Hypercalcemia and primary hyperparathyroidism in dogs. Hyperparathyroidism in dogs and cats

Hyperparathyroidism in dogs and cats is an endocrine pathology that occurs due to excessive production of parathyroid hormone. With this pathology, there is an increase in calcium levels and a decrease in phosphorus levels in the blood, and damage to bone tissue in the form of increased fragility. Hyperparathyroidism can be primary or secondary. The secondary form of pathology in cats is called juvenile osteopathy.

Causes of the disease

More often primary hyperparathyroidism in dogs and cats it appears as a result of adenoma, cancer, hyperplasia of the parathyroid glands.

The cause of secondary hyperparathyroidism in animals is considered to be an insufficient amount of calcium in the diet with an excess of phosphorus. This pathology may develop as a result of destructive kidney damage and chronic dystrophic changes small intestine.

Pathogenesis

A pathological increase in the production of parathyroid hormone leads to disruption of the metabolism of phosphorus and calcium. With hyperparathyroidism, bone degeneration develops. As a result of increased resorption of bone tissue, calcium moves from the bones into the bloodstream. This is accompanied by increased excretion of this element in the urine. There is a restructuring of the bone and an acceleration of the processes of resorption of its parts. The bone apparatus of animals becomes soft and flexible.

A manifestation of kidney damage is increased urination as a result of increased calcium excretion. A large amount of calcium in the urine and bloodstream causes the formation of urinary stones.

Clinical picture and symptoms of hyperaparathyroidism

Development initial stages hyperparathyroidism is slow and asymptomatic. The early stages of hyperparathyroidism are characterized by muscle weakness, depression, and deterioration in performance in dogs.

As the disease progresses, thirst, increased urination, and decreased appetite are noted. The animal tries more and more to avoid contact with people, sometimes this behavior reaches the point of aggression towards humans.

In advanced cases, hyperparathyroidism in dogs and cats leads to lameness and even paralysis of the limbs. Fibrous bone degeneration is manifested by curvature of the limbs, swelling and pain in the joints. There is also frequent loosening and loss of teeth, and bone fractures.

Diagnosis of hyperaparathyroidism

The main method for detecting hyperaparathyroidism in dogs and cats is to study the calcium and phosphorus levels in the blood. To detect pathology of the bone apparatus, it is necessary to conduct an X-ray examination. X-ray sign pathology is considered to be a thin cortical layer of bone and the detection of bone cysts.

Hyperparathyroidism must be distinguished from diseases such as nutritional osteodystrophy, malignant hypercalcemia, etc.

Hyperparathyroidism in dogs and cats - treatment and prevention

In the early stages of development, the disease can be successfully treated. Moreover, for this it is enough to switch to super premium food or create a balanced diet. Typically within a couple of months proper feeding The calcium/phosphorus balance in the body is completely restored.

In advanced cases, surgery is necessary. Parathyroid adenoma is considered an indication for its surgical removal. After surgery, treatment is indicated to improve metabolic processes in bone tissue. For this purpose, gluconate, calcium phosphate, vitamin supplements. Also important given to diet. Conservative therapy consists of a decrease in calcium in the blood and an increase in phosphorus levels. First of all, we are talking about a diet rich in calcium. As drug treatment you can use phosphosan, etc. For kidney damage, use intravenous administration sodium chloride. Large animals are given about a liter of this liquid. Sodium citrate is used to reduce calcium levels in the blood. To preserve calcium in bone apparatus calcitrin is used. With pronounced inflammatory process in joints they use corticosteroids (prednisolone).

Secondary hyperparathyroidism, due to proper nutrition, provides Calculation of a balanced diet. If the disease is not advanced, then properly selected super premium food or a balanced homemade diet is almost guaranteed to restore the calcium/phosphorus balance in the pet’s body within several months.

Common consequences of hyperaparathyroidism

This disease rarely goes away without a trace. Usually this always results in stunted growth. It is also possible that the pelvic bones may become permanently deformed, causing difficulty in bowel movements and urination. In advanced cases of the disease, it is not recommended for recovered animals to give birth.

Deformation chest often causes chronic diseases respiratory system. Neurological problems in animals also persist throughout life.

NUTRITIONAL (SECONDARY) HYPERPARATHYROSIS (NUTRITIONAL OR JUVINYL OSTEODISTROPHY)

An endocrine disorder characterized by excessive synthesis and secretion of the parathyroid hormone parathyroid hormone, which is involved in the regulation of extracellular calcium levels. Secondary hyperparathyroidism is a disease that occurs as a result of prolonged stimulation of the parathyroid glands by a reduced level of calcium in the blood, initially as a compensatory process, and then a chain occurs pathological processes developing in response to a chronic decrease in calcium levels (hypocalcemia) in the blood. The parathyroid gland controls the level of calcium in the blood; a hormonally caused disorder leads to impaired mineralization of the bones and abnormal development skeleton, which is a consequence poor nutrition when kittens or puppies do not get enough calcium in their diet. A diet consisting mainly of meat and organ meats such as heart, liver and kidneys, etc. contains too much high level phosphorus and very small amounts of calcium and vitamin D (vitamin D is necessary for the absorption of calcium in thin section intestines), which leads to impaired growth and development of the skeleton, spontaneous fractures and lameness.

Exchange of calcium and phosphorus in the animal's body.

Calcium is one of the essential elements in the life of mammals. Calcium homeostasis is a very complex, balanced and multicomponent mechanism, the main links of which are calcium receptors on cell membranes, recognizing minimal fluctuations in calcium levels and triggering cellular mechanisms control (for example, a decrease in calcium leads to an increase in the secretion of parathyroid hormone and a decrease in the secretion of calcitonin), and effector organs and tissues (bones, kidneys, intestines) that respond to calcium-tropic hormones by corresponding changes in Ca++ transport.

The main hormonal mediators of calcium homeostasis are parathyroid hormone, vitamin D and calcitonin.

Parathyroid hormone, produced by the secretory cells of the parathyroid glands, plays a central role in calcium homeostasis. Its coordinated actions on bones, kidneys and intestines lead to an increase in the transport of calcium into the extracellular fluid and an increase in the concentration of calcium in the blood.

Parathyroid hormone has both anabolic and catabolic effects on bone tissue, which can be distinguished as early phase actions (mobilization of Ca++ from bones for quick recovery balance with extracellular fluid) and a late phase, during which the synthesis of bone enzymes (such as lysosomal enzymes) is stimulated, promoting bone resorption and remodeling. The primary point of application of parathyroid hormone in bones is osteoblasts. Under the influence of parathyroid hormone, osteoblasts produce a variety of mediators that have a powerful stimulating effect on the differentiation and proliferation of osteoclasts. Thus, bone resorption by osteoclasts is stimulated indirectly through osteoblasts.

Vitamin D is the second strong humoral agent in the system of regulation of calcium homeostasis. Its powerful unidirectional effect causes an increase in calcium absorption in the intestines and an increase in the concentration of Ca++ in the blood.

ETIOLOGY, PATHOGENESIS OF HYPERPARATHYROIDSIS

The metabolism of calcium is closely interconnected with the metabolism of phosphorus (mainly phosphate -P0 4 ), and their concentrations in the blood are inversely related. The ratio of calcium to phosphorus in the diet should be no less than 1:1 for dogs and 0.9:1 for cats and should not exceed 2:1 for both species. In the blood, the ratio of calcium and phosphorus for dogs and cats from 3-9 months. - 0.9-1.3, over 9 months. - 1.6-2.3.

The disease is observed in small kittens and puppies, which are fed primarily with meat or offal, because meat food contains a lot of phosphorus and little calcium, a violation of the mineralization of the skeleton occurs, its deformation, and in the case long term diseases, limb fractures. A calcium-poor diet stimulates the production of parathyroid hormone, as a result of which the deposition of calcium salts in the bones decreases, and the body begins, on the contrary, to take calcium from the bones (osteoresorption) in order to preserve normal level calcium in the blood.

In turn, insufficient calcium intake is often reported when feeding dogs and cats diets consisting of meat or meat by-products. Typically, meat diets contain approximately 0.02% Ca and 0.3% P, which provides a Ca to P ratio of 1:15-1:20, which causes secondary hyperparathyroidism.

The maximum osteoresorptive effect is observed in bones with a pronounced cortical structure (long tubular bones), while bones with a trabecular structure (vertebrae, iliac crest) can maintain their density. This effect has a certain differential diagnostic value when, during an X-ray examination of patients with secondary hyperparathyroidism, a decrease in bone density is recorded in the radial and tibia, less in the femur and often absent in the vertebrae.

Bright clinical manifestations bones are accompanied by cases of secondary hyperparathyroidism in young, actively growing animals. In them, the effect of excess parathyroid hormone manifests itself faster - deformations of the bones of the limbs, spine, fractures, etc. occur. A clear example can serve clinical case cat Ushlepa, who was admitted to the clinic for observation by orthopedic doctors regarding an X-shaped curvature lower limbs, thoracic lordosis, lumbar kyphosis and pelvic canal stenosis, the cause of which turned out to be severe primary hyperparathyroidism caused by a mono-diet (feeding poultry meat).

Joints are also a weak link in the body of patients with primary hyperparathyroidism. The load on them increases due to erosive changes in the epiphyses and disruption of bone geometry. Another pathogenetic factor of arthropathy is the deposition of calcium salts in the synovial membranes, cartilage and periarticular, which leads to chronic trauma and severe pain syndrome throughout the animal's life.

Neuromuscular changes in secondary hyperparathyroidism manifest themselves in weakness and fatigue. This reversible syndrome, quickly disappearing after the appointment of adequate help.

CLINICAL SIGNS

The disease has a long-term hidden nature of development, the absence pathognomonic symptoms up to the development of severe osteodystrophy with destruction of the skeleton. As a rule, the disease manifests itself between the ages of 3 and 7-8 months; purebred cats (Scottish, British, Sphynx, exotic) are often affected.

Decreased activity and mobility, lack of interest in games, drowsiness;

Lameness, even after jumping or falling from a small height;

Incorrect positioning of the limbs (X-shaped);

Constipation;

Neatness of movement, lack of playfulness, curiosity and desire to “walk on the ceiling” characteristic of cats; the animal has difficulty overcoming obstacles and jumping on furniture.

Lameness is the most indicative symptom of the disease. The cause of lameness is calcium deficiency in the bones, as a result of which their fragility increases and stress tolerance decreases. In extreme severe conditions Subperiosteal greenstick fractures are possible.

LABORATORY DIAGNOSTICS OF SECONDARY HYPERPARATHYROIDIS

The key criteria for the laboratory diagnosis of hyperparathyroidism are three indicators: increased level parathyroid hormone and low or normal levels of calcium in the blood plasma, increased levels of phosphorus. Simultaneous detection of these three in a patient laboratory signs leaves virtually no doubt about the diagnosis of secondary hyperparathyroidism. Thus, with classic bright variants of the course of the disease, its laboratory diagnostics cannot help but amaze with its simplicity.

They learned to determine calcium in the blood a little over a hundred years ago - in 1907. In the blood, calcium is found in three main forms: the ionized fraction of the element - 50%, the fraction associated with proteins - 40-45%, the fraction consisting of complex phosphate and citrate connections - 5%. The main clinical laboratory parameters for studying this element in the body are concentration total calcium and the concentration of ionized (or free) blood calcium.

Range normal values total calcium in dogs - 2.25-2.85 and cats - 2.0-2.7 mmol/l; ionized calcium in dogs - 1.26-1.50 and cats -1.10-1.30 mmol/l.

Except diagnostic value(to confirm the diagnosis of secondary hyperparathyroidism), the level of phosphorus in the blood serves as a differentiating criterion for distinguishing primary (hyperfunction pair thyroid gland, as a rule, due to its degeneration) and secondary hyperparathyroidism caused by malnutrition during the period of intensive growth of the animal or chronic renal failure. In the second case, phosphorus levels tend to increase depending on the severity of renal dysfunction, which is associated with a loss of the ability to actively excrete phosphates. In addition to hyperphosphatemia distinctive feature secondary hyperparathyroidism will always have normal or decreased blood calcium levels.

The range of normal phosphorus values ​​in dogs is 1.1-2.0 up to 6 months. - 0.9-2.1 and cats - 1.0-2.3 up to 6 months. 2.1-2.8 mmol/l;

Useful for diagnosing and establishing the severity of the disease are indicators of increased reorganization of bone matter and osteoresorption under the influence of prolonged excessive release of parathyroid hormone into the blood. Markers of osteoresorption include increased levels alkaline phosphatase(its bone fraction). However, this indicator can increase in any form of hyperparathyroidism and other conditions associated with active restructuring of bone matter. Its values ​​are more informative as indicators of the severity of damage to the skeletal system.

INSTRUMENTAL DIAGNOSTICS

X-ray examination methods for secondary hyperparathyroidism include plain chest radiography, abdominal cavity(allows one to accidentally detect consolidated rib fractures and establish spinal curvatures), as well as targeted X-ray examination of skeletal bones (diffuse thinning cortex bones, decreased bone density, hypertrophy of the periosteum, traces of consolidated pathological fractures of the limbs, subperiosteal fractures, pronounced osteodystrophic changes in the skeleton).

The figures below illustrate these most common pathological changes in bones.

Secondary hyperparathyroidism can occur in older cats as a result of chronic renal failure.

Increased activity of the parathyroid gland is a compensatory reaction of the body to meat-food-induced hypocalcemia or low content calcium in the diet. The predominantly meat type of diet does not satisfy the cat’s body’s needs for microelements, primarily calcium, which is necessary for the normal growth of the animal.

This disorder occurs during periods of intense growth in young animals because they require a large number of calcium for growth and development.

TREATMENT

Treatment should be carried out by a specialist.

Treatment of patients with nutritional secondary hyperparathyroidism should be aimed at the main cause - normalization of the diet in terms of mineral composition.

Cage restriction to prevent bone fractures in animals with severe disease.

Laboratory studies and radiographs at intervals determined by your veterinarian are helpful in assessing improvement and response to therapy.

The purpose of monitoring is to trace the dynamics of restoration of impaired functions (primarily the state of the skeleton), and to ensure that calcium metabolism indicators are normalized.

Animals without severe bone deformities have a good prognosis. Bone mineralization returns to normal within two to three months.

Hyperparathyroidism is serious violation metabolism, in which calcium is washed out of the bones into the blood. Typically, 99% of calcium in the body is contained in bones and tooth enamel, 1% is in the form of ions in the blood plasma.

A constant level of calcium in the blood is maintained by hormones. Parathyroid hormone is produced in the parathyroid gland, under its action the level of calcium in the blood increases: the body borrows it from the bones, and the kidneys begin to retain these ions as much as possible. Calcitonin is a thyroid hormone that has the opposite effect. Violation of this balance is fraught with catastrophic consequences for the cat’s body.

Primary hyperparathyroidism

An increase in the level of parathyroid hormone can be caused by problems in the gland itself, then hyperparathyroidism is called primary. It is worth noting that this is very rare disease occurs predominantly in older animals. The cause is hyperplasia of the parathyroid glands due to growth.

• Benign neoplasia is an adenoma.
• Malignant – cancer of the parathyroid gland.

The symptoms will be similar. Manifestations of this pathology are associated with an increase in the level of calcium in the blood and are very diverse:

1. Bone syndrome: pathological, osteoporosis, bone pain.
2. Urinary system: nephrocalcinosis and, acute.
3. Digestive tract: , stomach ulcer.
4. Nonspecific signs: thirst and polyuria, weakness of all muscles, depression.

Secondary hyperparathyroidism

This form of the disease occurs disproportionately more often. The reason for the increased production of parathyroid hormone is an imbalance of calcium and phosphorus.

Hyperparathyroidism of renal origin

In adult cats with kidney disease, the body loses its ability to regulate electrolyte levels. Phosphorus in the blood increases, and calcium decreases. The body tries to correct the situation by increasing the production of parathyroid hormone. At the same time, the level of calcitriol (the active form of vitamin D), which is synthesized in the kidneys, decreases. Calcitriol is needed to ensure that calcium is absorbed from the intestines and not washed out by the kidneys. It is necessary for normal bone mineralization.

Symptoms of secondary renal hyperparathyroidism:

• Renal: dehydration, polyuria and polydipsia, depression and weakness, periodic vomiting, loss of appetite.
• Specific: abnormal mobility and , softening jaw bones(become rubbery to the touch).

The second name of the disease is rubber jaw syndrome.

Nutritional hyperparathyroidism (diet related)

The most frequent illness young animals, which out of habit is mistakenly called rickets, is nutritional osteodystrophy. The reason is excess phosphorus in the diet.

Everyone knows that bones are made of calcium, but the second, no less significant component is phosphorus. These elements are in close connection with each other, their ratio in the blood and skeleton must be constant.

The same balance of minerals should be supplied to the kitten with food. In balanced for cats, the level of calcium and phosphorus is at the proper level. Problems arise when feeding "" food. And not because the owners save on their pet, but rather from ignorance of the basic needs of cats.

Nutritional osteodystrophy develops rapidly when feeding predominantly meat foods. Bearing in mind that the cat is a predator, owners with the best intentions feed it chicken, beef or offal (liver, heart). A common mistake is buying meat baby food (supposedly of higher quality and safety) instead.

The proportions of calcium and phosphorus in beef are approximately 1:10, in the liver or heart - 1:50. Introducing cereals into the diet (meat porridge with oatmeal or buckwheat) does not help the situation: these products also contain 6-20 times more phosphorus than calcium. Even if the owner tries to provide the cat with other products, the animal can be picky, choosing only tasty morsels, and remains on a meat mono-diet.

An attempt to provide a kitten with calcium through products such as cottage cheese or milk is doomed to failure - again due to the phosphorus content in dairy foods (2 times more than calcium).

Kittens most often suffer from hyperparathyroidism. Although an adult animal on a meat diet begins to have certain problems, the need for calcium in growing young animals is tens of times higher. Breed is recognized as a predisposing factor for the occurrence of rickets: and cats are at risk.

Signs:

1. Nonspecific soreness.

The kitten refuses to run, play, and shows aggression when stroked or picked up. Lying or sitting a lot, lethargic.

1. Orthopedic problems.

Lameness, and may limp on one or the other paw. The bones become soft and deformed – you can visually notice the curvature of the limbs. The joints are sometimes enlarged.

A visit to a specialist is often caused by a spontaneous injury - a cat can get a fracture after jumping from a height of only 20 cm.

1. X-ray examination.

On an x-ray, the bones of a kitten with osteodystrophy may be almost invisible - they are transparent, fragile, like paper. Subperiosteal fractures of tubular bones and curvature of the spine are almost always visible. The older (and therefore heavier) the kitten, the more serious the pathology becomes, even leading to incurable consequences.

Excessive deflection lumbar region spine and compression spinal cord lead to chronic diseases, and in adulthood make normal labor. With spinal fractures, the hind legs may completely fail. Deformation thoracic spine and chest cause problems with heart function and breathing.

X-ray is the most accurate and visual diagnostic method for nutritional osteodystrophy in kittens. A blood test, on the contrary, is not informative:

• An increase in the enzyme alkaline phosphatase associated with bone lysis cannot be considered a specific sign of rickets, since it is observed normally in growing animals.
• And the ratio and level of calcium and phosphorus in the blood will be within normal limits - but at what cost!

Treatment of hyperparathyroidism in adult animals

At primary disease, that is, problems with the parathyroid glands, the only method of treatment is surgical removal adenomas. An expected complication after surgery is sharp drop level of calcium in the blood, so the cat must be kept under constant observation in a hospital for several days and the level of electrolytes adjusted.

For secondary renal hyperparathyroidism, the basis of treatment is with reduced content phosphorus. In addition to changing the diet, doctors are trying to take control of the underlying disease by prescribing drugs that bind phosphorus:

• If the blood test shows calcium and phosphorus levels within normal limits, calcitriol may be used.
• Serum calcium levels are monitored during treatment to prevent hypercalcemia.
• Stop using the drug as soon as parathyroid hormone levels return to normal.

Treatment of nutritional osteodystrophy in kittens

1. Diet.

Diet remains the main treatment measure. If the diet is changed in a timely manner, then it is not necessary to use medications or supplements, since within a week there will be a noticeable improvement.

The best solution is to use industrial complete nutritional supplements - this is the only way to confidently say how much calcium, phosphorus, proteins and fats a growing body receives. Studies have shown that even inexpensive but balanced food works better than natural nutrition in combination with mineral supplements.

If the owner is fundamentally against ready-made food, the doctor should convince him to use it at least until the end of the growth period, and then return to “natural” food. In case of a categorical refusal, the nutritionist must create a diet, carefully calculating the norms for calcium and phosphorus. Some clinics have this payable service. The owner’s task is to force the kitten to eat the prescribed foods.

1. Limitation of mobility.

With advanced rickets, the only way to prevent multiple fractures is cellular maintenance. The kitten is kept in a smooth-sided plastic container or carrier for 1-2 weeks or longer until the danger has passed. It is possible to keep a pet in an empty room without furniture - where there is no opportunity to jump, but in practice this is difficult to achieve.

1. Drug treatment.

If hypocalcemia is diagnosed based on blood biochemistry, or if a young cat has been sick for a long time, and calcium reserves in the bones are completely depleted, calcium supplements are used by injection. The main indications for this are cramps and muscle weakness.

Calcium gluconate 10% is administered intravenously 1 ml/kg with isotonic solutions every day until the deficit is eliminated.

IN severe cases synthetic calcitonin, a parathyroid hormone antagonist, is administered. It helps restore bone mineralization and reduces pain caused by bone resorption. The drug Miacalcic 5 IU/kg body weight (0.05 ml) is administered intramuscularly 2 times a week.

1. Mineral supplements.

The kitten should receive at least 200 mg/kg of calcium per day in food. An additional 5-20 mg/kg can be administered as supplements. Mineral premixes are used for 1-3 months, after which a complete industrial diet will be sufficient.

What not to do

1. Insolation.

During treatment, many people mentally humanize their pet. But irradiating it with a quartz lamp or taking it out into the sun for “rickets” is useless: in cats, vitamin D is not synthesized in the body; the animal can only get it from food.

1. Anesthesia.

A kitten whose bones are literally “melting” is in severe pain. All joints ache, the pain is aggravated at the site of spontaneous fractures. However, even with severe lameness, the use of non-steroidal anti-inflammatory or other analgesics is contraindicated. If a young animal ceases to feel pain fully, it can easily harm itself by actively moving and aggravate the injuries.

Prevention

The best prevention Hyperparathyroidism in kittens and adult cats is balanced feeding with the correct ratio of calcium and phosphorus. Industrial feed should vary in composition for adult and growing animals. When feeding regular food, they resort to vitamin and mineral supplements.

Timely contact veterinary clinic and full diagnostics (x-ray for claudication) help detect and treat hyperparathyroidism at an early stage.

Conclusion

It is better to study the nutritional issues of a cat even before the tiny fluffy ball appears at home. It is recommended to evaluate your strengths and deepen your theoretical knowledge before deciding to feed your cat the “old fashioned way” - natural food.

It should be remembered that the problem is not caused by a lack of calcium, but by an excess of phosphorus. It is especially important to provide high-quality food for high-breed animals - British, Siamese. When feeding commercial diets, preference is given to high-quality feed of at least premium class.

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ETIOLOGY: idiopathic, sometimes congenital, but often caused by severe general hormonal disorders of the body:
More often this is insufficient production of parathyroid hormone by the parathyroid glands; as a casuistry - accidental removal of the parathyroid glands during surgical intervention on the thyroid gland.
Other causes: the disease can also be caused by for the following reasons:
- autoimmune disease;
- surgical destruction;
- neoplasms;
- atrophy associated with prolonged hypercalcemia;
- magnesium deficiency;
- congenital agenesis;
- infarction of parathyroid adenomas;

PATHOGENESIS: the disease greatly disrupts the balance of Ca and P in the blood and causes severe hypocalcemia with all the ensuing consequences and clinical signs that are a consequence of the inability to adequately retain serum levels calcium.
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).

PECULIARITIES:
Clinic: diarrhea, epilepsy, obstruction, vomiting, appendages, grand mal and petit mal attacks, hypocalcemia;

Summary clinic:
1. Abnormal behavior, aggression, change in habits;
2. Abnormal proprioceptive positioning;
3. Abnormal light reflex of the pupil;
4. Anorexia (lack of appetite, refusal to eat);
5. Ataxia;
6. Auscultation of the heart: Tachycardia, increased heart rate;
7. Bradycardia, slow heart rate;
8. Ventricular tachycardia, multifocal or monofocal;
9. Ventricular premature tone, multifocal or monofocal;
10. Excitement (delirium, mania);
11. Generalized weakness;
12. Generalized lameness, stiffness of movement;
13. Hyperesthesia, increased sensitivity;
14. Hypothermia;
15. Dehydration;
16. Dysuria, difficult, painful urination, stranguria;
17. Dysmetria;
18. Disorientation, memory loss;
19. Dyspnea (difficulty breathing, with open mouth);
20. Dysphagia (difficulty swallowing);
21. Trembling;
22. Slow growth;
23. Cataract (clouding of the lens);
24. Lymphadenopathy;
25. Fever, pathological hyperthermia;
26. Mydriasis, pupil dilation;
27. Fainting, syncope, convulsions, collapse;
28. Polydipsia, increased thirst;
29. Polyuria, increased volume of urination;
30. Precommon salivation, ptyalism, salivation;
31. Prolapse of the third eyelid, protrusion of the membrane of the nyctitans;
32. Vomiting, regurgitation, emesis;
33. Photophobia;
34. Spasms of the head, neck, face;
35. Spasms of the hind limbs;
36. Spasms of the forelimbs;
37. Back spasms;
38. Tachypnea, Increased frequency breathing movements, polypnea, hyperpnea;
39. Tenesmus. pushing;
40. Tetany,
41. Tetraparesis, paresis of all limbs;
42. Tremor;
43. Depression (depression, lethargy);
44. Photophobia,

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.
Lean bone replaced by fibrous. 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.

Breeds.
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").

The diagnosis is made taking into account clinical and radiological signs and by determining the concentration of calcium in the blood.
- Clinical signs;
- rejection of other reasons;
- measurement of serum levels of Ca and P;
- amenability to treatment;

TREATMENT: synthetic parathyroid hormone according to an individually selected dosage regimen - constantly taking into account changes in the patient’s health status.
In acute cases, calcium gluconate and diuretics are administered intravenously, and CO2 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.

DEVELOPMENT: prolonged.

FORECAST: doubtful to unfavorable.

Secondary (food) hyperparathyroidism (butcher's dog disease, paper bone disease).

Secondary nutritional hyperparathyroidism is a compensatory hyperfunction of the parathyroid gland that develops with prolonged hypocalcemia (decreased calcium levels) and hyperphosphatemia (increased phosphorus levels).

Doesn't sound quite clear to the average pet owner? Let's figure this out together actual problem in kittens and puppies.

We will look at the pathology associated with improper feeding of babies, because... it occurs most often.

In case of incorrect, unbalanced feeding of kittens and puppies in the diet there is a large amount of phosphorus and an insufficient amount of calcium. As a result, the growing body lacks building material for the development of organs containing large amounts of calcium - bones and joints. The bones become soft and bend easily even with a slight load. At increased activity which everyone demonstrates healthy puppies and kittens, this leads to multiple fractures like a “green branch”, causing the animal severe suffering. Not only the long bones of the limbs bend and break, but also the vertebrae. As a result, neurological problems may occur - paresis and paralysis of the limbs, disruption of the innervation of the bladder and intestines. Puppies and kittens suffering from secondary nutritional hyperparathyroidism often refuse to move, lameness and pain appear when moving. Their limbs may be deformed.

Why are all these horrors happening? The answer is improper feeding.. Although dogs and cats are carnivores, in nature they do not eat only meat, along with meat they eat bones, which are a source of calcium and help balance the phosphorus-calcium ratio.

Loving owners begin to feed their little charming treasure with delicacies - meat, fish, meat baby food, or, even worse, “from the table” - soup, sausages, cervelat. All these products contain a lot of phosphorus and little calcium. This metabolic disorder minerals, leads to a decrease in calcium levels in the blood and leaching it from the bones.

Most often, animals come to our clinic with fractures, neurological disorders, or severe pain of unknown origin. The diagnosis is confirmed x-ray the entire skeleton. Sometimes it can be very difficult to carry out this type of examination, since putting the animal down causes him great pain.

On x-rays we see transparent bones, multiple fractures on the bones, and in severe cases - deformation of the vertebrae, curvature of the spine, vertebral fractures, overcrowding bladder, "clogged" feces intestines. These animals need urgent help!

Drug treatment – pain relief. With neurological deficits, treatment is even more complex and does not always lead to recovery.

Only well-chosen diet animal, since the simple addition of vitamins and mineral supplements not effective! At home, it is difficult to create a diet so that the animal is provided with vitamins and minerals in the proper quantities and proportions. Even if you create such a diet, it is not a fact that the little picky eater will eat it entirely. A good solution is industrial feed (dry or wet). Animals must be accustomed to them from early childhood.

To prevent fractures of the limbs and spine, the animal's mobility is limited for up to 6 weeks (a carrier or crate may be required).

The practice of our clinic has shown that within 2-4 weeks after the start of proper nutrition, the bones of animals return to normal.

Chief physician of the Klyk clinic, Gady M.Yu.