Page 33 of 81

Nutritional anemia is understood as a disorder of the hematopoietic system that develops due to malnutrition and is observed mainly in infants and young children who are bottle-fed. Depending on the nature of the underlying cause, there are three main forms of nutritional anemia:

anemia due to one-sided milk feeding,
anemia due to one-sided carbohydrate feeding and
anemia due to various vitamin deficiencies.

In all forms of nutritional anemia, the importance of the endogenous moment is especially clearly revealed, since the same diet, prescribed for the same period, leads to the development of a severe anemic state in one child, while in another, under the same conditions, it has almost no effect on the composition blood.
IN practical activities Most often, we observe nutritional anemia in children aged 6-18 months, who receive significant amounts of cow or goat milk, but are completely or almost completely deprived of proper and timely complementary feeding. Clinical and hematological observations show that there is no reason to classify anemia that develops during breastfeeding as a special clinical form. goat milk, which was proposed by some authors (color table IV). Although it can be considered indisputably proven that the harmful effects of goat's milk are felt faster and more sharply than cow's milk, this difference is only quantitative, not qualitative.
The essence of the harmful effect on hematopoiesis of monotonous dairy nutrition, in other words, the pathogenesis of nutritional anemia cannot be considered definitively established. The old theory of progressive depletion of a child’s body with iron during monotonous milk feeding and the newer view of nutritional anemia as avitaminosis, if they cannot be accepted completely, then in any case should be recognized to a significant extent as justified.
Nutritional anemia due to inadequate feeding, especially with excessive and prolonged monotonous milk nutrition, should be classified as anemia with insufficient hemoglobin formation due to insufficient intake of iron from food; During the first 5-6 months of life, the child uses iron reserves that were deposited in the liver at birth and are largely depleted by the end of the first six months of life. Insufficient use by the body is also of undeniable importance. infant iron from food. A child's gastric juice is poor in hydrochloric acid; when breastfed, it is almost completely bound by milk casein and there is not enough of it to form an easily absorbed ferrous compound; as a result of this, iron taken with food is not absorbed in the child’s intestines; A shift in the reaction of intestinal contents to the alkaline side during monotonous milk feeding promotes the formation of poorly soluble phosphorus iron compounds in the intestines. Thus, both food and medicated iron are not used by the child's body. From what has been said it is clear that nutritional anemia- mostly glands are deficient in me. Undoubtedly, in the pathogenesis of nutritional anemia in infants, the lack of ascorbic acid, other vitamins, copper, cobalt, and possibly other microelements is important. Some authors admit the harmful effects of milk fat, others attribute this effect to soluble fatty acids and, finally, others believe that milk feeding leads to depletion in the body of the reserves of histidine and similar substances necessary for the intermediate formation of ammonia, as a result of which the acid-base balance is disturbed, which favors the development of anemia.
Modern data on exogenous and endogenous antianemic factors make it possible to partially reconsider the issue of the pathogenesis of nutritional anemia. The normal adult stomach secretes what is called internal factor(fundamental secretion, gastromucoprotein), which, interacting with an external factor (vitamin B12) found in meat, vegetables and other nutrients, acquires antianemic properties.
In light of these data, the pathogenesis of some anemias is based on the absence of internal or external factors or a violation of the normal interaction between them. In infants with immature secretory function gastrointestinal tract and in the absence of a sufficient amount of vitamin B12 in their diet conditions are inevitably created that are unfavorable for the activation of the antianemic principle, which makes them predisposed to states of anemia. One must, however, think that this point does not play a role in all forms of alimentary anemia, but only in some that take on a malignant nature with a tendency toward megalocytic erythropoiesis (severe forms with abuse of cow and goat milk, anemia of the Jaksch-Gayema type).
It is necessary to take into account, we think, the influence of the unique bacterial flora of the intestines in children with artificial feeding. Light invasion of Escherichia coli into the upper parts of the digestive tract, in combination with a primary or secondary disruption of the enzymatic energy of the stomach and intestines, can easily disrupt the impermeability of the intestinal barrier, which makes it possible for various products of incomplete breakdown of proteins and bacterial toxins themselves to pass beyond the intestinal wall.
Based purely external signs Two extreme forms of nutritional anemia of milk origin can be distinguished. With the first, mild, often escaping even the careful observation of not only the parents, but also the doctor, the child’s nutrition is almost or not at all disturbed, only some general pastiness, puffiness of the face and pallor of the outer integument are noted. The abdomen is large, peripheral lymph nodes and tonsils are moderately hyperplastic, the liver and spleen are either normal or slightly enlarged. The stool is dense, pale colored; there is often a tendency to constipation. The entire clinical picture, as can be seen from the above, gives the right to speak only about a more or less clearly expressed symptom complex of an eating disorder due to a monotonous milk diet. On the blood side, the main symptom is a decrease in the amount of hemoglobin, reaching 50-60%. The number of red blood cells decreases less clearly and usually fluctuates around 4,000,000, rarely dropping to 3,000,000. According to these ratios, the color index decreases noticeably and is usually equal to 0.5-0.7. There is clearly expressed oligochromemia, sometimes moderate polychromatophilia, almost always a slightly increased content of erythrocytes with vital granularity, and sometimes single normoblasts are found. There is no poikilocytosis. The number of leukocytes and platelets, as well as the leukocyte formula, do not deviate from the norm. From the above it is clear that the entire hematological picture gives the right to speak only about simple hypochromic anemia of the nature of chloranemia (see color table IV).
In the second, severe form, observed in young children, often even during the first six months there is a sharp lag in weight and less significant growth retardation. The skin is either deathly pale or has a waxy or yellowish tint. There is no real jaundice, and the bilirubin level in the blood usually remains at the upper limit of normal. On the eyelids, the back of the feet and at the ankles there is often more or less pronounced swelling, which is often subsequently joined by mainly pinpoint and sometimes more significant hemorrhages on the torso, limbs and face, indicating deep angioedema. Even in the absence of hemorrhages, it is almost always possible to obtain a positive Konchalovsky-Rumpel-Leede phenomenon (tourniquet). Progressive muscle hypotonia is noted. The abdomen is swollen, the liver and especially the spleen are enlarged; the latter sometimes protrudes only 1-2 fingers from under the costal arch and is not particularly dense. In other cases it is very large, reaches the navel and goes even lower into the cavity large pelvis, and to the touch it is dense, almost hard and has a clearly palpable notch (incisura) on the inner edge. In these severe cases, there are almost always clearly pronounced symptoms of rickets. Clinical observations do not give grounds to put the degree of spleen enlargement depending on the severity of rickets and vice versa, and it is also impossible to note the obligatory parallelism between the degree of anemic phenomena, on the one hand, and the severity of rickets and the size of the spleen enlargement, on the other.
As for the causes of splenomegaly, there are no comprehensive explanations for this, but one must think that the enlargement of the spleen is in a causal relationship with the death of red blood cells, lymphatic hyperplasia and myeloid metaplasia.
In such severe cases of nutritional anemia, the blood obtained by pricking a finger is already macroscopically striking in its pallor, sometimes almost watery. The duration of bleeding is noticeably prolonged. The amount of hemoglobin is sharply reduced and often reaches 15-25%, the number of red blood cells fluctuates around 1,500,000-2,000,000, falling in rare cases even below 1,000,000. Despite such pronounced anemia, the child’s lack of subjective signs is almost always striking oxygen starvation. The color index most often fluctuates around one; in especially severe cases it increases, reaching 1.2-1.5, but it is often less than one. Accordingly, the degree of saturation of erythrocytes with hemoglobin is also not always the same, and they can be either hypo- and hyperchromic, or with a normal content of the dye. Almost always, aniso- and poikilocytosis, polychromatophilia and a tendency to megalocytosis are clearly expressed. The number of red blood cells with intravital staining granularity is always more or less sharply increased, the number of nucleated red blood cells sometimes reaches a huge number, up to 50-100 per 100 white blood cells; in other cases there are relatively few of them or even none at all. Jolly bodies and Cabo rings are often found in red blood cells. The picture of red blood with the same degree of anemia can vary significantly, sometimes approaching the little characteristic picture noted in mild cases of nutritional anemia, and sometimes completely reminiscent of the blood picture in malignant anemia. The osmotic resistance of red blood cells usually remains within normal limits. Changes in white blood cells can also vary widely. Their total number is sometimes normal, less often slightly reduced and most often moderately increased. There is usually more or less pronounced lymphocytosis; according to some authors, there may be significant monocytosis, and almost always in moderate quantities there are young forms of granulocytes - myelocytes, myeloblasts and promyelocytes. Basophils are mostly completely absent. Eosinophils are contained in small quantities (0.5-1%) or may also be completely absent. According to the leukocyte formula, the hemogram is close to leukemia (pseudo-leukemia). The number of blood platelets in seriously ill patients can be significantly reduced (less than 100,000), although this is not a constant symptom, in milder patients it fluctuates within normal limits. Retraction of the blood clot is poorly expressed.
A symptom complex characterized hematologically by a sharp decrease in the number of red blood cells and hemoglobin, with a color index greater than one, an abundance of normoblasts and significant leukocytosis, and clinically by severe pallor, loss of nutrition, enlarged liver and a very large enlargement of the spleen, was described by Yaksh and Gayem as independent disease called anaemia splenica infantum or anaemia pseudoleucaemica (see color table VI).
As can be seen from all of the above, there is no reason to isolate this form as an independent nosological unit, and the indicated symptom complex can develop both due to purely nutritional hazards and as a result of the influence of other factors, for example, congenital syphilis and others chronic infections. Depending on the etiology, the leukocyte formula changes slightly; with Jaksh-Hayem's anemia of purely nutritional origin, as a rule, lymphocytosis is observed, while with a completely similar clinical syndrome, but of a toxic-infectious etiology, neutrophilia is observed.
The clinical and hematological picture of nutritional anemia due to dairy hazards is characterized by great polymorphism. We have described two extreme states - light form type of chloranemia and an extremely severe picture corresponding to pseudoleukemic anemia of the Yaksh-Gayema type. Between them there are a number of very diverse intermediate states, differing from each other not only in the intensity of identifying the main clinical and hematological signs, but also in the originality of their combination. We have already indicated that there can be severe nutritional anemia without a significant enlargement of the spleen and, conversely, a large spleen with relatively moderate anemia; to this we add that there are cases of significant normoblastosis without severe splenomegaly and with a low color index and, conversely, a huge spleen is not always combined with a large number of nucleated red blood cells in the peripheral blood.
An example of anemia of the Yaksh-Gayem type of purely nutritional etiology is the following observation.

Girl R.I., 2 years old, born several ahead of schedule, birth weight was 2350 g, breastfeeding for up to 1.5 months, and then was transferred to artificial feeding, and was often sick. Doesn't walk and doesn't stand. The skin is pale with a yellowish tint. The spleen is dense, reaching the level of the navel. Distinct symptoms of rickets. Weight 7,600 g. Blood test: hemoglobin 30%, erythrocytes 2,650,000, color index - 0.6, polychromasia, anisocytosis, moderate poikilocytosis, erythrocytes with supravital granularity 197%, normoblasts 95:300 white blood cells, leukocytes 31,600, neutrophils 41.2% (of which large myeloblasts 2%, micromyeloblasts 5.6%, promyelocytes 2.6%, myelocytes 4%, young 3%, stab 6%, segmented 18%, basophils 0.3%, eosinophils 2, 5% (mature 1.3%, young 0.6%, myelocytes 0.6%), monocytes 2.3%), lymphocytes 52.7%, plasma cells 1%. ROE - 39 mm per hour. This patient had a typical picture of hypochromic anemia of a pronounced regenerative nature, accompanied by splenomegaly.
Point (lifetime) bone marrow gave the following picture: myeloblasts 59.6%) (macromyeloblasts 5.6%), micromyeloblasts 54%)), neutrophils - 39%) (of which promyelocytes 3.3%), myelocytes 5.6%), young 8, 5%), rods 13.6%, segmented 8% (eosinophils 0.6%, lymphocytes 0.3%, reticular cells 0.6%), erythroblasts 15.6 per 100 white cells (basophilic megaloblasts 1.6, polychromatophilic 4.6, orthochromic 3.6).
The myeloblastic nature of the bone marrow and a sharp increase in erythropoiesis indicate a sharp increase in bone marrow function (see color table VI), and, despite this, anemic phenomena rapidly progressed, the amount of hemoglobin decreased to 20%, red blood cells to 124,000, the child died after 17 days with symptoms of associated pneumonia.
Clinical experience provides no basis for the assertion that severe forms of nutritional anemia develop gradually from the lungs, passing through intermediate stages. In many patients, mild and moderate anemia, despite prolonged exposure to a harmful moment, does not show a tendency to develop into a severe form; in others, on the contrary, an extremely severe form develops very quickly, apparently almost suddenly, within a few weeks. The decisive factor explaining this uniqueness, presumably, is the known functional insufficiency of the hematopoietic apparatus of the patient himself.
Nutritional anemia itself occurs without fever, and frequent febrile conditions are explained by a secondary infection that easily affects the weakened body of the patient. This decrease in resistance, decrease protective immunity One must be especially wary of children with anemia, since they, as a rule, die not from anemia as such, but from an intercurrent infection (sepsis, pneumonia, pyuria, etc.). Baar even admits a dual etiology of nutritional anemia: nutritional hazards (vitaminosis) create only a predisposition, causing the development of dystrophy, and the anemic effect is exerted by a secondary infection.
Diagnosis Nutritional anemia can be diagnosed only on the basis of a careful weighing of the medical history and the results of an objective general and hematological examination.
In the differential diagnostic relation, one must keep in mind post-infectious anemia (history, see below), sepsis (general picture, neutrophilia, shift of the Arnett formula to the left), hemolytic anemia(reduced osmotic resistance of red blood cells, microcytosis, jaundice, bilirubinemia) and leukemia. Some authors were even inclined to consider anaemia pseudoleucaemica infantum as a unique form of childhood leukemia; the difference in anatomical changes in both forms makes this view unfounded, and at present it is abandoned by everyone. When differentiating myelosis from Jaksch-Hayem anemia, one must keep in mind the following: the first disease is observed less frequently in early childhood; it occurs more or less acutely, in children who were previously healthy, without signs of severe rickets; with leukemia there is no lymphocytosis, there are almost always basophils (almost never with pseudoleukemic anemia), the number of ellinophils is significantly increased, the liver and spleen are evenly enlarged (with Jaksh-Gayema anemia, an enlargement of the spleen prevails), the disease always ends in death. In some cases, the diagnosis can be very difficult, especially with Guglielmo leukanemia. Intravital examination of bone marrow puncture makes it quite possible correct diagnosis during life, even in very severe cases (see colors, Table VI).
You should never abandon the Pirquet-Mantoux and Wasserman reaction, and it is often more advisable to check the latter with the parents rather than with the patient himself (especially in the case of very young children).
On section, an abundance of normo- and megaloblasts is found in the bone marrow, which indicates a former state of enhanced erythropoiesis; usually contains many myeloblasts and myelocytes. Extramedullary foci of hematopoiesis are found not only in the spleen and liver, but often also in the kidneys and lymph nodes.
Along with myeloid metaplasia, it is often possible to observe the proliferation of lymphoid tissue in the bone marrow (although, apparently, single lymphatic follicles are also found in normal bone marrow). Hemosiderosis of organs indicates increased breakdown of red blood cells during life.
Treatment, of course, should be based on adjusting the diet by reducing the amount of milk and introducing a variety of complementary foods. In mild cases, even under the influence of one diet it is possible to restore normal composition blood within 4-8 weeks. In seriously ill patients, it is often very difficult to diversify the diet, which is hampered not only by the child’s lack of appetite, but also by his persistent reluctance to accept new, especially denser foods. In such cases, it is advisable to first somewhat stimulate the child’s entire body by prescribing large doses of iron, liver, nonspecific protein therapy, hemotherapy, ultraviolet irradiation and enzyme therapy, and only with an improvement in appetite gradually diversify the diet. In especially severe cases, it is not possible to start with these relatively slow-acting drugs and you have to resort to blood transfusions, which usually has a brilliant effect, quickly eliminating severe anemic phenomena, improving the child’s well-being and appetite and increasing his resistance to all sorts of random infections. Indications for transfusion are: 1) low (less than 2,000,000) content of erythrocytes and hemoglobin, 2) the presence of secondary complications that occur sluggishly due to the reduced resistance of the body and, in turn, complicate the treatment of anemia with conventional means, and 3) lack of adequate effect from conventional methods dietary and drug treatment.
It is necessary to improve the general sanitary and hygienic living conditions of the child. Wide use of air, light - necessary condition correct therapy. Massage and gymnastics provide a good auxiliary effect.
The second form of nutritional anemia, which develops due to monotonous and excessive feeding of carbohydrates, is rarely observed, occurs with a general picture of flour disorder, usually with dyspeptic symptoms, and in terms of the hematological picture is no different from the first form.
Treatment consists of eliminating feeding defects and using the above remedies.
Finally, the last form of nutritional anemia is observed with hypo- and vitamin deficiencies, in particular with childhood scurvy, or the so-called Möller-Barlov disease.
The clinical picture is determined by the severity of the general phenomena of vitamin C deficiency, which primarily include loosening and bleeding of the gums in children with teeth, subperiosteal hemorrhages, especially in the area of the lower epiphyses femur, - in young children, subcutaneous and intramuscular hemorrhages, sometimes hematuria, poor weight gain, loss of appetite. It should be noted that there is no parallelism between the severity of morbid symptoms and the degree of anemia.
From the blood side - the phenomenon of more or less pronounced hypochromic anemia. The amount of hemoglobin is reduced, the number of red blood cells is significantly reduced, the color index is less than one. Anisocytosis and polychromatophilia are common. There are almost always single normo- and megaloblasts. The number of leukocytes is normal or, more often, slightly reduced. Always relative and sometimes absolute lymphocytosis and often a more or less significant shift of neutrophils to the left.
The number of plaques is mostly within normal limits, sometimes slightly increased and much less often decreased. The osmotic resistance of red blood cells is slightly increased. ROE has been significantly accelerated.
Clotting time and bleeding duration are normal or slightly increased. Retraction of the blood clot is well expressed, less often slightly reduced.
During the recovery period, with phenomena of enhanced regeneration, a picture of true polycythemia is sometimes noted.

The degree of anemia in a child with scurvy largely depends on the amount of hemorrhage and the frequency and severity of bleeding. Anemic phenomena develop especially easily in young children. The leukocyte formula and the total number of white blood cells are affected by the influence of random secondary infections.
An example of anemia in a child with scurvature is the following observation.
In a child K.V., 2 years 11 months old, who was in a state of severe nutritional dystrophy with very severe symptoms of scurvy, a blood test showed the following: Sali hemoglobin 25%, red blood cells 2,070,000, color index 0.6. Anisocytosis, poikilocytosis, oligochromemia. 4 normoblasts per 200 leukocytes. White blood cells 5700. Blood platelets 102,000. Leukocyte formula: lymphocytes 55.5%, segmented neutrophils 39.5%, band neutrophils 1.5%, and monocytes 3.5%, ROE 25 mm per hour.
Anemia due to prolonged insufficient administration of factor B2 gives approximately the same clinical picture. In children suffering from pellagra, anemia rarely reaches such levels severe degrees, as with vitamin C deficiency, and the leukocyte formula for the most part remains within the age norm.

Submitting your good work to the knowledge base is easy. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Posted on http://www.allbest.ru/

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

Abstract

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 the pathological process developed and physiological characteristics those that predispose to disease

Organs of hematopoiesis and immune defense. They are divided into central (red bone marrow and thymus) and peripheral (spleen, lymph nodes, lymphoid formations of the 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. In cattle, it is flat, elongated with rounded ends, lies in the left hypochondrium between the rumen 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, rapid growth, and gastrointestinal disorders. In addition, - low digestibility of Fe taken orally due to insufficient content hydrochloric acid in the stomach and imperfection of the hematopoietic function of the bone marrow at an early age. 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, lambs need nutrients ah is provided by mother's milk, which provides the average daily gain of lambs 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 food.

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 the summer, the killed young animals should be allocated the best pastures and should be fed concentrate fertilizers.

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 of 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 inadequate feeding of the ewe (this can be seen from the diet indicated below, see below). 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 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. 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 more high content gland. 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.

Absorption of iron from natural feed in adult animals it ranges from 8-10% of the accepted level. 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, 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 found in varying amounts in medicinal drugs, obtained from animal liver (see Vitohepat).

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

Cyanocobalamin has high biological activity. It is a growth factor, necessary for normal hematopoiesis and red blood cell maturation; 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 the function of the liver and nervous system.

Cyanocobalamin activates the blood coagulation system; V 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 has been successfully used to treat malignant anemia, for posthemorrhagic and iron deficiency anemia, aplastic anemia, anemia of a nutritional nature, anemia caused by toxic and medicinal substances, and other types of anemia.

Also prescribed for radiation sickness, dystrophy in premature and newborn babies after past 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, 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, and a 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 the physiological state and growth energy.

Early signs of the disease also include a decrease in the level of serum iron 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.

In addition to the above changes, in animals suffering from nutritional anemia, a decrease in 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).

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. 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, and 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. 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 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. With hypocobaltosis, weakly colored microcytes, increased ESR, low content cobalt in the body. 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.

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, with therapeutic purpose in a dose of 1-2 ml based on their content of 150-200 mg of iron.

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 acute deficiency vitamin E.

Currently, practical veterinary specialists of the republic have the opportunity to choose from a wide selection of iron dextran preparations imported production. 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 to prevent diseases caused by deficiency of iodine, selenium, magnesium, iron, to treat animals with 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, prevention they have postpartum complications.

DOSES AND METHOD OF APPLICATION: the drug is administered intramuscularly or subcutaneously: heifers and cows once per 45-- 25 days before calving at a dose 15--20 ml, for calves the therapeutic dose is 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 preparation 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, the nature and stage of the pathological process, as well as the general condition of the 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. The extensive clinical trials showed 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.

Posted on Allbest.ru

Boar No. 3 large white breed

Diagnosis of “Nutritional anemia (Anemia alimentaris)”

Start of supervision:

End of supervision:

student of group 607

correspondence department

Medical history

1. Diagnosis: Nutritional anemia (Anemia alimentaris)

Patient's owner and address:

Genus, gender, age, color, weight and breed of the animal: piglet, 2.5 months, boar, large white breed, weight 10 kg, white color.

Dropped out

Resident:

Curator: Brem M.A.

Anamnesis

vitae the animal was kept in a standard pigsty, in cages in groups of 15-20 animals. The cages were overcrowded; the bedding was not changed regularly and was sometimes absent. There was dampness, drafts, and a large accumulation of harmful gases, ammonia, and carbon dioxide in the room. There was no vitamin and mineral supplementation. There was no ultraviolet radiation. Maciona doesn't. Diet: rye bran 1.5 kg, skim milk 2 liters, well water ad libitum, often cold.

morbi The animal was admitted on October 21, 1998 with the following symptoms: lethargy, stunted growth, decreased and perverted appetite, depression, pale visible mucous membranes, dull bristles, pale skin and hooves, first symptoms in the form of seizures, bleeding gums, desquamation of the epithelium of the skin.

1. General condition

Temperature 38.0 0 C, pulse 89 beats per minute, respiration 25 per minute.

The animal is depressed, assumes the pose of a sitting dog, has an average build, a phlegmatic temperament, a gentle constitution type, and fatness below average.

2. External integument, mucous membranes, lymph nodes.

Upon examination of the animal, no damage to the skin was found. The skin is elastic, dry, pale, and desquamation of the skin epithelium is noted. The bristles are dull, brittle, and hold well in hair follicles. The mucous membranes are moist, without damage. The submandibular lymph nodes are enlarged and have a dense consistency.

3.Circulatory system.

There was no pain in the heart area. The cardiac impulse is localized on the left in the third intercostal space. The heartbeat was weakened during auscultation and no extraneous noise was heard. Arterial pulse arrhythmic. The content is satisfactory. No undulation was observed. When auscultating the heart, two sounds are heard: systolic - long and low, after a silent pause, diastolic - shorter and high. Venous pulse is negative. Borders of the heart: upper - along the line of the anconeus, posterior - up to the 5th rib.

4.Respiratory system.

Breathing is rapid, shallow, uneven. There is a sharp dry cough. Auscultation revealed no wheezing or noise. Breathing hard vesicular. On percussion there is a clear pulmonary sound. No nasal discharge is observed. Front percussion lung border- from the posterior angle of the scapula down along the line of the anconeus to the sternum. The upper border is from the posterior angle of the scapula caudally, parallel to the spinous processes of the thoracic vertebrae, departing from them by the width of two fingers. The posterior border is determined along three lines: along the malock line - the 11th intercostal space; along the line of the ischial tuberosity - the 9th intercostal space and along the line of the shoulder joint - the 10th intercostal space.

5. Digestive system.

Appetite is reduced. The act of defecation: the posture is natural, painless, feces are formed. The pharynx and esophagus are painless on palpation. The act of receiving food and water is natural and painless.

6. Genitourinarysystem.

The act of urination is natural and painless. On examination, the kidneys are painless, located under the transverse processes of the first lumbar vertebrae. When performing deep palpation through the abdominal wall, an increase in bladder not identified.

7. Nervous system.

The animal is phlegmatic, depressed, inactive, head down. There was trembling of the pelvic limbs and decreased muscle tone. Pain sensitivity is good. The study also revealed good tactile and temperature sensitivity.

8. Organs of movement.

The animal often assumes a sitting dog pose, which indicates weakness ligamentous apparatus. All movements are well coordinated. Paralysis and paresis were not observed. Muscle tone is weakened. The backbone is weak. The costal rosary can be felt on the last ribs.

9. Resultsresearch (Status praesenslocalis).

The animal is depressed, assumes a sitting dog pose, and desquamation of the skin epithelium is noted. The bristles are dull, brittle, mucous membranes are pale pink; The submandibular lymph nodes are enlarged and dense, the heartbeat is weakened and arrhythmic. Breathing is rapid, shallow, uneven, and there is a sharp dry cough. Appetite is reduced. There is tremor of the pelvic limbs and decreased muscle tone. The skeleton is weak, on the last ribs there are rachitic rosaries.

10. Laboratory research

Laboratory tests of blood, feces, urine - 10.23.98 are attached below on special forms.

11. Diagnosis.

1. Initial: Nutritional anemia Anemia alimentaris

Rickets

2. Final: Nutritional anemia Anemia alimentaris

Rickets

Hypovitaminosis A, D, E, B

Course of the disease

The animal is depressed and often assumes a sitting dog pose. Satisfactory appetite. The tail is not curled. The bristles are dull, do not adhere to the body, and are brittle. The mucous membranes are pale pink color, wet. The skin is pale pink, dry, and desquamation of the skin epithelium is observed. Noted muscle tremors. The hooves are dirty, the hoof horn is dull. The feces have a mushy consistency, a dirty brown color, and undigested food particles are observed. Breathing is shallow and rapid. The abdomen is enlarged and disproportionate to the body of the animal. On the last ribs, during palpation, costal “rosaries” are felt.

Feeding, cleaning the animal, cleaning the cage. Treatment prescribed:

Rp.: Calcii carbonatis 20.0

Rp.: Natriumchloride 5.0

D.S. Internal. With food.

Rp.: Sol. Novocaini 0.5% - 5ml

D.S. For diluting an antibiotic.

Rp.: Acidi ascorbinici 1.0

Rp.: Trivitamini 1000ml

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

Sol. Glucosi 5% - 200 ml

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Sol. Cikloxyloli 200ml

Rp.: Sulfadimezini 1.0

D.S. Internal.

Rp.: Hydrolizini 2 ml

D.S. Internal.

Antibiotics and sulfonamides are prescribed as a result of the animal possibly contracting pneumonia. These drugs are prescribed to remove secondary microflora from the body.

The animal is depressed and often assumes a sitting dog pose. Satisfactory appetite. The tail is not curled. The bristles are dull, do not adhere to the body, and are brittle. The mucous membranes and skin are pale, desquamation of the skin epithelium is observed. Muscle tremors are noted. Breathing is shallow and rapid. The abdomen is enlarged and disproportionate to the body of the animal.

Feeding, cleaning the animal, cleaning the cage.

Rp.: Calcii carbonatis 20.0

D.S. Internal. With food for one meal.

Rp.: Benzylpenicillini - natrii 200000 ED

D.S. Intramuscularly, dilute in 5 ml of 0.5% novocaine solution.

Rp.: Acidi ascorbinici 1.0

D.S. Internal. For one appointment.

S. Intramuscularly, 0.2 ml.

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Sol. Cikloxyloli 200ml

S. Internal, 3 drops 1 time per day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Sol. Calcii chloridi 10% - 200ml

Sol. Glucosi 5% - 200 ml

M.D.S. Internally, 10 ml once a day.

The animal is depressed, but shows an active interest in the food. The sitting dog pose is adopted less frequently. The nasal planum is wet. Breathing is shallow. Pulse increased. The bristles are dull, do not adhere to the body, and are brittle. The tail is not curled. The hooves are dirty, the hoof horn is dull.

Rp.: Sol. Thiamini bromidi 0.5% - 1ml

S. Intramuscularly, 0.5 ml once a day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Benzylpenicillini - natrii 200000 ED

D.S. Intramuscularly, dilute in 5 ml of 0.5% novocaine solution.

Rp.: Sol. Camphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml.

Rp.: Trivitamini 1000ml

D.S. Internally, 3 ml once a day.

Rp.: Hydrolizini 2 ml

D.S. Internal. For one appointment.

The animal is active and has a good appetite. The bristles are dull, do not fit tightly to the body, and are brittle. The mucous membranes are pale. Desquamation of the skin epithelium is observed. The hooves are dirty, the hoof horn is dull. Breathing is shallow.

Cleaning the cage, feeding the animal.

Rp.: Natriumchloride 5.0

D.S. Internal. With food.

Rp.: Benzylpenicillini - natrii 200000 ED

D.S. Intramuscularly, dilute in 5 ml of 0.5% novocaine solution.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Acidi ascorbinici 1.0

D.S. Internal. For one appointment.

Rp.: Sulfadimezini 1.0

D.S. Internal.

Rp.: Sol. Cikloxyloli 200ml

S. Internal, 3 drops 1 time per day.

Rp.: Sol. Calcii chloridi 10% - 200ml

Sol. Glucosi 5% - 200 ml

M.D.S. Internally, 10 ml once a day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

The animal is active, shows a good appetite, the skin is pale, the stubble is dull. The tail is slightly curled. The mucous membranes and conjunctiva are pale. Desquamation of the skin epithelium is observed. The hooves are dirty, the hoof horn is dull.

Cleaning the animal and feeding it. Cleaning the cage.

Rp.: Sol. Thiamini bromidi 0.5% - 1ml

S. Intramuscularly, 0.5 ml once a day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Benzylpenicillini - natrii 200000 ED

D.S. Intramuscularly, dilute in 5 ml of 0.5% novocaine solution.

Rp.: Trivitamini 1000ml

D.S. Internally, 3 ml once a day.

Rp.: Hydrolizini 2 ml

D.S. Internal. For one appointment.

Rp.: Sol. Ferroglucini 5% - 200 ml

D.S. Intramuscularly, 0.3 ml once every 2 days.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

Ultraviolet irradiation DRT 400, 15 minutes a day.

The animal is active and has a good appetite. The mucous membranes and skin become pink. The bristles are dull on the sides, shiny in the area of the head and back. The tail is curled. The hooves are dirty, the hoof horn is dull.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Calcii carbonatis 20.0

D.S. Inside with food.

Rp.: Sol. Calcii chloridi 10% - 200ml

Sol. Glucosi 5% - 200 ml

M.D.S. Internally, 10 ml once a day.

Rp.: Acidi ascorbinici 1.0

D.S. Internal. For one appointment.

Rp.: Sulfadimezini 1.0

D.S. Internal.

Rp.: Sol. Cikloxyloli 200ml

S. Internal, 3 drops 1 time per day.

The animal is active and shows a good appetite. The mucous membranes and skin are pink. The stubble is dull on the sides, shiny on the head and back. The hoof horn is slightly pinkish. Feces formed with the remains of digested food.

Feeding, cleaning the animal, cleaning the cage and feeder.

Rp.: Sol. Thiamini bromidi 0.5% - 1ml

S. Intramuscularly, 0.5 ml once a day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Trivitamini 1000ml

D.S. Internally, 3 ml once a day.

Rp.: Hydrolizini 2 ml

D.S. Internal. For one appointment.

Rp.: Sol. Cyanocobalamini 10% - 2ml

D.S. Intramuscularly, 0.5 ml, 1 time every 2 days.

Ultraviolet irradiation DRT 400, 15 minutes a day.

Cleaning and feeding the animal. Cleaning the cage and feeder.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Calcii carbonatis 20.0

D.S. Inside with food.

Rp.: Sol. Calcii chloridi 10% - 200ml

Sol. Glucosi 5% - 200 ml

M.D.S. Internally, 10 ml once a day.

Rp.: Acidi ascorbinici 1.0

D.S. Internal. For one appointment.

Rp.: Sulfadimezini 1.0

D.S. Internal.

Rp.: Natriumchloride 5.0

D.S. Internal. With food.

The animal is active and shows curiosity. The mucous membranes are pink. Desquamation of the skin epithelium is observed. Appetite has a good tail curled.

Feeding the animal. Cleaning the cage.

Rp.: Sol. Thiamini bromidi 0.5% - 1ml

S. Intramuscularly, 0.5 ml once a day.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Trivitamini 1000ml

D.S. Internally, 3 ml once a day.

Rp.: Hydrolizini 2 ml

D.S. Internal. For one appointment.

Rp.: Sol. Ferroglucini 5% - 200 ml

D.S. Intramuscularly, 0.3 ml once every 2 days.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

The animal is active and shows a good appetite. Mucous membranes and skin are pink. The hooves are dirty, the hoof horn is dull and pink. The shiny bristles do not adhere to the body. The tail is curled.

Cleaning and feeding the animal. Cleaning the cage and feeder.

Rp.: Sol. Sulphocamphocaini 10% - 2ml

S. Intramuscularly, 0.2 ml 2 times a day.

Rp.: Doloroli 0.5

Da in tabulletis

S. Internal.

Rp.: Cobalti chloridi 2.0

Ferri sulfatis 2.5

Cupri sulfatis 1.0

Magnii sulfatis 1.0

D.S. Internal, dilute in 1 liter of water. 5 ml, 2 times a day.

Rp.: Calcii carbonatis 20.0

D.S. Inside with food.

Rp.: Sol. Calcii chloridi 10% - 200ml

Sol. Glucosi 5% - 200 ml

M.D.S. Internally, 10 ml once a day.

Rp.: Acidi ascorbinici 1.0

D.S. Internal. For one appointment.

Rp.: Sulfadimezini 1.0

D.S. Internal.

Conclusion

A boar from JSC “Berdskoe” was taken into care on October 22, 1998 at the age of 2.5 months. General condition as of 10/22/98: depression, stunted growth, perverted appetite, the animal often assumes the “sitting dog” pose. Pallor of the mucous membranes and hoof covers was noted. The bristles are dull, brittle, and do not adhere to the animal’s body. Pulse and breathing are increased, nervous phenomena in the form of convulsions, bleeding gums. When palpating the last ribs, “rosary beads” are detected.

When studying the systems: respiratory, cardiovascular, digestive, genitourinary, nervous and according to laboratory studies of feces, urine, blood, a final diagnosis was made:

Nutritional anemia, rickets, hypovitaminosis A, D, E, B.

Treatment was carried out aimed at increasing the level of hemoglobin in the blood: ferroglucin (0.3 ml), stimulation and normalization of metabolism: microelements (5 ml), vitamins B1, B12, C, trivitamin; antibiotic therapy: benzylpenicillin sodium salt, sulfonamide drugs were also used. Also ultraviolet radiation.

Two days after the start of treatment, the animal’s condition improved: the mucous membranes and skin became pink, the bristles acquired shine. The animal's appetite normalized. The animal became active and mobile. The general condition of the animal is satisfactory. The animal was handed over to further treatment.

Blood test No. 1

Type of animal: piglet, floor: boar, age: 2.5 months, suit: white, nickname (number): №3.

The owner of the animal and his address AOZT “Berdskoye”, Iskitimsky district, Novosibirsk region

Diagnosis: Nutritional anemia, hypovitaminosis A, D, E, B, rickets.

Number of gems

Number of erythras

Number of leukocytes.

Leukocyte formula

neutrophils

by method

discovered

Structural features of erythrocytes and leukocytes: erythrocytes and leukocytes are not changed.

ROE by method Panchenkova is 8 mm/g.

Reserve alkalinity by have not been studied.

Bilirubin by have not been studied.

Additional Research -

Conclusion

A blood test revealed a decrease in the number of red blood cells and hemoglobin content, which is characteristic of anemia. When analyzing the leukogram, the swelling showed a regenerative shift to the right.

The study was conducted

(Brem M.A.) 10.24.98

Urine examination No. 1

Type of animal: piglet, floor: boar, age: 2.5 months suit: white, nickname (number): №3

AOZT “Berdskoye”, Iskitimsky district, Novosibirsk region

Urine came in “ 23” October 1998

Physicalproperties

1. Quantity - 200 ml.

2. Color - yellow-green.

3. Transparency - transparent,

4. Consistency - liquid.

5. The smell is specific

6. Specific gravity - not studied.

Chemicalproperties

1. Urine reaction - pH=5 (to litmus).

2. Protein (with sulfasalicylic acid) - negative.

3. Albumosis - negative.

4. Glucose (with Gainess solution) - negative

5. Blood pigments (Collo test) - negative

6. Bilirubin - not tested

7. Urobilin - not studied

8. Indican - not studied

9. Acetone - negative

Conclusion

Laboratory examination revealed no pathological changes.

The study was conducted

(Brem M.A.) 10.24.98

Stool examination

Type of animal: piglet, floor: boar, age: 2.5 months; suit: white, nickname (number): №3

Owner of the animal and his address: AOZT “Berdskoye”, Iskitimsky district, Novosibirsk region

Physicalproperties

1. Quantity - 50 g.

2. Shape and consistency - formed

3. Humidity - about 80%.

4. Color - dark brown with a greenish tint.

5. The smell is specific

6. Digestibility is normal..

7. Pathological impurities - absent.

Helminthsand their parts

1. Round - no mature ones were found.

2. Ribbon - no sexually mature ones were found.

Chemicalproperties

1. Reaction - pH=7.

2. Protein - negative.

3. Blood pigments - negative.

4. Bile pigments - negative.

5. Test for starch (with Lugol solution) - negative.

Microscopic examination

1. Feed residues - no.

2. Inorganic components - no.

3. Helminth eggs - not found.

4. Test for fat - negative.

Conclusion

Digestibility is satisfactory. Blood pigments were detected.

The study was conducted

(Brem M.A.) 10.24.98

Tutoring

Need help studying a topic?

Our specialists will advise or provide tutoring services on topics that interest you.
Submit your application indicating the topic right now to find out about the possibility of obtaining a consultation.

Iron deficiency (nutritional) anemia of piglets

This is a hematological syndrome characterized by impaired hemoglobin synthesis due to iron deficiency and manifested by anemia.

In young animals, anemia is most common and is associated with a lack of iron.

Characterized by activity disorder hematopoietic organs and metabolic disorders, which leads to growth retardation in young animals and a decrease in disease resistance. Mostly piglets are affected.

Etiology. The main cause of the disease is a lack of iron in the body. The need of young animals for it is determined by two factors - the consumption of iron for the implementation of life processes and the increase in live weight, and thus the volume of blood. Due to the high growth rate of piglets, their need for iron is much greater. Animals satisfy the need for iron by receiving it through mother's milk or food, as well as through internal (endogenous) intake, mainly with red blood cells.

Sow milk, rich in plastic substances, is very low in iron. Endogenous iron, released from hemoglobin during the breakdown of red blood cells, is about 1% per day. From plasma, it is usually absorbed by the reticuloendothelial system and goes to the synthesis of new red blood cells, consumed in the body or deposited. However, a feature of young animals, including piglets, is that their reticuloendothelial system functions poorly.

A factor predisposing piglets to anemia is the fact that at birth their iron reserve is only 50 mg. Therefore, by the 7-8th day of life of piglets, they become iron deficient, and by 3-4 weeks of age, anemia reaches its climax.

Deficiencies in the body of nutrients, vitamins and minerals contribute to the occurrence and severity of the disease.

Pathogenesis. Iron deficiency in the body leads to a decrease in hemoglobin levels and a decrease in the activity of iron-containing enzymes, which are closely related to protein synthesis and other important cellular functions.

In addition, iron in hemoglobin plays an important role in the formation of the oxygen-hemoglobin complex and prolonging its existence, enough time 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. In case of iron deficiency, the duration of existence of such a complex is varying degrees contracts, a state of hypoxia occurs.

In this case, breathing and heart function become compensatory and cardiac hypertrophy develops.

Symptoms In the first 10-15 days, 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 in healthy piglets, usually well developed at 3-6 weeks of age.

Pallor of the skin and visible mucous membranes appear, which later acquire a yellow color, swelling of the eyelids, and lethargy. Adynamia, piglets bury themselves in the bedding, suckle the sow poorly, are stunted in growth, the stubble becomes rough, brittle, and the skin becomes wrinkled. There may be a perversion of appetite, digestive disorders. The abdomen is often swollen or pulled up, diarrhea alternates with constipation. There may be some mucus in the stool. Hemoglobin in the blood sharply decreases from 10 to 3-5 g/%. The number of red blood cells usually does not change. A change in the qualitative composition of erythrocytes is noted, accompanied by anisocytosis, poikilocytosis, polychromatophilia, and erythroblasts are detected.

Diagnosis. Early diagnosis involves determining the amount of iron in the blood, liver, spleen, and kidneys. In other cases, an analysis of piglet feeding is carried out, based on clinical symptoms and the results of hematological studies. Piglets with a hemoglobin content below 40% are considered sick. Determining the color indicator of blood is of great diagnostic importance.

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

diagnosis anemia animal