Nutritional dystrophy. Dystrophy in cats

Nutritional dystrophy (Dystrophia alimentaris) is a nutritional disorder of the body due to irrational feeding. She is accompanied varying degrees metabolic disorders, development of dystrophic and atrophic processes in parenchymal organs, muscles and other tissues.

Etiology. The main cause of nutritional dystrophy is prolonged underfeeding and underfed of animals, when the energy of the diet does not cover its consumption in the body. Dystrophy is also diagnosed in chronic digestive disorders, lung diseases, etc. Predisposing causes are excessive exploitation of working animals, unreasonable use of highly productive cows.

Pathogenesis. The mechanism of development of dystrophy is complex and not yet fully understood. Initially, malnutrition is compensated by one’s own fats, carbohydrates, and later proteins. Then due to lack nutrients deep, hard-to-reversible processes occur in organs and tissues. Function disorder gastrointestinal tract manifested by hyposecretion, decreased chemistry and absorption of nutrients. With this pathology, proteins, carbohydrates and fats are not completely broken down: for example, proteins break down to the stage of albumosis or peptones, carbohydrates - to dextrins; these products are poorly absorbed by the intestinal epithelium and are thrown out along with fecal matter. Absorbed toxic substances block the reticuloendothelial system, deepening serious condition sick animal. Loss of about 40% of the animal's weight leads to death.

Pathological changes: general exhaustion, bedsores on protruding parts of the body, lack of fat in subcutaneous tissue, omentum, mesentery, atrophy of all muscles, reduction in the volume of parenchymal organs and glands endocrine system. Gelatinous infiltrates are found in the subcutaneous tissue, epicardium, and fatty capsule of the kidneys yellow. In the abdominal and pleural cavities 2-4 l of transudate yellowish color. Atelectasis, lesions and picture of pulmonary edema.

Symptoms IN clinical practice nutritional dystrophy is conventionally divided into three stages. The first stage is characterized by a decrease in the animal’s weight by 15-20%, increased appetite, general lethargy, fatigue. Pulse, breathing, rumination and body temperature are at the lower physiological boundaries. The mucous membranes are anemic with a icteric tint. The elasticity of the skin is reduced, the hair is without shine and tousled, covered, like ash, with desquamated epithelium.

In the second stage, weight loss is 20-30%. Weakness and unsteadiness of gait are noted. Reflexes are reduced. The mucous membranes are anemic, dry, with a bluish tint. Hair is matte and tousled. The heartbeat is slightly increased, the pulse is low, breathing and body temperature are below normal. Secretion and motility of the gastrointestinal tract are reduced, defecation is difficult. With the predominance of putrefactive processes in the small and large intestines, peristalsis increases, diarrhea gives way to constipation.

In the third stage, weight loss reaches 30-40%. Sick animals lie down and cannot get up on their own. There is no appetite, slow peristalsis, dry feces, weakened anal tone. Temperature and breathing decrease. Heart sounds are weakened, pulse is rapid, small wave. Urine of low density, acidic reaction. Skin and tendon reflexes are reduced or absent. Soporous state. Sick animals refuse food and drink. The amount of hemoglobin and red blood cells decreases in all stages of dystrophy; leukopenia, hypoglycemia, hypoproteinemia. The animal's condition is serious and death often occurs.

The course is chronic.

Forecast. When conducting radical treatment In the first and second stages, the prognosis is favorable; in the third stage, death often occurs, as irreversible processes develop in organs and tissues.

Treatment. Diet therapy for animals in the first and second stages of the disease comes down to enriching the body with plastic substances, improving the secretory, chemical and motor functions of the gastrointestinal tract. For this purpose, they organize the supply of yeasted and malted food, sprouted grains, root tubers, especially sugar and semi-sugar beets, hydroponic greens; Root vegetables are used chopped and sprinkled with bran. The animals are provided with clover and alfalfa meal or hay, and in the summer - grass in abundance. Dietary feed is fed 4-5 times a day. IN large quantities give salted, good-quality water with bran. For seriously ill animals (in the third stage of exhaustion), it is advisable to give salted bran mash, oatmeal, rye flour, pulp from root vegetables.

Pharmacotherapy: subcutaneous or intravenous administration glucose for cows 1.5-2 l, for sheep intraperitoneally - liquid No. 3 or B at the rate of 15-20 ml per 1 kg of animal weight. Cardiac drugs are used: caffeine, cordiamine.

Physiotherapy: ultraviolet irradiation. Skin massage, autohemotherapy.

Prevention. Clinical examination, creation and improvement of a biologically complete feed base, veterinary control over the technology of preparation and storage of feed: hay, haylage and silage. Improve animal hygiene.

NUTRITIONAL DYSTROPHY -DYSTROPHIAALIMENTARISA

It is characterized by general exhaustion, metabolic disorders, dystrophic and atrophic processes in parenchymal and other organs.

Etiology. The main cause of wasting is the lack of nutrients in animal diets. Contributing cause emaciation is the overexploitation of working animals.

Pathogenesis. IN The body of starving animals first of all depletes carbohydrate reserves, mainly in the liver. Depletion of the liver with glshogen leads to excitation of its chemoreceptors. Irritation is transmitted to the central nervous system, from there along afferent nervous (mainly sympathetic) pathways to adipose tissue. Under the influence of adrenaline, norepinephrine, as well as glucocorticoids from fat depots (subcutaneous, perinephric fat, omentum), neutral fats and fatty acids. Lipemia promotes increased use of fat by organs and tissues as the main source of energy with overeducation interstitial toxic products - ketone bodies, butyric acid, etc. In addition, the abundance of chylomicrons in the blood leads to fatty infiltration of the liver, turning into fatty degeneration which can result in cirrhosis. Oppression of the most important functions of the body occurs. Thus, dysfunction of the gastrointestinal tract is manifested by hyposecretion, a decrease in the enzymatic processes of digestion and absorption of feed nutrients. As a result, proteins are broken down to the stage of albumosis or peptones, carbohydrates into dextrins, which are poorly absorbed by the intestinal epithelium and are excreted along with feces, which aggravates their deficiency.

Short-term insufficient feeding does not have a significant effect on the reproductive function of females and males. Long-term underfeeding is accompanied by a decrease in the secretion of pituitary gonadotropin, as a result of which in males there is a decrease in testosterone formation and spermatogenesis is suppressed. In females, the reproductive cycle is disrupted, the weight of the uterus decreases, atrophic changes occur in the ovaries, and follicle maturation worsens.

Symptoms. Depending on the weight loss of the animal, nutritional dystrophy is conventionally divided into three stages. The first stage is characterized by a loss of body weight by 15-20%, the second by 20-30% and the third by more than 30%. With a weight loss of up to 40% or more, the death of the animal usually occurs.

In the first stage of clinical symptoms the most characteristic are a decrease in fatness, productivity and performance. It can be considered as pathological condition, completely normalizing after eliminating the causes and providing the animals with a nutritious diet.

In the second and third stages of the disease, morphofunctional changes occur in organs and tissues. Emaciation, mucous membranes are anemic, dry with a bluish tint. The hair is tousled and dull. Sheep have thinning wool and areas of baldness (alopecia) appear. The growth of young animals stops or stops completely. Secretion and motility of the gastrointestinal tract are reduced, defecation is difficult, breathing is slow, body temperature is lowered, and heart sounds are weakened. With a loss of more than 30% of body weight (third stage), animals lose the ability to move, lie down, and cannot get up on their own. Appetite is absent or sharply reduced, peristalsis of the forestomach, stomach and intestines is slow, feces are dry, the tone of the anus is relaxed. Body temperature is low, breathing is slow, heart sounds are weak.

At all stages of the disease, a decrease in blood hemoglobin, the number of red blood cells, white blood cells (leukopenia), sugar (hypoglycemia), and total serum protein (hypoproteinemia) is noted. In the first stage of the disease, ketonemia and ketonuria are established. In the second and third stages of the disease, urine is of low relative density and acidic.

Current andforecast. The course is usually long-lasting. When transferring animals to complete diets and appropriate treatment in the first and second stages of the disease, the outcome is usually favorable. In the third stage, when deep, irreversible processes develop in organs and tissues, the death of the animal often occurs.

Pathomorphological changes. Atrophy and dystrophy of muscles and organs, yellowish gelatinous infiltrate in the subcutaneous tissue, omentum, mesentery, epicardium, and fatty capsule of the kidneys. In the abdominal and pleural cavities there is an accumulation of up to 2-4 liters of yellowish transudate. In the liver there is fatty infiltration and degeneration, cirrhosis is possible, most often atrophic. Amyloid deposition in the kidneys and spleen, development of glomerulonephritis.

Diagnosis. The diagnosis is based on anamnestic data, poor feeding, and characteristic clinical signs.

It is characterized by general exhaustion, metabolic disorders, dystrophic and atrophic processes in parenchymal and other organs.
Etiology. The main cause of wasting is the lack of nutrients in animal diets. A related cause of emaciation is the overexploitation of working animals.
Pathogenesis. In the body of starving animals, carbohydrate reserves are first depleted, mainly in the liver. Depletion of the liver glyc_)gene leads to excitation of its chemoreceptors. Irritation is transmitted to the central nervous system, from there along afferent nervous (mainly sympathetic) pathways to adipose tissue. Under the influence of adrenaline, norepinephrine, as well as glucocorticoids, neutral fats and fatty acids begin to enter the bloodstream in increasing quantities from fat depots (subcutaneous, perirenal fat, omentum). Lipemia promotes increased use of fat by organs and tissues as the main source of energy with excessive formation of interstitial toxic products - ketone bodies, butyric acid, etc. In addition, the abundance of chylomicrons in the blood leads to jaundice infiltration of the liver, which turns into fatty degeneration, which can result in cirrhosis. Oppression is coming essential functions body. Thus, dysfunction of the gastrointestinal tract is manifested by hyposecretion, a decrease in the enzymatic processes of digestion and absorption of feed nutrients. As a result, proteins are broken down to the stage of albumosis or peptones, carbohydrates into dextrins, which are poorly absorbed by the intestinal epithelium and are excreted along with feces, which aggravates their deficiency.
Short-term underfeeding does not have a significant effect on reproductive function females and males. Long-term underfeeding is accompanied by a decrease in the secretion of pituitary gonadotropin, as a result of which in males there is a decrease in testosterone formation and spermatogenesis is suppressed. In females, the reproductive cycle is disrupted, the weight of the uterus decreases, and atrophic changes in the ovaries, follicle maturation worsens.
Symptoms Depending on the weight loss of the animal, nutritional dystrophy is conventionally divided into three stages. The first stage is characterized by a loss of body weight by 15-20%, the second by 20-30% and the third by more than 30%. With a weight loss of up to 40% or more, the death of the animal usually occurs.
In the first stage, the most characteristic clinical symptoms are a decrease in fatness, productivity and performance. It can be considered as a pathological condition that is completely normalized after eliminating the causes and providing the animals with a nutritious diet.
In the second and third stages of the disease, morphofunctional changes occur in organs and tissues. Emaciation, mucous membranes are anemic, dry with a bluish tint (Fig. 144), the hair is tousled and dull. Sheep have thinning wool and areas of baldness (alopecia) appear. The growth of young animals stops or stops completely. Secretion and motility of the gastrointestinal tract are reduced, defecation is difficult, breathing is slow, body temperature is lowered, and heart sounds are weakened. With a loss of more than 30% of body weight (third stage), animals lose the ability to move, lie down, and cannot get up on their own. Appetite is absent or sharply reduced, peristalsis of the forestomach, stomach and intestines is slow, feces are dry, the tone of the anus is relaxed. Body temperature is low, breathing is slow, heart sounds are weak.
At all stages of the disease, a decrease in blood hemoglobin, the number of red blood cells, white blood cells (leukopenia), sugar (hypoglycemia), total protein blood serum (hypoproteinemia). In the first stage of the disease, ketonemia and ketonuria are established. In the second and third stages of the disease, urine is of low relative density and acidic.
Course and prognosis. The course is usually long-lasting. When transferring animals to complete diets and carrying out appropriate treatment in the first and

In the second stage of the disease, the outcome is usually favorable. In the third stage, when deep, irreversible processes develop in organs and tissues, the death of the animal often occurs.
Pathomorphological changes. Atrophy and dystrophy of muscles and organs, yellowish gelatinous infiltrate in the subcutaneous tissue, omentum, mesentery, epicardium, and fatty capsule of the kidneys. In the abdominal and pleural cavities there is an accumulation of up to 2-4 liters of yellowish transudate. In the liver there is fatty infiltration and degeneration, cirrhosis is possible, most often atrophic. Amyloid deposition in the kidneys and spleen, development of glomerulonephritis.
Diagnosis. The diagnosis is based on anamnestic data, poor feeding, characteristic clinical signs.
Treatment. Aimed at the gradual restoration of the most important vital functions body, normalization of metabolism, nutrition and productivity. Horses, cattle, sheep and other herbivores are given legume, legume-cereal hay good quality, oats, barley turf, compound feed, cake, meal, green feed, potatoes, carrots, beets, milk (for young animals); for pigs - mash of boiled potatoes, bran, grain dirt, mixed feed, grass flour, skim milk, combined silage, green feed; carnivores - meat, liver, fish, cottage cheese, meat soups, porridges. Some of the animal feed is given in malted or yeasted form, the grain is sprouted, and the root crops are crushed. Prescribe fresh fish oil, ABC, PABC. To restore motility of the gastrointestinal tract, increase its secretory function Carlsbad salt is given, small doses of magnesium sulfate or sodium sulfate (70-80 g), bitterness are prescribed. Hydrolysine L-103, amino-peptide-2 and other protein preparations are administered parenterally. Glucose is prescribed intravenously or subcutaneously at a dose of 0.3-0.5 g per 1 kg of animal weight in the form of 5-20% solutions. Injected orally or intramuscularly vitamin preparations.
Prevention. When animal fatness decreases, the rate of energy and protein nutrition is increased by 10-15% until it is restored. If there is a shortage of feed, use nitrogen-containing non-protein products, feed yeast, twig feed, processed wood waste, by-products leather industry, animal fat, sunflower processing waste, grass meal, algae and other non-traditional feed.

CLASSIFICATION OF DYSTROPHIES. .

It is associated with the type of metabolic disorder, and in addition, with the localization, prevalence of morphological changes and the influence of genetic factors (see diagram). Depending on the type of metabolic disorder, protein, fat, carbohydrate and mineral dystrophies are distinguished. Considering that metabolic processes are closely interconnected and represent a single whole, dystrophies in different diseases are of a mixed nature.

by origin

acquired
hereditary

by pathogenesis

decomposition
infiltration
transformational
altered synthesis

by prevalence

by type of metabolic disorder
1. protein
  1. cellular (parenchymal) dysproteinoses
    1. grainy
      healine drip
      hydrolytic

DYSTROPHY PATHOGENESIS MACRO AND MICRO CHANGES

Damage, or alteration, is called changes in the structural organization of cells, intercellular substance, tissues and organs, which are accompanied by disruption of their vital functions.

Damage is caused by a wide variety of causes of exogenous or endogenous origin. The type and degree of damage depend on the nature and strength of the pathogenic factor, the duration and frequency of its exposure, the structural and functional characteristics of the organ or tissue and the reactive state of the body. According to the mechanism of action of an aggressive stimulus on cellular and tissue structures, direct and indirect (through reflex, humoral and immunopathological influences) damage are distinguished. Damage in the phase of initial changes is usually reversible, i.e., when the cause of its occurrence is eliminated, the damaged organs and tissues are restored. Damage during the phase of profound changes becomes irreversible, i.e., it can lead to the death of cells and tissues or the organism as a whole. The main types of damage to cells, intercellular substance, tissues and organs are atrophy, dystrophy and necrosis.

DYSTROPHY

Dystrophy - qualitative changes chemical composition, physical and chemical properties and morphological type cells and tissues of the body associated with metabolic disorders. Changes in metabolism and cell structure, reflecting the adaptive variability of the organism, are not related to dystrophic processes.

Etiology. Disruption of metabolic processes, leading to structural changes in tissues, is observed under the influence of many external and internal factors. Pathogenic factors act on organs and tissues either directly or reflexively through the neurohumoral system, which regulates metabolic processes. The nature of dystrophic processes depends on the strength, duration and frequency of exposure to a particular pathogenic stimulus on the body, as well as the reactive state of the body and the type of damaged tissue. Essentially, dystrophic changes are noted in all diseases, but in some cases they arise primarily and determine the nature of the disease, and in others they represent a nonspecific or secondary pathological process accompanying the disease.

Pathogenesis. The basis of any dystrophic process is a violation of enzymatic reactions (enzymopathy) in metabolism with damage to the structure and functions of the cellular tissue systems of the body. At the same time, metabolic products accumulate in the tissues, physiological regeneration and the functions of one or another organ, as well as the vital functions of the body as a whole, are disrupted.

Mechanismdevelop I and the essence of changes in different dystrophies are not the same. According to the mechanism of the process of dystrophic changes, they distinguish: decomposition; infiltration; transformation and altered, or perverted, synthesis.

Decomposition- changes in ultrastructures, macromolecules and complex (protein-fat-carbon-water and mineral) compounds of cellular and tissue systems. As a result of changes in the basic parameters of cell-tissue systems, complex biological compounds are modified and disintegrated into simpler compounds. Free proteins are hydrolyzed with the participation of lysosome enzymes or denatured. In this case, along with primary damage to ultrastructures, secondary processes may occur (for example, the formation of complex compounds such as amyloid, hyaline, etc.).

Pathological infiltration characterized by the deposition and accumulation in cells and tissues of metabolic products and substances carried through the blood and lymph flow.

Transformation(from Latin transformatio - transformation) - the process of chemical transformation of compounds into others, for example fats and carbohydrates into proteins or proteins and carbohydrates into fats, increased synthesis of glycogen from glucose, etc., with excessive accumulation of newly formed compounds.

Changed synthesis of any compounds is expressed in increased or decreased formation of them with accumulation or depletion and loss in tissues. Pathological synthesis is possible with the appearance and accumulation in tissues of compounds that are not characteristic of them under normal metabolic conditions

These pathogenetic mechanisms of dystrophies can appear simultaneously or sequentially as the process develops.

In morphologicalrespect Dystrophies manifest themselves in a violation of the structure of ultrastructures of cells and tissues. IN physiological conditions the restructuring of cell organelles and intercellular substance is combined with the processes of their restoration, and in dystrophies, regeneration at the molecular and ultrastructural levels is disrupted. In many dystrophies, inclusions, grains, drops or crystals of various chemical natures are found in cells and tissues, which under normal conditions do not occur or their number increases compared to the norm. In other cases, on the contrary, in cells and tissues the amount of their inherent compounds decreases until they disappear completely. In both cases, cells and tissues lose their characteristic fine structure, and in severe cases, discomposition of cellular elements is observed (for example, the beam structure of the liver is disrupted).

Macroscopicchanges. With dystrophies, the color, size, shape, consistency and pattern of organs change. The change in the appearance of the organ served as the basis for calling this process degeneration, or degeneration - a term that does not reflect the essence of dystrophic changes.

Functionalmeaningdystrophies. It consists of a violation of the basic functions of the organ. After eliminating the cause that caused the development of the dystrophic process, metabolism in cells, tissues and the whole organism, as a rule, is normalized, as a result of which the organ acquires functional usefulness and normal appearance. However, severe dystrophic changes are irreversible, that is, the growing disproportion between the increased disintegration of one’s own structures and insufficient restoration ends in their necrosis.

MINERAL DYSTROPHY - FORMATION OF CONCREMENTS

type of calculus stones

salt disturbance (reduction of Ca salts; deposition of Ca salts (dystrophic calcification; metastatic calcification; metabolic calcification))

macronutrientsmicroelementYoumicroelements.

In cells and tissues, calcium is detected when its salts precipitate from complex compounds in mitochondria and lysosomes (parenchymal dystrophies) or in the ground or fibrillar substance of connective tissue (mesenchymal and mixed dystrophies). Calcium deposits in the mitochondrial matrix are found in the form of small and very dense granules. When exposed to any strong acid, calcium carbonate dissolves, releasing gas. When reacting with sulfuric acid, gypsum crystals are obtained. If calcium metabolism is disturbed, the amount of its salts in tissues can be reduced, increased, or they fall out in unusual places.

Formation of stones). Stones are dense or hard formations that lie freely in the natural cavities of organs and excretory ducts of glands. They arise from organic matter of protein origin and salts of various compositions, which fall from the secretions and excreta of the abdominal organs.

The composition, size, shape, consistency and color of stones depend on the conditions and place of their formation. In farm animals, stones are most often found in the gastrointestinal tract, kidneys and urinary tract, gallbladder and bile ducts, pancreas and salivary glands, less often in other organs.

Gastrointestinal stones They are divided into true, false, phytobezoars, pilobesoars, conglobates and plumoconcretions.

True stones, or enteroliths, consist mainly (up to 90%) of ammonia-magnesium phosphate, calcium phosphate and other salts. They are spherical or irregular in shape, have a hard consistency and resemble cobblestones. Their surface is rough, smooth, sometimes polished (faceted) as a result of the tight fit of the stones. The color of freshly removed stones is dark brown, and after the surface layer has dried, it is grayish-white. A characteristic feature of enterolites is the layered structure of the cut surface (Fig. 16); on the fault there is radial radiance, which indicates the staged nature of their growth. In the center of the stone there may be a foreign body (a piece of metal, brick, felt, bone, etc.), which served as the basis for crystallization. These stones are primarily found in the large intestine of horses. Their size varies from a pea to 20-30 cm in diameter, weight - up to 11 kg. Up to tens and hundreds of small stones are found, large stones are usually single.

False stones, or pseudoenteroliths, have a round shape, consist mainly of organic matter, but contain small amounts of mineral salts. They are most often found in the colon of horses, as well as in the proventriculus and intestines of ruminants. Formed by eating food mixed with soil and sand. Their surface resembles peeled walnut(Fig. 17), diameter from 1-2 to 20 cm or more, weight up to 1 kg (sometimes more), quantity - from one to several dozen.

Phytoconcrete(from Latin phyton - plant) are formed from rasgel fibers. They are light, spherical or irregular in shape, their surface is smooth or rough-lumpy, and the consistency is loose. Easily broken. There are single and multiple. They are more common in ruminants in the forestomach.

Saw Concrete or hair balls, bezoars, found in the stomach and intestines of large and small cattle. Animals, especially young animals, with a lack of salts in the diet and a violation of mineral metabolism, lick their coats and each other (licker), swallow wool, which becomes enveloped in mucus and falls off to form balls.

Conglobats- stones from undigested food particles and stuck together feces with an admixture of foreign bodies (rag, earth, etc.). Most often found in horses in the large intestine with atony. Dogs and cats sometimes have feather growths.

Urine stones found in cattle, horses, fur-bearing animals (mink, etc.), including at a young age. Their formation in the renal tubules, pelvis and bladder is associated with urolithiasis, which occurs with excessive feeding of mineral salts, general violation mineral and protein metabolism, as well as with a lack of vitamins, especially A. In birds, their appearance in the kidneys is associated with gout due to a violation of nucleoprotein metabolism. The structure, shape, size and color of stones depend on the chemical composition and type of animal. They consist of uric acid, urates, oxalates, carbonates, phosphates, cystine and xanthium. Therefore, according to their composition, stones are distinguished between urate, phosphate, oxalate, calcareous and mixed. Often the stones have the form of casts, repeating the shape of the cavities (renal pelvis). There are single and multiple stones. The surface of the stones is usually smooth, granular or prickly; the cut pattern can be layered.

Salts can also fall out in the form of sand (urosedimenta).

Gallstones found in the gall bladder and bile ducts of cattle and pigs when gallstone disease. They are single and multiple. Their size varies from a few millimeters to 10 cm or more. A stone the size of a goose egg was found in a pig after fattening. The shape of the stones copies the cavity in which they are formed. Their composition: organic protein base, calcium salts, bile pigments and cholesterol. Depending on the composition, calcareous, pigment and mixed stones are distinguished. Cholesterol stones are practically never encountered.

Salivary stones (sialols) more often observed in horses in the excretory duct salivary gland. In ruminants, it is found in the pancreatic duct. Sometimes a foreign body is found in the center: oatmeal, straw, etc. The mineral base is calcium salts. Therefore, they are usually white and dense. Their size and number vary.

The functional significance and outcome of stone formation are different. Many stones have no clinical significance and are discovered only incidentally during sectioning. However, the formation of stones, especially enteroliths, can have significant consequences. Stones cause tissue atrophy, inflammation of the cavitary organs, necrosis of the walls of cavities, their perforation with the formation of penetrating ulcers, fistulas, as well as blockage of the excretory ducts, which prevents the movement of contents. In the latter case, due to irritation of nerve receptors, spastic contractions of the ducts with painful attacks (colic) are noted. Due to the pressure of the stone on the tissue when the intestines are blocked, the intestinal wall becomes dead and on this basis intoxication of the body develops with a fatal outcome.

MINERAL DYSTROPHY - DEPOSITION OF CA SALT

Dystrophy (from the Greek dys - disorder, trophe - nutrition) - qualitative changes in the chemical composition, physicochemical properties and morphological appearance of cells and tissues of the body associated with metabolic disorders. Changes in metabolism and cell structure, reflecting the adaptive variability of the organism, are not related to dystrophic processes.

mineral

type of calculus stones
salt violation
1. reduction of Ca salts
  deposition of Ca salts
  1. dystrophic calcification
    metastatic calcification
    metabolic calcification

Minerals, entering the body with food and water, play an important role in metabolism. Some of them are found in the body in significant quantities and are called macronutrients(sodium, potassium, calcium, magnesium, phosphorus, chlorine, sulfur, iron), others are present in tissues in small quantities - microelementYou(cobalt, copper, manganese, zinc, molybdenum, boron, iodine, bromine, etc.) or in very small quantities - microelements.

Morphologically, calcium metabolism is the most studied. Calcium salts entering the body are adsorbed in the small intestine, absorbed with the participation of vitamin D and enter all tissues and cells. Calcium is found in complexes with proteins in the blood (10-12 mg%), tissue fluid, cells, and also in milk (caseinates). 97% of it is included in the skeleton in the form of phosphoric acids, carbon dioxide (80% Cas(P04>

In cells and tissues, calcium is detected when its salts precipitate from complex compounds in mitochondria and lysosomes (parenchymal dystrophies) or in the ground or fibrillar substance of connective tissue (mesenchymal and mixed dystrophies). Calcium deposits in the mitochondrial matrix are found in the form of small and very dense granules. When exposed to any strong acid, calcium carbonate dissolves, releasing gas. When reacting with sulfuric acid, gypsum crystals are obtained. Calcium reduces metallic silver as a black precipitate in the Coss reaction with silver nitrate. Hematoxylin turns the precipitated calcium salts dark blue. If calcium metabolism is disturbed, the amount of its salts in tissues can be reduced, increased, or they fall out in unusual places.

Deposition of calcium salts on cells and tissues. This process is calledcalcification! orpetrification. Depending on the origin and mechanism of development, metastatic, dystrophic and metabolic calcification is distinguished.

Metastatic calcification, or calcareous metastases, occur with a general disturbance in the metabolism of calcium salts in the body with the development of hypercalcemia. The latter occurs with the destruction of bone tissue, with damage to the glands that secrete calcium salts from the body, with hypervitaminosis D and hyperparathyroidism. In this case, ionized calcium in increased concentration is not retained in solution, interacts with acids and precipitates in the form of salts in various organs and tissues (systemic calcification). Given the special nature of the exchange, they most often fall out in the kidneys, lungs, myocardium, in the gastric mucosa and in the walls of arteries. These glandular organs secrete acidic products (which causes them to become alkalized) and have less ability to hold these salts in solution. Salts precipitate in the stroma of organs, in cells and in the secretions of glands. The precipitation of calcium salts in the walls of the arteries is due to the fact that the tissue itself is in close contact with blood, which is poor in CO2.

Most often, calcification is observed in the elastic membrane of the vessels of the spleen, liver and heart. In the lungs, calcium salts are found in the alveolar walls; in the kidneys - in the walls of the interlobular arteries, the basement membrane of the convoluted tubules, the epithelial cells of the collecting ducts and the connective tissue base; in the gastric mucosa; in interglandular tissue; in the basement membrane; in the walls of blood vessels and in the elastic fibers of the muscle layer.

Dystrophic calcification occurs as a result of local metabolic disorders in organs with reduced vital activity, in dystrophic and atrophic tissues and necrotic foci.

Due to physicochemical changes in the environment, ionized calcium interacts with protein phosphate groups, which are cleaved off under the action of phosphatases, to form calcium phosphate.

Metabolic calcification(lime gout, calcification) can in some cases be systemic with the deposition of salts in the skin, tendons, fascia and aponeuroses, muscles, nerves, blood vessels and other tissues. In other cases, it manifests itself as a local process with the deposition of salts in the skin of the fingers. Unlike metastatic calcification, it is not associated with hypercalcemia, but develops at normal salt concentrations based on the special nature of metabolism, instability of buffer and colloid systems of blood and tissue, as well as the special condition of tissues in this area with their increased sensitivity to calcium (calciphylaxis ). The appearance of tissues and organs with slight deposition of calcium salts may remain unchanged. They are detected only by histological or electron microscopic examination. With increased accumulation of calcium salts in tissues, the appearance of whitish specks in the organ is observed macroscopically, which are felt in the form of grains of sand and crunch under the knife. With a large deposit of salts, the organ acquires a hard consistency and is difficult to cut with a knife or not cut at all.

The functional significance of calcium dystrophies is different. A lack of calcium salts in the body causes such functional and structural disorders that only in the initial stage can be reversible, and subsequently lead to functional failure of the organ and death. Deposits of calcium salts in the vessel wall, cardiac muscle and heart valves cause significant functional changes that are life-threatening. Vessels lose elasticity, become brittle, and prone to rupture. At the same time, calcification of dead caseous masses in tuberculosis stops the infectious process and indicates healing, although incomplete.

The outcome of calcium deposition in tissues. It has been proven that calcium salts can be absorbed from foci of calcification. Their resorption can occur enzymatically (halisteresis) or with the participation of phagocytes (lacunar resorption). At the same time, clusters of histiocytes and lymphocytes form around the calcified lesion, and in some cases giant cells such as osteoclasts appear, partially resolving lime, for example, in calcified tuberculosis lesions (N. A. Naletov, 1949). However, reversal of pathological calcium deposits is rarely observed. Calcified tissues usually retain calcium salts persistently. Often petrified tissue is encapsulated, and the calcification of dead masses does not significantly affect the functions of the organs.

MINERAL DYSTROPHY - REDUCTION OF CA SALT

mineral

type of calculus stones
salt violation
1. reduction of Ca salts
  deposition of Ca salts
  1. dystrophic calcification
    metastatic calcification
    metabolic calcification

In cells and tissues, calcium is detected when its salts precipitate from complex compounds in mitochondria and lysosomes (parenchymal dystrophies) or in the ground or fibrillar substance of connective tissue (mesenchymal and mixed dystrophies). Calcium deposits in the mitochondrial matrix are found in the form of small and very dense granules. When exposed to any strong acid, calcium carbonate dissolves, releasing gas. When reacting with sulfuric acid, gypsum crystals are obtained. Calcium reduces metallic silver as a black precipitate in the Coss reaction with silver nitrate. Hematoxylin turns the precipitated calcium salts dark blue. If calcium metabolism is disturbed, the amount of its salts in tissues can be reduced, increased, or they fall out in unusual places.