Edema in case of thyroid disease

Page 4 of 6


.
ENDemicheskiy ZOB - STRUMA ENDEMICA, ZOB ENZOTIC - STRUMA ENZOOTICA

Chronic disease characterized byan increase in the thyroid gland (goiter) and a violation of its function due to iodine deficiency. Iodine deficiency foci are found in the CIS, USA, Egypt, Brazil, India, Switzerland, Algeria, Ethiopia and other countries. They are mainly located in the depths of the continent, in the highlands, on the plains along the watershed of rivers in areas with high water cut, with hard calcareous waters, podzolic and acid soils.

Etiology.
The main cause of endemic goiter islack of iodine in the body due to its deficiency in water and feed. It was found that the disease appears in areas where the iodine content in the soil is below 0.1 mg / kg, in drinking water is less than 10 mg / l. These values ​​in different areas of iodine endemia may fluctuate in one direction or another, since the degree of assimilation of iodine is influenced by other minerals.

Iodine deficiency is aggravated by excesscalcium, magnesium, lead, fluorine, bromine, strontium, iron, as these substances worsen the absorption of iodine. In the foci of endemic goiter in the Chita region, iodine content in water is less than 2 μg / l, in feeds 0.06-0.25 mg / kg dry matter. In Ukrainian Polesye, iodine deficiency in animals is noted in the foci where the iodine content in water is 1.3-2.58 μg / l, and in some sources 0.9-1.0 μg / l. In the Ivanovo region in the foci of endemic goiter in 1 kg of dry matter for winter rations feed, the content of iodine is 0,039-0,323 mg / kg, in safe areas - 0,071-0,393 mg / kg.

The appearance of goiter is promoted by eating animalsa large number of feeds containing thyreostatic substances (goitrogenic substances) that are found in rapeseed, rape and other cruciferous, in white clover, beetroot, trout, turnip, rye, and some cabbage varieties. Iodidepressive action has nitrates, paraaminosalicylic acid, thiourea compounds, thiosuracil, sulfonamides, cyanogenic glucosides.

An aggravating factor in the onset of the disease is the deficiency in feed and water of cobalt, zinc and other microelements, as well as vitamins.

Pathogenesis.
Coming with food and water, iodine is absorbed intostomach and intestines and penetrates into the blood mainly in the form of iodides (KI, Nal). In the thyroid gland, iodides are oxidized and converted to molecular (elementary) iodine. The process of iodide intake into the thyroid gland and their oxidation into molecular iodine stimulates the thyroid-stimulating hormone of the pituitary gland. In the thyroid gland, molecular iodine is used for the synthesis of thyroxine (T4) and triiodothyronine (T3). The secretion of thyroxin by the thyroid gland is 10-20 times greater than that of triiodothyronine. The iodine in the blood plasma in the thyroid hormone bound to the protein is called organic iodine or protein-bound iodine (SIB). Iodine, associated with protein, is 90-95% composed of thyroxine. It serves as a criterion for assessing the functional state of the thyroid gland. Mineral (dialyzed) iodine plasma in adult animals is 15-20% of the total.

With prolonged deficiency in the body of iodinethe synthesis of thyroid hormones decreases, compensatory adaptive reactions appear in the form of increased secretion of the thyroid-stimulating hormone of the pituitary gland, which causes hyperplasia of the thyroid gland and its increase. In the compensation stage, the thyroid gland produces a sufficient amount of thyroid hormones, so there is no pronounced metabolic disorder. With prolonged exposure to iodine deficiency and other aggravating factors in the thyroid gland, it is no longer a simple hyperplasia, but a specific one - the goiter. In it connective tissue proliferates with simultaneous atrophy of glandular elements.

Deficiency in the body of iodine and thyroid hormonesaccompanied by a violation of carbohydrate, fat, protein and mineral metabolism, a slowdown in growth and development, a decrease in the reproductive function, a decrease in the activity of the cellulolytic microflora of the prednis, that is, processes that are inherent in hypothyroidism develop. The severe course of the disease is accompanied by a violation of glycoprotein metabolism and accumulation in the tissues of mucin, the appearance of myxedema.

Symptoms.
In adult animals, clinical signs are expressedweakly. In the foci of iodine deficiency, the animals notice short stature, an elongated torso, a decrease in milk, meat, wool and other productivity. The skin is mostly dry, stiff, and wrinkles form on the neck of some cows. Observe the keratinization of the surface layer of the skin - hyperkeratosis.

There is a delay of the afterbirth, subinvolution of the uterus,lengthening the time from calving to fertilization, anovulatory sex cycles, the formation of follicular cysts, ovarian hypofunction. Often there are abortions, the birth of a dead or non-viable offspring. Iodine deficiency is more often manifested by symptoms of hypothyroidism, for which endophthalmos (eyes westernization) and the phenomenon of myxedema in the form of mucosal edema of the premaxillary space are characteristic. In hypothyroidism caused by iodine deficiency, bradycardia is observed (in cows 32-28 per minute). In areas of pronounced iodine endemia, goiter occurs more often on the background of hypothyroidism of the thyroid gland, in regions of moderate iodine deficiency it can occur with normal or increased function (hypertension, rheose). Endemic goiter in newborn calves is characterized by hyperfunction of the thyroid gland. The degree of hyperthyroidism is low and is manifested by moderate tachycardia and pop-eyed.

The enlargement of the thyroid gland can be established in adult sheep and goats only with strong iodine deficiency, in other species of animals - no.

Due to a sharp increase in the thyroid glandthere is compression of the larynx, trachea and esophagus, difficulty breathing and reception of food. The sick young grows poorly and develops, it is susceptible to various diseases and often dies. The surviving goiter gradually decreases and disappears within 3-5 months. With an insignificant deficiency of iodine, an increase in the thyroid gland may not be present, but the young are born weak, grow poorly, differ in short stature, a rare and coarse woolly covering, and poor fatness. Piglets are born with a rare coat, often die at birth or a few hours after birth. The surviving pigs have cyanotic skin, wrinkled, neck and limbs shortened. In piglets, suckers, eyelids, an increase in the tongue (the first period of the disease), then swelling of the subcutaneous tissue in the head, neck and groin, eyelid (second period of the disease). Edema of the eyelids is accompanied by narrowing of the eye slits. The body temperature at the beginning of the disease is normal, but decreases with deterioration.

In adult animals and in young animals,decrease in the content of iodine bound to protein in the blood serum (norm 4-8 μg%, 315-630 nmol / l), iodine concentration in milk also decreases. In the milk of cows from free from goiter areas, the content of iodine is 60-80 μg / l, in areas of iodine deficiency is much lower.

In patients with calves, the serum T3is 1.55-4.36 nmol / L, T4 is 7.8-2.92 nmol / L, in healthy individuals of the same age, respectively, 2.8-4.74 and 44.26-39.72 nmol / l. With a decrease in blood levels of T3 and T4, the level of thyroid-stimulating hormone in sick animals is almost twice as high as in healthy individuals (0.74 ± 0.23 vs. 0.37 ± 0.14 mIU / L). In young animals, there is a decrease in calcium in blood, an increase in phosphorus.

Pathological changes.
According to morphological changes, there are three formsendemic goiter: a) diffuse - the thyroid gland is uniformly hyperplastic, there are foci of small adenomas; b) nodular - the thyroid gland is enlarged, more often in the form of one or several large nodes bounded by a capsule (Figure 162); c) mixed - the thyroid gland is significantly enlarged and has one or more small nodes. Histologically, in turn, is divided into parenchymal and colloidal. When the parenchymal goiter of the gland is dense, fleshy, pale brown with a reddish tinge. When the colloid goiter of the gland is swollen, its surface is smoothed, yellowish-gray or pale brown, half-luminescent follicles are visible on the incision. With the development of secondary destructive changes in the thyroid gland, cysts of the size from millet grains to chicken eggs are formed. Histologically, with parenchymal goiter, small follicles are usually established, the colloid is thick, intensely colored, or it is not detected. With colloid goiter, the follicles are large, their epithelium sharply compacted. The colloid is thick, intensely colored. Simultaneously with proliferative processes, destructive fibrosis and cyst formation are noted.

Diagnosis.
The diagnosis of endemic goiter is set tobased on the nature of the biogeochemical zone, the content of iodine in water, soil and fodder, the clinical symptoms of the disease, the results of biochemical studies of blood, milk, pathomorphological changes in the thyroid gland. To diagnose endemic goiter from dead or fallen animals, thyroid glands are taken and their mass is determined (1 g per 100 kg of animal weight). The relative weight of the thyroid gland above 7 g in cattle, 8 g in sheep and 10 g in pigs indicates its increase.
In areas with severe iodine deficiency, the thyroid gland in newborn calves sometimes reaches 500 g, in lambs and piglets - 100 g.
Iodine deficiency often occurs with a deficiency in the body of other macro- and microelements, with signs of osteodystrophy and rickets.
Endemic goiter should be differentiated from hypothyroidism and thyrotoxicosis of another origin, inflammation (thyroiditis), thyroid tumors.

Current and forecast.
The course of the disease is chronic. With the timely elimination of the causes and the appointment of appropriate therapy, the forecast is favorable or cautious.

Treatment and prevention.
In endemic areas, in animal rationsinclude iodized table salt (25-40 g of potassium iodide per 1 ton). Standard iodized table salt is used in the form of free mineral top dressing or fed in quantities corresponding to the norms of ordinary table salt. Pigs, poultry and horses, in order to avoid poisoning, the salt is only given in doses mixed with food. With the preventive and curative purpose, additives of potassium iodide salts, Lugol solution, kayod, amyloyodine and other preparations are used. They are dosed based on iodine deficiency in the main diet or use indicative tabular data. To meet the need for iodine, cattle should consume a ration with an element content of 0.8-1.5 mg / kg dry matter for highly productive cows and 0.2-0.7 mg / kg for the remaining cattle groups. The content of iodine in the rations of sows is 0.4-0.5 mg / kg dry matter, pigs young - 0.2-0.3 mg / kg, adult sheep - 0.2-0.6 mg / kg, lambs up to 6 months - 0,2-0,4 mg / kg, young sheep older than 6 months - 0,2-0,3 mg / kg. Such fluctuations in the level of iodine in the diet are determined by the productivity and the presence in feed of gutrogenic substances that reduce the absorption and metabolism of iodine.

Approximate preventive doses of the additivepotassium iodide in mg per day per animal: cattle adult - 1.5-8, young cattle older than 6 months - 0.5-5, calves up to 6 months - 0.2-1.5, sheep and goats adults - 0.2-0.9, lambs and kids - 0.1-0.4, pigs of all ages per 100 kg of animal weight - 0.3-0.4 mg, sucking pigs - 0.05-0.2 mg. For high-yielding and deep-shelled cows, the dose should be increased by 50%. Treatment doses are 2 times higher than preventive. This drug is recommended to be fed daily for 1.5-2 months, then take a break for 2-3 weeks.

Iodine salts and additives are added together with substances,stabilizing iodine (sodium bicarbonate, sodium thiosulfate, etc.). Iodine in stabilized form is applied in the form of preparations Kayode, amiloyodina et al. Potassium iodide stabilized with sodium carbonate to sodium chloride. Daily doses Kayode (tablet) on the head: the dry cows 2-6, cows lacto-al from 1 to 5, heifers 1-2, 2-3 heifers, bulls-producing (per 200 kg of animal weight) - 1, large cattle for fattening and young for up to 300 kg - 1, young animals over 300 kg - 2, adult animals 3-4.

Amyloyodine is a preparation containing potassium iodide, crystalline iodine and starch. It is prescribed in the form of additives in concentrated feed in doses: cows 0.1 grams, ewes 0.01 g per day.

Antistrum contains in 1 tablet 1 mg of potassium iodide, it can be used 2-3 times a week in a dose covering the iodine deficiency in the diet.

In regions where endemic goiterbackground of the insufficiency of other macro- and microelements, for the prevention and treatment of the disease, polymineral top dressings are used. In the Chita region, for example, for the prevention of endemic goiter in sheep and cattle, polymineral fertilizing has been developed and tested, including amyloyodine, copper sulfate, cobalt carbonate, sodium selenite, sulfur, microvit A feed and bran.

When prescribing iodine preparations are not allowedtheir overdose, since this results in the death of embryos and fetus, the birth of a non-viable offspring, a decrease in productivity. If the disease is accompanied by the phenomena of pronounced hypothyroidism, myxedema, treatment with thyroid medications is indicated.