ZOB DIFFUSION TOXIC

ZOB DIFFUSION TOXIC (syn: Graves disease) is a disease characterized, as a rule, by a small diffuse increase in the thyroid gland and persistent excess secretion of thyroid hormones, which causes disturbances in all kinds of metabolism and energy, as well as the functions of various organs and systems. Often, along with the term "diffuse toxic goiter", the terms "hyperthyroidism" and "thyrotoxicosis" are used as its synonyms. However, hyperthyroidism is a physiological increase in the thyroid function, for example, hyperthyroidism in pregnant women is caused by an increase in the formation of serum proteins of blood that bind thyroid hormones. Clinical manifestations of physiological hyperthyroidism have not been observed, and sometimes minimal hyperplasia of the thyroid gland tissue is observed. Thyrotoxicosis (a pathological excess of thyroid hormones) develops with diffuse toxic goiter, thyrotoxic adenoma, in the initial stage of subacute or chronic autoimmune thyroiditis, in certain forms of thyroid cancer, hormone-active adenoma of the pituitary gland producing thyroid stimulating hormone or, more rarely, growth hormone, and also With uncontrolled use of drugs containing thyroid hormones or iodides.

The clinical manifestations of thyrotoxicosis of any etiology are similar. It is proved that diffuse toxic goiter is an autoimmune disease that develops in people with hereditary predisposition, having a defect in the immune control system. Such individuals develop thyroid-stimulating antibodies. The trigger mechanism of this autoimmune process can be a trauma, a constant emotional tension, infectious diseases, etc.

Long-term increased formation of thyroid hormones leads to the development of a picture of thyrotoxicosis, but its severity does not correspond to the degree of enlargement of the thyroid gland. Thyrotoxicosis is accompanied by cardiovascular damage (thyrotoxic heart) - widening the heart to the left, strengthening the tone, sinus tachycardia, turning into paroxysmal or permanent ciliary arrhythmia with extrasystole and the development of heart failure, high pulse pressure due to an increase in systolic and a decrease in diastolic blood pressure, etc. For patients characterized by chaotic, unproductive activities, increased excitability, irritability, tearfulness, trembling of fingers and whole body; Working capacity reduced. Patients lose weight sharply, despite a good appetite, they have a negative nitrogen balance. Characterized by a constant low-body temperature and intolerance to heat, myopathy, osteoporosis. In addition to the thyroid gland, other glands of internal secretion are affected, functional insufficiency of the adrenal cortex is observed, a violation of carbohydrate metabolism, up to the development of diabetes mellitus, in women - dysfunction of the ovaries (meager menstruation or amenorrhea), fibrocystic mastopathy , sometimes with galactorrhea Outside pregnancy and the period of feeding the child), in men - impotence and gynecomastia .

There are three degrees of severity of thyrotoxicosis. At a mild degree heart rate does not exceed 100 beats per minute, arrhythmia and other symptoms are absent, the patient's working capacity is reduced slightly, the body weight loss is no more than 3 - 5 kg. With thyrotoxicosis of moderate severity, the heart rate does not exceed 120 beats per 1 minute, the body weight of the patient is reduced by 8-10 kg, the work capacity is significantly reduced. In severe thyrotoxicosis, the heart rate exceeds 120 beats per minute, the patient is diagnosed with atrial fibrillation, extrasystole, circulatory failure IIB -III stage, thyrotoxic hepatitis, functional insufficiency of the adrenal cortex, and work capacity is sharply reduced. A terrible complication of thyrotoxicosis is thyrotoxic crisis .

Approximately half of the patients, mainly women over the age of 40, develop a syndrome of endocrine ophthalmopathy due to edema and infiltration of orbital tissues with various cellular elements along with thyrotoxicosis. In patients, exophthalmos (eyelashes), photophobia , and lacrimation are noted.

The diagnosis is established on the basis of a characteristic clinical picture and data from a number of laboratory and instrumental studies: the determination of thyroid hormone (thyroxine and triiodothyronine) in the blood, the reduction of the level of thyroid-stimulating hormone, increased thyroid absorption of iodine or technetium radionuclides in comparison with the norm, the uniform distribution of the absorbed radionuclide Iodine or technetium in the enlarged thyroid gland determined by scanning.

Treatment depends on the severity of thyrotoxicosis, the degree of enlargement of the thyroid gland, the development of complications of the disease, the degree of exophthalmos. With conservative treatment, the most commonly used are mercazolil - a thyreostatic drug that blocks the biosynthesis of thyroid hormones. After reaching the euthyroid state, i.e. Such a physiological state of the body, when clinical manifestations of thyroid dysfunction are absent, the dose of Mercazolilum is gradually reduced to maintenance, which patients take for 1 to 1.5 years. The complex therapy includes glucocorticoids, beta-adrenoblockers, sedatives, anabolic hormones, cardiac glycosides and diuretics for heart failure, etc. Treatment is carried out under the constant supervision of an endocrinologist or therapist.

In the absence of a stable effect of conservative therapy, in large craw, severe thyrotoxicosis, contraindications to the use of thyreostatics (mercazolil, etc.), blood diseases and a number of other conditions, subtotal removal of the thyroid gland is indicated. With contraindications to surgical intervention (severe somatic diseases), a radionuclide of iodine is prescribed.

The prognosis with proper treatment is favorable. With a timely diagnosis and the correct treatment tactics, the illness ends with complete recovery.

A thyrotoxic crisis can develop after a mental trauma, physical overwork, an acute infectious disease, an operation, radionuclide treatment of iodine or technetium. The clinical picture of the crisis consists of signs of damage to the nervous, cardiovascular system and the gastrointestinal tract. Thyrotoxic crisis is characterized by a rapid and sharp increase in the severity of thyrotoxicosis, psychomotor agitation, fever to 38 - 40 ° C, worsening of heart activity and increased symptoms of hypocorticism (decreased functional activity of the adrenal cortex). Abdominal syndrome includes abdominal pain, diarrhea and persistent vomiting, leading to dehydration of the body. With a thyrotoxic crisis, paresis, paralysis, bulbar symptoms (swallowing on swallowing, difficulty in pronouncing certain sounds, etc.) can be observed. At a distance; The development of a crisis is possible for the onset of a coma.

The clinical picture of thyrotoxic coma is very characteristic. The first signs indicating a threat to its development are progressive inhibition, confusion, loss of orientation in space and time. The patient takes a characteristic posture (diluted and half-bent legs, scattered arms), frequent and erratic movements of the limbs are noted, after 12-24 h, a sharp muscle weakness develops to complete adynamia, prostration and loss of consciousness. The body temperature rises to 41-42 ° C, the pulse disappears, the blood pressure drops. Thyrotoxic coma often leads to death.

The diagnosis of thyrotoxic crisis is based on the data of anamnesis (presence of diffuse toxic goiter, stress situation, operation, etc.), the characteristic clinical picture and the results of biochemical studies, primarily on the concentration of thyroid hormones in the blood.

Treatment of urgent conditions, such as thyrotoxic crisis and thyrotoxic coma , requires immediate measures aimed primarily at reducing the concentration of thyroid hormones in the blood, fighting adrenocortical insufficiency, dehydration, cardiovascular and neuro-vegetative disorders. Intravenous or intramuscular injection of 100-300 mg hydrocortisone per day, 5-10 ml Lugol solution, in which potassium iodide is replaced by sodium iodide, drip with glucose; Cautiously in small doses apply cardiac glycosides (korglikon or strophanthin), with severe tachycardia and arrhythmia - beta adrenoblockers (anaprilin or obzidan) or calcium antagonist diltiazem , intravenously injected 5% glucose solution with insulin. As a rule, the patient must be administered 1-2 liters, sometimes up to 3 liters of liquid (the amount of liquid administered is controlled by the volume of urine allocated to the patients and the intensity of sweating). Bubbles with ice can be applied to the region of the main blood vessels of the thighs and liver. The patient must be hospitalized.