Functional features of the endocrine glands in dogs. Endocrine disorders in dogs

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 (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 the age of 30 months.

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 gonadotropic hormones - follicle-stimulating and luteonizing hormones (FSH, LH), which, in turn, also leads to ovarian hypofunction. In the development of anesthesia, both genetic (breed, inbreeding, constitutional characteristics) and external (underfeeding of growing animals, unfavorable macro- and microclimate, isolated housing, insufficient exercise, etc.) factors can play an important 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 months of age. 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 introduction into the body of drugs with FSH and LH activity, 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 bitches

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) are used. 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 occurs quite often. The development of this disease is facilitated by the fact that the corpus luteum of the reproductive 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 vary in severity and are usually diagnosed 50-80 days after estrus. With this syndrome, lactation is usually 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

Smirnova O. O., Candidate of Biological Sciences, veterinary therapist. Veterinary clinic of neurology, traumatology and intensive care, St. 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 mellitus
Endocrine diseases that interfere with skin healing in cats include HAC; OKN, secreting excess sex steroids; diabetes mellitus; cellulite.

The most common among these pathologies in everyday veterinary practice are HAC, hypothyroidism in dogs and diabetes mellitus in both types of animals. The likelihood of developing the remaining listed diseases is lower, but nevertheless, they should not be forgotten and should be included in the list of differential diagnoses if the corresponding 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 with radioactive iodine in patients with hyperthyroidism) or congenital. Since these cases are casuistic, we will not consider them. In addition, radioactive iodine treatment is currently not available in the Russian Federation.
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.
The skin of healthy dogs and cats is colonized by a variety of 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 the 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 is characterized by a bacterial infection localized in the stratum corneum of the skin and in the hair follicles. This form of 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 latter two bacterial species are likely 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 a surgical stitch placed several years ago. Atrophy of subcutaneous tissue 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. It is possible that the edges of skin wounds may diverge 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. These inflammatory skin diseases, in turn, also prevent tissue regeneration 2.
It should also be remembered about secondary hyperparathyroidism, which develops against the background of GAC. This pathology contributes to the activation of osteoclasts and, accordingly, osteodystrophy. A decrease in bone 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 found to have OKNs that secrete sex hormones. In this case, patients had low serum cortisol concentrations, but clinical signs, presumably due to sex hormones, were consistent with OAB. 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 are common 12. Changes in the 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 the effects of concomitant diseases. However, no skin disease directly related to diabetes was identified. The most common pathology in dogs with diabetes was a superficial bacterial skin infection. 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 of veterinary diagnostics and methods of treating pathologies of the endocrine system, feline HA 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.

OKNs that secrete excess sex steroids

The number of cats described in the literature with acute intestinal tract hypersecretion of progestogens or other sex hormones is relatively small. Excess progestogens with typical symptoms of OAB have been described in some cats. 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 of 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 listed in the reference list 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 inflammation,10 but the most studied of these 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 of the inflammatory process in obesity and is expressed by a variety of 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.

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, and weakness of the pelvic limbs during movement. 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 area of ​​the genitals, groin and armpits. In the 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, and 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 weight gain, 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), lower abdomen, tail	Apathy, weakening of muscles kulov, polydipsia, poly- uria, obesity, stomach pear, sexy functions are limited or none	Lymphopenia, eosinopenia, blood sugar N-P, more local phosphatase P, ho- Lesterol P-SP, cortisol SP differential test (see text)
Hypothyroidism	thickened, peels off, 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 lower abdomen)	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 corticosteroid hormones for a long time.

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 to genetic reasons that cause 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). Care must be taken to ensure that side effects do not overshadow 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. Apparently, there is a genetic predisposition to hyperadrenocorticism, since German boxers have a tendency to tumor degeneration of the adrenal cortex, and poodles have a tendency 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 the typical clinical picture of Cushing's syndrome occurs.

Symptoms. The appearance of the animal is an obese body on thin atrophied legs. Characterized by lordosis of the spine, hanging belly, atrophy of the temporal muscles, and alopecia. Equally specific are exophthalmos and increased blood pressure. The skin becomes very thin; when stretched, large blood vessels are clearly visible in it. To the touch, the skin is cold, dry, hyperpigmented, as if “sprinkled with black pepper” (lived hair follicles are 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, only the head, neck and limbs remain covered with long hair. 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 normal. 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. It has a dense consistency, is inactive, and does not cause pain at the onset of the disease. 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. The thyroid gland consists of isolated left and right lobes. 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 of the 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 site of 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. The parathyroid glands are the size of a grain of rice or hemp. 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 mellitus . 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 are predisposed to it. 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 by the thyroid gland (thyroidogenic 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 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 a complete diet, 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 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 mellitus	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 of gluten- 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 to severe stress (falling from 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 are disrupted, 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 show a symptom of “bloating” of the bones of the upper and lower jaws; their cortical layer is in some places susceptible to osteolysis, alternating with areas of thickening. A general depletion of skeletal bones in calcium is noted - osteoporosis. In adult females of small and toy breeds, hypoparathyroidism occurs as a latent form of tetany, becoming active only before estrus or during whelping 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. For chronic hypoparathyroidism, dihydrotachysterol is prescribed to regulate the phosphorus-calcium balance: 1-15 drops of a 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.

0

Endocrine, or endocrine glands, are all glands or groups of cells whose products, hormones or secretions, due to the lack of their own excretory tracts, are secreted into the blood and lymphatic capillaries and distributed throughout the body through the circulatory system. When hormones entering organs located near, and often far from the place of hormone production, come into contact with specific receptors, they have an inhibitory or activating effect, and often with the autonomic nervous system, on organs involved in metabolism and morphological changes. This contributes to the adequate adaptation of organs involved in metabolism to environmental conditions. Unlike hormones, paracrine signaling substances, when diffused into interstitial tissue, influence cells or groups of cells that are located near the site of product production.

In what follows, only the macroscopically visible hormone-producing glands, paraganglia, and pancreatic islets will be examined in detail. Thus, in the wall of the stomach and intestines there are numerous, separately lying cells, which, despite differences in structure and produced products, are united into the enteroendocrine system. Cells of similar structure are located in the mucous membrane of the bronchi and urethra, as well as in the kidneys (Andrew, 1981; Bohme, 1992; Grube, 1986; Hanyu et al., 1987; Kitamura et al., 1982; Pearse, 1980). The myocardium contains cells that, due to atrial natriuretic peptide (ANP) during sodium production in the kidneys, have an indirect effect on the volume of extracellular fluid (Forssmann, 1987).

How closely the interaction between endocrine organs and the autonomic nervous system occurs, which can be considered as a functional unity in the regulation of processes occurring in the body, can be understood from the following: 1) in the central nervous system there is an intensive interaction of the nuclei of the diencephalon with the pituitary gland and pineal gland, 2) both cells of the enteroendocrine system and the autonomic nervous system produce and secrete neuropeptides.

PITUITARY

The pituitary gland, hypophysis, glandula pituitaria, is an unpaired small organ located between the chiasma opticum and the corpus mamillare ventral to the diencephalon. It consists of the neurohypophysis, which forms on the basis of the diencephalon, and the adenohypophysis, which arises from the pituitary recess lining the roof of the oral cavity. The neurohypophysis is divided into the infundibulum, or pituitary stalk, and the lobus nervosus, or posterior lobe (-/2). The adenohypophysis includes the pars tuberalis, or funnel-shaped lobe (-/3), pars distalis, or anterior lobe (-/3"), pars intermedia, or intermediate lobe (-/4). The pituitary gland is an integral part of the hypothalamic-pituitary system. This is expressed The fact is that the hormones released into the blood in the neurohypophysis are formed by neurosecretory neurons, the bodies of which are located in the nucleus supraopticus and nucleus paraventricularis of the hypothalamus, and the functioning of the adenohypophysis is controlled by liberins and statins, which are secreted by the neurons of the small cellular nuclei of the gray tuberosity, tuber cinereum.

Rice. 1. Schematic representation of the pituitary gland along the midline of a dog (A) and a cat (B)

1 recessus infundibuli; 2 infundibulum, 2" lobus nervosus neurohypophysis; 3 pars tuberalis, 3" pars distalis adenohypophysis; 4 pars intermedia adenohypophysis; 5 cavum hypophysis; 6 dura mater

The pituitary gland in dogs is somewhat flattened, oval, in cats it is spherical. Not only does the size of the pituitary gland vary by breed, but even within the same breed there are individual differences (Latimer, 1942, 1965; White/Foust, 1944; Hanstrom, 1966). The size of the pituitary gland of a dog with an average head size is 10 x 7 x 5 mm, of a cat - 5 x 5 x 2 mm. Under the same housing conditions, the pituitary gland in females is slightly larger than in males, and in pregnant animals it is larger and heavier than in non-pregnant animals (Latimer, 1942; White/Foust, 1944). The mass of the pituitary gland in males of various breeds with an average body weight of 11 kg is 0.0658 g, in females with an average body weight of 8.93 kg - 0.067 g (Latimer, 1942).

The neurohypophysis, neurohypophysis, through the stalk or funnel of the pituitary gland, infundibulum, is in direct connection with the tuber cinereum of the hypothalamus. The pituitary stalk is cylindrical, very short and contains a short recess in the form of a depression in the proximal part, and in cats, reaching the lobus nervosus, recessus infundibuli (-/1). Distally, the pituitary stalk is thicker and passes without a clear boundary into the lobus nervosus, or posterior lobe (-/2’).

The adenohypophysis is larger than the neurohypophysis. Its pars tuberalis, the tuberal or funnel-shaped part, covers the pituitary stalk in dogs and cats. In dogs, the anterior and intermediate lobes of the adenohypophysis (-/3", 4) cover the posterior lobe of the neurohypophysis on all sides, while in cats the proximal portion of the caudal surface of the posterior lobe remains uncovered. With the development between the anterior and intermediate lobes of the adenohypophysis in dogs and In cats, there remains a pituitary cavity, cavum hypophysis (-/ 5), which varies significantly in its length and width.

In a fresh organ, the cut surface of the neurohypophysis appears homogeneous and glassy due to the large number of neurites and glial cells; the cut surface of the adenohypophysis, in which epithelial cells and sinusoidal capillaries predominate, has a granular consistency denser than that of the neurohypophysis. The microscopic structure of the pituitary gland, as well as the role of different cell types in the production of individual hormones, as well as the influence on other hormone-secreting glands or other organs, are described in textbooks on histology and physiology (e.g. Mosimann / Kohler, 1990; Scheunert / Trautmann , 1987).

Only aa go directly to the posterior lobe of the pituitary gland. hypophysiales caudales. They arise in dogs from the caudal communicating branch of a. intercarotica caudaiis, which runs in the hard shell along the body of the basisphenoid. In cats, these vessels come from the rete mirabile epidurale. After passing a. carotis interna through the diaphragm sellae, diaphragma sellae from it, or from the a. cerebri rostralis, separated by aa. hypophysiales rostrales, which go to the pituitary stalk and the posterior lobe of the adenohypophysis. Often small aa. hypophysiales rostrales arise on each side of the caudal communicating artery, a. communicans caudaiis, and run radially, converging on the pituitary stalk. In the dura mater of the brain at the pituitary gland, the pituitary arteries are connected into one thin network, a plexus (Green, 1951), from which the arteries primarily go to the median eminence, eminentia mediana and infundibulum of the neurohypophysis, as well as to the pars tuberalis of the adenohypophysis. From this primary capillary region in the pituitary stalk, numerous veins are formed, which run distally along the ventral surface of the adenohypophysis, and then into the voluminous sinusoids of the anterior and intermediate lobes. This system makes possible the influence of liberins and statins produced in the tuber cinereum, and then moving along the tractus tuberoinfumdibularis into the pituitary stalk, after their further transport in the blood, on various cells of the anterior lobe. Numerous veins that drain blood from the pituitary gland soon flow into the sinus cavernosus or the caudal sinus intercavemosus.

Sympathetic nerve fibers from the cranial cervical ganglion go to the pituitary gland or in the form of a perivascular plexus with aa. hypophysiales or in the form of branches n. caroticus internus.

On the outer surface of the pituitary gland, the dura mater forms a thin connective tissue capsule, which at the same time represents a strong connection of the pituitary gland with the flat pituitary fossa, fossa hypophysiales, on the body of the basisphenoid. In the region of the pituitary stalk, the dura mater protrudes above the free edge of the sella turcica, sella turcica in the form of diaphragma sellae, covers most of the pituitary gland on the dorsal side and leaves only a small hole for the passage of the pituitary stalk. In this area, in relation to the pituitary gland, the cavum subarachnoidale ends, which is especially extensive on the dorsal side of it in the form of an interpeduncular cistern, cisterna interpeduncularis. Between the two plates of the dura mater on both sides of the pituitary gland there passes the sinus cavernosus, and caudally from it the sinus intercavernosus. In the region of the latter, a. go to the pituitary gland on each side. carotis interna, or, respectively, in cats - rete mirabile epidurale, n. oculomotorius, n. trochlearis and n. ophthalmicus, as well as n. abducens.

Sh PIROID GLAND (EPIPHYSUS)

The pineal gland, glandula pinealis, is an unpaired organ. Its cross section is circular. The pineal gland lies between the cerebral hemispheres in front of the roof of the midbrain, tectum mesencephali. Its size varies among animals, and in medium-sized dogs the length reaches approximately 3 mm and the diameter reaches 2 mm. In cats, this ratio is 2x1 mm. Being part of the diencephalon, the pineal gland is connected to the caudal portion of its roof through frenulums, habenulae with a short stalk, pedunculus. The fibers of the commissure of the frenulum, comissura habenularum, pass through this junction. In the body, corpus, pineal gland, in addition to nerve fibers, there are pinealocytes, which, depending on the duration and intensity of light, produce the hormone melatonin. In dogs and cats, regardless of age, especially on the ventral surface of the pineal gland, some pinealocytes contain melanin. The functional significance of these pigmented cells has not yet been studied (Calvo et al., 1992). Considering the connection with the diencephalon, as well as humoral interaction with other glands that secrete hormones, through melatonin, the pineal gland represents an important central organ of neurovegetative regulation. At night, melatonin production is more active than during the day, and with the participation of feedback through the cranial cervical ganglion of the sympathetic part of the nervous system and with innervation by sympathetic fibers, the pineal gland can have a controlling effect on biological rhythms. The arteries that supply the pia mater near the pineal gland send thin branches to the interior of the organ. In the pineal gland, the branches branch into sinusoids.

SCH ITIC gland

The thyroid gland, glandula thyreoidea, consists of the left and right lobes, lobus sinister

A) et lobus dexter, as well as the isthmus connecting them, isthmus. The shape of each lobe varies considerably in dogs and cats, being oval and slightly flattened at the sides, and in cats, most often thinner than in dogs. The lobes, from dark red-brown to gray-red in color, have a consistency similar to that of the liver. In adult animals, the thyroid gland may be denser, while in cats it may be softer. The incidence of isthmus in cats varies (16-87%). In dogs it depends on body size. An isthmus is present in half of large dogs, a third of medium-sized dogs and a quarter of small dogs (Heller, 1932). Both lobes are located in dogs on the dorsolateral surface of the trachea and run parallel to it. In rare cases, the gland may be located slightly cephalad or caudally. On ultrasound examination in dogs, the thyroid gland appears caudal to the larynx as a homogeneous fusiform structure and is clearly demarcated from surrounding structures (Wisner et al., 1991). In cats, both lobes are higher on the dorsal side than in dogs, so they can be located between the trachea and esophagus and be covered dorsolaterally by m. longus capitis. In the presence of an isthmus, the caudal poles of both lobes are connected, and the isthmus passes along the ventral surface of the trachea. The epithelial cells of the thyroid follicles produce the hormones thyroxine and triiodothyronine, which play an important role in metabolic processes. These epithelial cells are separated from the epithelium of the root of the tongue during development. Then they reach the lateral surfaces of the first tracheal ring through the ductus thyreoglossus. Between these cells there are always so-called C-cells. They produce calcitonin, which, together with parathyroid hormone, is involved in maintaining a constant calcium level.

The relative mass of the thyroid gland in dogs and cats is maximum at the time of birth, and decreases in the first weeks after birth. Regardless of breed, the absolute and relative mass of the thyroid gland varies.

Absolute and relative weight of the thyroid gland in dogs and cats

(Haensly et al., 1964; Heller, 1932; Latimer, 1939; Meissner, 1924; Meyer, 1952; Schneebeli, 1958; Schweinhuber, 1910):

Table 1

Accessory thyroid glands, glandulae thyroideae accessoriae, can form during development from separated parts of the thyroid gland, which is more common in dogs than in cats. They can occur at the base of the tongue, along the neck, in the mediastinum near the heart, or near the aortic arch. Their size varies greatly and they can often only be detected by histological examination. If part of the ductus thyreoglossus remains during development, it may develop into a cyst in the neck area.

The main vessel supplying the thyroid gland is a. thyreoidea cranialis. It arises from a. carotis communis at the level of the annular tracheal membrane (ligament), membrana cricotrachlealis or the first tracheal cartilage. In addition to branches to the pharynx, larynx and adjacent muscles, this artery gives off ramus dorsalis et ramus ventralis along the corresponding parts of each lobe of the thyroid gland to both the thyroid gland and the epithelial bodies. The area where thin a. thyreoidea caudalis (-/1) varies. Most often, it arises from the brachiocephalic trunk, truncus brachiocephalicus or the costocervical trunk, truncus costocervicalis. Less commonly, it is formed from the right subclavian artery, a. subclavia dextra. A. thyreoidea caudalis always accompanies n. laryngeus recurrens (-/5) and connects through anastomoses with the dorsal branch of a. thyreoidea cranialis.

Extraglandular veins are different not only in different animals, but also on different sides of the body of the same animal, and connect with each other. V. thyreoidea cranialis (-/ n) and often double v. thyreoidea media (-/t) drains blood into v. jugularis is on its side. Arcus laryngeus caudalis (-/p) represents the connection between the left and right v. thyreoidea cranialis, as well as the cranial part of the unpaired v. thyreoidea caudalis (-/u). The last vessel passes along the midline along the ventral surface of the trachea and flows into either the left or right v. brachiocephalica or v. jugularis externa, or interna of the right side.

Rice. 2. Topography of the thyroid gland and left outer epithelial bodies of the dog (according to Borer, 1990)

A glandula thyreoidea; In glandula parathyreoidea; With trachea; D oesophagus; E m. hyopharyngeus; F m. thyreopharyngeus; G m. cricofaringeus; Hm. thyreohyoideus; Lm. sternothyroideus; To cartilago thyreoidea; Lm. cricothyreoideus; Mm. sternohyoideus

a a. carotis communis; b a. thyreoidea cranialis; c - k branches a. thyreoidea cranialis; with ramus dorsalis; dramus ventralis; e ramus sternoclei domastoideus; f ramus laryngeus caudalis; g ramus pharyngeus; h ramus cricothyreoideus; i ramus muscularis; k ramus laryngeus; I a. thyreoidea caudalis; m v. jugularis interna; n v. thyreoidea cranialis; o - s aste der v. thyreoidea cranialis; t v. thyreoidea media; u v. thyreoidea caudalis; v v. laryngea impar; w arcus hyoideus; x anastomose zwischen arcus hyoideus und v. jugularis interna

1 truncus vagosympathicus; 2 n. laryngeus cranialis; 3 ramus internus n. laryngeus cranialis; 4 ramus externus n. laryngeus; 5 n. laryngeus recurrens; 6, 7 rami musculares from ansa cervicalis; 8th connecting branch to the 1st cervical nerve

In the thyroid gland, lymphatic capillaries form a dense network around individual follicles (Rusznyak et al., 1967), and draining lymphatic vessels go to In. retropharyngeus medialis.

Sympathetic nerves to the thyroid gland are formed from the cranial cervical ganglion, and parasympathetic nerves from n. laryngeus cranialis. Individual fibers may emerge from the n end. laryngeus recurrens.

E PITHELIAL BODIES (PARATYROID GLANDS)

After developing from the epithelium of the third and fourth gill pouch, the outer epithelial body, glandula parathyreoidea externa, also called glandula parathyreoidea IV, and the inner, glandula parathyreoidea interna, also called glandula parathyreoidea III. The parathyroid hormone they produce, together with calcitonin secreted by the C-cells of the thyroid gland, regulates calcium metabolism.

In dogs, the outer epithelial body has a lenticular or rice grain shape with a smooth surface and is located at the cranial pole or cranial half of the thyroid lobe, less often - near the dorsal edge. In cats, the outer epithelial body is usually located laterally in the caudal half of the thyroid lobe. The size and weight of epithelial bodies in dogs under one year of age depend little on age. The size of the outer epithelial body in large dogs is 3-7 x 2-5.5 x 1.5-2.5 mm, the inner epithelial body is slightly smaller. The color varies from golden yellow to reddish brown and often stands out well against the background of the thyroid gland.

In dogs and cats, the internal epithelial body lies in the middle part of the thyroid lobes in the parenchyma of the thyroid gland, somewhat distant from the medial or dorsal surface and not always noticeable from the outside. In some cases it may be absent (Pinto and Silva, 1947).

The outer epithelial body receives 1-2 rami glandulares from a. thyreoidea cranialis, and venous outflow is carried out through rami glandulares, which flow into v. thyreoidea cranialis or arcus laryngeus caudalis. The internal epithelial body does not have its own arterial or venous branches, but is adjacent to the vessels of the thyroid gland (Orsi et al., 1975).

Sympathetic fibers from the cranial cervical ganglion reach the epithelial bodies, accompanying the arteries; parasympathetic fibers originate from n. laryngeus recurrens.

ADRENAL GLANDS

The adrenal gland, glandula suprarenalis or adrenalis, is a paired organ that consists of the cortex, cortex and medulla, medulla (-/C, 2). On the outside, this organ has a thin connective tissue capsule and is surrounded by connective tissue with fat cells, located retroperitoneally on the medial side of the cranial pole of the kidney. The adrenal cortex develops from the mesoderm and is influenced mainly by ACTH of the adenohypophysis. The adrenal medulla produces epinephrine and norepinephrine and is primarily regulated by the sympathetic nervous system. On the cut surface of a fresh adrenal gland, the border between the light cortex and the dark medulla is clearly visible macroscopically. In dogs, each adrenal gland (-/A) is elongated, dorsoventrally flattened and has a light gray to white color. In cats, the yellowish-white adrenal glands (-/B) are shorter than in dogs, oval and disc-shaped. The common trunk of the caudal phrenic vein, v., runs along the ventral surface. phrenica caudaiis, and cranial abdominal vein, v. abdominalis cranialis, leaving a superficial groove in cats and a deep groove in dogs. Due to the presence of this deep groove in dogs, two elongated lobes, not completely separated from each other, and two rounded lobes on the right adrenal gland can be distinguished on the right adrenal gland. Common trunk a. phrenica caudaiis and a. abdominalis cranialis passes the adrenal glands from the dorsal side and does not leave a groove.

Rice. 3. Adrenal glands of a dog (A) and a cat (B), view from the ventral side; C - cross section of 1 cortex; 2 medulla. Life size

In adult females, as well as pregnant and lactating ones, the size and weight are larger than in males, as well as in young animals.

In dogs and cats, the adrenal glands are located retroperitoneal and medial to the cranial half of the kidneys, or medial to their cranial pole. The left adrenal gland is connected to the left wall of the aorta caudaiis, the right adrenal gland is connected to the right wall v. cava caudaiis.

The blood supply to the adrenal glands is carried out by numerous aa. suprarenales or directly from the aorta abdominalis, or from a. phrenica caudaiis, a. abdominalis cranialis or a. renalis. After passing through the connective tissue capsule, these branches branch and give off radially voluminous capillaries throughout the entire circumference to the medulla. From the capillary network of the medulla, blood collects in a large central vein and then flows through several vv. suprarenales in v. cava caudalis, v. phrenica caudalis, v. abdominalis cranialis or v. renalis. There are significant individual differences in the number and length of blood vessels. In dogs and cats, tiny vessels are combined in the connective tissue between the kidneys and adrenal glands, which probably explains why at least a small part of the catecholamines produced in the adrenal medulla can reach the kidneys by the shortest route (Christe, 1980; Dempster, 1978 ; Earle/Gilmore, 1982). Lymphatic capillaries are numerous in all parts of the adrenal glands and are located in the form of a network. Through several lymphatic vessels, lymph is collected in the Inn. lumbale aortic.

Rice. 4. Location of the adrenal glands of the dachshund with nearby ganglia and sockeye salmon (according to Seiferle, 1992) a left, a’ right adrenal gland; b left, b" right kidney; c ureter; d oesophagus; e ventral leg, e' lateral leg of the right part of the diaphragm. f left part of the diaphragm; g pars costalis musculature of the diaphragm; h v cava caudaiis; i. i" mirror of the diaphragm; k m. psoas minor; l m. psoas major; IX. -XIII. 9-13. ribs

1 aorta abdominalis; 2 a. hepatica, 7 a. gastrica sinistra, 2" splenic artery a. coeliaca; 3 a. mesenterica cranialis 4 a. phrenica caudaiis; 5 a. und v. renalis, 6 a. mesenterica caudaiis; 7 a. tcsticularis; 8 vv. phrenicac, 8" common trunk v. phrenica caudaiis and v. abdominalis cranialis; 9 truncus vagalis ventralis, 9" his rami gastrici parietales; 10 truncus vagalis dorsalis, 10" his rami gastrici viscrales, 10" his rami cocliaci; 11 ganglion cocliacum; 12 ganglion mesentericum craniale; 13 branches of plexus suprarenalis; 14 ganglion renale and plexus renalis ; 15 plexus aorticus abdominalis; 17 left and right n. hypogastricus; 19 branch n. iliohypogastricus lateralis;

Table 2

Numerous autonomic nerve fibers to the adrenal glands arise either directly from nearby n. splanchnicus major, or from ganglion coeliacum and ganglion mesentericum craniale. In the form of plexus suprarenalis, they reach the adrenal glands directly or with blood vessels and enter the organ with them. The nerve fibers form a plexus in the capsule, from which numerous bundles of nerve fibers extend into the cortex and adrenal medulla.

O lines of the pancreas

Inside the pancreas, between the exocrine cells of the terminal sections of the gland, endocrine cells of the pancreas, endocrinocyti pancreatici, are united into small groups, the islets of the pancreas or islets of Langerhans, insulae pancreaticae. Individual islands of unequal size, including a large number of vessels, consist of 10-100 endocrinocytes. The number of islets varies significantly in dogs and cats, reaching several thousand. In the lobus sinister of the pancreas, the islets of Langerhans are larger and more numerous than in the lobus dexter. The capillary region of the endocrine and exocrine parts of the pancreas are connected to each other, and the lumen of the capillaries in the islets is larger and the capillaries are more numerous than in the exocrine part of the pancreas. The transition to the boundary surface between the two parts is very pronounced.

Upon microscopic examination, 3 types of cells are distinguished in the islets. A cells make up 10–20% of endocrine cells overall, but are absent from the islets of the caudal lobus dexter of the pancreas. This may be due to the fact that the caudal part of the lobus dexter and the remaining parts have different origins. A-cells produce glucathone and regulate carbohydrate metabolism with insulin-producing B-cells. B cells make up 80-90% of endocrine gland cells. In addition to somatostatin-producing D cells, which make up 1% of all islet cells, there are also other, individually occurring cells that, for example, can produce gastrin and serotonin. These cells are compared to the cells of the enteroendocrine system (Mosimann/Kohler, 1990). Electron microscopy revealed the presence in A-cells of electron-dense granules with a diameter of up to 0.5 μt. In B cells, the granules are larger than in A cells, have lower electron density, but contain crystalline inclusions. In D cells, the granules are smaller and have less electron density than the granules in A cells.

PARAGANGLIA

There is no precise definition of what paraganglia are. Most often, paraganglia are large or small clusters of devoid of processes, catecholamine-containing, chromaffin cells, which are located in close proximity to the ganglia of the autonomic nervous system or from large arteries. Most often, these clusters are distinguished only using macro-microscopic research methods. Since these cells, as well as the cells of the adrenal medulla, have a common origin, it has long been believed that paraganglion cells have endocrine activity. Today it is known that the adrenal medulla, as the largest paraganglia, according to this definition, actively produces hormones, but the carotid glomerulus, glomus caroticum, as well as the aortic glomerulus, glomus aorticum, function as chemoreceptors and record the partial pressure of CO 2 in the blood.

Glomus caroticum in dogs has a very thin capsule of loose connective tissue, which passes into the surrounding tissues without a clear boundary. Therefore, the boundaries between the glomus and surrounding tissues are little noticeable when viewed through a magnifying glass. It is located, most often, craniomedial from the terminal division of a. carotis communis in the area where a. pharyngea ascendens or a. occipitalis, less often - in the area of ​​occurrence of a. carotis interna. Glomus caroticum is spherical or elongated, sometimes covering, like a ring or semiring, the area of ​​origin of one of the named arteries (Cantieni/Frewein, 1982). Accurate data on the size of glomus caroticum can be obtained from histomorphometric studies. The volume of the glomus caroticum in an adult German Shepherd and an adult Boxer is 3-16 mm 3 . A dense network of voluminous capillaries contacts parenchymal cells (Type I and Type II). On average, dogs have 3.3% Type I cells and 2.2% Type II cells (Frei-Kuchen, 1981; Pallot, 1987).

Rice. 5. Topography of the right glomus caroticum, view from the medial side. A - German shepherd (according to Cantieni/Frewein, 1982) and B - cat (modified, according to Pallot, 1987)

1 glomus caroticum; 2 a. carotis communis; 3 a. carotis externa; 4 a. carotis interna; 5 sinus carotis; 6 a. occipitalis; 7 a. pharyngea ascendens; 8 a. larvngea cranialis; 9 ramus sinus carotici glossopharyngeal nerve; 10 branch n. vagus; 11th branch from ganglion cervicale craniale; 12 plexus caroticus externus

Rice. 6. a. Schematic representation of the paraganglia of the head, neck and thoracic region (after Seiferle, 1992)

1 aorta descensens; 2 arcus aortae; aorta thoracica; 4 a. subclavia sinistra; 5 truncus brachiocephalicus; 6 a. subclavia dextra; 7 a. carotis communis dextra; 8 a. carotis communis sinistra; 9 a. carotis interna; 10 a.m. carotis externa;

11 sinus caroticus; 12 glomus caroticum; 13 glomus aorticum; 14 ramus sinus carotici; 15 ganglion distale of the vagus nerve; 16 no. laryngeus cranialis; 17 no. depressor; 18 ganglion cervicale craniale; 19 sympathetic part

IX n. glossopharyngeus; X n. vagus

Rice. 6. b. Schematic representation of the large abdominal paraganglia of a dog at 24 weeks of age. Ventral view (after Mascorro/Yates, from Seiferle/Bohme, 1992)

1 aorta abdominalis; 2 a. renalis; 3 a. testicularis (ovarica); 4 a. mesenterica caudalis; 5 adrenal gland; 6 paraganglion aorticum abdominale

In cats, glomus caroticum, due to its powerful connective tissue capsule, is separated from surrounding tissues more easily than in dogs. In general, glomus caroticum is spherical in diameter, 2 mm and is located at the site of origin of either a. pharyngea ascendens, or a. occipitalis. Components, according to Seiferleet al. (1977), include: vessels 22.3%, specific tissue 16.9% and remaining tissue 60.8%.

In dogs and cats, the glomus caroticum is innervated by branches from the ramus sinus carotici of the glossopharyngeal nerve, as well as branches of the ganglion cervicale craniale. In dogs, in addition, thin branches come directly from n. vagus or its rami pharyngei. All named branches are connected to each other, and in dogs they are attached to the part of the plexus caroticus externus, with significant variations.

Glomus aorticum includes groups of chromaffin cells that lie on the aortic arch and are not clearly demarcated from surrounding tissues. These cells, like the cells of glomus caroticum, record CO2 pressure in the blood and transmit information along the branches of n. vagus to the nuclei of the medulla oblongata. The meaning and functions of the efferent fibers that end in the glomus caroticum and glomus aorticum are not yet precisely known.

Paraganglion aorticum abdominale is located near the ventral surface of the aorta abdominalis and the place of origin of a. mesenterica caudalis, and is better developed in newborn animals than in adults. Its functions, as well as those of small groups of chromaffin cells, for example near n. tympanicus or in a. subclavia are unknown.

Literature used: Anatomy of a dog and a cat (Coll, authors) / Transl. with him. E. Boldyreva, I. Kravets. - M.: “AQUARIUM BUK”, 2003. 580 pp., ill. color on

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Veterinary endocrinology, based on clinical and experimental research, is an actively developing science. Over the past decades, significant success has been achieved in the study of pathologies of the endocrine glands in animals: previously undetected disorders have been described, diagnostic methods and treatment methods have been improved. At the same time, endocrine diseases in productive animals, cats and dogs, are far from a rare phenomenon, which is facilitated by the increasingly complex environmental situation, unbalanced feeding, the use of hormonal drugs, infections, etc.

Diseases of the endocrine system in animals are caused by dysfunction of the hypothalamus and pituitary gland, thyroid and parathyroid glands, adrenal cortex, islets of Langerhans of the pancreas, thymus and gonads. As a rule, endocrine diseases in animals of complex origin are manifested by a variety of clinical signs, including combined lesions of the nervous system, heart, liver, kidneys and other organs and tissues. The determining factor for endocrine diseases in animals is a deficiency or excess of hormone synthesis.

Next, we will look at the most common endocrine pathologies of dogs and cats.

DIABETES MELLITUS
Clinical manifestations of diabetes mellitus in animals are as follows: increased thirst (polydipsia), frequent urination (polyuria), decreased body weight in the presence of increased appetite (polyphagia). In isolated cases, animals experience decreased activity, weakness of the pelvic limbs, plantigrade gait, refusal to feed, vomiting, lack of bowel movements or diarrhea, dull and poorly maintained coat. In some cases, cataracts develop.

CUSHING'S SYNDROME
Clinical signs of Cushing's syndrome in animals: in 80-90% of cases, increased thirst and urination; a painful state similar to sleep and accompanied by immobility, lack of reactions to external stimuli; note sagging of the abdomen (“pot-bellied” appearance); muscle weakness and atrophy; noisy and rapid breathing; up to 70% of cases are symmetrical alopecia and skin atrophy. Testicular atrophy occurs, the sexual cycle in females is absent, obesity develops against the background of increased appetite. The presence of long-term non-healing wounds, corneal ulceration, hidden urinary tract infections and the formation of phosphate stones are often detected.

ADDISON'S DISEASE
Symptoms of hypoadrenocorticism in animals include: lack of sexual activity, poor appetite, weight loss, dehydration, fatigue and weakness (some individuals are unable to stand). With the acute development of the disease, weakness, vomiting, and diarrhea (often with blood) are observed. When palpating the abdomen, pain is noted. The most characteristic of hypoadrenocorticism is a decrease in blood pressure, weakening and slowing of cardiac activity, a drop in muscle tone, a decrease in general excitability, the appearance of collapse and fainting.

HYPERTHYROIDISM is more often diagnosed in cats than in dogs. As a rule, this endocrinopathy occurs in middle-aged and old cats. Most of the sick cats were between 6 and 10 years old; no breed or gender dependency was identified. In dogs, hyperthyroidism occurs between the ages of 8 and 13 years. In most cases, dogs are brought to the veterinarian because of shortness of breath, coughing, difficulty swallowing and the appearance of a mass on the neck.

HYPOTERIOSIS
Clinical manifestations of hypothyroidism in animals: an increase in the size of the thyroid gland - goiter. The development of hypothyroidism in young cats leads to stunted growth and development; they have a disproportionate appearance with a round and short body, a round and thick head, and abnormally short limbs. Such animals often have difficulty defecating.

In dogs with hypothyroidism, lethargy, increased drowsiness, decreased interest and decreased response to external stimuli are noted, a decrease in body temperature and increased thermophilia are recorded. Their appetite is preserved and the individual has a tendency to obesity. In dogs with hypothyroidism, the condition of the skin, subcutaneous layer, and coat worsens. It becomes dull, poorly maintained, symmetrical alopecia appears with hyperpigmentation of the skin on the back of the nose, chest, sides, tail and thighs on the inside. The skin becomes cool and dry. Peeling and blockage of the follicle openings with keratin plugs are often observed, which leads to the appearance of inflammatory processes and acne. When examining your pet’s head, you can see a “sad” face – puffiness (myxedema). Sick animals often have a decreased heart rate.

At the Aibolit veterinary clinic you can conduct a comprehensive examination of a pet with pathology of the adrenal glands, pancreas and thyroid glands, carry out diagnostic studies, conservative and, if necessary, surgical treatment.