite this, because of the intensive filtration of fluid from the vessels into the tissues, the lymphatic system is not able to return to the total lymphatic drainage of the blood significant volumes of tissue fluid. In connection with the overload of lymphatic ways, lymphatic insufficiency arises, and it plays an important role in the pathogenesis of edema.
2. Symptoms and classification of edema</ b>
1. Increase the organ or tissue in the volume.
2. The edematous tissue has a dough-like consistency, with pressure, a slowly fading pit remains.
3. When the tissue is cut from its surface, the edematous fluid flows.
4. The function of swollen tissue or organ decreases.
5. There is a local decrease in the temperature of the tissues.
6. The oedematous tissue is gray.
There are two classifications of edema:
According to the pathogenetic classification, all swellingdivide: on hydrodynamic - if the main contributing factor is the hydrodynamic factor, oncotic - if the main contributing factor is the change oncotic pressure, osmotic - if the main contributing factor is the change in membrane osmotic pressure and - if the main contributing factor is the change in the permeability of cell membranes.
The division of edema into hydrodynamic, osmotic, oncotic and membranous is somewhat arbitrary, in real conditions all 4 factors take part in the development of all edema.
Depending on the reasons, the following types are distinguished:edema: cardiac (stagnant), stagnant edema of non-cardiac origin, renal, hungry (cachexic), toxic, inflammatory, neurotic, hormonal, allergic.
Cardiac edema occurs as a result of cardiacinsufficiency, caused by myocardial damage (myocarditis, infarction) or endocardium (endocarditis, decompensated defects). The main contributing factors for the development of cardiac edema are hydrodynamic, osmotic, oncotic and membrane.
Insufficiency of the left half of the heart leads tovenous stasis, increase of pressure in the system of a small circle of blood circulation. Stagnation of blood in the vessels of the lungs develops. Insufficiency of the functional activity of the right side of the heart, accompanied by increased pressure, venous stasis in the system of a large circulation, which is accompanied by increased infiltration of blood plasma and a decrease in fluid resorption in capillary vessels. Edema in animals in this case is found on the sites of the bodies removed from the heart - in the subcutaneous tissue of the stomach, thoracic and pelvic extremities, in the subsidence area.
The hypoxia and acidosis that develops when the blood stasis leads to disruption of the trophic to an increase in the permeability of the walls of the vessels, and their output is enhanced in water tissues and plasma proteins.
Heart failure leads to that. That increases the production of aldosterone, while the sodium content in the blood is delayed, hyperosmia develops, this serves as a signal for activating the production of vasopressin, which causes a water retention in the body.
Any cardiac edema is a stagnant swelling, but notevery stagnant swelling is cardiac. Stagnant edema of non-cardiac origin occurs with embolism, vein thrombosis, compression of the vessels with an improperly applied bandage, a tourniquet, tightly tightened cinch. Congestive edema of non-cardiac origin occurs in all cases when the outflow of intermuscular fluid through the lymphatic vessels is disturbed. The main factors in the development of these edema are hydrodynamic and membrane. When the veins are squeezed in them, the hydrodynamic pressure rises, the vessels expand, the outflow of interstitial fluid stops. Transsudation in the focus of stagnation is promoted by hypoxia and acidosis, which lead to an increase in the permeability of membranes. The transudate, squeezing the lymphatic ducts, prevents the lymphatic drainage. Increased pressure in the hollow veins (lack of right half of the heart) causes a reflex spasm of the lymphatic vessels, leading to lymphatic insufficiency. Disturbance of lymph circulation is an important link in the formation of cardiac edema.
Cardiac edema appears most often towards the endday, especially with increased physical exertion, congestive edema of non-cardiac origin is distinguished by the fact that they are limited, localized in those places where the blood vessels are squeezed and there is no dependence of their formation on the time of day.
The development of renal edema is due to twofactors. The first factor is the diffuse lesion of the glomerular apparatus by the inflammatory process (glomerulonephritis), as a result of which the filtration capacity of the kidneys sharply decreases. The resulting circulatory disturbance in the kidney itself stimulates an increased production of aldosterone, which contributes to the retention of sodium in the body. Increased sodium content in the blood activates the secretion of antidiuretic hormone, which enhances the reabsorption of water in the distal sections of the renal tubules, increases the permeability of capillaries in the body. A distinctive feature of edema with glomerulonephritis is the increased hydrophilicity of loose connective tissue, which occurs under the action of aldosterone, antidiuretic hormone and other biologically active substances released by the kidney.
The second factor determining the development of renaledema is the primary lesion of the renal tubules. Acutely and chronically occurring nephroses are characterized by the release of large amounts of protein (mainly albumins) by the kidneys. Developing hypoproteinemia causes the development of blood hypochondria, which facilitates the movement of fluid from the bloodstream into the tissues. Gipoonkiya and its accompanying hypervolemia, irritating osmo - and volyumoretseptory reflexively stimulates the release of aldosterone and increased retention of sodium and water in the body. Some importance in the mechanism of sodium and water retention with nephrosis may have increasing renal tissue sensitivity to aldosterone and antidiuretic hormone.
In diseased animals, renal edema can be observedin the abdomen, podgorudka, groin, sacrum, larynx. Especially clearly manifested puffiness of renal origin in the eyelid, often in dogs and pigs. This is explained by the fact that these areas are rich in loose fiber, which readily adsorbs electrolytes. Renal edema is most often expressed in the morning.
5. Cachectic (hungry) swelling</ b>
Cachexia edema occurs as a result ofinsufficient intake of nutrients in the body or their inability to digest. Alimentary insufficiency can develop with poor protein feeding, chronic severe diseases (malignant tumors, infectious diseases, gastrointestinal lesions, chronic anemia). In the pathogenesis of cachexia edema, hypoproteinemia plays a leading role. Reducing the concentration of proteins in the blood leads to a drop in the oncotic pressure, so that water does not remain in the lumen of the vessels and moves into the tissues. In case of starvation, life continues due to the use of the body's own reserves (interorgan metabolism is established), while in tissues and organs molecular concentration increases, osmotic pressure increases and water intake by starving animals increases. When starvation develops cardiovascular insufficiency, leading to an increase in venous pressure, a violation of lymph circulation - creates favorable conditions for the release of fluid from the vascular system into the tissues. An important role in the development of cachexic edema is played by an increase in the permeability of the wall of capillary vessels, associated with trophic disturbances. Hungry edema can appear everywhere, while cachexia is accompanied not only by swelling of the tissues, but also by mucous membranes, serous membranes, accumulation of transudate in various cavities. The appearance of hunger edema does not depend on the time of day.
Toxic edema is most often observed inanimals after the bites of poisonous snakes, bees, other stinging insects. The causes of such edema can be poisoning by fighting toxic substances (phosgene, diphosgene), chlorine, ammonia.
In the pathogenesis of toxic edema, the main roleplays the permeability of the walls of blood vessels. In connection with the destruction of cells, hyperonchia and hyperosmia can develop in tissues and organs. The transition of water to tissues, organs is facilitated by biologically active substances, such as histamine, serotonin, bradykinin, prostaglandins, that are damaged by cellular elements. Toxic edema is local, their boundaries are determined by the nature of the intake of toxic substances into the body. Inhalation of gaseous toxins leads to pulmonary edema, defeat of the skin with mustard gas, lewisite, croton oil leads to its edema, if poisons enter the large circulation, swelling can be ubiquitous.
Inflammatory edema occurs as a result ofdamage to cells, tissues in the focus of inflammation. Unlike other forms of edema, their development is due to increased permeability of histohematological barriers. This is due to the numerous inflammatory mediators released by the damaged cells. The main role is played by histamine, serotonin, lysosomal hydrolases, prostaglandins, leukotrienes, adenosinephosphoric acids (ATP, ADP, AMP).
Important role in the development of inflammatory edemaplays an oncotic factor. As a result of damage to cell membranes, an inflammatory fluid (exudate) that contains a significant amount of protein (up to 9%) leaves the blood vessels. The content of proteins in the tissue fluid increases in the first 15-20 minutes after the action of the pathogenic factor, stabilizes during the next 20 minutes, and from 35-40 minutes the second wave of increase in the concentration of proteins in the tissue begins, associated with impaired lymphatic flow and the difficulty of transport of proteins from the source inflammation. Infringement of permeability of vascular walls at an inflammation is connected not only with accumulation of mediators of damage, and also with frustration of nervous regulation of a tone of vessels. With a decrease in the value of the oncotic blood pressure, (and with inflammation it can decrease by 1/3 in the inflammation focus), edema develops, the development of which is associated with the release of fluid from the vessels into tissues in quantities that do not have time to be transported back to the general bloodstream. There is fluid retention in the tissues and edema formation. Dystrophic, necrotic and atrophic processes occur in the focus of inflammation in the tissues, which leads to an increase in the molecular concentration and, according to the law of osmosis, the water goes towards greater osmotic pressure.
Inflammatory edema is limited, their appearance does not depend on the time of day, and they accompany many animal diseases of an infectious and non-contagious origin.
Allergic edema develops insensitized animals in response to repeated exposure to the allergen. Allergic edema is manifested with hyperergic inflammation in the form of urticaria, allergic rash, sharp edema at the site of the allergen injection. The main role in the pathogenesis of allergic edema is attached to the formation of immune complexes, which lead to cell damage (damage), the formation of biologically active substances and as a result of increased blood vessel permeability.
The most common edema of endocrine originare found in animals suffering from hypothyroidism of the thyroid gland. Deficiency of thyroid hormones leads to disruption of protein, fat, carbohydrate, water-salt metabolism. The pathology of glycoprotein metabolism leads to the accumulation in the tissues of mucin - a mucus-like substance that binds water and to the appearance of myxedema - mucous edema.
In the mechanism of development of any kind of edema,there is a violation of the water-electrolyte balance. However, with certain types of edema, the role of the nervous system appears most clearly and directly. such edema is called neurogenic. They arise as a result of the disturbance of the nervous trophism of tissues and vessels, the neural-reflex regulation of water metabolism. The decisive role in the development of edema of neurogenic origin has increased permeability of the vascular wall and a disorder of metabolic processes in tissues with impaired innervation. Swelling of the skin, mucous membranes can be observed with neuralgia, in particular the trigeminal nerve, damage or compression of nerve trunks.
The consequences of edema depend on localization,duration and severity. Very dangerous pulmonary edema, larynx, the accumulation of edematous fluid in the hearth, pleural cavity, in the cavities of the brain. Prolonged accumulation of fluid in tissues disrupts blood circulation, reduces the supply of nutrients to cells, causes them to squeeze, the structure and function of the injured organ and a number of located disrupt, the resistance decreases.
Pulmonary edema leads to asphyxia, edema of the pericardial cavity - to cardiac tamponade, ascites disrupts the function of the abdominal cavity organs.
Sometimes swelling performs a protective function. So, with inflammatory, toxic edema, edematous fluid reduces the concentration of toxic substances in the tissues.
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