Treatment and prevention of fatty liver disease in piglets using Hepatovex

TOXIC LIVER DYSTROPHY IN PIGLETS -DISTROPHIA HEPATIS TOXICA PORCELLORUM

The disease is characterized by degenerative and necrotic changes in the liver, manifested by its functional insufficiency, intoxication of the body and metabolic disorders. Suckling piglets and weaners are susceptible.

Etiology. The disease occurs when there is a deficiency of selenium in feed, which is associated with its deficiency in soil and water. It can also develop with long-term feeding of pregnant sows with rancid fats and other poor-quality feeds. One of the contributing factors of the disease is the deficiency in the diet of vitamin E, sulfur-containing amino acids. Bad hygiene conditions content, the action of various stress factors significantly weaken the body and predispose to disease.

Pathogenesis. The development of the disease is associated with insufficient formation of phospholipids in the body of piglets due to a deficiency of antioxidants, in particular selenium and tocopherol (vitamin E) in feed. This leads to an increase in lipolytic processes that contribute to the release of fat from the depot into the general circulation, and then to the transition to the liver cells, which leads to fatty degeneration of the liver, and subsequently to necrobiosis of the liver cells. Functions of a liver, and especially antitoxic, are broken. This condition contributes to an imbalance of metabolism throughout the body, a disorder of other functions occurs in the patient, and especially the digestive, central nervous system and cardiovascular.

Symptoms. The disease in an acute form often occurs in suckers with signs of lethargy, loss of appetite, often a slight increase in temperature, muscle tremors, and unsteadiness of the backside. In patients, the pulse and respiration become more frequent, at times there are convulsions, soreness of the abdominal walls, liver, and an increase in its boundaries. The disease lasts up to 3-6 days, and if timely measures are not taken, it often ends in death. The subacute course of the disease continues 8-10 days. Both suckling piglets and weaned piglets get sick. They gradually develop general depression, weakness, loss of appetite, staggering gait. Often the disease is accompanied by yellowness of the mucous membranes and skin, swelling of the skin around the eyes and on the lower abdominal wall. In the area of ​​the liver - soreness, its posterior border is enlarged, body temperature, as a rule, is not increased.

The chronic form of the disease is characterized by a mild manifestation of clinical signs. The disease often develops in weaned piglets and is manifested by a weakening vitality. In sick piglets, fatness decreases, weakness develops, sometimes a shaky gait, convulsive twitches

individual groups muscles. In some cases, yellowness of the mucous membranes and skin is noted. The amount of bilirubin in the blood can rise up to 10 mg%. Anemia often develops, which usually occurs in the presence of hemorrhagic diathesis, hemolysis of red blood cells due to intoxication of the body. Sick piglets gradually turn into slugs, other diseases join, which often leads to death of young animals.

pathological changes. Characteristic of this disease is an enlarged liver, which has a variegated color from yellow, clay-gray to brown-cherry. Its consistency is flabby, the parenchyma is easily torn, the cut surface is dull. In a chronic course, the liver tissue becomes hard, brittle. Yellowness of the subcutaneous tissue and internal organs is pronounced. Histological examination reveals fatty degeneration of liver cells and their necrosis. Diagnosis. When setting it up, it is important to take into account the results of the analysis of feed, conditions of detention, symptoms, lab tests blood, pathoanatomical changes and well-being of farms for this disease.

Treatment and prevention. For treatment, sodium selenite is used at a dose of 0.1-0.2 mg (0.1-0.2 ml of a 0.1% solution) per 1 kg of body weight once every 20 days by subcutaneous or intramuscular injection. The meat may be suitable if the gilts are compulsorily slaughtered no earlier than 45 days after the last injection of sodium selenite. Used to treat tocopherol acetate, which reduces the need for selenium, as well as methionine and other therapeutic agents, depending on the symptoms of the disease.

For the prevention of disease, it is important to create favorable conditions feeding and maintenance of breeding stock and young. The minimum physiological requirement of pigs for selenium is 0.111-0.103 mg/kg dry matter of feed. If necessary, in order to prevent the disease, sodium selenite is used for 7-10-day-old piglets, one injection at a dose of 0.15 mg/kg. The effectiveness of the fight against toxic liver dystrophy in piglets is directly dependent on organizational, economic and veterinary and sanitary measures, and especially in biogeochemical provinces that are unfavorable for this disease.

DISEASES OF OLDER AGE (POSTNATAL DISEASES)

PERIODIC TYMPANIA RUMEN V CALVES -TYMPANIA PERIODICA RUMENiS VITULORUM

A frequently recurring disease in the same animal aged 20-60 days and older, characterized by swelling of the scar and deterioration of the general condition of the body.

Etiology. The cause of the disease is the impact of stress factors caused by violations in the feeding and maintenance of young animals. This includes a rough transition to dairy-free feeding and giving unusual food, hypothermia of the animal, feeding spoiled feed: frozen potatoes, beets, rotten and moldy feed, caked grass, low-quality stillage, brewer's grains, too much liquid feed, overfeeding with beets, potatoes and others. easy-bearing feed. Periodic morbidity contributes to the unsuitability of the functions of the proventriculus in the early period of life of calves to the assimilation of succulent and other types of feed. Predispose to the disease lack of exercise, unsanitary conditions.

Pathogenesis. The mechanism of the development of the disease is associated with a weakening of the motor function of the proventriculus and a violation of the regurgitation of gases resulting from enhanced fermentation processes in the rumen. The secretory function of the abomasum in this disease is sharply inhibited, which is expressed in a low concentration of free hydrochloric acid, a decrease in total acidity, and a weakening of pepsin activity; gastric juice in patients, the consistency is mucous. The digestive and absorption functions of the intestine are disturbed (B. M. Anokhin).

Stretched by gases, the proventriculus puts pressure on the organs of the chest cavity, impeding the functions of the heart and lungs, resulting in disturbances in the activity of the central nervous system and other organs and tissues.

Symptoms. The characteristic signs of the disease are periodic swelling of the scar and diarrhea, which usually appear 40-60 minutes after feeding. During the initial development, swelling of the scar does not reach a sharp degree and for the most part soon disappears, repeating again after the next feeding.

Gradually, with repeated illness, the swelling of the scar becomes stronger and lasts much longer, disappearing only by the end of the day. Sometimes the meteorism of the scar reaches such a degree that life-threatening phenomena occur - shortness of breath, a sharp weakening of cardiac activity, squeezing the intestines.

The sick calf stretches its neck, its back is hunched over, stops taking food, the region of the left hungry fossa quickly begins to swell, and soon its surface is at or even above the line of the lumbar vertebrae. With percussion of the scar, a tympanic sound is heard. In some cases, test-like mushy masses are felt below the layer of gases, sometimes pain. Hypersensitivity in the region of the abomasum. The general condition is disturbed, which is expressed by the anxiety of the animal, especially at the beginning of the disease, the calf often steps over its hind limbs, as the disease develops, its pulse, breathing become more frequent, there are no movements of the scar, belching, chewing gum. Diarrhea is another significant symptom. At the same time, feces of a liquid, watery consistency are mixed with gas bubbles.

At the beginning of the disease, the act of defecation is accompanied by straining and veins, later defecation occurs without tension, becomes involuntary, the tail, perineum and hocks are usually contaminated stool and with frequent recurrence of the disease are covered with dried crusts of feces.

The corpse of a calf is often emaciated, the volume of the abdomen is sharply increased. The region of the left hungry fossa is swollen. The tail and crotch are stained with feces. Peripheral veins filled with blood. There is a large amount of gases and contents in the rumen. There may be ruptures of the diaphragm and scar.

Diagnosis. Attention is drawn to the conditions of feeding and keeping sick calves, age, characteristic symptoms, their frequency.

Forecast. With the elimination of the causes of the disease and timely treatment, calves usually recover within 3-6 days. In other cases, the disease may recur periodically after 10-20 days or more. Severe bloating, profuse diarrhea, emaciation, lethargy, and lack of appetite are considered severe prognostic signs.

Treatment. For therapeutic purposes, probing and washing the scar with 1-2% sodium bicarbonate solution is indicated. Of the medicines are recommended: ichthyol - 2.0-3.0 ml (diluted with water), carbolene - 5.0-8.0 g, gastric juice - 20.0-40.0 ml, resorcinol in the form of 0.5-1 % solution for 0,5-10,0 ml, tympanol - 0.4-0.5 ml/kg with preliminary dilution of the drug with drinking water in a ratio of 1:10, and if necessary again, but at a dilution of 1:5. Wormwood tincture of 1-3 ml, juniper fruits, as well as various astringents and others are used. disinfectants. Elimination of the causes of the disease is an important factor recovery of sick young.

We studied the effect of oral administration of naftalan on the body of healthy and calf rumen patients with tympani. It was found that under the influence of naftalan at a dose of 0.05 ml/kg, the secretory function of abomasum in clinically healthy calves, both on an empty stomach and during feeding, is enhanced. Juice secretion increases, the concentration of free hydrochloric acid and total acidity increase. The activity of pepsin increases. The introduction of naftalan against the background of feeding at a dose of 0.3 ml/kg also leads to an increase in gastric secretion and its motor function. However, under the influence of the drug at a dose of 1 ml/kg, inhibition of the functions of the stomach and the general condition of the calves is observed. It was also found that naftalan at a dose of 0.3 ml/kg has good medicinal properties in calf rumen tympania. Under the influence of the drug in this dose in sick animals, the motor function of the abomasum increases, gas formation in the proventriculus weakens, belching of accumulated gases occurs or becomes more frequent, which contributes to the recovery of sick calves (B. M. Anokhin).

Prevention. Prevention of the disease is based on the hygiene of feeding and keeping animals, the elimination of stress factors and the increase in natural resistance in young animals.

BEZOARUM DISEASE -MORBUS BEZOARUM

The disease is characterized by the presence in the abomasum of young animals of various sizes of lumps and balls of wool, hair, plant fibers and is manifested by a perversion of appetite, gastroenteritis. The disease develops more often in lambs and less often in calves and usually in the winter-spring period.

Etiologyand pathogenesis. With inadequate or insufficient feeding of lambs in milk period content, a metabolic disorder occurs, and in some cases it is accompanied by a perversion of appetite. Sucker lambs eat wool from ewes in the circumference of the udder, contaminated with urine and feces. Subsequently, they gnaw the wool not only from mothers, but also from other sheep, lambs. Less commonly, the cause is an unsatisfied sucking reflex. The background for the onset of the disease in calves, lambs can be diseases of the breeding stock, manifested by the phenomena of "lizuha".

The ingested wool in the abomasum is not digested and concentrates on curdled milk clots. Gradually, under the influence of the peristaltic movements of the abomasum, the wool falls into spherical bodies or woolen cords, similar to felt. These formations are called pylobezoars. If their formation is based on plant fibers-phytobezoars, the latter often develop in transition period from milk feeding to vegetable feeding. Bezoars of various origins irritate the abomasum mucosa, contributing to the development of gastritis and indigestion. They can close the pyloric opening of the abomasum, causing increased pain syndrome due to an obstruction to the movement of the contents of the stomach into the intestines. It continues to develop a violation of motor and secretory functions, which contributes to the development of enteritis. When analyzing the biochemical composition of blood in a sick young animal, a pathology of mineral-vitamin and protein metabolism is ascertained.

Symptoms. The sick young animals have a perverted appetite, eating wool and other inedible or contaminated objects is noted. Gradual emaciation, pallor of the mucous membranes, dryness of the coat and skin, an increase in general depression. Diarrhea alternates with constipation. When a blockage occurs, the lambs are worried, refuse to suckle. During this period, an increase in body temperature is possible, breathing quickens, becomes shallow, the cardiovascular system cannot cope with the load under these conditions, asphyxia increases, and after a few hours of blockage, patients die.

Less often, bezoars move back into the stomach cavity as a result of activation of the motor function of the abomasum and small intestine.

pathological changes. Most characteristic in the stomach, where bezoars are found spherical or roller-shaped and ranging in size from walnut to the chicken egg. Their consistency is dense, the color is mostly brownish-brown. Strangulated bezoars are usually found in the pyloric part of the abomasum at the entrance to the duodenum. Their number in the stomach is different. Usually the stomach is full of contents, the mucosa of the abomasum and small intestine is reddened, edematous, contains a lot of mucus.

Diagnosis. It is set on the basis of complex studies of the conditions of feeding and maintenance of the breeding stock and young animals, characteristic clinical signs, as well as data from the pathoanatomical picture.

Treatment and prevention. It is necessary to improve the veterinary and sanitary culture on the farm in every possible way, to observe the care of the udder, to organize a balanced feeding of the breeding stock and a sufficient supply of young animals with milk. Train lambs to eat hay and concentrates as early as possible.

For the treatment of young animals, various symptomatic agents are used, depending on the manifestation of the disease. Drugs are used that increase the body's supply of vitamins, minerals, protein, improve digestion and digestibility of feed, and, if necessary, painkillers.

Lick briquettes, polymineral premixes containing salts of cobalt, copper and other trace elements are used as means of prevention and treatment.

GASTROENTEROCOLITIS -GASTROENTEROCOUTIS

This is an inflammatory disease, manifested by damage to the wall of the stomach, intestines, indigestion and a violation of other body functions. According to the nature of the inflammatory process, gastroenterocolitis is divided into catarrhal, hemorrhagic, fibrinous, phlegmonous, ulcerative, and along the course - into acute, subacute and chronic. Along with a non-contagious etiology, the disease is often of an infectious or invasive origin. The disease usually occurs in the post-colossive period of feeding and more often in calves older than 15 days, in piglets - at 30 days of age or in the first days after weaning from sows, in lambs - at the age of 1.5-4.0 months and older. It causes significant economic damage due to loss of weight gain in young animals, in some cases loss of livestock, the cost of caring for and treating sick people, as well as weakening resistance and susceptibility to other diseases.

Etiology. The occurrence of gastroenterocolitis in calves occurs as a result of various stress factors: abrupt change fodder, their poor quality, low or high acidity, the temperature of the milk being drunk, the transportation of young animals in unsatisfactory conditions, prolonged exposure to cold, overheating. Contribute to the disease hypovitaminosis A, dyspepsia, poisoning, transfer in early

age for whole milk substitutes, etc. In pig complexes, the onset of the disease is preceded by feeding feeds with a lack of vitamins A, D, E, C, B, lysine, choline, lecithin, calcium, phosphorus, cobalt or affected by fungi, as well as hypogalactia of sows , a sharp transition of weaned piglets to other types of feed. In lambs, along with the above reasons special place It has autumn period maintenance, and especially in those years when pastures are covered with green young grass after autumn rains, during a period when there are frosts in the mornings and warm days. Alternate freezing and thawing of juicy young grass causes changes in its physico-chemical composition, which can be the cause of the disease. The occurrence of gastroenterocolitis is facilitated by a decrease in the resistance of lambs and sheep due to a cold.

There may also be regional factors. Drinking cold or contaminated water, drinking low-quality milk from mastitis-affected breeding stock, heat air often predispose to disease.

Pathogenesis. Under the influence of one or more given reasons the development of the disease against the background of a weakened resistance of the body And enhancing vital activity in the digestive tract conditionally pathogenic microflora.

In calves with acute catarrhal gastroenteritis, the acid-forming function of the abomasum is most often inhibited, and the juice secretion, on the contrary, increases. An increase in juice secretion is associated with an increase in mucus secretion, which is accompanied by a change in the consistency of gastric juice due to an increase in its viscosity (B. M. Anokhin). The excitability of the neuromuscular apparatus of the stomach and intestines is disturbed, which is expressed by a sharp increase in peristalsis due to the impact of various irritations that occur when using poor-quality food, which is accompanied by a hemodynamic disorder of the digestive apparatus and the development of inflammatory processes in the wall of the stomach and intestines.

With their significant manifestations, mucus secretion into the intestinal cavity increases, its digestive capacity weakens, incomplete decay products are formed, which are usually toxic to the body, favorable conditions are created for the activation of opportunistic microflora, which worsens the course of the disease. The most severe are fibrinous, hemorrhagic and ulcerative gastroenterocolitis, accompanied by the above inflammatory processes and significant severity. general reaction organism.

Symptoms. More often there is a catarrhal form of the disease. Clinically, acute catarrhal gastroenterocolitis with a mild course is characterized by normal or slightly elevated temperature body and fluctuations in the number of pulse beats, respiration within physiological boundaries.

Disturbances from the digestive organs are expressed by a decrease in appetite, increased intestinal motility and frequent release of liquid feces with a small amount of mucus in it. The severe course of the disease in animals is usually manifested by a decrease or lack of appetite, increased intestinal motility, frequent release of liquid, and sometimes sharply fetid feces with mucus. The general condition is depressed, the temperature is often elevated, there are signs of pathology of the cardiovascular system.

Sick young animals move sluggishly, lie more with half-closed eyes and react poorly to environmental stimuli. Often there are signs of hypovitaminosis A or rickets, growth retardation, development, emaciation, the level of albumin in the blood decreases.

In chronic catarrhal gastroenterocolitis, diarrhea alternates with constipation. There is a lot of mucus in the feces, sometimes blood and other impurities.

Intestinal peristalsis may increase, and at times it is weakened. Intestinal noises in different periods of the disease of unequal strength. Appetite is reduced. A decline in strength and significant emaciation develops. The coat is tousled, the shedding is delayed.

In lambs in the second half of summer, against the background of the disease, a secondary disease often develops - bronchopneumonia.

With traumatic ulcerative inflammation of the abomasum in two and four-week-old calves, the appearance of colic-like attacks of the disease is observed. They appear in calves shortly after drinking, while the pulse and respiration are quickened, the body temperature is lowered, and there is a slight tympania of the scar. A prerequisite for the appearance of the disease is the transfer from milk to various feed mixtures and roughage.

Toxic dystrophy of the liver(dystrophy hepatis toxica) – the disease is accompanied by pronounced dystrophic and necrotic processes in the liver. It occurs in all animals, but especially in omnivores and carnivores. Of the farm animals, piglets are the most commonly affected. With the industrial technology of keeping animals, the disease is observed at all times of the year.

Etiology . The disease most often occurs on farms where animals long time receive biologically inferior food and are kept in an unsatisfactory microclimate. The main cause of the disease is feed intoxication. Secondary toxic dystrophy of the liver can be observed with gastroenteritis of various origins.

Predisposing causes of toxic liver dystrophy may be violations in the diet of protein-carbohydrate ratio, lack of vitamins A and E, selenium and cobalt, essential amino acids, especially methionine, and lipotropic factors in feed.

Symptoms. Toxic dystrophy of the liver occurs mainly acutely, less often chronically.

The disease occurs suddenly. The condition of the animal is extremely depressed, rarely excited.

There is an increase in heart rate, respiration, body temperature sometimes rises, and then decreases. In most cases, there are signs of gastroenteritis and mild parenchymal jaundice.

On palpation and percussion, pain is noted in the liver area.

The content of albumins in the blood is reduced, the activity of hepatospecific enzymes is increased - sorbitol dehydrogenase, orginase, alkaline phosphatase, glutamine transpeptidase, alanine aminotransferase, as well as high level bilirubin, liver antigens appear.

In the urine, the content of urobilin, bilirubin increases, protein appears.

At chronic course periodic indigestion is observed, signs of jaundice increase, the content of albumin, fibrinogen, prothrombin decreases in the blood, the level of bilirubin increases, autoantibodies to hepatic antigens appear.

Diagnosis and differential diagnosis. When making a diagnosis, the quality of the feed, the presence of poisonous plants, fungal infection, vitamin content, minerals, protein-carbohydrate ratio in the diet, correct application antimicrobials and anthelmintics, as well as characteristic Clinical signs, pathological changes and laboratory results. Important diagnostic value has a decrease in blood albumin content, an increase in bilirubin, hepatospecific enzymes and the appearance of liver antigens. To clarify the nature of the disease, toxicological examination of feed and bacteriological examination of cadaveric material are decisive.

It is necessary to differentiate toxic hepatodystrophy caused by intoxication from liver damage associated with the disease of young animals with leptospirosis, colienterotoxemia, salmonellosis and dysentery.

Treatment. Eliminate the cause of the disease. In acute cases, the stomach and intestines are washed warm water or 0.01% potassium permanganate solution using a probe. Give cleansing enemas. Oily laxatives are given inside and kept on a starvation diet for 12-24 hours, water is given in plenty. Then sick animals are prescribed dietary feeding, mainly easily digestible carbohydrate feed, milk, skim milk, curdled milk, propionic acidophilus culture 2 times a day for 5-7 days.

At the onset of the disease, intravenous administration of a glucose solution with ascorbic acid, subcutaneously vitamins E and A or trivitamin in the accepted doses, 0.1% aqueous solution of sodium selenite at a dose of 0.1-0.2 mg / kg of body weight, inside choline- chloride and methionine - 30-60 mg/kg of animal weight.

If necessary, in order to suppress conditionally pathogenic microflora, antibiotics, sulfonamides and other antimicrobial drugs are prescribed. After completing the course of antimicrobial therapy, drugs from beneficial microorganisms are used.

Prevention includes monitoring the quality of feed, diet and the usefulness of diets. It is necessary to comply with zoohygienic standards of the microclimate in livestock buildings.

In disease-prone farms, for prophylactic purposes, piglets and calves are injected subcutaneously or intramuscularly with a 0.1% solution of sodium selenite in doses of 0.1-0.2 mg / kg or a complex preparation of selevit, tocopherol, methionine is included in the diet.

Hepatosis -- common name liver diseases characterized by dystrophic changes in the hepatic parenchyma in the absence of pronounced signs of inflammation.

Depending on the etiological factors, their strength and duration of exposure, fatty degeneration - fatty hepatosis, amyloid degeneration - liver amyloidosis and other types of dystrophy may prevail.

Fatty hepatosis (fatty degeneration, liver steatosis) is a disease characterized by the accumulation of triglycerides in hepatocytes and a violation of the basic functions of the liver. There are acute fatty hepatosis (toxic liver dystrophy) and chronic fatty hepatosis, which is much more common than the first. In conditions of livestock intensification, fatty hepatosis is the most common disease in highly productive cows, fattening livestock, including sheep. Pigs, fur-bearing animals, dogs, zoo animals often get sick.

Etiology. Fatty hepatosis is recorded as a primary, and more often as a secondary concomitant disease. The causes of primary hepatosis include feeding poor-quality, spoiled feed. Toxins of pathogenic fungi, protein decay products, rancid fats are especially dangerous for the liver. Hepatosis occurs when animals are fed poor-quality fish, meat and bone meal, fodder yeast, rancid fats, spoiled meat, fish, etc.

Liver dystrophy is caused by lupine alkaloids, potato solanine, gossypol of cotton cake. The possibility of liver damage by nitrates, nitrites, pesticides and other mineral fertilizers, which are contained in food in increased quantities, is not excluded. Cause fatty hepatosis there may be a lack of selenium in feed, as well as a deficiency in the diet of essential acids, trace elements and vitamins. In dogs, the most relevant deficiency in the diet of sulfur-containing amino acids - methionine, cystine, lysine, tryptophan, vitamins A, E, group B, selenium and zinc. Also in dogs common cause fatty liver becomes an introduction to large doses ivomeca or cidectin.

As a concomitant disease, hepatosis develops with obesity, ketosis, diabetes mellitus, poisoning, cachexia and many other diseases, which are based on metabolic disorders and the functions of endocrine organs.

In cats, in addition to obesity and diabetes, anorexia can lead to fatty liver disease, ulcerative colitis and drug therapy (catecholamines, steroids and corticosteroids), pregnancy and lactation. Stress can be one of the contributing factors.

Liver dystrophy is often the result of infectious and parasitic diseases, chronic diseases of the gastrointestinal tract, kidneys, uterus, heart and other organs.

Pathogenesis. Fatty hepatosis develops with intensive synthesis of triglycerides in the liver and the inability of hepatocytes to secrete them into the blood. The main pathogenetic role in this case is played by excessive intake to the liver. fatty acids and toxins. Under the influence of toxic products, the synthesis of the apoprotein protein, which is part of lipoproteins, is inhibited. Lipoproteins are the main transport form of triglycerides. It is in the composition of lipoproteins that triglycerides are secreted by hepatocytes into the blood. The accumulation of fat in the liver parenchyma is accompanied by a violation of its main functions, necrosis and lysis of hepatocytes. Dystrophy, necrosis and autolysis of liver cells leads to disruption of bile formation and biliary excretion, protein-forming, carbohydrate-synthesizing, barrier and other functions of the liver. This is accompanied by indigestion, metabolism, accumulation of toxic metabolic products in the body, etc.

Symptoms. Acute fatty liver develops rapidly, it clinical manifestation characterized by signs of general intoxication and jaundice. Sick dogs are strongly depressed, indifferent to others, body temperature may rise slightly by 0.5-1 ° C, but this level does not last long. Appetite is absent or reduced. The liver is often enlarged, soft, painless. Toxic effects on the brain due to the accumulation of ammonia, amines, phenols and other toxic substances in the body often lead to hepatic coma.

Piglets develop anorexia, numbness, loss of strength; vomiting, diarrhea, general muscle weakness, sometimes convulsions, often scaly or nodular skin rash. In acute hepatosis, animals can die in a very short time or after 1-2 weeks. Mortality reaches 90%.

In cows, acute liver dystrophy appears by the time of calving or during the first 2-4 days after it. The animal refuses to feed, hardly rises, stale, there is a sharp tachycardia, rapid breathing, atony of the proventriculus.

In sheep, symptoms of the disease often begin to appear 2-4 weeks before lambing. The sheep refuses to feed, the pupils are dilated and motionless, the animal moves in a circle, falls to the ground, after a while a coma occurs. The temperature is subnormal, fever is an exception.

In dogs, acute fatty hepatosis is accompanied by depression, parenchymal jaundice, and a decrease or lack of appetite. The temperature at the beginning of the disease can rise by 0.5-1.0? They note flatulence, persistent diarrhea and constipation, sometimes colic, with severe toxicosis - hepatic coma. The liver is enlarged, soft consistency, painless, the spleen is not enlarged.

In cats, the main symptom for a long time remains a sluggish appetite, sometimes the animal completely refuses to feed. The liver is enlarged, jaundice appears on late stage disease in the development of renal failure.

In chronic hepatosis, the symptoms are mild. Observe oppression, general weakness, loss of appetite. The liver is moderately enlarged, with smooth surface, painful on palpation and percussion. Yellowness of the mucous membranes and skin is not manifested or very slight. Body temperature is normal.

In the blood in acute and chronic hepatosis, there is a decrease in glucose (in cows below 2.22 mmol/l), an increase in bilirubin (more than 10.3 µmol/l), cholesterol (more than 3.9 mmol/l). With toxic liver dystrophy, an increase in the activity of AST, ALT, LDH is established. In the case of concomitant hepatosis, note characteristics underlying illness.

Current and forecast. Acute fatty hepatosis is accompanied by severe liver failure and often leads to the death of the animal. In chronic hepatosis, if the causes are eliminated and appropriate treatment is applied, the disease ends in recovery. Acute fatty hepatosis can turn into chronic, and the latter - into cirrhosis of the liver.

pathological changes. In acute fatty hepatosis, the liver is sharply enlarged, yellow or lemon-colored. yellow color, brittle or flabby, the pattern on the cut is smoothed. For chronic fatty hepatosis, an increase in the liver is more often, its edges are rounded, the organ has a motley mosaic pattern (brown-red areas alternate with gray or yellow). The predominance of fatty degeneration gives the liver fat look, clayey or ocher color. In dogs, the liver is often uniformly colored yellow, sometimes orange.

Histological examination reveals dystrophy of hepatocytes, mainly in the central parts of the lobes, observe disorganization in the structure of the liver lobes, the disappearance of their beam structure. With toxic liver dystrophy, necrosis and lysis of hepatocytes and other cells are detected. Cell nuclei reduced in volume irregular shape, located centrally, the protoplasm is filled with drops of fat of various sizes. Interlobular connective tissue without pronounced changes. The spleen is not enlarged.

The diagnosis is made on the basis of anamnesis, clinical signs, blood biochemistry, scatology, urinalysis. Acute fatty liver must be distinguished from acute hepatitis. In acute hepatitis, the spleen is enlarged. And with hepatosis, it is normal. The same sign allows us to confidently differentiate chronic hepatosis from cirrhosis of the liver.

Treatment. Eliminate the causes of the disease. In the diets of ruminants, hay, grass cuttings or flour, oatmeal, barley turd, root crops are introduced, carnivores and omnivores are given reverse, cottage cheese, benign lean meat, fish, oatmeal and other cereals, a bran mash. Rations are supplemented with the introduction of vitamin preparations. Patients with hepatosis dogs and cats are given food rich in L-carnitine, which activates fat metabolism in hepatocytes. Vigosine can be used as a source of L-carnitine and magnesium sulfate.

Lipotropic, vitamin and choleretic drugs. Of the lipotropic agents, choline chloride, methionine, lipoic acid, lipomide, lipostabil forte, Essentiale, Liv-52, vitamin U, etc. are used. Choline chloride and methionine emit methyl groups that prevent fatty infiltration and liver dystrophy. Choline chloride is also part of the lecithin involved in the transport of fats. Assign it inside in doses: cattle and horses 4-10g, pigs - 2-4g, sheep - 0.5-2g, dogs - 0.5-1g. The course of treatment is up to 30 days. Doses of methionine inside are indicated for cattle and horses from 3 to 20 g, for pigs - 2-4 g, for sheep - 0.5-1 g.

Vitamin U (the active form of methionine) is administered orally in doses (mg / kg): piglets - 10, sows - 3-5, cattle - 2-3. An approximate therapeutic and prophylactic daily dose of lipoic acid and lipomide is 0.5-1.0 mg/kg of animal weight. The course of treatment is 30 days. The hepatoprotectors hepabene and carsil, silitarin (legalon) and silybin used in medicine deserve attention.

Bile formation and bile excretion are stimulated by the use of magnesium sulfate orally at a dose of large animals - 50-70 g, pigs - 5-10, sheep - 3-5 g, daily dose should be divided into 2 doses. Cholagol, allochol and others are also prescribed. Allahol dosages: large animals - 30 mg / kg, pigs and sheep - 50, small animals - 70 mg / kg.

Dogs and cats are prescribed sorbents and probiotics. Cats that refuse to eat are force-fed. Corn stigmas and immortelle flowers are used as phytotherapeutic agents.

Prevention. Good quality nutrition. Use in poisoning sorbents. Regular provision of probiotics. Providing animals with the necessary amount of carbohydrates, complete protein, selenium, zinc and other trace elements, water and fat soluble vitamins. In carnivores, avoid food with high content fats.

All toxic drugs are strictly dosed and used together with hepatoprotectors. Carry out preventive measures against infectious and parasitic diseases.

Amyloidosis of the liver is a chronic disease characterized by the deposition in the intercellular tissues of the liver and other organs of a dense protein-saccharide complex - amyloid. Liver amyloidosis usually occurs in combination with the deposition of amyloid in the kidneys, spleen, intestines and other organs. The disease is more common in horses than in large cattle and animals of other species.

Etiology. The disease is often caused by purulent chronic processes in the bones, skin, internal organs (arthritis, osteomyelitis, ulcers, tumors, pleurisy, bronchopneumonia, mastitis, endometritis). Often the disease appears in horses - producers of hyperimmune sera. Cachexia in most cases is accompanied by amyloidosis of the liver, although amyloidosis of the kidneys is not detected.

Pathogenesis. The waste products of microbes, the breakdown of tissue proteins cause metabolic disorders, the deposition of amyloid on the walls of the vessels of the liver, kidneys, spleen, and intestines. In the liver, this process begins in the peripheral parts of the hepatic lobules, then spreads to the entire lobule. Hepatic beams atrophy, continuous homogeneous areas are formed from amyloid masses with compressed intralobular capillaries. Due to impaired blood supply, tissue trophism decreases, hepatocyte dystrophy occurs, and functional liver failure occurs.

Symptoms. The most characteristic signs are pallor of the mucous membranes, emaciation, enlargement of the liver and spleen (hepatosplenomegaly). The liver is dense, painless, accessible parts are even, smooth. The percussion borders of the liver are dilated. The spleen is greatly enlarged and hardened. Jaundice is rare, it is not intense. Digestion is disturbed. Protein is often found in the urine.

pathological changes. The mass of the liver in large animals reaches 23 kg or more, its capsule is tense, the edges are rounded. The color is brown-clay, the pattern on the section is unclear. The spleen is enlarged, dense. Amyloid lesions are often found in the kidneys, intestines, and inflammation in the joints, bones and other tissues.

Diagnosis. Based on the data of anamnesis, liver biopsy, characteristic clinical signs. In the differential diagnosis, other liver diseases are excluded by the absence of symptoms specific to them.

Forecast. The disease can continue for years. The prognosis is unfavorable.

Treatment. treated for the underlying disease. Apply funds.

Normalizing metabolism in the liver (sirepar, prohepar, heptral).

Prevention. Timely elimination of purulent-inflammatory processes in organs and tissues.

Colostrum toxicosis is an acute disease of newborns, characterized by diarrhea and general toxicosis. Calves get sick more often, but it can also occur in young animals of other species.

Etiology and pathogenesis. The main reason for calves is feeding dry and calving cows (heifers) straw, hay, silage, haylage or other feeds affected by toxic fungi (mycotoxicosis). A possible cause is toxicity, which occurs when pesticides and other toxic substances penetrate into the fetus and colostrum. As well as pathogens of mastitis and their toxins.

The pathogenesis of this disease is similar to toxic dyspepsia. The central link in the pathogenesis of colostrum toxicosis is fermentopathy due to inhibition of digestive enzymes by toxins with the subsequent development of toxicosis.

Symptoms. The disease begins after the first drinking of colostrum on the 1st-2nd day after birth. Manifestations of the disease increase rapidly: loss of appetite, indomitable diarrhea, liquid feces, severe depression up to a coma, sunken eyes. Body temperature is within normal limits or below it. Reserve alkalinity is reduced.

Pathological changes are uncharacteristic. The mucous membrane of the abomasum and small intestine swollen with petechial hemorrhages. Liver, kidneys and heart muscle in the stage of protein-fatty degeneration. The spleen is not enlarged.

Diagnosis. Established on the basis of clinical signs, the results of mycological and toxicological studies of feed, colostrum (milk), abomasum contents. It is necessary to differentiate the disease from toxic dyspepsia of a different etiology, bacterial, viral and other diseases.

Current and forecast. The disease is transient. The prognosis is cautious and unfavorable.

Treatment. Calves are prescribed a strict diet using a decoction of flaxseed, rice. Oak bark, oatmeal jelly, yarrow infusion, horse sorrel and other medicinal herbs. Instead of two regular feedings, young animals are fed 0.5 -1% sodium chloride solution or the above decoctions.

The volume of the first portion of colostrum after fasting for a calf does not exceed 0.25 - 0.5 liters, but as it recovers, it is gradually increased. Sick calves are fed 4 times a day. To suppress the secondary microflora, antimicrobials are prescribed orally 2-3 times a day, the course is 3-7 days. Antibiotics are prescribed after determining the sensitivity of pathogenic intestinal microflora to them. Farmazin is used orally at 1 ml / kg 2 times a day, ampioks, oksikan (calves, lambs 8-15 mg / kg, piglets 10-20 mg / kg 2 times a day).

To prevent dysbacteriosis, probiotics are prescribed (vetom, lactobacterin, bifikol). To normalize water-electrolyte metabolism and acid-base balance, a 1% solution of sodium chloride is prescribed orally (calves 2-4 liters per day); subcutaneously, intravenously or intraperitoneally alkaline solution Chappot (equal volumes of 0.9% sodium chloride solution and 1.3% sodium bicarbonate solution, 5% glucose solution), Ringer-Locke solution and other salt mixtures.

To eliminate acidosis, 40-50 ml of a 6-7% solution of sodium bicarbonate is injected subcutaneously, the injection is repeated as it dissolves. To relieve toxicosis, adsorbents are used inside 2-3 times a day: activated carbon, lignin (calves 50-100 g), enterosorbent (0.1 g / kg), polysorb VP (calves 200 mg / kg, piglets - 50-100).

Hemodez is administered intravenously (calves 50-100 ml), polyglucin (calves on the 1st day 10-15 ml/kg, on the 2-3rd day 5-7 ml/kg). To restore enzymatic processes in the gastrointestinal tract, they are prescribed orally 2-3 times: natural gastric juice, trypsin (0.1-0.3 mg / kg), enteroform (0.1-0.15 g / kg), lysozyme or lysosubtilin. Of the means of stimulating therapy, glucose-citrate blood, lactoglobulin, dostim are used. The greatest attention is paid to the use of adsorbents and antitoxic drugs.

TOXIC HEPATITIS (TOXIC LIVER DYSTROPHY)

Hepatitis is an inflammation of the liver, characterized by alterative (dystrophic, necrotic and atrophic) changes in the parenchyma, exudative and proliferative changes in the stroma of the organ, accompanied by a violation of its functions. Inflammation of the liver is diffuse. At the same time, the division of liver diseases into inflammatory and dystrophic is largely arbitrary. It is known that dystrophic processes in the organ occur against the background of an inflammatory reaction, and the course of inflammation is associated with the development of various types of dystrophies in hepatocytes.

From hepatitis in pigs, its autoimmune nosological form was isolated. Such liver lesions according to L.M. Pivovara (1987) arise as a result of sensitization of the body by liver antigens and are characterized by an immune inflammatory process, a recurrent course, the presence of immunocompetent lymphocytes and antihepatic autoimmunoglobulins.

In a number of papers published in last years in the CIS countries and abroad, an experimental viral hepatitis E for piglets. Although susceptibility to this virus in pigs in vivo has not been fully proven, further study of this issue may make some adjustments to the nosology of liver diseases in pigs.

Pathology of the liver among diseases of the digestive system in young animals occupies one of the leading places. This is due to the fact that diseases of the stomach and intestines directly correlate with liver damage, which are recorded on average in 8.3 - 32.5% of young animals, more often in piglets of 2-4 months of age. In this case, up to 50 - 60% of diseased animals die.

Etiology and pathogenesis. The disease has a polyetiological origin. All factors that can cause inflammatory and degenerative lesions in the liver can be divided into two groups: exogenous and endogenous origin. The first group includes poisons of plant, animal and chemical origin, as well as operating beginnings in poor quality food. The second group includes mainly intermediate metabolic products accumulated in the blood and the body. However, it should be noted that this division is conditional. In practice, there is a complex of causes of exogenous and endogenous origin. According to B.V. Usha (1990) often the first causes are exacerbated by the second, and a "vicious" circle is formed.

The greatest danger is the feeding of grain waste to young animals that has been exposed to rain, snow or moisture during the harvesting period. Such feeds are often affected by toxic fungi and toxic liver damage is noted in animals. The same changes in the body are caused by mineral fertilizers that are accumulated in plants in an unused form with their irrational use. In addition, there may be other toxic substances of chemical (pesticides, herbicides, etc.) and vegetable origin (alkaloids, saponins) in feed.

According to many authors, liver damage can occur with prolonged and unsystematic use of tetracycline antibiotics and other antibacterial drugs. So in Germany, a case of salinomycin poisoning of fattening pigs was noted. This antibiotic has been used in Germany since December 1987 as a means of increasing the efficiency of fattening pigs. In some animals under its influence, liver damage was observed, as well as ulceration of the gastric mucosa.

It should be noted that antibiotics are not the only group medicines widely used in veterinary medicine and capable of causing toxic liver dystrophy. These include drugs from the groups of sulfonamides and nitrofurans. All fundamental guidelines on medical hepatology published over the past 15 years include chapters or sections on acute toxic and drug-induced liver damage.

Our observations in recent years on industrial complexes and experimental studies suggest that the development of toxic liver dystrophy in weaned piglets can be caused or provoked by the uncontrolled use of erythromycin, chloramphenicol, norfloxacin, tylosin and sulfadimesin.

Many authors note that toxic dystrophy occurs most often in those farms where pigs are fed biologically defective feed for a long time and kept in an unsatisfactory microclimate. In the works of N.I. Kuznetsova (1995) proved the significance of deficiency in feed of sulfur-containing amino acids (methionine, cystine, choline), folic acid and vitamins A, E, C in the development of toxic liver dystrophy in piglets. The damaging effect on the liver in this case is associated with under-oxidized products formed in the body in large quantities with a lack of the above nutritional factors. The disease is also often recorded in areas characterized by a deficiency in the soils of assimilable forms of selenium.

In studies conducted by I.M. Karput, L.M. Pivovar and A.G. Ulyanov, it is indicated that chronic disorder metabolism, as well as repeated feed intoxication in animals can lead to autoimmune liver damage. In this case, autoantibodies to liver antigens are detected, both in blood serum and colostrum.

In recent years, it has become known that the normal microflora of the gastrointestinal tract takes part in the detoxification of various compounds that enter the body from the outside or are formed in the digestive tract. With gastroenteritis, this process is disrupted, which leads to increased absorption of toxic products into the blood and the development of toxic liver dystrophy.

There is an opinion that a significant load on the liver in the period after calving of cows and farrowing of sows is one of the causes of inflammatory and degenerative liver lesions in offspring.

The pathogenesis of hepatitis can be represented as a process triggered by toxic substances that come with food and are formed in the body in violation of digestion and interstitial metabolism. After absorption into the blood, they enter the liver, where they act on the hepatocyte. Depending on the dose and duration of their intake, various processes occur in the parenchyma of the organ: the activity of oxidative enzymes decreases, the content of glycogen drops sharply, fatty infiltration develops, decay of liver cells is observed, and later liver necrosis. The main differences in pathogenesis come down to a different interpretation of the cause-and-effect relationships leading to the death of the hepatocyte.

According to V.N. Baimatov, first of all, glycogen is consumed in the liver, as it is used in the detoxification process. Accordingly, reserve and compensatory-adaptive mechanisms are mobilized in the body to restore homeostasis. This is, first of all, the activation of the process of gluconeogenesis and ketogenesis. In the blood, the concentration of intermediate products of the main metabolism increases: pyruvic and lactic acids, ketone bodies, amino acids. The accumulation of these products causes a "vicious" cycle. Overexcitation of the sympathetic nervous system leads to an acceleration of gluconeogenesis. The resulting acetone increased amount is a hepatotropic poison, acts on the hepatocyte.

At the same time, fat tends to accumulate in the cytoplasm of liver cells. Fatty degeneration is a compensatory-adaptive reaction of the body to a lack of energy and plastic reserves. However, an increase in ketone bodies as a result of gluconeogenesis can lead to morphological and functional damage to the liver. The development of fatty degeneration of the liver is aggravated by the fact that acidosis develops in the blood due to advanced education pyruvic and lactic acids. Moreover, the activity of fibroblasts in the connective tissue of the liver is stimulated and its intensive growth begins. As a result, the nutrition of hepatocytes worsens. Severe fatty degeneration of the liver develops. With its appearance, the physicochemical relationship between the structural cytoplasmic protein and cellular fat is disrupted, and this leads to necrobiosis, and then necrosis of liver cells.

It is also important that poisons of various origins enter the liver through portal vein and systemic circulation, initially affect capillary endothelium, Kupffer cells and connective tissue cells. Dystrophic changes in the liver cells are a consequence of the inflammatory process of the above cells. Hepatic cells initially swell diffusely, compress and clog the bile ducts. The function of hepatic, endothelial and connective tissue cells weakens, and then they die. At the same time, pigment, protein and carbohydrate metabolism are disturbed.

The described processes especially progress with a deficiency in the diet of methionine, cystine, choline and tocopherol. The absence or deficiency of these lipotropic factors leads to the fact that the newly formed fatty acids are not involved in the synthesis of phospholipids, but are deposited in the liver as part of triglycerides. The deposition of fat in the liver is facilitated by a decrease in the level of its oxidation as a result of a drop in lipolytic activity. There is a quantitative and qualitative change in enzyme systems. In the liver cell itself, an increase in enzymes occurs due to the breakdown and release of enzymes from the lysosomes of the cytoplasm. If hepatocytes were in a state of necrobiosis, then proteolytic enzymes transfer it to a state of necrosis.

Selenium deficiency also plays a fundamental role in the development of toxic dystrophy (hepatitis). Here, profound and versatile disorders of redox processes and cellular respiration acquire significant significance. Violation of redox processes in inflammation of the liver is manifested in violation of all types of metabolism.

In recent years, the leading role in the pathogenesis of acute toxic liver damage is assigned to lipid peroxidation (LPO). So, in the works of L.L. Akhundzhakova points to the intensification of lipid peroxidation in toxic liver damage. At the same time, in hepatocytes, there is a decrease in energy-producing ability, suppression of protein synthesis function and, as a result, an increase in the level of endotoxemia due to the formation of medium molecular weight peptides that have an inhibitory effect on the processes of respiration and oxidative phosphorylation in hepatocyte mitochondria, which, ultimately, can lead to their death.

Ways of pathogenesis can be variable and not fit into the designated framework. It should be taken into account the state of other organs and systems. First of all, the gastrointestinal tract, which is in direct contact with toxic substances that violate its structure and function. Changes in the motor-evacuation, secretory and synthetic functions of the stomach and intestines, in turn, affect the pathogenesis of hepatitis. Taking into account the state of the body, endogenous and exogenous causes acting on the body, a different course of liver diseases is possible.

The organs of the abdominal cavity have topographic relationships with each other through the circulatory, lymphatic and nervous systems, as well as through biologically active substances produced and released by these organs under the coordinating action of the central nervous system. A number of organs have a common blood circulation due to the existing anastomoses. As a result, blood from one organ can enter another. The close relationship of the abdominal cavity organs in ontogenesis often causes their combined pathology in a number of ways.

There is evidence that in the pathology of the liver there are also functional, and then morphological changes in the endocrine system. It has been established that in hepatitis in the adrenal glands, the excretion of ketosteroids is impaired, and the secretion of oxycorticosteroids increases. The inactivation of insulin, thyroxine, and estrogens in the liver is also disrupted, which leads to morphofunctional changes in the endocrine organs that produce these hormones. In the future, the function of the hypothalamic-pituitary-adrenal system may be impaired.

Symptoms. Diagnosis of hepatitis is difficult due to the lack of typical symptoms and the same type of clinical picture of the disease. The manifestations of the disease largely depend on the degree of intoxication of the body. In acute hepatitis, the disease lasts 1-2 days. During this period, lethargy, loss of appetite are noted. Body temperature sometimes rises to 40.5 ° C, then decreases and becomes subnormal. Some animals develop muscle tremors, unsteadiness of the backside, anorexia. In some cases note nervous excitement, circling and convulsions. Palpation and percussion of the liver area is painful. There is vomiting, indigestion, the volume of the abdomen increases. In patients, the pulse and respiration become more frequent, cyanosis of the skin and mucous membranes is noted, then a coma and death occur.

The subacute course of the disease is more common in weaned piglets and nursery calves. At the same time, oppression of animals is clinically noted varying degrees, body temperature rarely rises, there is no appetite, vomiting, constipation, followed by diarrhea. Intestinal flatulence appears, feces are light clay in color. Sometimes the mucous membranes and skin turn yellow. There are violations of cardiac activity. Some animals have tremors.

In the chronic course of the disease, weakness gradually develops, appetite decreases, a shaky gait appears, convulsive contractions of the muscles of the body. In some animals, trophic disorders of the skin are noted - toxicoderma, which is characterized by necrosis of the upper layer of the skin of the ears. Sometimes noticeable yellowness of the skin and mucous membranes, swelling of the subcutaneous tissue and lower abdomen.

All of the above clinical signs are in many ways similar to the symptoms observed in a number of other diseases of the digestive system, so the final diagnosis should be made on the basis of laboratory tests. In sick animals, the concentration of hemoglobin decreases by an average of 15-20%. The number of leukocytes increases with a high degree of certainty by an average of 3540%, in the leukogram, a hyperregenerative shift of the nucleus to the left in the neutrophilic group is noted.

More specific in the diagnosis of hepatitis are biochemical blood tests. They can be divided into the following groups:

^ tests aimed at studying the metabolism of pigments, proteins, carbohydrates, lipids, vitamins and minerals;

^ samples to control the activity of hepatospecific enzymes;

^ trials studying the detoxification function;

> sample analysis of excretory function.

The study of pigment metabolism includes the determination of bilirubin in the blood serum, urobilin in the urine and stercobilin in the feces. According to most researchers, the dynamics of bilirubinemia in animals quite clearly reflects the phase and severity of the disease process. The content of bilirubin in the blood 2-3 times higher than normal is a sign of bilirubinemia (jaundice). Simultaneously with an increase in serum bilirubin, there is an increase in the concentration of urobilin in the urine and strecobilin in the feces.

Violation of protein metabolism in hepatodystrophy is accompanied by hyper- or hypoproteinemia and dysproteinemia. The latter occurs due to an increase in the concentration of y-globulins and a significant decrease in albumin. In order to control disorders of carbohydrate metabolism, the content of glucose in serum is determined and carbohydrate loads are applied using glucose, galactose, sucrose.

Of the disorders of lipid metabolism, lipidemia, hypercholesterolemia, an increase in ketone bodies and non-esterified fatty acids are noted. Of the changes in mineral and vitamin metabolism, the most typical is a decrease in the concentration of fat-soluble vitamins and a violation of calcium and phosphorus metabolism, with the development of hypocalcemia and hypophosphatemia. According to A.P. Kudryavtsev toxic liver dystrophy in piglets is accompanied by an increase in the concentration of iron in the blood. In his opinion, this feature can be used for differential diagnosis.

Hidden liver diseases are accompanied by slight changes in the biochemical state of the blood. Importance in this case, it acquires the definition of enzyme activity, which changes earlier than others biochemical samples. In liver pathology, the activity of aspartate and alanine aminotransferases, cholinesterase, lactate dehydrogenase, alkaline phosphatase, gamma-glutamyl transpeptidase, aldolase, fructose-1-phosphoaldodase, sorbitol dehydrogenase, leuciaminopeptidase, ornithinecarbamoyltransferase, glutamyl dehydrogenase undergoes significant changes.

For the differential diagnosis of liver diseases, the most reliable is the histological examination, which in 100% of cases gives the correct morphological characteristics of the organ. These methods are simple, easy to implement and have little effect on the health and productivity of animals.

Pathological and anatomical changes. They largely depend on the etiological factor. In the early stages of the development of the disease, the liver is slightly enlarged, flabby, sometimes ocher-yellow in color. With necrosis of the parenchyma, flabbiness and wrinkling of the liver are more pronounced, the color is gray-clay or dark red. There are degenerative changes in the heart muscle and kidneys. Swollen, loosened, hyperemic, sometimes with hemorrhages, the mucous membrane of the gastrointestinal tract is covered viscous mucus. Erosions and ulcerations are observed. In addition to the above changes, there is often an increase in the size of the gallbladder and its wall due to the growth of connective tissue.

Treatment. The effectiveness of therapeutic and preventive measures largely depends on the degree of intoxication of the body and the period of the disease. In the case of the development of irreversible changes in the liver, the prognosis is unfavorable, the treatment is long, expensive and ineffective. It is economically more expedient to send such sick animals for forced slaughter.

Therefore, holding medical measures it is necessary to start as early as possible using the methods of etiotropic, pathogenetic and replacement therapy. First of all, it is necessary to eliminate the effect of the etiological factor that caused liver damage. It is also mandatory to improve the conditions of keeping and caring for animals. It is desirable to introduce carbohydrate foods into the diet and limit the use of proteins and fats to optimal values.

Young animals are kept on an 8-12-hour starvation diet without water restrictions. In the acute course of the disease, oily laxatives, such as castor, sunflower, and flaxseed oils, are used internally to remove toxic substances from the gastrointestinal tract at a dose of 40-80 ml / head. Also for this purpose, you can use sodium sulfate (25-50 g) or Karlovy Vary artificial salt (2-5 g). In order to suppress the toxigenic microflora, antibiotics and sulfonamides are prescribed orally in therapeutic doses. In the future, sick animals are fed dietary feed (milk, skim milk, oatmeal jelly, liquid cereals from barley and oatmeal, yogurt). In addition, acidophilic broth culture, propionic-acidophilic broth culture, etc. are prescribed 2 times a day for 4-5 days.

Medical pathogenetic treatment should be aimed at restoring the metabolism in hepatocytes, for which they use glucose, lipotropic drugs, vitamins, as well as agents that stimulate bile secretion. If necessary, prescribe cardiac drugs: camphor oil, sodium caffeine benzoate solution. Of the lipotropic agents, choline chloride, methionine, methylmethionine sulfonium chloride, lipoic acid, lipomide, etc. are used. Of the agents that enhance bile formation and bile secretion, chologon, allochol, corn stigmas, etc. are used.

In the presence of convulsions, seizures are removed by injecting analgin. To increase the output of bile into the duodenum during the period of reducing the inflammatory reaction in the liver, in the chronic course of hepatodystrophy, the use of allochol (pills containing dry bile) or hologon is indicated inside the pigs.

In order to stimulate the detoxification function of the liver, the binding of toxins and their rapid elimination from the body, there are recommendations for the use of 0.037% sodium hypochlorite solution intraperitoneally in piglets, as well as inside with feed of the SV-1 sorbent [S.S. Abramov et al., 2000; E.A. Pankovets et al., 2000]. There is information in the literature about the good therapeutic and prophylactic efficacy of sodium selenite and vitamin E [Sh. M. Abdullaev, 1985; L. F. Vinogradova, T. S. Illarionova et al., 1998]. The disadvantage of selenium preparations is its high toxicity, and vitamin E - its use in the form of oil solutions.

Thus, for the treatment of young animals with diseases of the liver and other digestive organs in the conditions of industrial technology of animal husbandry, the most rational and effective is the use of complex preparations containing lipotropic substances, antioxidants and vitamins. The use of these drugs is also indicated for mass treatment of piglets and calves with antibacterial drugs in order to reduce the negative impact of the latter on the liver.

Prevention. When carrying out preventive measures, measures are taken to prevent the ingress of toxic substances into the body of animals. To this end, it is necessary to constantly monitor the nutritional value of the diet, the sanitary quality of feed, the conditions of keeping both offspring and mothers. The composition of the diet should include, in accordance with existing standards for each age group animals, essential amino acids(lysine, methionine, cystine), as well as an appropriate set of vitamins and minerals. All feeds should be regularly examined for toxicity.

The rationale for taking preventive measures to prevent liver damage in animals can be the results of a biochemical blood test. At the same time, liver damage is evidenced by a decrease in the amount of total protein due to a decrease in the level of albumin, an increase in the concentration of total lipids, cholesterol and bilirubin, an increase in the activity of AST, ALT, GGTP and alkaline phosphatase. It is advisable to carry out such studies regularly as part of medical examinations, which in the conditions of the complex is an integral part of the technological cycle.

When opening the corpses of dead animals or anatomy of the internal organs of the forcedly killed young animals, it is necessary to conduct a pathomorphological assessment of the state of the liver. Its lesions in 20 or more percent of cases in the absence infectious diseases serves as an indicator of the unfavorable condition of the economy in terms of toxic liver damage and requires appropriate veterinary measures.

For this purpose, it is recommended to use a 0.1% solution of sodium selenite for young animals, vitamin preparations, lipotropic agents. To prevent drug-induced liver damage, it is necessary to strictly follow the recommendations for the dosage of drugs and control functional state liver during the treatment of animals. Giving antibacterial drugs together with hepatoprotectors can serve as an effective preventive measure, which significantly reduces the toxicity of the former.

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Toxic dystrophy of the liver

Vveating

The autopsy was performed on October 27, 2014 at 9:20 am under mixed lighting in the sectional hall of the department general pathology them. V.M. Koropova by students Andronova Anastasia Alexandrovna, Borisova Anastasia Andreevna and Filippova Alena Yurievna.

The history of the animal is not known.

The clinical diagnosis is not known.

1. External inspection

I. Identification features

The corpse of a cat, a half-breed British shorthair cat, gray-blue color, aged about 6 years, weighing about 6 kg, correct physique, above average fatness (obesity), castrated.

II. Corpse changes

The corpse is cold, rigor mortis is well expressed in all muscle groups. Cadaverous spots and signs of decay were not found.

III. Special part.

Visible mucous membranes

conjunctiva and mucosa oral cavity without damage, smooth, moderately moist, shiny, gray Pink colour with a yellowish tint.

The mucous membrane of the nasal cavity without damage, gray-pink, moist with bloody discharge (mucous, transparent, red).

Mucous prepuce without damage, smooth, moderately moist, pale pink.

Anus is gaping. The anal area is stained with feces. Visible rectal mucosa without damage, smooth, moderately moist, gray-pink.

Leather and skin derivatives

The integrity of the skin is not broken, the skin is malelastic, dry. The hairline is dull, well kept. On the abdominal wall and in the sternum, the hair is shaved.

Subcutaneous adipose tissue- well developed, a large amount of fatty deposits of a white-pinkish color with a yellowish tint. There is a small hemorrhage in the region of the xiphoid process on the left side (a spot with a diameter of about 3 cm, dark red, does not expire). The same spot is on the abdominal wall on the left side in the region of the last rib with a diameter of about 2.5 cm.

somatic lymph nodes

The left mandibular lymph node is round, white, not enlarged, the cut surface is smooth, juicy, moderately moist.

The right mandibular lymph node is round, pink, blood-filled, slightly enlarged, the cut surface is smooth, juicy, moderately moist.

The left prescapular lymph node is fusiform, white, not enlarged, the cut surface is smooth, juicy, moderately moist.

The right prescapular lymph node is fusiform, pink, blood-filled, slightly enlarged, the cut surface is smooth, juicy, moderately moist.

Inguinal lymph nodes- rounded, pink, filled with blood, enlarged, the cut surface is smooth, juicy, moderately moist.

Skeletal muscles

The muscles are poorly developed, red in color with a yellowish tint, the fibrous pattern is smoothed, the cut surface is moderately moist.

Bones, joints, ligaments

Teeth are white with a grayish tinge and yellow coating are firmly held, integrity is preserved.

Bones without violation of integrity, gray-white color, strong, even.

The joints are mobile, without breaking the integrity. On the section of the hip and shoulder joints: cartilage is smooth, shiny, white, moist, synovium is transparent.

2. Internal inspection

Abdomen

The position of the internal organs is anatomically correct. In the abdominal cavity there is a free clear liquid dark red, about 7 ml in volume (transudate).

The peritoneum is smooth, shiny, even, moist, transparent, with a yellowish tint and abundant fat deposits.

chest cavity

The position of the organs is anatomically correct. In the chest cavity there is a free transparent liquid of red color, with a volume of about 5 ml (transudate).

The costal pleura is even, smooth, shiny, moist, the intercostal blood vessels are dilated and filled with blood.

The integrity of the diaphragm is not broken, the sternum is attached at the level of the 9th rib. Violet-red diaphragm, with dark red hemorrhage on the left side.

pericardial cavity

The pericardium is smooth, shiny, moist, with a small amount of fatty deposits. The pericardial cavity contains a small amount (about 0.5 ml) of a clear reddish fluid.

Language

Gray-pink color, moderately moist, rough, fleshy, integrity is preserved, elasticity is weakly expressed.

Salivary glands

Not enlarged, light beige in color, lobulation clearly expressed, scraping moderately moist.

Pharynx and esophagus

The mucous membrane of the pharynx is smooth, shiny, moderately moist, bluish-red in color, no damage.

The esophagus is empty, collected in folds, which are easily straightened. The mucous membrane of the esophagus is even, smooth, shiny, moderately moist, bluish-red in color, without damage.

Larynx and trachea

The mucosa of the larynx is smooth, shiny, moderately moist, bluish-pink in color, no damage, cartilage intact.

The integrity of the tracheal rings is not broken. The mucosa is dark red, smooth, shiny, moderately moist, without damage. IN lower sections trachea there is a small amount of clear foam with mucus from the lungs.

Bronchi

The bronchi contain mucus and clear, pale pink foam. The mucous membrane is smooth, pale pink.

Heart

Teardrop-shaped heart, slightly enlarged.

The pericardium is transparent, smooth, shiny, moist, with a small amount of fatty deposits, integrity is not broken.

The epicardium is even, smooth, shiny, red-gray in color, in some places there are small areas of a grayish-pink color. coronary vessels heavily bled. The ratio of the walls of the right and left ventricles is 1.5:1.

The myocardium is well developed, flabby, red-gray in color, in some places there are small areas of a grayish-pink color, the fibrous pattern is slightly smoothed.

The integrity of the heart valves is not broken. The cavities of the ventricles and atria without thrombi. There are small blood clots in half of the ventricles.

Aorta and pulmonary artery

Holistic. The surface is even, smooth, moderately moist, dark red. The valves are saved.

Lungs

The lungs are enlarged and uneven in structure. There are areas of crepitus of a pale pink color, as well as dark red, unevenly colored, soft, doughy consistency, crepitus is pronounced along the edges. The edges of the lungs are slightly pointed. There is a lot of bleeding on the surface of the incision.

When pressing on the lungs, a small amount of pink foamy liquid comes out of the bronchi.

Swimming test: all pieces from different areas swim heavily, plunging into the water by more than 2/3.

Bronchial and mediastinal lymph nodes

Rounded, pink, blood-filled, slightly enlarged, the cut surface is smooth, juicy, moderately moist.

Stuffing box

The omentum is smooth, shiny, even, moist, uniformly yellow in color with abundant fatty deposits.

Spleen

Not enlarged, regular shape, dark red color, smooth surface. The capsule is not tense, its integrity is not broken. On the tail of the spleen there is a petechial hemorrhage of a dark cherry color with a diameter of about 1 mm.

On the section moist, juicy, the follicular structure is clearly visible, the scraping is plentiful.

Liver and gallbladder

The liver is of the correct form, smooth, elastic doughy consistency, enlarged, filled with blood, the edges are rounded, the integrity is not broken. The capsule is tense, its integrity is not broken. The liver is colored unevenly - there are areas of red-brown and greenish-brown. On the section - juicy, abundant scraping (a small amount of dark brown gruel), the lobed structure of the liver is smoothed.

The gallbladder is full, greenish-red in color, biliary tract patency is preserved. The mucosa is thickened, smooth, shiny, velvety. Bile is viscous-watery, dark red, with solid particles (sand).

Pancreas

Not enlarged, pale pink, soft, doughy texture.

kidneys

Greatly enlarged (occupying more than half of the abdominal cavity), rounded, smooth surface, the integrity of the capsules is not broken. Left kidney larger, black-red, with bright red spots. The right one is red-blue, with yellow spots.

The capsules of both kidneys are very tense, difficult to separate. Under the capsules - multiple hemorrhages, black-red blood clots. On the section - there is no differentiation of layers, multiple hemorrhages and cysts (cavities) in the entire parenchyma, the kidney parenchyma itself is melted, connective tissue cords are visible, in the cavities there are blood clots, there are no formed renal pelvises.

Bladder

Contains a small amount of urine with blood, mucus and a small amount of fine sand.

The mucosa is uneven, rough, strongly thickened, dark pink in color with black-red multiple ulcerations. The serous membrane is dark red, the vessels are filled with blood. patency urinary tract not broken.

Stomach

There is no food mass in the stomach, there is only a small amount of bile and clear mucus.

The serous membrane of the stomach is gray-pink in color, smooth, the blood vessels are moderately filled with blood.

The mucosa is gray-red in color, thickened, covered with poorly washed off mucus and collected in folds. The folds are hard to straighten out. The cardiac sphincter has several dark red ulcers.

Small intestine

The mesentery is uniformly colored, pale pink, smooth, shiny, with a large amount of fatty deposits, the blood vessels are moderately filled with blood.

The duodenum is bright pink, covered with a large amount of mucus, the wall is slightly swollen, all over the mucosa there are ulcerations of a dark red color. There are no feed masses in the duodenum.

skinny and ileum all over filled with mucous mass, a small amount of mushy digested food. The mucous membrane is pale pink, slightly darker and thicker in places.

Large intestine

The caecum is enlarged, it contains a large amount of food masses with wool. The mucosa is bright pink, swollen, covered with a large amount of mucus.

The colon and rectum throughout contain a large amount of soft digested food with wool and mucus. The mucous membrane is gray-pink, reddish and thickened in places.

Mesenteric lymph nodes

Slightly enlarged, rounded, gray-pink, juicy on the cut, filled with blood.

Brain

Not researched.

Spinal cord

Not researched.

3. Pathological anatomical diagnosis

Toxic dystrophy of the liver; acute serous hemorrhagic cholecystitis and cholestasis

Polycystic kidney disease with atrophy of the parenchyma and hemorrhages under the capsule

Acute hemorrhagic urocystitis and urolithiasis

Acute catarrhal gastroenteritis; stomach and duodenal ulcers

Protein myocardial dystrophy

Pulmonary edema and acute congestive hyperemia

Compensatory focal alveolar emphysema

Conclusion

cadaveric cat autopsy dystrophy

Based on the results of the pathoanatomical study, it should be concluded that the death of the cat “Boni”, which belongs to Ivanova O.Yu., occurred as a result of respiratory arrest, which occurred against the background of severe intoxication of the body caused by toxic liver dystrophy, as well as polycystic kidney disease with parenchyma atrophy and hemorrhages under capsule.

Analysis of diagnostic data

Toxic degeneration of the liver (Dystrophiahepatistoxica) is characterized by severe toxicosis, fatty degeneration and necrosis of liver cells. Suckling piglets, weaners and gilts are predominantly ill.

Etiology

Fatty degeneration is recorded as a primary, and more often as a secondary concomitant disease. The causes of primary hepatosis include feeding poor-quality, spoiled feed. Toxins of pathogenic fungi, protein decay products, rancid fats are especially dangerous for the liver. Also, liver dystrophy is caused by lupine alkaloids, potato solanine, gossypol of cotton cake. The possibility of liver damage by pesticides, nitrates and nitrites, urea and other chemicals is not excluded. The disease is often registered in areas characterized by a deficiency in the soils of assimilable forms of selenium. The cause of toxic liver dystrophy can be a violation of the protein-carbohydrate ratio in the diet and a deficiency in it of cystine, methionine, choline and vit. E. As a concomitant disease, hepatosis develops with obesity, ketosis, diabetes mellitus, cachexia and many other diseases, which are based on metabolic disorders and the function of endocrine organs. Liver dystrophy is often the result of infectious and parasitic diseases, chronic diseases of the gastrointestinal tract, kidneys and other organs.

Pathogenesis

Toxic substances that come with food and are formed in the body when digestion and interstitial metabolism are disturbed, after being absorbed into the blood, enter the liver, where, depending on the dose and duration of their intake, various processes develop: the activity of oxidative enzymes decreases, the glycogen content drops sharply, fatty tissue develops. infiltration, there is a breakdown of hepatocytes, and later - liver necrosis. Suppression of the synthesis of fatty acids in the liver leads to an increase in the formation of triglycerides. Along with this, the formation of lipoproteins in the liver is inhibited - the main transport form triglycerides from liver cells. The intake of hepatotropic poisons inhibits the synthesis of apoprotein - a protein that is part of lipoproteins, the transport of triglycerides is inhibited, so they accumulate in the liver cells. Dystrophy, necrosis, autolysis of hepatocytes lead to impaired bile formation and biliary excretion, protein-forming, carbohydrate-synthesizing, barrier and other functions of the liver.

Clinical signs

In suckling piglets, the disease occurs more often in an acute form and is characterized by signs of arousal, increased heart rate and respiration, and a state of depression. Body temperature in some cases rises to 40.5-40.8C, then decreases and becomes subnormal. Sometimes there is yellowness of the mucous membranes and skin, vomiting, constipation are replaced by diarrhea. Piglets develop anorexia, torpor, generalized muscle weakness, sometimes convulsions, and often a scaly or nodular skin rash. A significant amount of bilirubin enters the blood. Oliguria develops. High specific gravity urine contains urobilin, bilirubin and protein. In heart failure, cyanosis of the skin and mucous membranes is observed. Animals can die in a very short time or after 1-2 weeks. Mortality reaches 90%. In the blood, the content of albumins is reduced, the activity of hepatospecific enzymes sorbitol dehydrogenase, arginase, alkaline phosphatase, glutamine transpeptidase, alanine aminotransferase, as well as a high level of bilirubin are increased, liver antigens appear. In the urine, the content of urobilin, bilirubin increases, protein appears.

Subacute and chronic forms of the disease are more often recorded in weaned piglets and gilts. They are characterized by less pronounced features. Watching the oppressed general state, lack of appetite, sometimes vomiting, diarrhea. Body temperature - within normal limits or lowered. Yellowness of the mucous membranes and skin is not manifested or very slight. In the blood of sick animals with chronic hepatodystrophy, the content of albumin, fibrinogen, prothrombin is sharply reduced, coagulability is reduced, the content of bilirubin is increased, autoantibodies to hepatic antigens are detected. Their titers naturally increase after the exacerbation of the process.

Live morphological study of the obtained methods of puncture biopsy of liver samples reveals a picture of degenerative changes in liver cells. In the tissue, the appearance of vacuoles, and in some cases even necrotic foci, is noted. The vessels are hyperemic with slight lymphoid infiltration. In the hepatic lobules, where necrosis is detected, the beam structure is disturbed, while necrotic cells are in the stage of autolysis. In slightly affected and healthy hepatic lobules, pathological regeneration of hepatocytes is noticeable.

In a cytological study of liver punctates, various dystrophic changes in liver cells, which are detected in stained preparations, are clearly determined. Marked granular, vacuolar, fatty degeneration.

Pathological changes

In acute dystrophy, the liver is sharply enlarged, yellow or lemon-yellow, brittle or flabby, the pattern on the cut is smoothed. For chronic process characteristically more often an increase in the liver, its edges are rounded, the organ has a motley mosaic pattern (brown-red areas alternate with gray or yellow). With necrosis of the parenchyma, flabbiness and wrinkling of the liver is more pronounced, the color is gray-clay or dark red. Degenerative changes are noted in the heart muscle and kidneys. The mucous membrane of the digestive tract is covered with viscous mucus, swollen, loosened, hyperemic, sometimes with hemorrhages, erosions and ulcerations are observed.

Diagnosis and differential diagnosis.

When making a diagnosis, the quality of the feed, the presence of poisonous plants in it, the infestation with fungi, the content of vitamins, minerals, the protein-carbohydrate ratio in the diet, the correct use of antimicrobials and anthelmintics, as well as characteristic clinical signs, pathological and anatomical changes and laboratory results are taken into account. An important diagnostic value is a decrease in the blood content of albumin, an increase in bilirubin, hepatospecific enzymes and the appearance of liver antigens. To clarify the nature of the disease, toxicological examination of feed and bacteriological examination of cadaveric material are decisive.

It is necessary to differentiate toxic hepatodystrophy caused by intoxication from liver damage associated with the disease of young animals with leptospirosis, colienterotoxemia, salmonellosis and dysentery.

Treatment

Eliminate the causes of the disease. In the acute form of toxic dystrophy, the stomach and intestines are washed with warm water or a 0.01% solution of potassium permanganate using a probe and an enema. Inside injected laxatives (castor, sunflower or linseed oil). Sick animals are prescribed a starvation diet for 12 hours, then they are fed dietary feed (milk, skim milk, oatmeal jelly, liquid porridge from barley and oatmeal, yogurt). In addition, an acidophilic broth culture, a propionic-acidophilic culture are prescribed 2 times a day for 5-7 days. Subcutaneously injected hydrolysin and inside lipotropic substances: choline chloride, tocopherol acetate, methionine. In the future, animals are transferred to a diet of carbohydrate feed with the required level of protein, amino acids, vitamins and minerals. At the onset of the disease, subcutaneous injections of a glucose solution, a 0.1% aqueous solution of sodium selenite, and intramuscular injection calcium gluconate solution. The drugs are prescribed 2 times a day, in the absence of glucose, sugar with milk, hay infusion, jelly and cereals can be given inside. If necessary, prescribe cardiac drugs. Bile formation and bile secretion are stimulated by the use of magnesium sulfate, as well as cholagol, allochol, etc.

Prevention

It is necessary to constantly monitor the nutritional value of the diet, the sanitary quality of feed, the conditions of keeping pigs. All feeds should be regularly examined for toxicity. In disadvantaged farms, for prophylactic purposes, it is recommended to administer a solution of sodium selenite intramuscularly (to sows once 25 days before farrowing and to piglets for the first time at the age of 5 days and the second at 15 days).

List of used literature

1. Zharov A.V. Forensic veterinary medicine. - M.: Kolos, 2001.

2. Zharov A.V., Shishkov V.P., Zhakov M.S. pathological anatomy farm animals. - M.: Kolos, 2003.

3. Zharov A.V., Ivanov I.V., Strelnikov A.P. Autopsy and pathomorphological diagnosis of animal diseases. - M.: Kolos, 2000.

4. Belkin B.L., Zharov A.V., Prudnikov V.S. et al. Pathological diagnosis of animal diseases. Atlas-album / Ed. prof. Belkina B.L. and Zharova A.V. - M.: Aquarium-Print, 2013.

5. Internal illnesses animals / Under the general. ed. G.G. Shcherbakov. A.V. Korobov. - St. Petersburg: Publishing house "Lan", 2002.

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