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Nutritional anemia - pediatric hematology. Nutritional anemia: causes, symptoms, diagnosis and treatment methods. Iron deficiency in the body: consequences

NUTRITIONAL ANEMIA OF YOUNG CALM

nutritional anemia of young animals(Anaemia alimentaris), a disease of newborns with a characteristic disorder of hematopoiesis. It is observed in the autumn-winter period and early spring, more often among piglets raised in industrial complexes.

Etiology: the main cause of the disease is a deficiency of mainly iron, as well as copper and cobalt in the newborn’s body. Suckling piglets with mother's milk receive up to 1 mg of iron with a daily requirement of 7 x 10 mg. In this regard, by the end of the first week, iron deficiency occurs. In the next two weeks, iron deficiency reaches 100 x 200 mg and A. a. m. takes on a severe manifestation, especially in animals that have had dyspepsia and are kept on inadequate diets (lack of lysine, histidine and trace elements).

Course and symptoms. The disease is usually acute, especially in winter and early spring. Pale mucous membranes, skin white; Animals are lying down, tachycardia, shortness of breath, and periodic diarrhea are noted. The feces are whitish in color. Hemoglobin content decreases to 25%; when it decreases to 24%, the piglets die. Lambs are inactive and refuse milk. Calves lick wool, swallow foreign objects. Foals are delayed in growth and development.

Pathological changes. The muscles are pale colored, the liver is enlarged, kidneys are noted degenerative changes. Extramedullary foci of hematopoiesis are found in the spleen, liver and lymph nodes.

The diagnosis is made on the basis of a comprehensive comparison of epizootological data (absence of infectious diseases on the farm, age of young animals, etc.), clinical examination, pathological changes and results laboratory research.

Treatment and prevention. Sick piglets are prescribed 0.3 x 1 g of iron glycerophosphate daily. Granular feed containing up to 1.5% glycerophosphate is convenient. Granules are fed to piglets or lambs from 5-7 days of age for 25-30 days (30-50 g per day), calves and foals for 30 days (150-200 g per day). When using granules, provide free access to a watering hole. For treatment and prevention, on the 2nd x 5th day of a piglet’s life, intramuscular injections of 1 x 2 ml of solutions of iron-dextran preparations: ferroglucin, imferon and myofer are also used twice. Nutritious diets prevent the occurrence of A. a. m.

Literature:
Karelin A.I., Anemia of piglets in industrial complexes in different seasons of the year, in: Problems of veterinary sanitation. Proceedings of VNIIVS, 1978, vol. 62.


Veterinary encyclopedic Dictionary. - M.: "Soviet Encyclopedia". Chief Editor V.P. Shishkov. 1981 .

See what "NUTRITIONAL ANEMIA OF YOUNG CALM" is in other dictionaries:

    Nutritional anemia of young animals- (Anaemia alimentaris) iron deficiency anemia, disease p. X. animals with predominant damage to the hematopoietic organs. A. a. m. occurs everywhere, mainly in the autumn-winter and early spring periods, especially in piglets in ... Big Soviet encyclopedia

    - (from the Greek an negative particle and haima blood), anemia, pathological condition body, when rom per unit volume of blood the number of red blood cells decreases, and the hemoglobin content also decreases. Blood volume in A. may be normal,... ... Veterinary encyclopedic dictionary

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MINISTRY OF AGRICULTURE AND FOOD OF THE REPUBLIC OF BELARUS

VITEBSK ORDER“BADGE OF HONOR” STATE ACADEMY OF VETERINARY MEDICINE

Faculty of Veterinary Medicine

Department of Internal Non-Contagious Animal Diseases

Essay

Nutritional anemia (anemia alimenta)

Curator: 3rd year student Kovalchuk Nikolay Nikolaevich

Head of supervision: assistant Shabusov Nikolay Nikolaevich

VITEBSK-2011

1. Definition of disease

2. Anatomical data of the organ or area where the pathological process developed and physiological characteristics predisposing to the disease

3. Etiology of the disease

4. Pathogenesis

5. Symptoms of the disease

6. Diagnosis of the disease

7. Differential diagnosis

8. Forecast

9. Treatment of the disease

10. Exodus

11. Prevention

List of used literature

1. DEFINITION OF DISEASE

Alimencontainer anemia (anemia alimenta)- an animal disease characterized by a disorder of hematopoiesis due to iron deficiency in the body, metabolic disorders, decreased growth and development, increased susceptibility to other diseases and large economic damage.

The disease is diagnosed in young animals of all types of farm animals, but especially often in piglets, pregnant and lactating females.

2. Anatomical data of the organ or area where it developed pathological process and physiological characteristics those that predispose to disease

Organs of hematopoiesis and immune defense. Divided into central (red bone marrow and thymus) and peripheral (spleen, lymph nodes, lymphoid formations) digestive tract- tonsils, Peyer's patches).

Red bone marrow in young animals it lies in tubular and spongy bones, in adults - only in spongy bones.

Thymus or thymus has cervical and thoracic parts. The cervical part is a steam room, located on the sides of the trachea to the larynx, the thoracic part is in the mediastinum in front of the heart. After puberty, the gland gradually undergoes involution and disappears over time. Dogs and horses have a highly developed thoracic part thymus, the cervical part in the form of two paired processes protrudes slightly into the neck area due to the first rib.

Spleen-a compact organ located in the abdominal cavity near the stomach. In a horse, the spleen is triangular in shape with a wide dorsal end, lying in the left hypochondrium, on the greater curvature of the stomach. At the large cattle flat, elongated with rounded ends, lies in the left hypochondrium between the scar and the diaphragm, with its caudal end reaching the 9th rib. In pigs, the spleen is long with narrowed ends, located to the left of the stomach, protruding beyond the last rib. In dogs, the spleen is flat, irregularly triangular in shape, lies in the left hypochondrium, extends far beyond the last rib.

3 . ETIOLOGY OF THE DISEASE

The main cause of nutritional anemia is a low supply of iron in their body at birth, insufficient content of this element in colostrum and milk, intensive growth, gastrointestinal disorders. In addition, the low digestibility of Fe taken orally due to insufficient hydrochloric acid in the stomach and imperfection in early age hematopoietic function bone marrow. At the same time, the concentration of hemoglobin in the blood decreases to 5-6 mg% or lower, appetite decreases, growth and development slows down.

There are two periods in feeding young animals: suckling and after beating.

In the first month of life, the lambs' need for nutrients is met by the mother's milk, which provides the lambs with an average daily gain of 250-300g. Starting from 2-3 weeks of age, lambs begin to be accustomed to eating various feeds: oatmeal, chopped root vegetables, well-leafed hay and twig feed.

In the second month of lambs’ life, the approximate feeding rate should be 0.2-0.25, in the third - 0.35-0.40 and in the fourth - 0.6-0.65 feed units.

When feeding culled lambs, gender, age and breed differences should be taken into account. Thus, the need for feed in rams is 25-30% higher than in lambs. In the first 4-6 months. During their lifetime, they gain 180-200 g of live weight per day and by 7-9 months of age reach a live weight of 40-45 kg, while 6.7-7.0 units of feed are consumed per kilogram of live weight gain.

IN summer period Killed young animals should be allocated the best pastures and should be fed concentrates.

In winter, young animals should receive only high-quality feed in abundance: at least 1.0-1.5 kg of good hay, 1-2 kg of root vegetables and concentrates up to 300 g.

Numerous factors that reduce the resistance of newborns contribute to the disease: lack of protein, cobalt, zinc, manganese, vitamins A, B12, E in the diets of ewes and lambs; low level hemoglobin in the blood of the uterus, etc. The course of anemia worsens, the mortality rate of lambs increases due to violations of maintenance technology and sanitation rules.

However, in our supervised animal the cause of the disease was malnutrition ewes (this can be seen from the diet below, see Table No. 1 - Ewe diet), a contributing factor was also the lack of preventive treatments with vitamins and minerals.

Table No. 1 - Ewe diet.

Indicators

Loose timothy hay field dried, 2nd grade

Raw potatoes

Rye bran

Amount of feed, kg

Digestible protein, g

Crude fiber, g

Crude fat, g

Iron, mg

Cobalt, mg

Zioncobalamin, mg

Calcium, g

Phosphorus, g

Feed units

2.Ca/P ratio is 1:1

Conclusion: from the analysis of the diet it is clear that it lacks cobalt and cioncobalamin; and it is also not balanced in terms of nutritional value and digestible protein content.

4. PATHOGENESIS

The main amount of iron in the body of animals is associated with proteins, i.e. is in the form of organic compounds. Most of them contain iron in the heme form, while the rest contain iron in the non-heme form. Heme iron accounts for 70-75% and is represented by hemoglobin, myoglobin and heme-containing enzymes - cytochromes, cytochrome oxidase, catalase, peroxidase. The share of non-heme iron is 25-30%. It includes transferrin, ferritin, hemosiderin and some iron proteinates.

Hemoglobin belongs to the group of chromoproteins. It consists of a prosthetic group - heme, which is a complex of divalent ferrous form of iron with protoporphyrin and a protein component - globin.

In the body of adult animals, the iron concentration averages 0.005-0.006% based on fresh tissue and 0.14-0.17% based on ash. This is approximately twice as much as zinc and 20 times more than copper.

In newborn animals, with the exception of rabbits, the concentration of iron in the body is lower than in adults.

In feed, iron is in the form of a trivalent ion complex with proteins. In animals with a single-chamber stomach, this complex is broken down under the influence of hydrochloric acid and pepsin in the gastric juice and trivalent iron, being restored, turns into divalent iron. The salts formed in this case (in particular FCl) are well ionized and absorbed.

Iron absorption occurs mainly in the duodenum. This process is complex and step-by-step. It proceeds faster when animals are sufficiently supplied with protein, vitamins A, C, E, folic acid, cobalt, copper, amino acids, glutathione and others nutrients. Absorption is inhibited by organic acids that form insoluble iron salts (oxalates, citrates), as well as accelerated transit of chyme and excess phosphates.

From the intestinal mucosa, part of the iron enters the blood and binds to transferrin, which is subsequently converted into ferritin. Last in large quantities deposited in the liver and spleen. In addition to ferritin, iron is stored in the body in the form of hemosiderin, which is a derivative of ferritin with a higher iron content. It is found in macrophages of the bone marrow, spleen, and Kupffer cells of the liver. A lot of hemosiderin is found in the spleen of healthy animals. Endogenous iron losses are small and are associated with its excretion in bile and desquamated epithelium of the intestinal mucosa, and in females, with the secretion of the mammary glands. After the destruction of red blood cells, the released porphyrin ring is mainly used again for the synthesis of hemoglobin. Balance is maintained between iron-containing proteins of the mucous membrane, blood, liver and spleen. When the level of plasma iron decreases for the synthesis of hemoglobin, myoglobin, enzymes or during blood loss, iron from the organs is mobilized into the plasma. At the same time, the absorption of iron in the intestines increases, which contributes to the resumption of its introduction into the depot. The mechanism of iron metabolism in the body is complex and not fully known.

The level of iron in the liver and spleen of animals (especially young animals) correlates with its content in the diet and can be used as a diagnostic test for the body's supply of this metal.

The absorption of iron from natural feed in adult animals ranges from 8-10% of the intake. It increases to 15-20% with a deficiency of the element in the diet, insufficient accumulation in the body, or increased erythopoiesis.

Iron compounds perform oxidative functions in the body. Hemoglobin transports oxygen, myoglobin binds and reserves it. They are able to attach an oxygen molecule to form oxyhemoglobin and oxymyoglobin, respectively, and then release it to tissues. In this case, the valence of iron does not change; it remains divalent. Cytochromes, cytochrome oxidase, catalase, peroxidase play an important role in the processes of tissue respiration. Iron is contained in the prosthetic group of ferroflavoprotein enzymes, and is also part of the cofactors fumaric acid dehydrogenase and acyl-CoA.

Iron deficiency in the body is accompanied by microcytic hypochromic anemia, which occurs against the background of insufficient hemoglobin synthesis and a decrease in its quantity in red blood cells.

The importance of iron for the body.

Iron is part of hemoglobin and stimulates the activity of iron-containing enzymes, which are closely related to protein synthesis and other cellular functions. It also plays an important role in the formation of the oxygen-hemoglobin complex and increasing the duration of its existence, providing time sufficient for this complex to reach the most peripheral parts of the body, where it gradually disintegrates along the way and releases released oxygen to the tissues. With a lack of iron, the duration of existence of such a complex is reduced and animals develop a state of hypoxia. In this case, breathing becomes compensatory and cardiac hypertrophy develops. In addition, iron deficiency in the body leads to a decrease in hemoglobin levels and a decrease in the activity of iron-containing enzymes.

CYANOCOBALAMIN (Cyanocobalaminum).

VITAMIN B 12 (Vitaminum B 12).

Co a -[ a -(5, 6-Dimethylbenzimidazolyl)-Co b-cobamide cyanide, or a -(5, 6-dimethyl-benzimidazolyl)-cobamide cyanide.

Synonyms: Actamin B12, Almeret, Anacobin, Antinem, Antipernicin, Arcavit B12, Bedodec, Bedoxyl, Bedumil, Berubigen, Biopar, Catavin, Cobastab, Cobavite, Cobione, Curibin, Cycobemin, Cycoplex, Cytacon, Cytamen, Cytobex, Cytobion, Dancavit B12 , Distivit, Dobetin, Dociton, Dodecavit, Emobione, Grisevit, Hepagon, Lentovit, Megalovel, Novivit, Pernapar, Redamin, Reticulogen, Rubavit, Rubivitan, Rubramin, Vibicon, etc.

Dark red crystalline powder, odorless. Hygroscopic. Slightly soluble in water; solutions are red (or pink) in color. Sterilize solutions at a temperature of + 100 C for 30 minutes. Prolonged autoclaving destroys the vitamin. Oxidizing reducing agents (e.g. ascorbic acid) and salts heavy metals contribute to the inactivation of the vitamin. Microflora quickly absorbs vitamin B12, so solutions must be stored under aseptic conditions.

A characteristic chemical feature of the cyanocobalamin molecule is the presence in it of a cobalt atom and a cyano group, forming a coordination complex.

Vitamin B 12 (cyanocobalamin) is not produced by animal tissues. Its synthesis in nature is carried out by microorganisms, mainly bacteria, actinomycetes, and blue-green algae. In humans and animals, it is synthesized by the intestinal microflora, from where it enters the organs, accumulating in the largest quantities in the kidneys, liver, and intestinal wall. Synthesis in the intestines does not fully satisfy the body's need for vitamin B 12; additional amounts come from animal products. Vitamin B 12 is contained in varying quantities in medicinal preparations obtained from animal liver (see Vitohepat).

In the body, cyanocobalamin is converted into the coenzyme form adenosylcobalamin, or cobamamide (see), which is active form vitamin B 12.

Cyanocobalamin has high biological activity. It is a growth factor, necessary for normal hematopoiesis and maturation of red blood cells; participates in the synthesis of labile methyl groups and in the formation of choline, methionine, creatine, and nucleic acids; promotes the accumulation of compounds containing sulfhydryl groups in erythrocytes. Has a beneficial effect on liver function and nervous system.

Cyanocobalamin activates the blood coagulation system; in high doses causes an increase in thromboplastic activity and prothrombin activity.

It activates the metabolism of carbohydrates and lipids. In case of atherosclerosis, it slightly lowers the cholesterol level in the blood and increases the lecithin cholesterol index.

Cyanocobalamin has a pronounced healing effect with Addison-Beermer disease, agastric anemia (after gastrectomy), with anemia due to polyposis and syphilis of the stomach, with anemia accompanying enterocolitis, as well as with other pernicious anemia, including that caused by tapeworm infestation, during pregnancy, sprue and etc.

For use as a medicinal product, vitamin B 12 is obtained by microbiological synthesis.

Vitamin B 12 is a highly effective antianemic drug. This drug is successfully used for the treatment of malignant anemia, post-hemorrhagic and iron deficiency anemia, aplastic anemia, nutritional anemia, anemia caused by toxic and medicinal substances, and for other types of anemia.

Also prescribed for radiation sickness, dystrophy in premature and newborn babies after infections, with sprue (together with folic acid), liver diseases (Botkin's disease, hepatitis, cirrhosis), polyneuritis, radiculitis, neuralgia trigeminal nerve, diabetic neuritis, causalgia, migraine, alcoholic delirium, amyotrophic lateral sclerosis, children's cerebral palsy, Down's disease, skin diseases(psoriasis, photodermatoses, dermatitis herpetiformis, neurodermatitis, etc.).

Cyanocobalamin is administered intramuscularly, subcutaneously, intravenously and intralumbarally.

Vitamin B 12 is poorly absorbed when taken orally. Absorption is slightly improved when administered together with folic acid.

For anemia associated with vitamin B12 deficiency, 100 - 200 mcg (0.1 - 0.2 mg) is administered once every 2 days; for anemia with symptoms of funicular myelosis and for macrocytic anemia with lesions of the nervous system - 500 mcg or more per injection (daily in the first week, and then at intervals between injections of up to 5 - 7 days). At the same time, folic acid is prescribed.

During the period of remission, in the absence of symptoms of funicular myelosis, 100 mcg 2 times a month is administered for maintenance therapy, and in the presence of neurological phenomena - 200 - 400 mcg 2 - 4 times a month.

For posthemorrhagic and iron deficiency anemia, 30-100 mcg are prescribed 2-3 times a week; for aplastic anemia in childhood- 100 mcg until clinical and hematological improvement occurs; for anemia of a nutritional nature in early childhood and anemia in premature infants - 30 mcg for 15 days.

Cyanocobalamin is contraindicated in acute thromboembolism, erythremia, erythrocytosis.

5. SIMPVOLUMES OF DISEASE

Sick animals are inactive, do not suckle the uterus well, are stunted in growth, and lose weight. They experience anemia of the mucous membranes, swelling of the eyelids, perversion of appetite, gastrointestinal disorders, polypnoea, tachycardia, wrinkled skin, dry and brittle hair. Such lambs are more susceptible to infectious pneumoenteritis and often die.

In lambs, the disease is manifested by a decrease or absence of appetite, pallor of the mucous membranes, increased fatigue, gastrointestinal disorders, hypothermia, delayed growth and development, high susceptibility to infectious diseases.

The earliest laboratory diagnostic tests for nutritional anemia are a significant decrease in liver iron reserves and low activity of heme-containing enzymes. Reserve iron is used primarily to maintain hemoglobin levels. Therefore, initially the body, under conditions of iron deficiency, maintains the level of oxygen consumption by tissues at a physiologically sufficient level, and therefore, the hemoglobin content of the blood at the onset of the disease remains within the normal range. Increased consumption of iron for hemoglobin synthesis negatively affects the activity of cytochromes and other respiratory enzymes that ensure interstitial respiration, and therefore physiological state and growth energy.

Early signs of the disease also include a decrease in the level of serum iron and content ascorbic acid in internal organs. With further progression of the disease, a significant decrease in the amount of hemoglobin (oligochromemia) is established in the blood of sick animals. This indicator is a reliable diagnostic test for iron deficiency, since at least 65% of this element is found in blood hemoglobin.

In addition to the above changes, in animals suffering from nutritional anemia, a decrease in the color index (less than one), nonspecific resistance, cellular and humoral immunity factors, general iron-binding capacity and an increase in latent iron-binding capacity (free transferrin) are recorded.

6. DISEASE DIAGNOSIS

Diagnosis is based on medical history, clinical signs, pathological changes, and blood test results. In this case, the level of hemoglobin in the blood and iron in the blood serum is crucial.

Early diagnosis consists of determining the amount of hemoglobin in the blood, liver, spleen, and kidneys. In other cases, a feeding analysis is carried out based on clinical symptoms and the results of hematological studies. Lambs with hemoglobin levels below 40 g/l are considered sick. Important diagnostic value has a definition of the color indicator of blood. Normally, this indicator is close to one; with anemia it drops to 0.6-0.5.

When differentiating the disease, anemia that occurs due to the influence of other factors on the body of young animals, in particular infectious and invasive ones, is excluded.

In our case, the diagnosis was made on the basis of clinical signs, epidemiological data, and laboratory blood tests.

7. DIFFERENTIAL DIAGNOSIS

Differential diagnosis . It is necessary to exclude hemolytic disease of the newborn, posthemorrhagic anemia, B12 and folate deficiency anemia, hypocobaltosis, hypocuprosis. For hemolytic disease Newborns are characterized by an age aspect. In addition, with this pathology, along with anemia, yellowness of the mucous membranes and sometimes hemoglobinuria are also noted. Changes in color (anisochromia) and size (anisocytosis) of red blood cells are the most characteristic feature posthemorrhagic anemia. For anemia caused by vitamin B12 deficiency and folic acid, take into account the results of blood tests and the effectiveness of prescribing appropriate therapy. In hypocobaltosis, weakly colored microcytes are more often found, increase in ESR, low cobalt content in the body. Hypocuprosis is characterized by nervous disorders and low copper levels in the liver and blood. For differentiation iron deficiency anemia from the last two diseases, an analysis of the mineral composition of the diet can be very valuable.

8. FORECAST

Based on clinical and laboratory studies during the course of the disease, as well as the results of the treatment, a diagnosis was made - Anutritional anemia. According to the results of the study, the prognosis is favorable.

nutritional anemia hematopoiesis pathogenesis

9. TREATMENT

Currently, injectable iron-dextran preparations are more often used to prevent anemia and treat sick animals. The most effective are iron dextran preparations (ferrodextran, ferrodex, ferroglucin, dextrafer, impoferon, impozil-200, myofer, armidextran, ferrobal, DIF-3). They are administered intramuscularly in the thigh area for therapeutic purposes in a dose of 1-2 ml based on their iron content of 150-200 mg.

The widely used domestic ferroglucin-75 was first tested as an antianemic agent in 1963 (D.P. Ivanov et al., 1971). The drug is a complex compound of low molecular weight dextran with ferric iron, which contains about 75 mg in 1 ml. The drug is injected into calves and foals with 5-8 ml on the 3-4th day of life, and in lambs with 3-4 ml on the 5-6th day of life.

For therapeutic purposes, ferroglucin-75 is administered to young animals over two weeks of age in mg at the rate of ferric iron per 1 kg of body weight: piglets 50-100; calves and foals 15-20; lambs and fur-bearing animals 50. If necessary, injections of the drug are repeated in the same doses after 10 days. The use of ferroglucin-75 is contraindicated in cases of acute vitamin E deficiency.

Currently, practical veterinary specialists of the republic have the opportunity to choose from a wide selection of imported iron dextran preparations. All of them, as a rule, differ only in iron content, but some additionally include vitamin B12.

Considering that in practice nutritional anemia is often diagnosed with iodine deficiency, as well as the role of this microelement for newborns, the drug sedimin was introduced into production.

To treat the supervised animal, Sediminum Plus and Multivit were used.

Pharmacological description of some medicines used in the treatment of animals.

Multivit injection includes: vitamin A 50,000 I.E.; vitamin D3 25,000; vitamin E 4 mg; vitamin B1 10 mg; vitamin B2 0.04 mg; vitamin B6 1 mg; vitamin B12 0.01 mg; D-panthenol 2 mg; nicotinamide 5 mg.

INDICATIONS FOR USE: n lack of vitamins, especially in diseases during the growth period. Muscular dystrophy, growth disorder, nervous diseases, recovery period, stressful situations. Achieving good activity and stimulating development.

DOSES AND METHOD OF APPLICATION: Intramuscular injection and oral administration to cattle, horses, camels: 10-30 ml. Calves, foals: 10-20 ml. Sheep, goats, pigs: 5-10 ml. Small animals 1-5 ml.

NOTES: There is no waiting period for human consumption of milk and meat after treatment.

STORAGE CONDITIONS. Store in a cool place, protected from light and out of reach of children.

RELEASE FORM: Bottles of 50 and 100 ml.

Sediminum plus, COMPOSITION: w liquid dark brown, V 1 ml of which contains 13--18 mg iron, 6,0--7,0 mg iodine, 5,4--6,6 mg magnesium and 0,30---0,40 mg selenium.

INDICATIONS FOR USE: p the drug is used for the prevention of diseases caused by deficiency of iodine, selenium, magnesium, iron, treatment of animals suffering from enzootic goiter, white muscle disease, iron deficiency anemia, hypomagnesemia, as well as to stimulate the growth of increased nonspecific resistance of the body of young animals, the reproductive ability of cows and sows, and the prevention of postpartum complications in them.

DOSES AND METHOD OF APPLICATION: the drug is administered intramuscularly or subcutaneously: heifers and cows once a day 45-- 25 days before calving at a dose 15--20 ml, calves therapeutic dose amounts to 2,5 ml on10 kg of live weight (but not more than 10 ml per head), prophylactic -- 1,5 ml per 10 kg live weight; main sows are prescribed for 12-8 days before piglets are weaned and 25--20 days before farrowing in position 12--15 ml per injection, and for replacement sows - per 14--7 days before the expected insemination (covering) and 25--20 days before farrowing at a dose 8 ml; To prevent anemia, suckling piglets are injected with the drug twice on3-5 th And 10--15 th days of life based on 1,5 ml/kg live weight. For gilts a drug prescribed based on 0,5 ml/kg live weight (but not more than 5 ml per head). At If additional prescription is necessary, the drug is administered in the same doses, but Not earlier than in 10 days after the first treatment of animals.

CONTRAINDICATIONS: p a contraindication to the use of the drug is the treatment of animals for 10 the last days with preparations containing selenium and iodine.

WAITING PERIOD: m After administering the drug to animals, the jar can be used for food through 7, and the liver, kidneys... 14 days, milk - without restrictions.

STORAGE CONDITIONS. List B. Store in a dark place at a temperature from +2 to +25°C. Shelf life: 2 years.

RELEASE FORM: in are released packaged in glass bottles made of neutral glass according to 50, 100, 200,250,400,500 ml.

10. EXODUS

As a result of the treatment provided ( complex treatment through a rational combination of local and general therapy taking into account environmental factors, nature and stage of the pathological process, as well as general condition animal) clinical recovery occurred.

The therapy provided a generally positive result. The outcome is clinical recovery.

11. PREVENTION

Prevention carried out with the same drugs that are used to treat anemic piglets.

It is necessary to accustom lambs to feeding early. They grow faster, develop better, and are more resistant to disease.

An effective means of preventing and treating iron deficiency anemia is Ferrovit, a new injectable veterinary drug containing iron and vitamin B12. It is a sterile, dark brown liquid with a weak specific odor. Our extensive clinical trials have shown that ferrovit has antianemic and restorative effect. The iron contained in it, after being included in metabolic processes, stimulates hematopoiesis. Vitamin B 12 also has a positive effect on hematopoiesis, increasing the efficiency of iron use and growth energy.

Ferrovit is used to prevent and treat nutritional anemia, normalize metabolism, and increase the safety and growth rate of young animals.

The drug is administered subcutaneously or intramuscularly. No more than 10 ml of the drug can be injected into an animal at one injection site.

LIST OF REFERENCES USED.

Anatomy of domestic animals: textbook for universities / I. V. Khrustaleva [etc.]; edited by I. V. Khrustaleva. - M.: Kolos, 2000. - 704 p.

Karput, I. M. Immunology and immunopathology of diseases of young animals / I. M. Karput. - Minsk: Urajai, 1993. - 288 p.

Kondrakhin, I. P. Nutritional and endocrine diseases animals / I. P. Kondrakhin. - M.: Agropromizdat, 1989. - 287 p.

Fundamentals of the physiology of farm animals: textbook. allowance / N. S. Motuzko [etc.]. - Vitebsk: OU VGAVM, 2004. - 125 p.

Workshop on internal non-contagious animal diseases / V. M. Danilevsky [et al.]; edited by V. M. Danilevsky, I. P. Kondrakhin. - M.: Kolos, 1992. - 271 p.

Directory of clinical and biological parameters of animals / N. S. Motuzko [et al.]. - Gorki, 2001. - 72 p.

Telepnev, V. A. Basic symptoms and syndromes of animal diseases: educational method. allowance. - Vitebsk: OU VGAVM, 2000. - 76 p.

Private animal science: textbook. manual for secondary special education. agricultural institutions / Ya. V. Vasilyuk [etc.]. -Minsk: Urajai, 1999. - 416 p.

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Nutritional anemia of piglets is a disease of piglets, accompanied by a decrease in the number of red blood cells and hemoglobin content per unit volume of blood and a change in the properties of the blood, leading to stunting of animals and a decrease in the body’s resistance to various diseases. Nutritional anemia belongs to the group of hypoplastic deficiency anemias.

The disease is widespread in all natural climatic zones, more often in conditions of industrial technology, and causes great economic damage to farms. Piglets are affected mainly before 3 weeks of age.

Historical reference. Nutritional anemia in piglets was first described by the German scientist W. Brush in 1890.

Etiology. Most common cause The widespread spread of nutritional anemia is iron deficiency in the body of piglets. The daily iron requirement of one piglet is up to one month old compared to young animals of other species, it is very large and averages 8-10 mg, which is associated with a rapid increase in body weight in the piglet (the piglet’s weight doubles by 6-8 days, and by two months, i.e. by the weaning period increases by 14-16 times). Newborn piglets can satisfy their need for iron only by:

  • alimentary route (sow's milk);
  • endogenous pathway, 65% associated with red blood cells.

Sow's milk is very poor in iron (2 times less than that of a cow), which is why a piglet can receive only 1-1.5 mg of iron per day with milk, or only 15-20%. Due to endogenous iron (during the breakdown of red blood cells) 1%.

A newborn piglet is born with a reserve of iron in the body of approximately 50 mg; it can receive about 1 mg per day through mother’s milk. Hence, already from the second week from birth, iron deficiency is observed in the piglet’s body, which ultimately leads to the development of hypochromic iron deficiency anemia. The disease is promoted by numerous factors that lead to a decrease in the body's resistance in newborn piglets: lack of protein, microelements (cobalt, zinc, manganese), vitamins (A, B12, E) in the diet of the sow and piglet; low level of hemoglobin in the blood of the sow, etc. Feeding to sows and piglets can lead to nutritional anemia toxic feed, as well as feed containing alkaloids (compound feed affected by mold, cotton cake, peanut flour, etc.). Violations in housing technology and zoohygienic rules (crowded housing, insufficient air exchange, high air humidity in the pigsty, great content ammonia, high microbial contamination, etc.).

Pathogenesis. Considering that by the 5th – 7th day of life a newborn piglet develops iron deficiency in its body, the formation of the hemoglobin molecule is disrupted. At the same time, endogenous iron metabolism in a piglet at this age is not developed.

Newly formed red blood cells are hypochromic. Nutritional deficiency disrupts not only the synthesis of the hemoglobin molecule and the formation of red blood cells, but also the synthesis of plasma proteins.

With nutritional anemia in piglets, redox processes are disrupted and oxygen starvation of tissues develops, which leads to under-oxidized products of interstitial metabolism entering the blood, causing spasms of peripheral vessels, increased cardiac activity and accelerated blood flow; the alkaline reserve of the blood, protein content and especially gamma globulins decrease. Fatty degeneration of the heart muscle and liver parenchyma is noted. Large deposition of fat in tissues contributes to mechanical effects on the walls blood vessels, stagnation of blood, disruption of peripheral nutrition of the skin, dryness occurs, the color and elasticity of the bristles changes, necrosis of the tips of the tail and ears develops. Abnormal supply of nutrients with the blood to organs and tissues contributes to the development of catarrhal inflammatory process of the intestinal mucosa and anemia. Iron deficiency eliminates the stimulating effect of this microelement on the bone marrow, leading to impaired erythropoiesis. There is a gradual decrease in the number of red blood cells circulating in the blood. In anemic piglets, the body's resistance to secondary diseases decreases.

Clinical signs. On pig farms where anemia is common, already from 7-10 days of age, normally developed and healthy piglets develop weakness, lethargy, inactivity, reduced sucking ability and even loss of the sucking reflex, increased heart rate and breathing. Characteristic signs of anemia appear - pallor of the skin, especially the ears (“white ears”), mucous membranes, swelling of the eyelids. These signs of growth retardation and anemia are recorded during a clinical examination in almost all piglets, even those that are normally developed at birth. Subsequently, piglets who become ill with nutritional anemia are stunted even more; their stubble becomes ruffled, rough and brittle, and their skin becomes dry and wrinkled. Most piglets with nutritional anemia experience gastrointestinal disorders, cyanosis of the mucous membranes, the tip of the tail and ears. As the disease progresses, the piglets weaken, become stunted, and skin folds appear in the neck and shoulder joints. On the part of the muscles, progressive hypotension is noted. IN severe cases We almost always note clearly expressed symptoms of rickets. The blood becomes watery and its coagulability is reduced. The hemoglobin content in the blood decreases to 25%, the hemoglobin content in the blood reaches 7-5% and lower (with an average of 11-12 g/%), the color index decreases to 0.6-0.5 (with a norm of 1) , and the number of red blood cells - up to 3 -1.3 million. In the blood smear, young formed elements indicating bone marrow regeneration are not detected. We discover a large number of pale colored red blood cells (hypochromic anemia).

Flow. Anemia in piglets develops relatively quickly, and the pathological process ends just as quickly. If left untreated, piglets die on the 10-14th day from the onset of the disease.

Pathological changes. Characteristic changes revealed during autopsy of a piglet that has died from nutritional anemia are pallor of the mucous membranes, skin, skeletal muscles and all internal organs. In severe cases of nutritional anemia, the mucous membranes and skin have a pale porcelain color. Often at autopsy we find enlargement of the heart, dystrophic changes in the liver, kidneys, and sometimes an enlargement of the spleen. In the chest and abdominal cavities contains varying amounts of serous transudate.
At histological examination establish an increase in the volume of bone marrow cells, the accumulation of a significant number of megakaryocytes in the spleen and their single presence in lymph nodes, changes in the structure of the heart muscle, metaplasia of the squamous epithelium of the glomerular capsule of the kidneys and swelling of reticulo-endothelial fibers in the liver, and sometimes atrophy of liver cells.

Diagnosis put in a comprehensive manner: analyzing the diets of sows, taking into account the provision of their diets with protein, iron and microelements; clinical signs of the disease; data from a blood test for the content of hemoglobin and red blood cells, as well as taking into account the data of the pathological autopsy.

Differential diagnosis. Veterinary specialists have to differentiate nutritional anemia in piglets from other factors, such as infectious and invasive ones.

Treatment. If there is nutritional anemia in piglets on the farm, animal owners must eliminate the causes of nutritional anemia. The breeding stock and young animals are provided with a complete feeding ration. Deficiency of iron or microelements is replenished by introducing into the diet of suckling sows and piglets the missing ingredients in the form of premixes or mixtures prepared for this group of animals. To replenish the missing iron and trace elements, sick piglets are prescribed preparations of iron, manganese, cobalt, zinc, B vitamins, hematogen, liver preparations, etc. For group treatment with good results iron glycerophosphate is used internally in the form of powder, paste or as part of granulated feed at the rate of 1-1.5 g per piglet once a day for 6-10 days in a row. IN last years On pig farms, for the treatment and prevention of anemia in piglets, special iron dextrin preparations, both domestic and imported, are used: imposil-200, imferon, myofer, ferrodex, armidextran, ferroglucin, etc. They are administered to piglets intramuscularly once at the age of 5-7 days from calculating 150-200 mg of iron per injection. Gives a good healing effect intramuscular use microanemin, consisting of iron sulfate, copper sulfate and cobalt chloride. In the absence of the above drugs, fresh citrated blood of the sow can be administered subcutaneously in a dose of 5-7 ml per piglet, a total of 2-3 injections every other day.

Prevention. To prevent nutritional anemia in piglets, it is necessary to eliminate the causes that cause it. Sows in the second period of gestation and farrowing are provided with a diet complete in protein, iron, cobalt, zinc, manganese, vitamins A, group B and E. At industrial complexes in the workshops of pregnant sows, farrowing and suckling, specialists should pay special attention to the introduction of for animals, primexes containing iron and vitamin B12 preparations. Operating personnel must follow the rules of farrowing, and give newborn piglets iron glycerophosphate as a supplement at the rate of 0.2-0.3 g per piglet starting from the 2nd birthday and for 10-15 days in a row. Piglets 2-3 days of age are intramuscularly injected with ferrodextrin preparations at a dose of 1.5 -2 ml at a rate of 150-200 mg of iron per piglet, but it is better to use specially prepared iron dextrin preparations for internal use, which allows you to avoid stress due to injections and save time for veterinary specialists serving the pig farm. For this purpose, piglets 5-6 days of age are given orally a single dose of ferrous galactan in a dose of 2 ml (200 mg of iron). It is advisable to combine the enteral use of iron-containing preparations with the simultaneous administration of ascorbic acid to animals with food (5-7 mg per piglet once), which helps improve iron absorption.

Nutritional anemia- an animal disease characterized by a disorder of hematopoiesis due to iron deficiency in the body, metabolic disorders, decreased growth and development, increased susceptibility to other diseases and large economic damage.

The disease is diagnosed in young animals of all types of farm animals, but especially often in piglets, pregnant and lactating females.

Etiology. The main cause of nutritional anemia is a low supply of iron in their body at birth, insufficient content of this element in colostrum and milk, rapid growth, and gastrointestinal disorders. It has been established that for the normal development of a piglet in the first days of life, 7-10 mg of iron is required, and with mother’s milk it receives only about 1 mg, i.e. the need is satisfied by no more than 15%. If we consider that the reserves of this bioelement in the body of newborn sucklings are no more than 50 mg, then it becomes obvious that by the end of the first week of life they begin to experience iron deficiency. In addition, piglets have a physiological predisposition to the disease - low digestibility of Fe taken orally due to insufficient hydrochloric acid in the stomach and imperfection of the hematopoietic function of the bone marrow at an early age.

In complete colostrum of cows, the iron content is quite high, and in milk it is much lower - 2-4 mg/kg of dry matter. Daily Need for calves it is estimated at 15-30 mg/kg. They receive no more than 4 mg per day with milk, and if we take into account that only 26% of iron is absorbed from milk, then it is obvious that its total absorption will be no more than 1 mg. A number of researchers believe that the actual supply of iron to young animals, taking into account its absorption, should be ensured at a level of 125-130 mg per day. Iron reserves in the body of calves at birth are estimated at 3000 mg. Consequently, by the end of the third week of life, if additional iron-containing drugs or supplements are not prescribed, iron deficiency occurs. At the same time, the concentration of hemoglobin in the blood decreases to 5-6 mg% or lower, appetite decreases, growth and development slows down. Considering that milk and skimmed milk form the basis of the calf diet milk period, it is very important to organize a full-fledged mineral nutrition dairy herd.

Pathogenesis. The main amount of iron in the body of animals is associated with proteins, i.e. is in the form of organic compounds. Most of them contain iron in the heme form, while the rest contain iron in the non-heme form. Heme iron accounts for 70-75% and is represented by hemoglobin, myoglobin and heme-containing enzymes - cytochromes, cytochrome oxidase, catalase, peroxidase. The share of non-heme iron is 25-30%. It includes transferrin, ferritin, hemosiderin and some iron proteinates.

Hemoglobin belongs to the group of chromoproteins. It consists of a prosthetic group - heme, which is a complex of divalent ferrous form of iron with protoporphyrin and a protein component - globin.

In the body of adult animals, the iron concentration averages 0.005-0.006% based on fresh tissue and 0.14-0.17% based on ash. This is approximately twice as much as zinc and 20 times more than copper.

In newborn animals, with the exception of rabbits, the concentration of iron in the body is lower than in adults.

In feed, iron is in the form of a trivalent ion complex with proteins. In animals with a single-chamber stomach, this complex is broken down under the influence of hydrochloric acid and pepsin in the gastric juice and trivalent iron, being restored, turns into divalent iron. The salts formed in this case (in particular FCl) are well ionized and absorbed.

Iron absorption occurs mainly in the duodenum. This process is complex and step-by-step. It proceeds faster when animals are sufficiently supplied with protein, vitamins A, C, E, folic acid, cobalt, copper, amino acids, glutathione and other nutrients. Absorption is inhibited by organic acids that form insoluble iron salts (oxalates, citrates), as well as accelerated transit of chyme and excess phosphates.

From the intestinal mucosa, part of the iron enters the blood and binds to transferrin, which is subsequently converted into ferritin. The latter is deposited in large quantities in the liver and spleen. In addition to ferritin, iron is stored in the body in the form of hemosiderin, which is a derivative of ferritin with a higher iron content. It is found in macrophages of the bone marrow, spleen, and Kupffer cells of the liver. A lot of hemosiderin is found in the spleen of healthy animals. Endogenous iron losses are small and are associated with its excretion in bile and desquamated epithelium of the intestinal mucosa, and in females, with the secretion of the mammary glands. After the destruction of red blood cells, the released porphyrin ring is mainly used again for the synthesis of hemoglobin. Balance is maintained between iron-containing proteins of the mucous membrane, blood, liver and spleen. When the level of plasma iron decreases for the synthesis of hemoglobin, myoglobin, enzymes or during blood loss, iron from the organs is mobilized into the plasma. At the same time, the absorption of iron in the intestines increases, which contributes to the resumption of its introduction into the depot. The mechanism of iron metabolism in the body is complex and not fully known.

The level of iron in the liver and spleen of animals (especially young animals) correlates with its content in the diet and can be used as a diagnostic test for the body's supply of this metal.

The absorption of iron from natural feed in adult animals ranges from 8-10% of the intake. It increases to 15-20% with a deficiency of the element in the diet, insufficient accumulation in the body, or increased erythopoiesis.

Iron compounds perform oxidative functions in the body. Hemoglobin transports oxygen, myoglobin binds and reserves it. They are able to attach an oxygen molecule to form oxyhemoglobin and oxymyoglobin, respectively, and then release it to tissues. In this case, the valence of iron does not change; it remains divalent. Cytochromes, cytochrome oxidase, catalase, peroxidase play an important role in the processes of tissue respiration. Iron is contained in the prosthetic group of ferroflavoprotein enzymes, and is also part of the cofactors fumaric acid dehydrogenase and acyl-CoA.

Iron deficiency in the body is accompanied by microcytic hypochromic anemia, which occurs against the background of insufficient hemoglobin synthesis and a decrease in its quantity in red blood cells.

Pathological changes. There is pallor of the skin and mucous membranes, atrophy of skeletal muscles, granular and fatty degeneration in the liver, kidneys and myocardium, and sometimes hemorrhages. The cavities of the heart are dilated, the myocardium is flabby, anemic. Most animals have an accumulation serous exudate in the abdominal and chest cavities, catarrh gastrointestinal tract, slight enlargement of the spleen. It is dense and purple in color. The liver is enlarged, light brown, the lungs are often swollen. In fur-bearing animals, areas of gnawing are often noted on the skin.

Histological examination reveals a decrease or absence of hemosiderin in the spleen, bone marrow hyperplasia, extramedullary foci of hematopoiesis in the liver, spleen, and lymph nodes. In fur-bearing animals, foci of hematopoiesis are sometimes found in the kidneys, as well as hemorrhages and necrosis in the liver.

Symptoms. In piglets, the disease can be observed already in the first days after birth. Moreover, only about 10% of suckers have clinical, and about 50% subclinical anemia. Characteristic symptoms Nutritional anemia occurs more often in well-developed piglets aged 10-15 days. Sick animals are inactive, do not suckle the uterus well, are stunted in growth, and lose weight. They experience anemia of the mucous membranes, swelling of the eyelids, perversion of appetite, gastrointestinal disorders, polyps, tachycardia, wrinkled skin, dry and brittle stubble. Such piglets are more susceptible to infectious pneumoenteritis and often die. By the end of the first month of life, the surviving sucklings have a noticeable sharp retardation in growth (by 35% or more) compared to their healthy peers.

In calves and lambs, the disease is manifested by a decrease or absence of appetite, pallor of the mucous membranes, increased fatigue, gastrointestinal disorders, hypothermia, delayed growth and development, and a high susceptibility to infectious diseases.

In fur-bearing animals, paleness of visible mucous membranes, nose, paw pads, discoloration and fragility of hair, decreased fatness, slowed growth, cannibalism, and impaired reproductive function are noted.

The earliest laboratory diagnostic tests for nutritional anemia are a significant decrease in liver iron reserves and low activity of heme-containing enzymes. Our studies showed that at 25 days of age, the iron content in the liver of piglets treated parenterally with ferroglucin and DIF-3 was 249.2 +33.6 and 212.4 +18.5 μg/g dry tissue, respectively, and in sucklings control group only 98.8 + 21.4 µg/g.

Reserve iron is used primarily to maintain hemoglobin levels. Therefore, initially the body, under conditions of iron deficiency, maintains the level of oxygen consumption by tissues at a physiologically sufficient level, and therefore, the hemoglobin content of the blood at the onset of the disease remains within the normal range. Increased consumption of iron for hemoglobin synthesis negatively affects the activity of cytochromes and other respiratory enzymes that provide interstitial respiration, and therefore the physiological state and growth energy.

Early signs of the disease also include a decrease in serum iron levels and ascorbic acid content in internal organs. With further progression of the disease, a significant decrease in the amount of hemoglobin (oligochromemia) is established in the blood of sick animals. This indicator is a reliable diagnostic test for iron deficiency, since at least 65% of this element is found in blood hemoglobin. It is believed that 90 g/l of hemoglobin in the blood of piglets is sufficient for their satisfactory development. At 80 g/l hemoglobin, there is a decrease in the intensity of growth, development and resistance to infectious diseases. In the blood of such animals, the activity of catalase, peroxidase, and carbonic anhydrase is inhibited, the content of ascorbic acid decreases, and the amount of reduced glutathione increases. A decrease in the level of hemoglobin to 60 g/l, erythrocytes to 4 thousand/ml, hematocrit below 0.30 L/l and serum iron to less than 70 mg% indicates the disease of piglets with nutritional iron deficiency anemia.

Literary data and the results of our research indicate that in calves, a decrease in blood hemoglobin below 70 g/l, erythrocytes below 4.5 T/l, hematocrit below 0.28 L/l reliably correlate with clinical signs of the disease.

In addition to the above changes, in animals suffering from nutritional anemia, a decrease in the color index (less than one), nonspecific resistance, cellular and humoral immunity factors, general iron-binding capacity and an increase in latent iron-binding capacity (free transferrin) are recorded.

Diagnostics based on medical history, clinical signs, pathological and morphological changes, and blood test results. In this case, the level of hemoglobin in the blood and iron in the blood serum is crucial.

Differential diagnosis. It is necessary to exclude hemolytic disease of the newborn, posthemorrhagic anemia, B12 and folate deficiency anemia, hypocobaltosis, hypocuprosis. Hemolytic disease of newborns is characterized by an age aspect. In addition, with this pathology, along with anemia, yellowness of the mucous membranes and sometimes hemoglobinuria are also noted. Changes in color (anisochromia) and size (anisocytosis) of red blood cells are the most characteristic sign of posthemorrhagic anemia. For anemia caused by deficiency of vitamin B12 and folic acid, the results of blood tests and the effectiveness of appropriate therapy are taken into account. With hypocobaltosis, weakly colored microcytes, increased ESR, and low cobalt content in the body are more often found. Hypocuprosis is characterized by nervous disorders and low copper levels in the liver and blood. To differentiate iron deficiency anemia from the latter two diseases, analysis of the mineral composition of the diet can be very valuable.

Treatment and prevention. Considering the role of iron in the etiology of nutritional anemia, the basis of treatment and preventive measures for this disease should be drugs that include this bioelement. They can be administered orally or parenterally. Of the first, iron glycerophosphate, proposed in 1961, is very effective (D.P. Ivanov et al., 1971). It is a light yellow powder containing 18% iron and 15% phosphorus. It is administered to piglets in the form of powder (0.5-1.0 g) or paste (2.5-3.0 g) daily or every other day starting from 5-7 days of age for 5-7 days. The powder is mixed with water, skim milk, fish oil and put it in the mouth. In large farms and complexes, it is more advisable to use iron glycerophosphate as part of granulated feed, which piglets begin to feed from 5-7 days of age. The drug is also prescribed to sows before insemination, 15-20 days before farrowing and for 2 weeks suckling period 5-10 g per head per day.

Currently, injectable iron-dextran preparations are more often used to prevent anemia and treat sick animals. The widely used domestic ferroglucin-75 was first tested as an antianemic agent in 1963 (D.P. Ivanov et al., 1971). The drug is a complex compound of low molecular weight dextran with ferric iron, which contains about 75 mg in 1 ml. Ferroglukin-75 s for preventive purposes is administered to piglets into the muscles of the thigh or neck in a dose of 2-3 ml (150–225 mg of iron) at 3-4 days of age. The drug can also be administered orally in the first 8-12 hours after birth of sucklings at the same dose. If necessary, the injection is repeated on the 10-14th day of the animals’ life at a dose of 3 ml. The drug has good preventive effectiveness, stimulates the growth and development of piglets, and reduces waste. Ferroglucin-75 is prescribed to sows 15-20 days before farrowing in a dose of 10 ml. The drug is injected into calves and foals with 5-8 ml on the 3-4th day of life, and in lambs with 3-4 ml on the 5-6th day of life.

For therapeutic purposes, ferroglucin-75 is administered to young animals over two weeks of age in mg at the rate of ferric iron per 1 kg of body weight: piglets 50-100; calves and foals 15-20; lambs and fur-bearing animals 50. If necessary, injections of the drug are repeated in the same doses after 10 days. The use of ferroglucin-75 is contraindicated in cases of acute vitamin E deficiency.

Currently, practical veterinary specialists of the republic have the opportunity to choose from a wide selection of imported iron dextran preparations. All of them, as a rule, differ only in iron content, but some additionally include vitamin B12.

Considering that in practice nutritional anemia is often diagnosed with iodine deficiency, as well as the role of this microelement for newborn piglets and sows, we tested and introduced the drug DIF-3 into production. The drug is a complex compound and contains 48.0-50.0 mg/ml iron and 4.8-5.6 mg/ml iodine. It is a sterile, non-volatile, dark brown liquid with a slight specific smell, mixes well with water.

Antianemic effectiveness of the drug Dif-3 and its effect on nonspecific resistance, immune reactivity, functional activity thyroid gland suckling piglets were studied in comparison with other parenteral and iron preparations oral administration for 86 animals, divided according to the principle of analogues into 4 groups. The piglets of the first group were fed individually from the 5th to the 10th day of life 0.5 g daily, and from the 11th to 21st day 1.0 g every other day with iron glycerophosphate. The sucklings of the second group received at the same time a mixture of this drug with iodinol (before the 10th day of life, 0.5 g of iron glycerophosphate + 0.5 ml of iodinol, and from the 11th day - 1.0 g + 1.0 ml, respectively). Animals of the third and fourth groups at 5 and 15 days of age were administered parenterally, respectively, DIF-3 and ferroglucin-75 in an amount of 2 ml per injection. At 25 days of age, 3 sucklings from each group were killed, and samples of the liver, muscles and thyroid gland were collected.

During clinical observation of piglets that were fed iron glycerophosphate (group 1), administered DIF-3 (3) and ferroglucin-75 (4), it was found that they developed well, were mobile, willingly suckled the queens and ate feed. Many animals that received a mixture of ferric glycerophosphate and iodinol experienced gastrointestinal dysfunction, and by the end of the second week of life, most of them developed Clinical signs nutritional anemia.

The results of a blood test showed that at 15 days of age, piglets treated with DIF-3 had the highest rates of erythropoiesis. Moreover, the differences in hematocrit value, compared with animals of the fourth group (ferroglucin-75), were significant (P< 0,05). В конце опыта морфологические показатели крови между группами достоверно не отличались (Р >0.05), however, all of them, with the exception of leukocytes, were lower in animals that received a mixture of iron glycerophosphate and iodinol.

The iron content in the liver and muscles of piglets fed iron glycerophosphate and administered DIF-3 and ferroglucin-75 did not differ significantly. It was significantly lower in piglets of the second group - 98.8 ± 21.4 and 51.1 ± 3.6 μg/g of dry matter, respectively. They also established a minimum level of manganese in the muscles - 1.1±0.2 μg/g dry tissue, which is reliable (R<0,05) ниже, чем у животных, обработанных ДИФ-3.

It was found that of all the tested drugs, DIF-3 had the most pronounced effect on the natural resistance of the piglets. Thus, on the 12th day of the experiment, phagocytic activity and phagocytic index of leukocytes in animals of the third group amounted to 46.1 ± 4.17% and 3.10 ± 0.17 microbial cells, respectively, which is 23.6 (P > 0.05) ) and 16.5% (P< 0,05) выше, чем у поросят, которым инъецировали ферроглюкин –75. Обработка сосунов ДИФ-3 сильнее повышала также бактерицидную и лизоцимную активность сыворотки крови. Самыми низкими в 15 и 26-дневном возрасте показатели nonspecific protection were in anemic piglets of the second group.

Intramuscular administration of DIF-3 increased the level total protein blood serum. At 26 days of age in piglets of the third group, this figure was 11.5% (P< 0,05), чем у животных четвертой группы.

In piglets of the third group, on the 12th and 23rd days of the experiment, the highest absolute and percentage content of T-lymphocytes was established, which was significantly higher (P< 0,05), чем у животных, которым скармливали смесь глицерофосфата с йодинолом (2 группа).

Determination of the level of thyroid hormones in the blood showed that on the 12th day of the experiment in piglets of the second and third groups, the amount of T3 was 3.6, respectively; 7.7, and T4 – 9.5 and 12.1% lower than in animals treated with ferroglucin-75 (group 4). By the end of the experiment, the T4 content in piglets of the first, second and fourth groups increased slightly, and in young animals treated with DIF-3, on the contrary, it decreased by 5.6% and amounted to 87.12 ± 6.42 nmol/l, which is significantly less than animals of the fourth group (P< 0,05). В этот период уровень Т3 у поросят второй, третьей групп составил лишь соответственно 87,0 и 91,5% относительно сосунов, обработанных ферроглюкином –75.

The highest average live weight of piglets during the weaning period (28 days) was found in the third group - 6.19 kg, which is higher than that of the young animals of the first, second and fourth groups, by 17.9, respectively; 21.6 and 7.8%.

Analysis of the results showed that ferroglucin-75, DIF-3 and iron glycerophosphate approximately equally stimulate hematopoiesis, ensure the supply of iron to the body and prevent iron deficiency anemia. Feeding piglets a mixture of iron glycerophosphate and iodinol (group 2) significantly reduces the absorption of iron in gastrointestinal tract, which is apparently associated with the unfavorable effect of the combination of elements used and their forms in the gastrointestinal tract of animals. The presence of iodine in the injectable iron dextran preparation DIF-3 has virtually no effect negative influence for iron absorption. In addition, iodine itself normalizes the function of the thyroid gland, significantly increases natural resistance and stimulates the growth of animals.

To clarify the effect of DIF-3, ferroglucin-75 and iron glycerophosphate on hematopoiesis, natural resistance, immune reactivity of the body of pregnant sows and to determine the effectiveness of the use of these drugs for the prevention of iron iodine deficiency in the mother-offspring system, two experiments were conducted. In the first of 48 sows that had 2-3 farrows, 4 groups of 12 animals each were formed. Animals of the first group were kept on a normal household diet (control). Sows of the second group, three weeks before the expected farrowing, during the first three weeks of the suckling period, were fed iron glycerophosphate at a rate of 5 g per head per day. Three weeks before farrowing, animals of the third and fourth groups were injected intramuscularly with DIF-3 and ferroglucin-75 at a dose of 10 ml, respectively. 4 sucklings from each group of sows were killed in the first hours of life, and the remaining piglets were treated with the same iron preparations as their mothers to prevent iron deficiency anemia. Iron glycerophosphate sucklings of the second group received from the 5th to the 21st day of life 0.5 g daily, or 1.0 g every other day. DIF-3 and ferroglucin-75 in an amount of 2 ml per injection were administered at 3 and 10 days of age. As a control (without treatment with iron preparations), 5 piglets from 6 sows of the first group were left.

Administration of iron-containing drugs to pregnant sows did not cause negative changes in their clinical condition. A blood test revealed that 5-6 days before farrowing, the hemoglobin level in animals treated with DIF-3 (group 3) and those receiving iron glycerophosphate (2) increased accordingly by 5.6 and 2.6%, and in sows of the first and fourth groups it decreased by 5.8 and 2.6%. The content of erythrocytes during this period decreased and was minimal in animals of the control (1) group - 6.50±0.35 T/l, and the number of leukocytes increased, and the maximum (by 30.3%) in the second group (P> 0, 05).

On the 4-5th day after farrowing, no significant intergroup differences in morphological blood parameters were detected, but they were higher in sows of the experimental groups.

On the 14-15th day of the suckling period, the highest content of leukocytes was observed in animals of the second and third groups, which was significantly higher than in the control group (P< 0,05). Остальные показатели гемопоэза существенно между группами не отличались.

When analyzing the leukogram, the most significant changes were detected in lymphocytes, segmented neutrophils, eosinophils and basophils.

The amount of iron in the blood of sows of the experimental groups from days 93-94 to 108-109 of gestation decreased by 11.2-11.8%, and in control animals - by 13.2%. During this period, the iodine content in sows of groups 1-4 decreased by 31.6, respectively; 30.0; 6.2 and 38.1%. Moreover, the absolute amount of this element in animals treated with DIF-3 was 382.18 ± 33.88 nmol/l, which was significantly higher than in other groups.

In the first days after farrowing, iron levels increased in the first group by 7.3%, and in the second, third and fourth groups - by 11.1, respectively; 17.2 and 16.0%. This is due to different reserves of the microelement and the unequal reaction of the body of control and experimental queens to its loss with colostrum and milk. During this period, an increase in blood levels of copper and zinc was also noted. In contrast to these microelements, the iodine content decreased, but was highest in animals that were administered DIF-3, -223.08 ± 26.79 nmol/l, which is 41.4% more than in the control group (P< 0,05).

The effect of DIF-3 on the level of iodine in the body of pregnant sows is evidenced by the results of determining thyroid hormones. Thus, the amount of T4 in the blood of animals treated with this drug by the end of pregnancy decreased by only 12.8%, and in sows of the first, second and fourth groups - 43.4; 50.4 and 71.6%. The T3 content under the influence of DIF-3 decreased more significantly and amounted to 0.77±0.03 nmol/l, which is significantly lower than in animals of the control group (P< 0,01).

Thus, the administration of iron supplements to pregnant sows has a positive effect on the morphological and microelement composition of the blood. In addition, the administration of DIF-3 prevents iodine deficiency.

The results of studying the tested drugs for nonspecific resistance, immune reactivity and productivity of sows have important scientific and practical significance.

Their analysis showed that 5-6 days before the survey, in animals that were administered DIF-3 (group III), the bactericidal and lysozyme activity of blood serum, phagocytic activity and the phagocytic index of neutrophils were significantly higher than in the control group. On the 4-5th day after farrowing, significant differences remained only in relation to humoral factors of nonspecific protection. In animals receiving iron glycerophosphate, the phagocytic index on the 14-15th day after farrowing was 20.48±1.11 microbial bodies, which is also significantly higher (P<0,05), чем у контрольных.

In the blood serum of sows treated with DIF-3, the content of total protein by the end of pregnancy increased by 2.7%, and in animals of groups I, II and IV it decreased slightly. At the same time, the administration of DIF-3 and ferroglucin-75 led to a decrease in the level of transferrins. In sows of groups I and II, this indicator, on the contrary, increased during the same period. Moreover, the differences between animals of groups I and III were significant (P<0,01). Одновременно у свиноматок всех групп снизилось количество Ig G.

After farrowing, the content of total protein in the blood serum remained the same as in the last period of pregnancy. Of its fractions, an increase in a-globulins and transferrins was noted in all animals, as well as a further decrease in IgG.

On the 14-15th day after farrowing, the highest amount of IgG was in sows receiving iron glycerophosphate (16.66±0.76%), which was significantly higher than in the control group (14.06±0.63%). During this period, animals of all experimental groups showed a higher content of Ig A and M, as well as T and B lymphocytes.

The use of iron supplements for sows also had a positive effect on their productivity. Thus, the yield of piglets per queen in groups II, III and IV was higher than that of the control group (9 animals) by 5.5, 12.2 and 6.7%, respectively. At the same time, the live weight of newborn sucklings obtained from group III queens was 8.1% higher than the offspring of control sows.

Summarizing these results, we can conclude that of the tested drugs, the most active stimulator of resistance and immune reactivity of pregnant uteruses is DIF-3.

The use of iron supplements in pregnant sows also affects the rates of phagocytosis and hematopoiesis in newborn piglets. It was found that the hemoglobin level and hematocrit in the offspring of group II queens were especially high (P< 0,05). Уровень железа в крови поросят, полученных от свиноматок, обработанных ДИФ-3, составил 6,02±0,26 ммоль/л, что достоверно выше (Р < 0,05), чем у сосунов контрольных маток.

On the 12th and 26th days of life, the indicators of erythropoiesis and the iron content in the blood of young animals in the experimental groups were significantly higher than in the control groups, which were characterized by the presence of clinical signs of iron deficiency anemia. By the end of the 2nd week of life, cellular and humoral indicators of natural resistance were maximum in piglets treated with DIF-3. Its administration also contributed to an increase in the level of total serum protein, mainly due to IgG and a - globulins. Under the influence of ferroglucin –75 and DIF-3, a significant decrease in the concentration of transferrins was noted.

Determination of thyroid hormones in the blood of newborn piglets showed higher activity of the thyroid gland than in sows, which indicates its important role in adaptation to new environmental conditions. It should be noted that suckers from different litters exhibit significant fluctuations in T4. Moreover, as a rule, piglets with a high content of T4 also had an increased amount of T3.

At 12 days of age, the lowest level of T4 was in anemic piglets of group I, and the minimum level of T3 was in animals injected with DIF-3 (group III). Their iodine content, on the contrary, was the highest – 618.58±18.12 nmol/l, which is significantly higher than in other groups (P<0,001). К концу подсосного периода минимальный уровень тиреоидных гормонов сохранился у животных, обработанных ДИФ-3, а количество йода по-прежнему было достоверно выше, чем у поросят других групп (Р < 0,01). Увеличение запасов йода и организме поросят III группы способствовало снижению заболеваемости, гибели и повышению среднесуточного прироста живой массы. Так, средняя живая масса одного поросенка III группы к отъему (26 дней) составила 6,37±0,17 кг, что на 34,9; 15,4 и 10,5% выше,чем в I, II и VI группах соответственно.

The second experiment was carried out on 24 sows, divided into three equal groups, and the offspring obtained from them. Animals of group I were kept on a normal diet (control). Three weeks before expected farrowing, sows of groups II and III were administered a single parenteral dose of ferroglucin-75 and DIF-3, respectively, at a dose of 10 ml per animal. Immediately after birth, 4-5 sucklings from each group of sows were killed and liver, spleen and muscle samples were collected. The remaining piglets obtained from sows of the control group were divided into three (1, 2, 3), and from sows of groups II and III - into two equal subgroups (4, 5 and 6, 7, respectively). One subgroup of sucklings from each group of queens (3, 5, 7) served as a control and were not subsequently treated with iron supplements. The first and second subgroups of piglets from control sows at 3 and 12 days of age were injected intramuscularly with ferroglucin-75 and DIF-3, respectively, at a dose of 2 ml per animal. The fourth and sixth subgroups of piglets were treated with the same iron supplements as their mothers, i.e. ferroglucin-75 and DIF-3 at the same age periods and in the same doses as sucklings from sows of the control group.

Observations of piglets from sows treated with DIF-3 and ferroglucin-75 showed that the most characteristic clinical signs of anemia (pallor of the skin and mucous membranes, rapid and shallow breathing, tachycardia, swelling of the eyelids, lethargy) in animals of all control groups began to appear on 9-12 days of life, and the severity of the disease was approximately the same.

The number of erythrocytes, leukocytes, hemoglobin level and hematocrit in the 2-day offspring of control sows were not significantly inferior to those of piglets whose mothers were administered ferroglucin-75 (group II) and DIF-3 (III). At 10 days of age, the differences in erythropoiesis indicators between the control and experimental subgroups were more pronounced in groups II and III. By the end of the experiment, the morphological parameters of the blood of control piglets, except for leukocytes in group I, were significantly lower than those of sucklings treated with iron-dextran preparations.

The amount of iron in the blood of newborn piglets obtained from queens of groups II and III was 5.96±0.27 and 5.52±0.23 mmol/l, respectively, which is significantly higher (P< 0,001), чем у приплода контрольных свиноматок. С одержание этого микроэлемента в печени и селезенке потомства от опытных маток, напротив, оказалось достоверно ниже, чем у поросят от контрольных. Уровень железа в молозиве первых 12 часов лактации достоверных межгрупповых различий не имел, однако был выше у животных опытных групп.

Summarizing the results obtained, we concluded that the administration of ferroglucin-75 and DIF-3 to sows in the last period of pregnancy at a dose of 10 ml per animal does not completely prevent iron deficiency anemia in the offspring, but significantly increases the iron content in the blood of newborns and slightly in the colostrum of mothers , significantly reducing its accumulation in the liver and spleen of the fetus.

Further studies have shown that DIF-3 is an effective means of preventing iron and iodine deficiency in cattle and has a positive effect on the growth and development of calves and the reproductive ability of cows.

Taking this into account, DIF-3 is recommended for production as a means of preventing iodine deficiency (goiter), iron deficiency anemia in young farm animals, increasing the reproductive capacity of sows and cows, as well as the viability of newborn piglets and calves, and preventing postpartum diseases (retained placenta, endometritis).

The drug is administered intramuscularly into the thigh or neck area of ​​pigs and cattle and cows in doses:

· Piglets – 2.0-3.0 ml per head on days 3-5 of life; if necessary, the injection is repeated after 7-10 days at the same dose;

· For sows – 8-12 days before insemination and 20-30 days before farrowing, 8-10 ml per head;

· For calves - on days 1-2 of life, 5 ml per head once;

· For cows - 35-25 days before calving in a dose of 7-10 ml per head once;

There are no contraindications to the use of the drug.

Animal products after using DIF-3 are used without restrictions, however, it should be borne in mind that the staining of tissue at the injection site lasts up to 30 days.

An effective means of preventing and treating iron deficiency anemia in piglets is Ferrovit, a new injectable veterinary drug containing iron and vitamin B12. It is a sterile, dark brown liquid with a weak specific odor. Our extensive clinical trials have shown that ferrovit has an antianemic and restorative effect. The iron contained in it, after being included in metabolic processes, stimulates hematopoiesis. Vitamin B 12 also has a positive effect on hematopoiesis, increasing the efficiency of iron use and the growth energy of piglets.

Ferrovit is used in pigs to prevent and treat nutritional anemia, normalize metabolism, and increase the safety and growth rate of young animals.

The drug is administered subcutaneously or intramuscularly. For piglets 3-10 days of age, the dose is 5 ml. For older young animals and adult pigs, ferrovite is injected in an amount of 10-20 ml. If necessary, the drug is re-prescribed in the same dose after 7-10 days. No more than 10 ml of the drug can be injected into an animal at one injection site. Caution should be exercised when prescribing ferrovit to piglets with significant vitamin E and selenium deficiency.

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Nutritional anemia.

Nutritional (nutritional) anemia (anaemia alimentaria (anaemia nutritiva)) is iron deficiency anemia that develops due to insufficient intake of iron from food, for example, when feeding children with cow's or goat's milk.

Nutritional anemia develops in children from 5 months to 2 years of age due to prolonged feeding with foods low in iron salts, lack of vitamins and proteins. Premature babies may develop the disease earlier.

Inspection reveals anemia in the visible mucous membranes, down-free areas of the skin, the crumbs of the paws and nose. Appetite decreases, animals lose weight, are stunted and die. When examining blood, the hemoglobin level decreases depending on the course of the disease. In puppies, the surviving ones have depigmented undercoats (bilopurosis). A study of sick females reveals their weight loss, loss of maternal instinct, the birth of dead, anemic or small puppies with impaired digestive function, low hemoglobin in the blood.

Etiology. The main cause of the disease is a lack of iron in the body. Numerous factors that reduce the resistance of newborns contribute to the disease: lack of protein, cobalt, zinc, manganese, vitamins A, B12, E in the diet; low level of hemoglobin in the blood, etc. It is also possible that the lifespan of red blood cells is 60 days, while in other animals it is 120 days. The course of anemia worsens, and the mortality rate of piglets increases due to violations of housing technology and sanitation rules.

Symptoms. In the first 10-15 days of life, young animals of all animal species experience a decrease in hemoglobin and the number of red blood cells. In foals, calves and lambs it is usually temporary, and in piglets it often develops into a severe form of the disease.

Iron deficiency anemia occurs between 3 and 6 weeks of age. Pallor of the skin and visible mucous membranes appears, which later acquire a yellow color, swelling of the eyelids, and lethargy. Mobility noticeably decreases, they become inactive, bury themselves in the litter, suckle poorly, quickly lag behind in growth, and their skin becomes wrinkled. There may be a perversion of appetite. Digestion is disrupted. The abdomen is often swollen or pulled up, and there is diarrhea, alternating with constipation. There may be some mucus in the stool. Hemoglobin in the blood sharply decreases from 100 to 30-35 g/l. The number of erythrocytes usually does not change, but sometimes it can decrease to 2 million per 1 mm3, and their qualitative composition can also transform, accompanied by anisocytosis, poikilocytosis, and polychromatophilia.

Diagnosis and differential diagnosis. Early diagnosis consists of determining the amount of hemoglobin in the blood, liver, spleen, and kidneys. In other cases, a feeding analysis is performed based on clinical symptoms and the results of hematological studies. Determining the color indicator of blood is of great diagnostic importance. Normally, this indicator is close to one; with anemia it drops to 0.6-0.5.

When differentiating the disease, anemia that occurs due to the influence of other factors on the body of young animals, in particular infectious and invasive ones, is excluded.

Pathogenesis. The mechanism of development of nutritional anemia has not been sufficiently studied. Most researchers believe that the pathogenesis of anemia is based on a violation of the erythropoietic function of the hematopoietic system. With endemic nutritional anemia in sheep, bone marrow hematopoiesis is disrupted (A. D. Grachev, 1971). In the erythroblastic series, passive hyperplasia develops due to a delay in the maturation of orthochromic normoblasts. The erythroblast maturation index decreases. Normoblastic hematopoiesis is partially replaced by megaloblastic hematopoiesis. Mitotic division of cellular elements of the bone marrow is inhibited, and the number of primary forms of erytoblasts decreases. Deviations in erythropoiesis are most pronounced at the stage of differentiation of erythroblasts and their hemoglobinization.

The leukoblastic series changes. The accumulation of zosinophilic cells, a decrease in the neutrophil maturation index, and the appearance of pathological forms of leukocytes are noted.

Hematopoiesis disorders affect the morphological composition of peripheral blood. Due to passive hyperplasia of erythroblastic tissue, the release of mature red blood cells into the bloodstream is delayed. Megalocytes, polychromatophils, and reticulocytes appear in the peripheral blood, and the number of young and band neutrophils increases. The content of segmented neutrophils, on the contrary, decreases.

The amount of copper, cobalt and manganese in the blood decreases. In young animals with anemia, the iron content in the blood increases, which is believed to be due to the body’s loss of ability to absorb this element. The level of boron and molybdenum in the blood may be increased.

In animals suffering from nutritional anemia, phosphorus-calcium, protein, carbohydrate and fat metabolism are disrupted. The activity of the heart, liver and other organs is disrupted. The disease is often complicated by bronchopneumonia and gastroenteritis.

Pharmacocorrection:

  • Periodic monitoring of the blood picture;
  • eating foods high in iron (meat, liver, etc.);
  • preventive administration of iron supplements in risk groups.
  • prompt elimination of sources of blood loss.

Treatment is carried out only with long-term intake of ferrous iron preparations orally in moderate doses, and a significant increase in hemoglobin, unlike improvement in well-being, will not be immediate - after 4-6 weeks.

Usually, any ferrous iron preparation is prescribed - most often it is ferrous sulfate - its prolonged dosage form is better, in an average therapeutic dose for several months, then the dose is reduced to the minimum for several more months, and then (if the cause of anemia is not eliminated), the maintenance minimum continues doses for a week every month for many years. Thus, this practice has proven itself well in the treatment of women with chronic posthemorrhagic iron deficiency anemia due to long-term hyperpolymenorrhea with tardiferon - one tablet in the morning and evening for 6 months without a break, then one tablet a day for another 6 months, then for several years every day for a week on days menstruation. This provides an iron load during the appearance of prolonged, heavy periods during menopause. A senseless anachronism is determining hemoglobin levels before and after menstruation.

For agastric (gastrectomy for a tumor) anemia, a good effect is achieved by taking a minimum dose of the drug continuously for many years and administering vitamin B 6 200 micrograms per day intramuscularly or subcutaneously for four weeks in a row every year for life.

Pregnant women with iron deficiency and anemia (a slight decrease in hemoglobin levels and the number of red blood cells is physiological due to moderate hydremia and does not require treatment) are prescribed an average dose of ferrous sulfate orally before birth and during breastfeeding, unless the child develops diarrhea, which usually happens rarely.

  1. Ursoferran-100 – IM 0.3ml

A sterile, slightly viscous solution for injection, dark brown in color with a specific odor, containing iron (Fe3+) in the form of iron (III)-dextran-heptonic acid as an active ingredient. Produced in glass bottles of 100 ml.

pharmachologic effect

After parenteral administration of ursoferrane, the iron (III)-dextran-heptonic acid complex slowly releases Fe3+, which ensures a prolonged effect of the drug in the body. Ursoferran stimulates erythropoiesis, due to the active inclusion of iron in hemoglobin and tissue enzymes (cytochromes, cytochrome oxidases, peroxidases, etc.), increases the body's resistance.

Indications

Iron deficiency anemia in piglets and minks.

Doses and method of administration

The drug is administered to piglets on the third or fourth day of life once deeply intramuscularly in the neck or in the upper third of the thigh at a dose of 1.5 - 2 ml per animal. For female minks, during the period of feeding puppies in the spring, the drug is administered once subcutaneously or intramuscularly at a dose of 0.3 ml per animal. For mink puppies aged 6 - 12 weeks, the drug is administered once subcutaneously or intramuscularly at a dose of 0.2 ml per animal.

Side effects

In rare cases, tissue redness or slight swelling may occur at the injection site, which disappear spontaneously within 2 to 3 days.

Rp.: Ursoferrani-100 – 0.3 ml

D.S. Once 0.3 ml IM

  1. Ascorbic acid 5% - 3 ml IM 1 time per day, 7 days

Pharmachologic effect:
It is important for the functioning of the body. Participates in the regulation of redox processes, carbohydrate metabolism, blood clotting, normal permeability of capillaries (the smallest vessels), the formation of steroid hormones, the synthesis of collagen and procollagen. Increases the body's resistance to infections.

Indications for use:
Prevention and treatment of vitamin deficiency and hypovitaminosis C (lack of intake and reduced intake of vitamin C into the body). Hemorrhagic diathesis (increased bleeding). Bleeding (nasal, pulmonary, hepatic, uterine, etc.). Infectious diseases. Intoxication (poisoning). Diseases of the gastrointestinal tract (achilia /lack of secretion of hydrochloric acid and enzymes in the stomach/, peptic ulcer, enterocolitis /inflammation of the small and large intestine/). Increased physical and mental stress.

Mode of application:
For prophylaxis, 0.05-1 g orally once a day for adults. For treatment in adults, 0.05-0.1 g 3-5 times a day. Parenterally (bypassing the gastrointestinal tract) it is administered in the form of sodium ascorbate, 1-3 ml of a 5% solution. A single dose is not higher than 0.2 g, a daily dose is 0.5 g. Children are prescribed orally for prophylaxis at 0.02-0.03 g per day; for treatment 0.05-0.1 g 1-2 times a day, parenterally 1-2 ml of 5% solution per day for 2-3 weeks.

Side effects:
Inhibition of the pancreatic insular apparatus (pancreatic cells that produce insulin), glucosuria (presence of sugar in the urine), inhibition of glycogen synthesis.

Contraindications:
Thrombophlebitis (inflammation of the vein wall with blockage). Tendency to thrombosis (formation of a blood clot in a vessel).

Release form:
Powder; dragees 0.05 g in a package of 50 g; For vitaminization tablets, write 0.5 g and 2.5 g; ascorbic acid tablets of 0.025 g with glucose weighing 3 g in a package of 10 pieces for children; tablets of ascorbic acid 0.1 g and glucose 0.877 g in a package of 12 pieces; ampoules of 5% solution in a package of 10 pieces of 1 ml, 2 ml and 5 ml; ampoules of 10% solution in a package of 10 pieces of 1 ml, 2 ml, 5 ml; combined tablets (0.1 g of ascorbic acid and 0.005 g of folic acid) in a package of 50 pieces.

Rp.: Sol. Ac. ascorbinici 5% 3 ml
D.t.d. N. 21 in ampull.
S. 3 ml IM 1 time per day, 7 days

  1. Calcium chloride 10% - 2ml IM once

Pharmachologic effect:
Calcium plays an important role in the functioning of the body. Calcium ions are necessary for the process of transmission of nerve impulses, contraction of skeletal and smooth muscles, activity of the heart muscle, formation of bone tissue, blood clotting, as well as for the normal functioning of other organs and systems.
A reduced calcium content in the blood plasma is observed in a number of pathological conditions. Severe hypocalcemia (low calcium levels in the blood) leads to the development of tetany (convulsions).
Correction of hypocalcemia is carried out with the help of calcium supplements, as well as hormonal drugs (see potassium tonin - p. 543, parathyroidin - p. 545), ergokaliferol, etc.

Indications for use:
In case of insufficient function of the parathyroid glands, accompanied by tetany or spasmophilia (a disease in children associated with a decrease in the content of calcium ions in the blood and alkalinization of the blood). With increased release of calcium from the body, which can occur during prolonged immobilization of patients. For allergic diseases (serum sickness, urticaria, angioedema, hay fever, etc.) and allergic complications associated with taking medications. The mechanism of the antiallergic effect is unclear; however, it should be noted that intravenous administration of calcium salts causes excitation of the sympathetic nervous system and increased secretion of adrenaline by the adrenal glands. As a means of reducing vascular permeability in hemorrhagic vasculitis (hemorrhage due to inflammation of the walls of blood vessels), radiation sickness, inflammatory and exudative processes (release of protein-rich fluid from small vessels of tissue) - pneumonia (pneumonia), pleurisy (inflammation of the membrane covering lungs and lining the wall of the chest cavity), adnexitis (inflammation of the uterine appendages), endometritis (inflammation of the inner surface of the uterus), etc. For skin diseases (itching, eczema, psoriasis, etc.). For parenchymal hepatitis (inflammation of liver tissue), toxic liver damage (damage to the liver by harmful substances), nephritis (inflammation of the kidney), eclampsia (severe form of late toxicosis of pregnancy), hyperkalemic form of paroxysmal myoplegia (paroxysmal / periodically occurring / paralysis occurring with an increase in the content of potassium in the blood).
Also used as a hemostatic agent for pulmonary, gastrointestinal, nasal, and uterine bleeding; in surgical practice, it is sometimes administered before surgery to increase blood clotting. However, there is no sufficiently reliable data on the hemostatic (hemostatic) effect of calcium salts introduced into the body from the outside; Calcium ions are necessary for blood clotting, but the amount of calcium normally contained in blood plasma exceeds the amount required to convert prothrombin into thrombin (one of the blood clotting factors).
It is also used as an antidote for poisoning with magnesium salts (see magnesium sulfate), oxalic acid and its soluble salts, as well as soluble salts of fluoric acid (when interacting with calcium chloride, non-dissociating / non-disintegrating / and non-toxic oxalate and calcium fluoride are formed).
The drug is also used in combination with other methods and means to stimulate labor.
When taken orally (8-10 g) it has a diuretic (diuretic) effect; According to the mechanism of action, it belongs to acid-forming diuretics (diuretics - see ammonium chloride).

Mode of application:
Calcium chloride is prescribed orally, intravenously by drip (slowly), intravenously by stream (very slowly!), and also administered by electrophoresis (percutaneous administration of medicinal substances through an electric current).
Taken orally after meals in the form of a 5-10% solution 2-3 times a day. Adults are prescribed 10-15 ml per dose (dessert or tablespoon of solution); children - 5-10 ml (teaspoon or dessert spoon).
6 drops per minute are injected into a vein, diluting before administration with 5-10 ml of a 10% solution in 100-200 ml of isotonic sodium chloride solution or 5% glucose solution. 5 ml of a 10% solution is injected intravenously slowly (over 3-5 minutes).
For the treatment of allergic diseases, the combined use of calcium chloride and antihistamines is recommended.

Side effects:
When taking calcium chloride orally, pain in the epigastric region and heartburn are possible; when administered into a vein - bradycardia (decreased heart rate); with rapid administration, ventricular fibrillation (chaotic contractions of the heart muscle) may occur. With intravenous administration of calcium chloride, a feeling of heat appears first in the mouth, and then throughout the body. This feature of the drug was previously used to determine the speed of blood flow; The time between the moment of its introduction into the vein and the appearance of a sensation of heat was determined.

Contraindications:
Calcium chloride solutions cannot be administered subcutaneously or intramuscularly, as they cause severe irritation and necrosis (death) of tissue.
Calcium chloride is contraindicated in cases of a tendency to thrombosis (blockage of a vessel with a blood clot), advanced atherosclerosis, or increased calcium levels in the blood.

Release form:
Powder in small well-sealed glass jars with a stopper filled with paraffin; 10% solution in ampoules of 5 and 10 ml; 5% and 10% solutions for oral administration.