Hormonal diseases and disruptions in dogs. Main endocrinological syndromes of dogs. The most common diseases of the endocrine system of dogs

Smirnova O. O., Candidate of Biological Sciences, veterinary therapist. Veterinary Clinic of Neurology, Traumatology and intensive care, Saint Petersburg.

List of abbreviations used: HAC – hyperadrenocorticism, OKN – tumor of the adrenal cortex, 17-GP – 17-hydroxyprogesterone.

Endocrine diseases that interfere with skin healing in dogs include HAC; hypothyroidism; diabetes.
Endocrine diseases that interfere with skin healing in cats include HAC; OKN, secreting excess sex steroids; diabetes; cellulite.

The most common among these pathologies in everyday veterinary practice are HAC, hypothyroidism in dogs and diabetes mellitus in both types of animals. Probability of developing the rest listed diseases below, but nevertheless we should not forget about them and should add them to the list differential diagnoses if appropriate symptoms are present. Also, the list does not indicate such a possible pathology in cats as hypothyroidism, since the likelihood of developing hypothyroidism in cats is extremely low and basically this pathology is either iatrogenic (as a consequence of thyroidectomy or treatment radioactive iodine patients with hyperthyroidism), or congenital. Since these cases are casuistic, we will not consider them. Besides, in Russian Federation Radioactive iodine treatment is not currently available.
At the same time, today the frequency of diagnosis of cases of both iatrogenic and spontaneous HAC in cats continues to increase. This is likely due to the development of specialization in small animal veterinary medicine, a better understanding of feline diseases, the desire of owners to provide more complex examinations to their pets, increasing awareness of this disease, greater familiarity of veterinarians with the many variants of disorders associated with excess glucocorticoids, and an increase in The lifespan of domestic cats is basically 2.
In this article we will consider only aspects of pathologies of the endocrine system, united by cause-and-effect relationships with impaired regeneration of soft tissues, without touching on other clinical, diagnostic and treatment issues that might be of interest to the clinician when establishing these diagnoses. To confirm any of the diagnoses, we will need specific laboratory tests and visual diagnostic methods, the choice of which will be based on the characteristics of the anamnesis and clinical picture demonstrated by the patient. Discussion of differential diagnostic methods is also beyond the scope of this article.
It is important to understand that some of these diseases do not always lead directly to impaired tissue healing. In certain cases, they simply contribute to the development of an infectious (secondary bacterial or fungal) process, which, in turn, is the reason for the absence or slowdown of normal regeneration 7, 8.
Leather healthy dogs and cats are colonized by various bacterial and fungal organisms. They are usually non-pathogenic and, moreover, prevent colonization by pathogenic species of microorganisms through competition. Potential pathogenic microorganisms, such as coagulase-positive staphylococci, often colonize mucous membranes, including - oral cavity. Thus, these microorganisms can be introduced when an animal licks a diseased body surface.
Infection with Gram-negative species can result from oral-fecal or environmental contamination.
Most skin infections develop when a combination of virulence factors and changes in skin condition allow microorganisms to overwhelm the skin's physical, chemical, and immunological defenses. Often recurrent pyoderma is secondary to primary skin or systemic diseases. This leads to epidermal damage, inflammation, and additional bacterial colonization and proliferation. Staphylococci and Malassezia also produce mutually beneficial growth factors. The vast majority of pyoderma in dogs is associated with coagulase-positive staphylococci. The most common species is Staphylococcus intermedius, and S. aureus, S. hyicus and S. schleiferi have also been isolated.
Superficial pyoderma characterized by a bacterial infection localized in the stratum corneum of the skin and hair follicles. This form The disease is much less common in cats and is associated with a wider range of microorganisms, including S. intermedius, S. felis, S. aureus, Pasteurella multocida and anaerobes (although the latter are more common in abscesses). Methicillin-resistant species, including S. intermedius, S. aureus, and S. schleiferi, have recently been isolated from dogs and cats. The last two types of bacteria are probably associated with deeper, opportunistic infections 12.
Secondary pyoderma is a common early manifestation of hypothyroidism and HAC, and this skin disorder may be noted even before systemic clinical signs appear 8.

A detailed consideration of these pathologies from the point of view of skin lesions that impede tissue regeneration

One of the most common among them is the HAK of dogs. Affected dogs exhibit a tendency to bruise, decreased subcutaneous fat, and stretched skin. The characteristic “fragility” appears not only in the skin, but also in the blood vessels. For example, after a banal puncture of a vein to take a blood sample or other even minor injuries, excessive bruising may occur. Rarely, bruising occurs due to metal staples in surgical suture installed several years ago. Subcutaneous tissue atrophy due to the catabolic effects of excess cortisol may also predispose to bruising. Wounds heal more slowly, probably due to the formation of a fragile, thin scar. Possible edge separation skin wounds due to insufficient fibrous tissue. For the same reason, long-healed wounds, including those from previous operations, can diverge (Fig. 1, 2) 2.

Atrophy of the glands of the hair root and epidermis is observed in 30–40% of dogs with HAC, which is likely due to the antiproliferative effect of glucocorticoids on fibroblasts with suppression of the synthesis of collagen and mucopolysaccharides. In humans, treatment with topical forms of glucocorticoids reduces the synthesis of collagen types I and III; this may also be the case with HAC in dogs 2. Quite often these patients develop pyoderma, apparently due to multiple local skin changes and immune suppression from excess cortisol, which may be difficult to treat. In approximately 10% of cases of spontaneous HAC, demodicosis is detected that developed in adulthood. Specified inflammatory diseases skin, in turn, also prevent tissue regeneration 2.
It should also be remembered about secondary hyperparathyroidism, developing against the background of GAK. This pathology contributes to the activation of osteoclasts and, accordingly, osteodystrophy. A decrease in bone tissue density and the process of its resorption prevent bone tissue regeneration during surgical interventions 2, 19.

Hyperandrogenism

The etiology and pathogenesis of the disease are associated with excessive androgenic stimulation. It may be caused by increased androgen production in testicular neoplasia (particularly interstitial cell tumors). Also, androgen stimulation may be associated with changes in peripheral metabolism of sex steroids and/or changes in the number or activity of peripheral receptors. Less commonly, in castrated males and females, pathology becomes a consequence of the synthesis of androgens in the OKN. The tissues of the perianal glands are androgen-dependent in males and females, so such patients are often diagnosed with gland hyperplasia or adenoma.
In male dogs (including castrated ones), the prostate gland will also respond to androgenic stimulation of OKN by developing hyperplasia.
Androgens stimulate epidermal hyperproliferation, increase sebum secretion and inhibit the onset of anagen. Dermatological manifestations include oily seborrhea, seborrheic dermatitis, otitis media, alopecia, hypertrichosis (caused by abnormal retention of hair in the follicles) 12.
There are anecdotal reports of dogs that have been diagnosed with OCs that secrete sex hormones. At the same time, patients had low serum cortisol concentrations, but Clinical signs, presumably caused by sex hormones, corresponded to HAC. Two dogs with ACC had clinical signs of HAC despite marked reductions in serum cortisol concentrations following ACTH administration. One tumor secreted progesterone, 17-GP, testosterone, and dehydroepiandrosterone sulfate, while the other secreted androstenedione, estradiol, progesterone, and 17-GP. In a publication describing 8 dogs with ACI and symptoms of HAC, three had decreased serum cortisol concentrations after an ACTH stimulation test, and one had an increased concentration of 17-GP; other sex hormones were not measured in these dogs, as were the other two dogs with cortisol concentrations below normal 2.

Hypothyroidism in dogs

Thyroxine plays a role in the normal immune response. Depletion of thyroxine stores suppresses humoral immunity and impairs T-cell function and also reduces the number of lymphocytes in the circulating blood. Dogs with hypothyroidism may develop superficial bacterial infections (folliculitis, superficial spreading pyoderma, rash) characterized by papules, pustules, collar-shaped scaling and/or patches of alopecia. Such infections are usually caused by Staphylococcus spp. and are accompanied by varying degrees of itching. Hypothyroidism may be a predisposing factor for the development of demodicosis in adult dogs and chronic otitis externa 2.

Pituitary dwarfism

With this pathology, secondary bacterial and/or fungal infections 12. Changes in coat are caused by the preservation of secondary hairs and the absence of primary (guard) hairs. The skin progressively becomes hyperpigmented and scaly (Fig. 3) 19.
Diabetes mellitus in dogs and cats
In diabetes mellitus, secondary pyoderma, Malassezia and other fungal dermatitis have been reported 8. In addition to a predisposition to chronic recurrent skin infections, these patients may exhibit xanthomas (dermal accumulation of lipids secondary to diabetes mellitus)5.
A common pathophysiological feature of microvascular disorders in diabetes is the progressive narrowing and eventual occlusion of the lumen of blood vessels, which leads to insufficient blood supply and dysfunction of the affected tissues, as well as the death of cells that form capillaries.
Table 1 provides a schematic and overview of the main consequences of insulin deficiency 2.


Results from a retrospective study of 45 diabetic dogs conducted between 1986 and 2000 suggest that most dermatological changes in diabetic dogs can be attributed to concomitant diseases. However, no skin disease directly related to diabetes mellitus. The most common pathology in dogs with diabetes was superficial bacterial infection skin. Otitis is also a common finding in these patients. The manifestation of deep infections was often interdigital furunculosis 7, 14.

GAK cats
Despite the development veterinary diagnostics and methods for treating pathologies of the endocrine system, feline HAC is still considered a rare disease and is accompanied by diabetes mellitus in approximately 80% of cats. Pituitary disease is present in 75–80% of cases of HAC, and 20–25% of cats suffer from cortisol-secreting tumors of the adrenal cortex (less commonly adrenal glands). In rare cases, adrenal tumors secrete steroid hormones other than cortisol. In addition to polyuria/polydipsia and weight loss, usually associated with concomitant diabetes mellitus, typical clinical signs of feline HAC include an enlarged abdomen, an unkempt coat with seborrhea, thinning of the coat, lack of hair regrowth, and muscle weakness. In severe cases, the skin becomes fragile and very easily damaged (the so-called fragile skin syndrome develops, Fig. 4)5.

Skin signs of HAC are not always observed. Alopecia is observed only in 60–80% of cases. Fragile skin syndrome is noted in 15–30% of cases and is a dermatological sign of HAC, characteristic specifically of cats 5.
OKN, secreting excess sex steroids
The number of cats described in the literature with OKN that oversecrete progestogens or other sex hormones is relatively small. Excess progestogens with typical symptoms GAK. A small number of cats experience increased androgen concentrations 2.
Progesterone-producing OCNs produce clinical signs identical to those caused by cortisol hypersecretion. This pathology, like GAK, contributes to the development of diabetes mellitus. This pathology, like GAC, is characterized by fragile skin syndrome. Skin signs are initially characterized by thinning of the skin, after which it spontaneously ruptures even from minor trauma (scratches, injections, etc.). In this case, bleeding and pain are usually absent. The skin of sick patients resembles tissue paper in appearance. Histological examination of such skin shows epidermal and dermal atrophy. The epidermis consists of only one layer of keratinocytes; there are very few collagen fibers 8.

Feline hyperthyroidism

Dermatological signs in cats with hyperthyroidism are secondary and are associated with worsening grooming, that is, their fur becomes dry, matted, and seborrhea appears. However, chronic and recurrent inflammatory skin diseases are not typical for such patients 8.

Obesity

Previously, the functions of fat were traditionally assessed as energy storage, thermal insulation, and structural support for certain organs. Classically, white adipose tissue was considered an inert and passive type connective tissue. But the discovery of leptin in the mid-1990s greatly increased interest in adipose tissue, which is now considered one of the important endocrine glands. Today it is known and generally accepted that adipose tissue is very active metabolically and is the largest endocrine organ in the body 6. The question of whether obesity in dogs and cats should be perceived as a disease still remains not fully resolved. Much remains unclear about obesity-associated diseases and their relationships in animals18. At the same time, there is a list of diseases that are considered to be associated with obesity. For cats, one of the sources indicated in the list of references for this article6 identified a list of diseases associated with obesity (type 2 diabetes mellitus, neoplasia, dental diseases, dermatological diseases, lower urinary tract problems, pregnancy complications, delayed wound healing, increased anesthetic/surgical risks) and likely leading to a reduction in life expectancy.

Cellulite

Cellulitis (inflammation of fatty tissue) in cats also interferes with tissue healing (Figure 5). Adipose tissue cells generate a wide variety of endocrine, paracrine and autocrine signals in the form of adipokines or adipocytokines, which are currently being intensively studied18. The metabolic role of most adipokines is complex and not fully understood18. However, perhaps one of their most important effects is their positive or negative impact on insulin sensitivity. Adipose tissue secretes more than 50 adipokines that influence metabolism, cell differentiation, tissue remodeling, immunity and inflammation10, but the most studied of them are leptin and adiponectin. In addition to adipokines, the following proinflammatory cytokines and acute phase proteins synthesized in adipocytes have now been identified: TNF-α, interleukin-1 and interleukin-6. They are quite well known and have both local and systemic pro-inflammatory effects4 and are also associated with the development of insulin resistance3.

TNF-α is a key component inflammatory process in obesity, which is expressed different cells, including macrophages, mast cells, neurons, fibroblasts and adipocytes 18 . One of the main physiological effects of TNF-α is the induction of local insulin resistance. In this case, TNF-α suppresses the expression of genes responsible for insulin-dependent glucose consumption by cells 13 ; 15; 16 . In addition to inhibiting glucose transport into the cell, TNF‐α reduces the uptake of free fatty acids by adipocytes and stimulates lipolysis and the release of free fatty acids into the systemic circulation 17 .

Literature:

  1. Fain J. N., Tagele B. M., Cheema P. et al. Release of 12 adipokines by adipose tissue, non-fat cells, and fat cells from obese women. // Obesity 2010, No. 18. – R. 890–896.
  2. Feldman E. C., Nelson R. W., Reusch C. and Scott-Moncrieff J. C. Canine and Feline Endocrinology, 4th Edition. – Imprint: Saunders, 2015. – 800 rub.
  3. Feve B., Bastard J. P. The role of interleukins in insulin resistance and type 2 diabetes mellitus. // Nature Rev Endocrinol. – 2009, No. 5. – R. 305–311.
  4. Greenberg A. S. and Obin M. S. Obesity and the role of adipose tissue in inflammation and metabolism. //Am J Clin Nutr. – 2006, No. 83. – R. 461–465.
  5. Guaguere E., Prelaud P. A Practical Guide to Feline Dermatology.
  6. Published by Merial, 1999.
  7. Hill's Global Mobility Fat: The Largest Endocrine Organ in Cats and Other Species, It's Not Just Energy Storage. P. Jane Armstrong, Julie A. Churchill; 29–34.
  8. Joyce J. Notes on Small Animal Dermatology. Wiley-Blackwell, 2010. – 376 p.
  9. Kern P. A., Ranganathan S., Li C. et al. Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. //Am J Physiol Endocrinol Metab. – 2001, No. 280. – R. E745–E751.
  10. Lago F., Dieguez C., Gomez-Reino J. et al. Adipokines as emerging mediators of immune response and inflammation. // Nature Clin Pract Rheumatol. – 2007, No. 3. – R. 716–724.
  11. Memon R. A., Feingold K. R., Moser A. H. et al. Regulation of fatty acid transport protein and fatty acid translocase mRNA levels by endotoxin and cytokines. // Am J Physiol. – 1998, No. 274. – R. E210–E217.
  12. Nuttall T., Harvey R. G., McKeever P. J. A Color Handbook of Skin Diseases of the Dog and Cat. 2nd edition. Manson Publishing Ltd, 2009. – 336 rub.
  13. Patton J. S., Shepard H. M., Wilking H. et al. Interferons and tumor necrosis factors have similar catabolic effects on 3T3-L1 cells. // Proc Natl Acad Sci. – 1986, No. 83. – R. 8313–8317.
  14. Peikes H., Morris D. O., Hess R. S. Dermatologic disorders in dogs with diabetes mellitus: 45 cases (1986–2000). //JAVMA. – 2001, Vol 219, No. 2. – R. 203–208.
  15. Peraldi P., Xu M., Spiegelman B.M. Thiazolidinediones block tumor necrosis factor-alpha induced inhibition of insulin signaling. // J Clin Invest. – 1997, No. 100. – R. 1863–1869.
  16. Qi C., Pekala P. H. Tumor necrosis factor-alpha induced insulin resistance in adipocytes. // Proc Soc Exp Biol Med. – 2000, No. 223. – R. 128–135.
  17. Ryden M. and Arner P. Tumor necrosis factor-alpha in human adipose tissue – from signaling mechanisms to clinical implications. //J Internal Med. – 2007, No. 262. – R. 431–438.
  18. Witzel A. New paradigms of adipogenesis. // VetPharma – 2013, No. 4.
  19. Nelson R., Feldman E. Endocrinology and reproduction of dogs and cats. – M.: “Sofion”, 2008. – 1256 p.
Pedigree breeding of dogs Sotskaya Maria Nikolaevna

Endocrine function of the gonads

The functions of the gonads are influenced by releasing hormones from the pituitary gland and hormones secreted directly by the gonads.

Male sex hormones.

Hormones secreted by the male gonads are steroids in nature and belong to the group androgens - male sex hormones. The formation of male sex hormones occurs in Leydig cells located in the testes. The male sex hormone is produced in the testes testosterone and its derivatives - androsterone and other androgens. Testosterone causes the development of genital organs, sperm maturation and male-type development. It, in turn, includes an increase in protein synthesis in the body, leading to the development of a positive nitrogen balance, as well as a decrease in the amount of fat in tissues, an increase in bone mass and muscle tissue and intensification of mucopolysaccharide metabolism. In addition to androgens, a certain amount of female sex hormones is produced in the testes - estrogen, the significance of which for males has not yet been sufficiently studied.

Female sex hormones

Hormones secreted by the female reproductive glands.

Female sex hormones are formed in the ovaries, combined into groups estrogen And gestagens. Small amounts of male sex hormones are also produced - androgens. Both androgens and estrogens accelerate maturation and reduce the period of bone growth. For example, estrogens activate osteoblasts, which leads to increased bone mineralization.

Hormones secreted by the pituitary-hypothalamic system.

In addition to the ovaries, sex hormones are also secreted by the pituitary-hypothalomic system. Among them: the so-called releasing hormones - follicle-stimulating (FSH) And luteinizing (LH), and gonadotropic hormones. Together they influence the maturation processes of germ cells. These hormones are secreted in both males and females, but in different quantities. In bitches, the synthesis of gonadotropic hormones occurs cyclically and determines the seasonality of reproduction. Prolactin causes the formation of milk in postpartum period, acting directly on the glandular cells of the mammary glands. In addition, it acts on the central nervous system, causing manifestations of the parental instinct.

From the book Treatment of Dogs: A Veterinarian's Handbook author Arkadyeva-Berlin Nika Germanovna

Examination of the reproductive system and mammary glands of bitches. Signs of concern include the presence of tumors, vaginal discharge, bleeding; hyperemia and soreness of the nipples. Prenatal pathologies include the occurrence of manifestations of the maternal instinct in bitches,

From the book Fundamentals of Neurophysiology author Shulgovsky Valery Viktorovich

Inflammation of the anal sacs and circumferential glands ¦ ETIOLOGY AND PATHOGENESIS Often inflammation of the paraanal glands begins as a result of their injury. It is accompanied by the appearance of protrusions on the side of the anus in the lateral and middle part of the perineum. Reason

From the book Breeding Dogs author Sotskaya Maria Nikolaevna

GLIA - MORPHOLOGY AND FUNCTION The human brain consists of hundreds of billions of cells, and nerve cells(neurons) are not the majority. Most of the volume of nervous tissue (up to 9/10 in some areas of the brain) is occupied by glial cells (from the Greek: glue). The fact is that

From the book Diseases of Dogs. Quick guide. External diseases author Georg Müller

Malformations of the gonads Disruption of the process of differentiation of the gonadsDescribed in fairly widespread hereditary anomalies that arise as a result of disturbances in the process of cell division - meiosis during the formation of germ cells in one of the

From the book Dog Diseases (non-contagious) author Panysheva Lidiya Vasilievna

Swelling and inflammation of the anal sacs and glands. Bursitis ani Anal sacs, Bursaeani, are two sacs the size of a hazelnut to a walnut, located on both sides of the anus between muscle layer and mucous membrane. Through a very narrow channel they communicate with

From the book Homeopathic treatment of cats and dogs by Hamilton Don

Diseases of the salivary glands Common diseases of the salivary glands in dogs include so-called mucous cysts. They develop when the patency of the excretory ducts is impaired and are located in the lower part of the pharynx, under the jaw (Fig. 87) or on the side of the upper part

From the book Genetics of Ethics and Aesthetics author Efroimson Vladimir Pavlovich

Inflammation of the sebaceous glands (acne) Inflammation of the sebaceous glands is usually observed in cats that are orange or yellow in color (and less often in cats with other coat colors). Inflammation is most often localized in the chin area and is one of the symptoms of deep

From the book Biology [Complete reference book for preparing for the Unified State Exam] author Lerner Georgy Isaakovich

Diseases of the mammary glands Insufficient milk production In some cases, milk production in the mother does not begin immediately after childbirth, as expected, but later. In addition, sometimes there is simply not enough milk to feed all the offspring. One of the herbal remedies

From the book Theory of Adequate Nutrition and Trophology [tables in text] author

11.1. Social function aggressiveness sympathetic nervous system, releasing adrenaline, sharply increases activity, speeds up running, enhances defense capability and determination. Its antagonist is the central nervous system, which balances the impulse

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From the book Brain, Mind and Behavior by Bloom Floyd E

From the book Behavior: An Evolutionary Approach author Kurchanov Nikolay Anatolievich

6.3. Endocrine function of the duodenum As noted above, by the beginning of the 50s we had overcome the technical difficulties associated with complete and atraumatic removal of the duodenum and transplantation of the pancreatic and common bile ducts into the jejunum

From the book Biological Chemistry author Lelevich Vladimir Valeryanovich

Endocrine system An endocrine organ is distinguished by the fact that it secretes a substance necessary to regulate the cellular activity of some other organs directly into the bloodstream (the term comes from the Greek endo - inside and krinein - to secrete). Such organs are called

From the author's book

8.4. Endocrine system Intensive study of biologically active substances that determine the functions of the whole organism begins at the very end of the 19th century. To designate these substances, the English physiologists W. Bayliss (1860–1924) and E. Starling (1866–1927) proposed in 1904

From the author's book

Hormones of the sex glands Male sex hormones Male sex hormones - androgens (from the Greek “andros” - male) - testosterone, dihydrotestosterone, androsterone. Synthesized in Leydig cells of the testes, prostate gland, and adrenal cortex. Not a large number of

From the author's book

Neutralizing function of the liver The liver is the main organ where it neutralizes natural metabolites (bilirubin, hormones, ammonia) and foreign substances. Foreign substances, or xenobiotics, are substances that enter the body from the environment

Disorders of the reproductive cycle in female dogs are quite common and occur at the level of the hypothalamic-pituitary complex and ovaries, manifesting themselves in the form of various symptoms, some of which may be pathognomonic signs of diseases of genital and extragenital nature.

Anestria (anestria, delayed puberty syndrome) - absence of estrus at puberty (sexually mature) age, is rare. According to Phemister R.D. (1980) only 2 clinically healthy beagle bitches out of 758 did not have a sexual cycle by 30 months of age.

The absence of estrus in the pubertal stage of development may be due to primary damage to the ovaries, or regulatory disorders at the level of the endocrine system of the brain. Consequently, dysfunction of the pituitary gland and hypothalamus leads to a decrease in the production of releasing factors (folliberin, luliberin) and gonadotropes - follicle-stimulating and luteonizing hormones (FSH, LH), which, in turn, also leads to ovarian hypofunction. In the development of anestriia important role Both genetic (breed, inbreeding, constitutional characteristics) and external (underfeeding of growing animals, unfavorable macro- and microclimate, isolated housing, insufficient exercise, etc.) factors can play a role.

Anestria is a mandatory symptom of some rare congenital malformations of the genital organs: agonadism, hermaphroditism, infantilism, etc.

Hormonal treatment and is carried out upon reaching 24 one month old. The basis of hormonal therapy is drugs with FSH and/or LH activity: pregnant mares serum gonadotropins (PSG), human chorionic gonadotropin (HCG), pituitary gonadotropins (FSH, FSH + LH). HSFAs have predominantly FSH activity, hCG - LH activity. Due to the combined administration of drugs with FSH and LH activity into the body, folliculogenesis and ovulation are stimulated. In addition to drugs with FSH and LH activity, some treatment regimens include estrogens, which cause an increase in the ovarian response to gonadotropins, as well as stimulation and more pronounced manifestation of signs of estrus in females (Table 1).

Table 1. Induction of sexual estrus in females

HYPOESTRAL SYNDROME (MILD AND SHORT DURATION HEAT)

In this case, the signs of proestrus and estrus are poorly expressed. Estrus is scanty and usually lasts no more than 7 days. The development of hypoestrous syndrome is based on insufficient production of estrogen by preovulatory follicles.

Treatment is hormonal. GSZhK, GSZhK are prescribed in combination with estrogens or with drugs that have LH activity (Table 2).

Table 2. Hormone therapy in bitches with hypoestrous syndrome

HYPERESTRAL SYNDROME (PROTECTIONAL AND EXTENSIVE HEAT)

Signs of proestrus and estrus are pronounced (the lips of the genital loop are very swollen, with copious hemorrhagic discharge). Estrus lasts for 40-60 days or more. General condition, as a rule, without the manifestation of a corresponding behavioral reaction (anxiety). However, with severe blood loss, increased thirst and, less commonly, anemia are possible. With the development of hyperestrous syndrome, persistent anovulatory follicles produce increased estrogen production. The absence of ovulation is due to insufficient secretion of LH by the anterior pituitary gland. After the spontaneous cessation of a prolonged estrus and/or its correction with the help of hormonal drugs, follicular and/or luteal cysts often form.

The presence of cysts in the ovaries (at the diestrus stage) causes a predisposition to the development of hydro- and/or pyometra.

In this case, methods of conservative therapy (exposure to hormones) or surgical intervention(ovaryhysterectomy). Bitches are prescribed drugs with LH, FSH/LH-releasing activity, as well as antibacterial agents to prevent the development of pyometra. According to Cain J.L. (1995), satisfactory treatment results in females with prolonged estrus were obtained with the administration of both hCG intramuscularly or subcutaneously at a dose of 100 - 500 units, and gonadotropin-releasing hormone (Gn-RH) intramuscularly or s/c at a dose of 50 mcg.

POLYESTRAL SYNDROME (VISION OF THE RHYTHM OF THE SEXUAL CYCLE)

In this case, the interval between estrus is reduced to 120-150 days. The interestrous period is shortened due to the anestrus stage. The cause has not been established. Females with a sexual cycle of 120 days or less are often infertile.

In this case, hormonal therapy is carried out, prescribing drugs with anti-gonadotropic activity (megestrol acetate, mibolerone), which ensures prolongation of the aestrous period (Table 2).

ANESTRAL SYNDROME (SECONDARY ANESTRIA)

In this case, a violation of the sexual cycle is noted, in which the interval between estrus exceeds 12 months. The interestrous period is lengthened due to the anestrus stage. This clinical picture is observed in bitches aged 8 years and older. Predispositions to the development of this syndrome are hypothyroidism and hyperadrenocorticism, obesity and cachexia. Anestral syndrome in bitches also occurs when androgenic hormones and drugs with antigonadal activity are prescribed.

Treatment is hormonal. The drugs and their prescription regimens correspond to anesthesia (Table 1).

POSTDIESTRAL SYNDROME (FALSE PUPTERY, FALSE LACTATION, PSEUDO-LACTATION)

This syndrome manifests itself as a result of regression of the corpus luteum after the completion of the sexual cycle and is characterized by the development in the bitch of signs of labor, lactation and a false idea that she has newborn puppies. This picture can be observed after oophorectomy in the diestrus stage, which is quite common. The development of this disease is facilitated by the fact that yellow bodies The sexual cycle and pregnancy function at the same time.

False lactation is the cause of mastitis, mastopathy and hormonally dependent neoplasms in the mammary glands.

The clinical picture of postdiestrous syndrome has three signs: false labor, established or unsteady lactation, as well as the manifestation of the maternal instinct. They have varying degrees severity and are usually diagnosed 50-80 days after estrus. At this syndrome, as a rule, lactation is noted. Developed lactation is characterized by the content of milk in the mammary glands, while unsettled lactation is characterized by the presence of a brown serous secretion. Bitches with developed lactation easily accept and feed newborn puppies from another litter (they often play the role of excellent nurses for orphan puppies). In the absence of suckling puppies, inanimate objects (dolls, slippers, etc.) become the object of maternal love. Bitches can be more aggressive towards other animals or people, protecting their adopted or “surrogate” cubs.

TREATMENT

In most cases, no treatment is required. Heavily lactating bitches are limited in water and food - factors that stimulate milk production. To suppress lactation, hormone therapy is performed, the purpose of which is to reduce the secretion of prolactin. Typically, bitches are prescribed megestrol acetate, bromocriptine and mibolerone. The drugs are administered orally every day: megestrol acetate at the rate of 0.5 mg/kg for 8 days; bromocriptine - 0.01 mg/kg for 2-3 weeks; mibolerone - 0.016 mg/kg for 5 days (Brown J.M., 1984; Cain J.L., 1995).

Ovariectomy is the most effective way to prevent false pregnancy.

GL. DULGER, GA BUROVA Moscow Agricultural Academy named after K.A. Timiryazeva

Today our guest is a specialist in laboratory diagnostics, a teacher at the Department of Biochemistry veterinary academy Vasilyeva Svetlana Vladimirovna. She was one of the first in our city to begin studying veterinary endocrinology and developing diagnostic algorithms, and is the author of 15 scientific papers in this field. The topic of our conversation is hormonal disorders in small pets.

Svetlana Vladimirovna, do dogs and cats really have hormonal disorders like people?

Yes, this is not surprising: all mammals have endocrine glands that work on the same principle as in humans and secrete hormones. A large number of endocrine diseases have been found and described in animals.

Why are they talking about this only now? It seems that animals have not suffered from such diseases before.

In fact, these diseases have always existed. However, previously they were practically not registered. There was no knowledge, no experience, and there were significantly fewer animals in the city. Indeed, more recently, veterinarians have realized that it is necessary to learn how to diagnose and treat hormonal diseases. Abroad, they have been underway for many years. Scientific research in this direction.

What endocrine diseases are most common?

I can say, based on my own research, that hypothyroidism, Cushing's syndrome, diabetes insipidus, type 1 diabetes mellitus, and polycystic ovary syndrome are most common in dogs. In cats, hormonal disorders are generally less common than in dogs, but non-insulin-dependent diabetes mellitus occupies a leading position.

How do they manifest themselves?

The fact is that every disease has a specific symptom complex. Much depends on how long the process has been and on the individual characteristics of the body. But any owner should know the basics characteristic features for which endocrinological examination is indicated. These include increased thirst and urination, changes in appetite, obesity or weight loss. With many hormonal disorders, areas of alopecia appear, the skin often darkens, and the quality of the coat deteriorates. As a rule, these symptoms develop over a more or less long period of time, and the disease has a chronic course.

Can there be congenital hormonal diseases?

Undoubtedly. In such cases, the growth and development of the animal is usually delayed, and rickets often develops.

How dangerous are these diseases?

They are dangerous because they cause significant disruptions in metabolic processes in the body, impair the functioning of organs and systems, especially the cardiovascular system. Sometimes the disease develops as a result of a tumor of the endocrine gland.

Are these diseases curable?

They respond well to replacement therapy diseases accompanied by decreased secretion of hormones. Syndromes of hyperfunction of the endocrine glands, especially tumors, are more difficult to treat.

What advice do you have for readers who notice these signs in their pets?

Be sure to undergo a comprehensive examination. To make a diagnosis, the doctor needs to examine the animal and analyze all the information about the development of the disease. The most important thing is to carry out laboratory diagnostics, including biochemical and clinical blood tests, as well as determination of the concentration of hormones in the blood. IN in some cases Urine examination, skin scraping, and ultrasound of the endocrine glands may be required. The examination can be done in the clinical-biochemical laboratory of the Academy of Veterinary Medicine.

The laboratory is located at st. Chernigovskaya house 5 in the building of the surgical building. By calling 388-30-51 you can find out more detailed information.

And the last question: after diagnosis, can patients receive your consultation?

Yes, after an appropriate comprehensive examination, we can give an opinion and prescribe a course of treatment.

Thanks for the interesting and important information.

MAIN ENDOCRINOLOGICAL SYNDROMES OF DOG

Relatively often, especially in older dogs, the functioning of the endocrine glands is disrupted. Diabetes mellitus, hormone-dependent hair loss, etc. occur. Unfortunately, in practice, doctors still incorrectly diagnose them as vitamin deficiencies, although it is unlikely that this kind of deficiency can be encountered. Most endocrine diseases are characterized by the simultaneous development of dermatopathies, which serves as a sign for recognizing these disorders. The connection between skin condition and dysfunction of the endocrine glands has now been scientifically proven. Thus, estrogens cause thinning of the epidermis, enrich it with pigment, and inhibit the development and growth of hair. Androgens cause thickening of the epidermis, they reduce the formation, but not the growth of hair, and activate the function of the sebaceous glands. The pituitary gland is involved in hair change; its adrenocorticotropic hormone inhibits the development of fur. On the contrary, thyroid hormone stimulates this process. When diagnosing endocrine diseases, it is necessary to know and use these patterns, since in veterinary medicine the determination of hormones in the blood is not carried out.

This section discusses the main endocrinological syndromes, taking into account their specific manifestations in the skin, which is important for practice. This division into main syndromes, and not into specific diseases, was not made by chance, since there are a lot of individual disorders, the frequency of their occurrence is different, and the functional manifestations and treatment are often the same.

Estrogeny. Feminizing syndrome . Hypergonadotropism in dogs is almost always associated with increased estrogen levels. In females, this occurs due to cystic or tumor degeneration of the ovaries, with cirrhosis of the liver; in males - with the development of sertolioma, long-term estrogen therapy, liver cirrhosis.

Symptoms. Disturbances in females are manifested by lethargy, adynamia, weakness pelvic limbs when moving. Females lose weight, their labia are swollen, along with this there may be an extended estrus or symptoms of chronic endometritis (see. Gynecological diseases)". With long-term estrogen, osteoporosis of the ribs and vertebral bodies, hyperreflexia of organs in the area of ​​the lumbosacral plexus develop. Changes in the coat usually begin with a prolonged molting period. The coat becomes dull and brittle. On the back, in the area of ​​the kidneys, symmetrical alopecia (symptom of "spectacles"), which, spreading, cover the genital area, groin and armpits. In an advanced stage of the disease, the hair falls out and remains only on the head, ears, limbs and the tip of the tail. The skin is dry, inelastic, sometimes, on the contrary, thickened and swollen, dark pigment inclusions are visible in places.

In males, the long-term influence of estrogen is manifested by feminization syndrome: libido (sex drive) fades, gynecomastia (female breasts) develops, and the male becomes attractive to same-sex men. The tissues of the prepuce swell, the testes become smaller and flabby to the touch. But spermatogenesis is preserved. Changes in the skin and coat are similar to those in females, however, alopecia is localized mainly on the sides. The results of laboratory tests are shown in Table 9. The course is chronic.

9. The main changes in the skin and coat of dogs due to various hormonal disorders

Hormonal
violations

Leather

Coat

Localization

results
clinical
research

results

laboratory
research

Estrogenemia
Femi syndrome
nization

Hyperkeratosis
and pigment-
tion, appearance
rash

Change of coat
pulled into
time, scrap-
cue hair,
rare + ob-
baldness

Back ("very-
ki"), area
genitals,
armpits, groin

Reluctance to move
ataxia, weight loss
body, genital hyper-
plasia and hypertrophy +
+ extended estrus Ti-
py A, B, C Endometritis,
after treatment with estrogen-
mi Male - feminized
aggravating syndrome: atro-
testicular fibrillation, preputial edema

Erythrocyte sedimentation H-

SG Number of leukocytes H-
SP, shift to the left is brightly high
affected by Urea

N-P,
creatinine N-P, choleste-
Rin N-P

Hypogonadotro-
pism

Soft, tone-
kaya, pliable-
vaya, later su-
hai, peels-
xia (parchment-
toe-shaped),
yellow-brown
Nevaya in white
stains

Fine-wallet-
viscous, sweaty
different color,
hair loss
los + bald-
tion, decrease-
growth rate

Neck, ears,
groin, tail,
limbs

Reluctance to move
addition body weight,
sexual dysfunction
(castration, genital
hypoplasia, senile,
testicular atrophy, crypto-
tumorous testicles)

Eosinophilia,
cholesterol N-P

Hyperadreno-

corticism

Thin, dry,
lethargic, hyper-
pigmentation
"peppered
black pepper"
or in white spots,
calcification,
hypothermia

Soft, straight
my, slightly
stretching
depigmented
bathroom, fall-
hair styling + +
baldness

Back (sides),
underbelly,
tail

Apathy, weakening of muscles
kulov, polydipsia, poly-
uria, obesity, stomach
pear, sexy
functions are limited or
none

Lymphopenia, eosinopenia,
sugar in blood N-P, more
local phosphatase P, ho-
Lesterol P-SP, cortisol
SP differential test
(see text)

Hypothyroidism

thickened,
peeling,
low elasticity,
cold,
diffuse or in
melanin spots
painted

Thin, dry,
matted,
the wool is dull,
rare, alopecia

Bridge of the nose,
neck, croup, ap-
tailing
hundred, groin, bad-
ra (chest and
underbelly)

Lethargy, hypothermia,
bradycardia, obesity
(late stage!), swollen
shaya muzzle, absence
sexual functions

Erythrocyte sedimentation SU,
cholesterol SP

Sazar diabetes

Wetting eco-
earth

In changed areas
skin loss
hair

No predisposition
proposals for lo-
calization
(absently)

Polydipsia, polyuria,
asthenia, severe itching

Blood sugar P-SP,
sugar in urine

DesignationsN - normal, P - increased, SP - strongly increased, U - accelerated, SU - strongly accelerated

Treatment. Castration is indicated for animals of both sexes. If castration is undesirable or cannot be performed due to the patient’s condition, females are treated with small doses of gestagens, males are prescribed long time corticosteroid hormones.

Hypogonadotropism syndrome occurs when the production of sex hormones is reduced and is characterized by the erasure of secondary sexual characteristics in animals. This is due genetic reasons, causing disruption of the regulation of the activity of the gonads by pituitary hormones, sometimes by castration of animals, especially if it was carried out before puberty.

Symptoms. The course of the disease is chronic. Specific lack of libido and sexual functions. Animals are apathetic, gain weight, and are reluctant to move. In males, the prepuce, penis, scrotum, and testes are atrophied. In females, weak development of the labia, vagina, and virgin cervix are noted. From the anamnesis of such animals it usually follows that they were castrated or “have never been in heat since birth,” or “sexual activity ceased after the first birth and lactation.” The skin is thin, parchment-like and slightly flaky. In places it is pigmented, yellow-brown spots are visible. The coat is thin, silky, devoid of color. In severe cases, alopecia develops in the neck, ears, tail, groin and limbs (see Table 9). The results of laboratory tests are close to normal readings. Sometimes cholesterol levels are increased, the number of eosinophils is decreased, and the function of the adrenal cortex is decreased.

Treatment consists of carrying out replacement therapy. Androgens or estrogens are prescribed for a long time in very small doses (0.1-0.01% of usual therapeutic doses). We must ensure that side effects did not block the therapeutic success. For this purpose, the animal’s condition is monitored every 3-6 months.

Cushing's syndrome . Changes in the activity of the adrenal cortex are almost always associated with hyperfunction, i.e., increased production of glucocorticoids. There appears to be a genetic predisposition to hyperadrenocorticism, since German boxers there is a tendency to tumor degeneration of the adrenal cortex, and in poodles - to hypertrophy of the cortex. Sometimes the disease can be caused by over-administration of hormones in the form of drugs.

Violation of the production of corticosteroid hormones initially leads to the development of hypogonadotropism (lack of libido, anostria, atrophy of the gonads). The disease progresses slowly until a typical clinical picture Cushing's syndrome.

Symptoms. The appearance of the animal is an obese body on thin atrophied legs. Characterized by lordosis of the spine, hanging abdomen, atrophy of the temporal muscles, and alopecia. Equally specific are exophthalmos and increased blood pressure. The skin becomes very thin; when stretched, large parts are clearly visible in it. blood vessels. To the touch the skin is cold, dry, hyperpigmented, as if “sprinkled with black pepper” (outdated hair follicles filled with keratin and detritus). White spots formed by lime deposited in these places are often found in the thickness of the dermis. The natural resistance of the skin decreases, their trophism deteriorates, resulting in the development of pyoderma (often in the corners of the lips) and bedsores (in the area of ​​bone protrusions). In rare cases remain covered long hair only the head, neck and limbs. X-rays reveal osteoporosis of the ribs, spine and hepatomegaly. Laboratory studies indicate steroid diabetes (see Table 9). The severe course of the disease ends with the inability of the pelvic limbs to support body weight, collapse and death.

Treatment. If the development of the syndrome is caused by excessive hormones, it is enough to cancel them. In case of hypersecretion of hormones by the adrenal cortex, Chloditan is used for 7-14 days, daily at 50 mg/kg, then only once a week at the same dose. The dog is re-examined after a month.

Hypothyroidism. Myxedema . Decreased thyroxine production due to congenital insufficiency of thyroid function or previous autoimmune thyroiditis. Cases of secondary hypothyroidism caused by pituitary disorders (tumor) have been described. English bulldogs, Irish setters, and spaniels are predisposed to the disease.

Symptoms. The dog exhibits a lethargic state, dullness, decreased temperament, thermophilia (lower body temperature), bradycardia, and a tendency to increase body weight (even with a reduced diet).

The coat is fine, matted, matte, sparse and depigmented. As the process progresses, alopecia develops, usually located on the sides, bridge of the nose, rump, base of the tail, thighs, groin, chest and abdomen. In bald areas, the skin is diffusely thickened, scaly, with melanotic spots (acanthosis nigricans). The muzzle appears swollen and the eyelids are narrowed. The loss of elasticity of the skin is clearly visible when it is gathered into a fold - the fold does not straighten out. The results of laboratory tests are shown in Table 9.

Replacement therapy: thyroxine is prescribed orally at a dose of 30 mg per day and Lugol's solution 5-10 drops per week. It is recommended to monitor the animal’s condition once every 3-6 months, and then determine the minimum required dose of the drug. The effect should be expected approximately 2 months from the start of treatment. There is a noticeable restoration of the skin and coat to a normal state. During estrus, the dose should be reduced by half, which corresponds to the least need for thyroxine.

Goiter . Pathological enlargement of the thyroid gland (struma), accompanied or not accompanied by a change in thyroxine production. The disease occurs mainly in mountainous regions and steppe regions, where factors of nutritional iodine deficiency and hereditary predisposition are combined.

Goiter in young dogs. The diagnosis is easily made based on palpation of the location of the soft swelling in the lower part of the neck, which distinguishes it from sialic cysts (upper part of the neck). The swelling can be uniform bilateral or uneven unilateral. Lugol's solution is prescribed as a remedy, 1-3 drops orally for several months. As the goiter decreases, the number of drops is reduced. Then small doses of vitamin A are prescribed and, if possible, the intake of calcium from food is limited, since it is involved in the development of goiter. It is recommended to include sea fish in the animal’s diet and add a little iodized salt.

Goiter in old dogs. There is one or two-sided enlargement of the thyroid gland. She dense consistency, sedentary, painful sensations at the beginning of the disease does not cause. The diagnosis is made taking into account the characteristic localization of the goiter: on the side of the trachea in the lower half of the neck. Goiter in old animals should be differentiated from thyroid tumors. The boundaries of the tumor are unclear, with signs of ingrowth of the surrounding tissue. The dog has difficulty swallowing and breathing. Atypical cells are found in the cell puncture from the tumor.

Treatment. Surgical removal of one lobe or the entire enlarged thyroid gland and subsequent drug replacement therapy.

Hemithyroidectomy technique. General anesthesia, intubation (insertion of a special tube through the mouth into the larynx); position on the side, the neck is fixed, the thoracic limbs are laid back (Fig. 47). Paramedian access to the thyroid gland, tissue incision between the sternothyroid and brachiocephalic muscles. Isolation and retraction of the ventral nerve of the neck (recurrent nerve). Revision of the thyroid gland. Thyroid consists of isolated left and right lobe. Determination of the extent of the lesion (unilateral or bilateral; often unilateral).

Rice. 47. Syntopy of the left lobe of the thyroid gland and stages of hemithyroidectomy:1 - position of the animal on the table and direction of tissue incision; 1 - enlarged left lobe thyroid gland - goiter; 3 - clamping of the cranial isthmus of the thyroid gland, including the anterior thyroid artery, the intersection of the isthmus; 4 - clamping of the caudal isthmus of the thyroid gland, including the caudal thyroid artery, the intersection of the isthmus; 5 - left ventral nerve of the neck; 6 - separating the goiter; 7 - sewing up fabrics

Separation of the goiter: first, the cranial isthmus of the gland, including the anterior thyroid artery, is isolated, then the caudal isthmus, including the posterior thyroid artery, is isolated. Ligation and intersection of isthmuses in the same sequence. Suturing the wound only by grasping the fascia of the neck and skin (without touching the muscles!). The parathyroid glands should be spared and preserved if possible. They are usually located on the lateral surface of the anterior pole of the goiter. Size parathyroid glands with rice or hemp grain. If during the dog’s life it becomes necessary to remove the second lobe of the thyroid gland, then after the operation thyroxine replacement therapy is carried out for life. You can gradually reduce the dose of the drug to determine whether the accessory thyroid glands are not producing enough hormone.

Diabetes . Diabetes diabetes caused by an absolute or relative lack of insulin. It is characterized by instability of blood sugar levels, a tendency to ketoacidosis and metabolic disorders.

The incidence of diabetes mellitus in dogs is 3% of all endocrine pathologies. Dachshunds, wire-haired terriers, somewhat less Scotch terriers, Spitz dogs and Irish Terriers. Diabetes mellitus occurs in dogs over 7 years of age. The ratio of sick males to females is approximately 1:4. In half of all females, the outbreak of the disease coincides with the end of estrus and occurs more often in autumn than in spring. As follows from the anamnesis, up to 25% of females have previously suffered from a disease of the uterus (endometritis, pyometra).

Diabetes mellitus, up to elementary glycosuria, is a disease caused by hormonal dysfunction. Dogs have predominantly insulin-deficient diabetes ("juvenile diabetes"), in contrast to humans, who more often have non-insulin-dependent "adult-onset diabetes". An increase in blood sugar is caused by a decrease in insulin levels due to:

Reducing its production by the pancreas (chronic sclerosing pancreatitis, cirrhosis, pancreatic atrophy);

Overproduction of corticosteroid hormones by the adrenal glands (steroid diabetes);

Overproduction of adrenocorticotropic hormone by the anterior pituitary gland (pituitary diabetes);

Overproduction of thyroxine thyroid gland(thyroid-induced diabetes, thyroxine provokes latent diabetes).

Symptoms. Polydipsia (thirst) and polyuria (increased urine output) are pronounced with simultaneous asthenia (weakness) and severe itching. Sometimes cataracts develop prematurely, and the smell of sour fruit is noted from the mouth. The wool is dull, brittle, and does not hold well. The skin is susceptible to pustular lesions, becomes wet, and has scaly defects.

In most cases, nephritis of varying degrees of severity occurs simultaneously, occurring with hypertension (increased arterial blood pressure). Liver damage is often diagnosed with increased activity of alkaline phosphatase and alanine aminotransferase; ESR over 3-6 mm, leukocytosis over 12,000, increased number of band leukocytes.

Diagnosis diagnosed by an increase in blood sugar and its presence in the urine (the renal threshold for sugar is 6.6 mmol/l.) If latent diabetes is suspected, they provoke it with thyroxine or perform another test. In a dog that has fasted for 24 hours, the blood sugar level is determined and 0.5 g/kg of glucose in the form of a 40% solution is injected intravenously. Blood sugar is re-determined after 90 and 120 minutes. By this time, a healthy animal should have restored its initial parameters.

Treatment. When blood sugar is below 11 mmol/l only complete diet feeding, including proteins, fats and carbohydrates. Feeding only meat should be prohibited! If the blood sugar level is over 11 mmol/l, 8-50 units of long-acting insulin are administered in the form of a suspension of crystalline zincinsulin (repeat the injection after 30-36 hours). At the same time, they maintain the same diet or reduce it by 1/4. Insulin administration is stopped after thirst disappears. If thirst has disappeared, but the sugar level remains high, above 11 mmol/l, then it is believed that even with such hyperglycemia, compensation has occurred in the body. Further attempts to reduce sugar levels to normal are fraught with an increase in cachexia and the risk of death of the animal. After stopping insulin administration and stabilizing the process, further monitoring of blood sugar levels is not necessary.

The dog owner should be warned that the dog should be fed immediately after administering long-acting insulin and again after 6-8 hours. With the onset of estrus, treatment is immediately resumed and the insulin dose is increased by half. Before and after estrus, repeatedly monitor the appearance of sugar in the urine! If the dog is in good general condition, it is better to neuter the dog, given the harmful effects of steroid hormones on the course of diabetes.

The life expectancy of a diabetic dog without treatment is short. With insulin therapy and elimination of thirst, the animal can live over 5 years.

Diabetes insipidus syndrome . A lesion of the hypothalamic-pituitary system, inherited in a recessive manner and manifested in a decrease in the production of the hormones oxytocin and vasopressin.

Oxytocin causes uterine contractions. Vasopressin causes vasospasm, stimulates the large intestine and inhibits diuresis.

Symptoms. Functional disorders: impaired ability of the kidneys to concentrate urine, polydipsia, polyuria, obesity, uterine atony. Animals show excruciating thirst, drinking several liters of water during the day. If there is no water, dogs can drink their own urine. Urine with a specific low specific gravity, below 1005. In addition, anarexia, weakness, and poor coat condition are noted. Females are more likely to get sick; poodles are more susceptible.

Diagnosis based on a simple test. If the dog is not given water for 8-12 hours, then in the case of a hypothalamic-pituitary disorder, the urine will not become more concentrated. (Do not limit water for more than 12-16 hours, as exicosis will develop - complete dehydration and death will occur!) The differential differences are as follows.

Diabetes

Sugar in urine, hyperglycemia

Nephritis

Proteinuria, epithelium in sediment

Azotemia, uremia

Increased urinary levels
we're in the blood

Pilmetra

Disease 3-10 weeks after estrus, leukocytosis, accelerated
elevated ESR, enlarged uterus, purulent discharge from the
Galishka

Posthemorrhagic anemia

Anamnesis data

Liver disease

Increased values ​​of alkaline phosphatase, alanine aminotrans-
ferases

Drug treatment glu-
cocorticoids, androgens,
estrogens,

Anamnesis data

Feeding dry concentrates
tami, swimming in the sea, etc.

Treatment. Sometimes thirst may suddenly stop spontaneously. There is evidence of the disappearance of thirst after exposure severe stress(falling off a bridge, car accident, pouring cold water on a dog sleeping in the sun). In other cases, adiurecrine is prescribed for insufflation in powder form into the nasal passages, 0.01-0.05 g 2-3 times a day. Young animals can recover; on adult animals, the effect of adiurecrine is not effective enough, then additional saluretics (diuretics) are given orally.

Hypoparathyroidism . More often this is insufficient production of parathyroid hormone by the parathyroid glands; as a casuistry - accidental removal of the parathyroid glands during surgery on the thyroid gland.

Parathyroid hormone is a polypeptide that takes part in the regulation of phosphorus and calcium metabolism in the body and facilitates their transfer through biological membranes. A decrease in the concentration of parathyroid hormone in the blood leads to the development of hypocalcemia, hyperphosphatemia, weakened excretion of calcium and phosphates, and alkalosis. Hypoparathyroidism occurs in two forms: chronic and latent (excluding postoperative complications).

Symptoms. A form of chronic intestinal osteodystrophy occurs in puppies. The processes of calcium resorption in the small intestine, and to restore its balance in the blood, calcium is mobilized from bone depots. Depleted bone tissue is replaced by fibrous tissue. The bones of the jaws are primarily affected, the widening of the nasal bridge becomes noticeable, teeth shift, and there is pain in the joints (especially in the maxillary joint).

Ectodermal disorders are observed in the form of cataracts, hair loss, brittle claws, defects in tooth enamel, and, in addition, cachexia. X-rays indicate a symptom of “bloating” of the bones of the upper and mandible, their cortical layer is subject to osteolysis in places, alternating with areas of thickening. A general depletion of skeletal bones in calcium is noted - osteoporosis. In adult females, small and dwarf breeds Hypoparathyroidism occurs as a latent form of tetany, becoming active only before estrus or during pregnancy and lactation (see Tetany).

Diagnosis placed taking into account clinical and radiological signs and by determining the concentration of calcium in the blood.

Treatment. In acute cases, calcium gluconate and diuretics are administered intravenously, and CO 2 inhalation is used to cause a shift towards acidosis. In case of chronic hypoparathyroidism, dihydrotachysterol is prescribed to regulate the phosphorus-calcium balance: 1-15 drops of 0.1% oil solution daily. The content of calcium and phosphate in the blood is determined again 5-7 days from the start of treatment, then once a month.



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