Diffuse toxic goiter, in most cases, is characterized by a relatively short history: the first symptoms usually appear 4-6 months before visiting a doctor and making a diagnosis. As a rule, the key complaints are associated with changes in the cardiovascular system, the so-called catabolic syndrome and endocrine ophthalmopathy.
  The main symptom of the cardiovascular system is tachycardia and quite pronounced palpitations. Patients can feel heartbeats not only in the chest, but also in the head, arms, and stomach. Heart rate at rest with sinus tachycardia caused by thyrotoxicosis can reach 120-130 beats per minute.
  With long-term thyrotoxicosis, especially in elderly patients, pronounced dystrophic changes in the myocardium develop, a frequent manifestation of which is supraventricular rhythm disturbances, namely atrial fibrillation (flicker). This complication of thyrotoxicosis rarely develops in patients under 50 years of age. Further progression of myocardial dystrophy leads to the development of changes in the ventricular myocardium and congestive heart failure.
  As a rule, catabolic syndrome is expressed, manifested by progressive weight loss (sometimes by 10-15 kg or more, especially in persons with initial excess weight) against the background of increasing weakness and increased appetite. The skin of patients is hot, sometimes there is severe hyperhidrosis. A feeling of heat is typical; patients do not freeze at a sufficiently low temperature in the room. Some patients (especially the elderly) may experience evening low-grade fever.
  Changes in the nervous system are characterized by mental lability: episodes of aggressiveness, agitation, chaotic unproductive activity are replaced by tearfulness, asthenia (irritable weakness). Many patients are not critical of their condition and try to maintain an active lifestyle against the background of a rather severe somatic condition. Long-term thyrotoxicosis is accompanied by persistent changes in the patient’s psyche and personality. A frequent but nonspecific symptom of thyrotoxicosis is fine tremor: fine trembling of the fingers of outstretched arms is detected in most patients. In severe thyretoxicosis, tremors can be detected throughout the body and even make it difficult for the patient to speak.
  Thyrotoxicosis is characterized by muscle weakness and a decrease in muscle volume, especially the proximal muscles of the arms and legs. Sometimes quite pronounced myopathy develops. A very rare complication is thyrotoxic hypokalemic periodic paralysis, which is manifested by periodically occurring sharp attacks of muscle weakness. Laboratory tests reveal hypokalemia and increased CPK levels. It is more common among representatives of the Asian race.
  Intensification of bone resorption leads to the development of osteopenia syndrome, and thyrotoxicosis itself is considered one of the most important risk factors for osteoporosis. Frequent complaints of patients are hair loss and brittle nails.
  Changes in the gastrointestinal tract develop quite rarely. Elderly patients may have diarrhea in some cases. With long-term severe thyrotoxicosis, degenerative changes in the liver (thyrotoxic hepatosis) can develop.
  Menstrual irregularities are quite rare. Unlike hypothyroidism, moderate thyrotoxicosis may not be accompanied by a decrease in fertility and does not exclude the possibility of pregnancy. Antibodies to the TSH receptor cross the placenta, and therefore children born (1%) to women with diffuse toxic goiter (sometimes years after radical treatment) may develop transient neonatal thyrotoxicosis. In men, thyrotoxicosis is often accompanied by erectile dysfunction.
  In severe thyrotoxicosis, a number of patients exhibit symptoms of thyroidogenic (relative) adrenal insufficiency, which must be differentiated from true. To the already listed symptoms are added hyperpigmentation of the skin, exposed parts of the body (Jellinek’s symptom), and arterial hypotension.
  In most cases, with diffuse toxic goiter, there is an increase in the size of the thyroid gland, which, as a rule, is diffuse in nature. Often the gland is significantly enlarged. In some cases, a systolic murmur can be heard over the thyroid gland. However, goiter is not an obligate symptom of diffuse toxic goiter, since it is absent in at least 25-30% of patients.
  Of key importance in the diagnosis of diffuse toxic goiter are changes in the eyes (“bulging”), which are a kind of “calling card” of diffuse toxic goiter, i.e. Their detection in a patient with thyrotoxicosis almost unambiguously indicates diffuse toxic goiter, and not about another disease. Very often, due to the presence of severe ophthalmopathy in combination with symptoms of thyrotoxicosis, the diagnosis of diffuse toxic goiter is obvious already upon examination of the patient.
  The clinical picture of thyrotoxicosis may differ from the classic version. Thus, if in young people diffuse toxic goiter is characterized by a detailed clinical picture, in elderly patients its course is often oligo- or even monosymptomatic (heart rhythm disturbance, low-grade fever). In the “apathetic” version of the course of diffuse toxic goiter, which occurs in elderly patients, clinical manifestations include loss of appetite, depression, and physical inactivity.
  A very rare complication of diffuse toxic goiter is a thyrotoxic crisis, the pathogenesis of which is not entirely clear, since a crisis can develop without an extreme increase in the level of thyroid hormones in the blood. The cause of a thyrotoxic crisis may be acute infectious diseases accompanying diffuse toxic goiter, surgical intervention or radioactive iodine therapy against the background of severe thyrotoxicosis, withdrawal of thyrostatic therapy, or administration of an iodine-containing contrast drug to the patient.
  Clinical manifestations of a thyrotoxic crisis include a sharp worsening of the symptoms of thyrotoxicosis, hyperthermia, confusion, nausea, vomiting, and sometimes diarrhea. Sinus tachycardia over 120 beats/min is recorded. Atrial fibrillation, high pulse pressure followed by severe hypotension are often observed. The clinical picture may be dominated by heart failure and respiratory distress syndrome. Manifestations of relative adrenal insufficiency are often expressed in the form of skin hyperpigmentation. The skin may be jaundiced due to the development of toxic hepatosis. Laboratory tests may reveal leukocytosis (even in the absence of concomitant infection), moderate hypercalcemia, and increased alkaline phosphatase levels. Mortality during thyrotoxic crisis reaches 30-50%.

A simple nontoxic goiter, which may be diffuse or nodular, is a nonneoplastic hypertrophy of the thyroid gland without developing a state of hyperthyroidism, hypothyroidism, or inflammation. The cause is generally unknown, but it is thought that it may be the result of prolonged hyperstimulation by thyroid-stimulating hormone, most often in response to iodine deficiency (endemic colloid goiter) or the intake of various dietary components or drugs that inhibit the synthesis of thyroid hormones. Except in cases of severe iodine deficiency, thyroid function is normal and patients are asymptomatic with a markedly enlarged, dense thyroid gland. The diagnosis is made based on clinical examination and laboratory confirmation of normal thyroid function. Treatment measures are aimed at eliminating the leading cause of the disease; in case of development of too large a goiter, surgical treatment (partial thyroidectomy) is preferable.

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ICD-10 code

E04.0 Non-toxic diffuse goiter

Causes of simple non-toxic goiter (euthyroid goiter)

Simple non-toxic goiter is the most common and typical cause of enlargement of the thyroid gland, most often detected during puberty, pregnancy and menopause. The reason is still unclear in most cases. Known causes are established defects in the production of thyroid hormones in the body and iodine deficiency in certain countries, as well as the consumption of foods containing components that suppress the synthesis of thyroid hormones (so-called goitrogens, for example cabbage, broccoli, cauliflower, cassava). Other known causes are due to the use of drugs that reduce the synthesis of thyroid hormones (for example, amiodarone or other iodine-containing drugs, lithium).

Iodine deficiency is rare in North America, but remains a leading cause of goiter epidemics worldwide (called endemic goiter). Compensatory low rises in TSH are observed, preventing the development of hypothyroidism, but TSH stimulation itself speaks in favor of non-toxic nodular goiter. However, the true etiology of most nontoxic goiters occurring in regions where iodine is sufficient is unknown.

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Symptoms of simple non-toxic goiter (euthyroid goiter)

Patients may have a history of low dietary iodine intake or high dietary intake of goitrogens, but this phenomenon is rare in North America. In the early stages, the enlarged thyroid gland is usually soft and smooth, and both lobes are symmetrical. Later, multiple nodes and cysts may develop.

The accumulation of radioactive iodine in the thyroid gland is determined, scanning and determination of laboratory indicators of thyroid function (T3, T4, TSH) are carried out. In the early stages, the accumulation of radioactive iodine by the thyroid gland may be normal or high with a normal scintigraphic picture. Laboratory values ​​are usually normal. Antibodies to thyroid tissue are tested to differentiate from Hashimoto's thyroiditis.

In endemic goiter, serum TSH may be slightly elevated and serum T3 at the lower limit of normal or slightly decreased, but serum T3 levels are usually normal or slightly elevated.

Treatment of simple non-toxic goiter (euthyroid goiter)

In regions with iodine deficiency, salt iodization is used; oral or intramuscular administration of iodine oil solutions annually; Iodizing water, cereals, or using animal feed (fodder) reduces the incidence of iodine deficiency goiter. The intake of goitrogenic components should be avoided.

In other regions, suppression of the hypothalamic-pituitary zone with thyroid hormones is used, blocking TSH production (hence the stimulation of the thyroid gland). TSH-suppressive doses of L-thyroxine required to completely suppress it (100-150 mcg/day orally, depending on serum TSH levels) are especially effective in young patients. The use of L-thyroxine is contraindicated in elderly and senile people with non-toxic nodular goiters, since these types of goiters rarely decrease in size and may contain areas with autonomous (non-TSH-dependent) function, in which case taking L-thyroxine can lead to development of a hyperthyroid state. Patients with large goiters often require surgery or radioiodine therapy (131-I) to reduce the size of the gland sufficiently to prevent the development of breathing or swallowing difficulties or problems associated with cosmetic correction.

Important to know!

Vascularization of the thyroid gland can be assessed using color flow and pulsed Doppler ultrasound. Depending on the clinical problem (diffuse or focal thyroid disease), the purpose of the study may be to quantify the vascularization of the thyroid gland or determine its vascular structure.

Such a nosological unit as nodular goiter, the ICD 10 code of which is from E00 to E07, respectively, is not one disease, but a clinical syndrome. It combines formations quite diverse in shape and structure that form in the area of ​​the thyroid gland. Most often, pathological changes in the structure of the organ are caused by a lack of iodine in the patient’s body.

The disease is usually endemic. It has been noted that in certain areas among the population the incidence rate may exceed 40%. Most often women in the age group of 40 years and over are affected. If we talk about characteristic symptomatic manifestations, they may be absent if the pathological process is mild. In more severe cases, nodular goiter can manifest itself in the form of various dysfunctions of this organ, as well as symptoms of compression of surrounding organs and tissues.

If we talk about the structure of such a human endocrine organ as the thyroid gland, then first of all we will determine that it consists of follicular cells. Each such cell is a microscopic ball that is filled with a specific liquid - keloid. As the pathological process develops, the follicle increases in size, forming a so-called node. The neoplasm can be represented by only one node or be formed from a large number of modified follicles. This is already the so-called diffuse nodular goiter.

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If we talk about the reason for the development of such pathological changes in the thyroid gland, it has not yet been precisely established. As mentioned above, most experts associate the formation of pathological changes in follicles with a lack of iodine in the human body. This theory is based on the fact that, according to statistical data, in areas with low levels of this chemical element in water and food, the incidence of nodular goiter among the population is quite high. However, how can we explain the fact that such a pathology is often detected in areas that are fairly free in iodine content?

According to another theory, diseases (classification code corresponds to column E0-07) develop as a result of increased load on the thyroid gland. As a rule, this is associated with a violation of the functioning of the entire human body. What factors can provoke an increase in the size of the follicles and form cystic formations on their basis?

1. Hereditary predisposition to disruption of the endocrine system.
2. Environmental factors. This may include increased radiation, water and air pollution with waste products from industrial enterprises.
3. Various human immune disorders or diseases.
4. Prolonged stressful situations.
5. Age-related changes in the tissues that form the thyroid gland can also contribute to the development of this pathology.

The difficulty of determining the cause of such a goiter (ICD 10 defines it as E01-07) may be due to the fact that the patient’s body is affected by not one, but several unfavorable factors. However, regardless of the determining factors, the symptomatic manifestations of the pathology are always the same.

Clinical picture

In the early and uncomplicated stages of the pathological process, it is almost impossible to determine the presence of nodular goiter without special studies. The patient has no specific complaints. The diagnosis in this case can be made by chance, for example, as a result of examining the thyroid gland using ultrasound. On the screen, the doctor notes the presence of nodes or cysts in the organ tissue.

Only at a later stage will the patient notice a change in the contours of the neck due to the growth of the cystic formation. This disease is called euthyroidism. The absence of clinical symptoms is due to the fact that hormone production in this case is not impaired. The patient will mainly be concerned about the resulting cosmetic defect. Only in some cases can unpleasant squeezing sensations appear in the throat area.

Diffuse goiter is considered the most severe in terms of symptomatic manifestations. The clinical course is very similar to thyrotoxicosis. When interviewing a doctor, the patient makes the following complaints:

1. Unpleasant sensations appear in the throat area. Sometimes it's just a feeling of pressure, but pain can also appear.
2. The patient complains of difficulty swallowing food.
3. When the cystic formation puts pressure on the trachea, complaints of impaired respiratory function appear.
4. Changes in the functioning of the cardiovascular system may be detected, for example, in the form of increased heart rate and arrhythmia. This symptomatic manifestation will have an additional code in the patient's medical history.
5. The patient notices that he has lost weight for no specific reason.
6. The work of the sweat glands increases.
7. The skin may be very dry.
8. The patient notes increased nervousness or, conversely, is prone to depression.
9. The process of memorizing a large amount of information may be disrupted.
10. Sometimes there are complaints of intestinal dysfunction or constipation.

Classification of the disease

If we talk about the classifications most often used in medical practice for this pathology, then those are used that are based on the characteristics of the degree of enlargement of the organ. An example would be the classification proposed by Dr. O.V. Nikolaev. Unlike ICD 10, it does not use coding, but simply indicates the degree of enlargement of the thyroid gland in the medical history:

1. Zero degree of pathology is characterized by the absence of obvious violations of the shape and size of the organ. Even palpation examination will not help make a diagnosis. The patient has no characteristic complaints.
2. In the first degree, there are no cosmetic defects in the neck area, but upon palpation, the doctor may note a slight enlargement of the thyroid gland. It is during this period that the first functional disturbances in the functioning of the organ may appear.
3. If the thyroid gland is clearly visible during the act of swallowing, then the patient is diagnosed with the second stage of the disease. During this period, the organ is easily palpable. The patient begins to complain of periodic difficulties when swallowing or breathing.
4. The third degree code for this pathology is set in the case when the patient’s gland is so enlarged that it changes the usual contour of the neck. During this period, all the main symptomatic manifestations of the disease can be identified in the patient.
5. If symptomatic manifestations increase and there is a significant cosmetic defect in the neck area, the person is given the fourth degree of the disease.
6. The fifth degree is the most severe. In this case, the gland grows to large sizes, which leads to compression of regional organs and tissues. The functioning of most organs and systems is disrupted.

There is a classification according to ICD 10. It is based not only on symptomatic manifestations, but also takes into account the causes of the development of the disease. There are 3 types of disease:

1. Endemic goiter, which is formed due to iodine deficiency.
2. A non-toxic form of goiter, in which the presence of one or several nodes is distinguished.
3. Thyrotoxicosis form of pathology.

Therapeutic measures

Experts believe that for mild forms of nodular goiter, therapy is usually not needed. The patient's health condition is monitored. And only in the presence of intensive cyst growth can treatment tactics be chosen. In this case, the question of which technique to use, conservative or operative, is decided.

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If a conservative, or, in other words, medicinal method is chosen, the patient is prescribed medications that can suppress the increased production of hormones by this gland. In addition to this, iodine preparations may be prescribed.

Surgical treatment is indicated for significant enlargement of cysts, for example, if the patient has a diffuse toxic goiter of severe severity. The surgical technique in this case is designed to remove the formed cysts. In this case, part of the affected gland (a lobe or half of the gland) is also removed. If a malignant neoplasm is detected, depending on the area of ​​the lesion, the entire thyroid gland may be removed.

Diffuse toxic goiter (synonyms: Graves' disease) is an organ-specific autoimmune disease in which thyroid-stimulating antibodies are produced.

ICD-10 code

E05.0 Thyrotoxicosis with diffuse goiter.

ICD-10 code

E05.0 Thyrotoxicosis with diffuse goiter

Causes of diffuse toxic goiter

Thyroid-stimulating antibodies bind to TSH receptors on thyrocytes, thereby activating the process normally triggered by TSH - the synthesis of thyroid hormones. The autonomous activity of the thyroid gland begins, not amenable to central regulation.

The disease is considered genetically determined. It is known that the production of thyroid-stimulating antibodies is caused by an antigen-specific defect in cellular suppression. A provoking factor for the formation of thyroid-stimulating immunoglobulins can be an infectious disease or stress. In this case, most patients are found to have a long-acting thyroid stimulant.

Pathogenesis of diffuse toxic goiter

An excess of thyroid hormones leads to uncoupling of respiration and phosphorylation in the cell, heat production and the rate of glucose utilization increase. gluconeogenesis and lipolysis are activated. Catabolic processes intensify, dystrophy of the myocardium, liver, and muscle tissue develops. A relative deficiency of glucocorticoids and sex hormones develops.

There are three stages in the development of the disease.

• I. Preclinical stage. Antibodies accumulate in the body, there are no clinical symptoms.
• II. Euthyroid stage. Hyperplasia of the thyroid gland increases progressively; thyroid hormones in the blood do not exceed normal values.
• III. The hyperthyroid stage is accompanied morphologically by lymphocytic infiltration of the thyroid gland, immunological reactions, and cytolysis. Clinical symptoms appear.

Symptoms of diffuse toxic goiter

There are three groups of symptoms:

• local symptoms - goiter;
• symptoms associated with overproduction of thyroid hormones;
• symptoms caused by concomitant autoimmune diseases. The thyroid gland is significantly enlarged; as a rule, the enlargement is noticeable upon examination. On palpation, a dense consistency is determined, and vascular murmurs are heard above the gland.

Symptoms caused by thyrotoxicosis increase gradually over several months. The child becomes whiny, emotionally unstable, irritable, and sleep is disturbed. Upon examination, the smooth, velvety skin attracts attention; there is pigmentation, especially in the eyelid area. Increased sweating and muscle weakness are often noted. The appetite is increased, but at the same time the child is progressively losing weight. Tremors of the fingers and increased motor activity appear. Tachycardia at rest and increased pulse arterial pressure are characteristic. Frequent stools are noted, and hepatomegaly is sometimes detected. Amenorrhea occurs in girls.

Sympathicotonia provokes the appearance of eye symptoms: Graefe's symptom - exposure of the sclera above the iris when looking down, Moebius' symptom - weakness of convergence of the eyeballs, von Stellwag's symptom - rare blinking, Dalrymple's symptom - wide open palpebral fissures, etc.

Thyrotoxicosis, depending on the severity of tachycardia, is divided into three degrees:

• I degree - heart rate increased by no more than 20%;
• II degree - heart rate increased by no more than 50%;
• III degree - heart rate increased by more than 50%.

Autoimmune diseases associated with thyrotoxicosis include endocrine ophthalmopathy, pretibial myxedema, diabetes mellitus, and juvenile polyarthritis. Endocrine ophthalmopathy is most often observed with diffuse toxic goiter. It is caused by the formation of antibodies to the membrane of the extraocular muscles and their lymphocytic infiltration, which also extends to the retrobulbar tissue. This causes swelling, hyperpigmentation of the eyelids, exophthalmos.

Complications of diffuse toxic goiter

If left untreated, the patient may develop a thyrotoxic crisis. At the same time, the temperature rises, motor restlessness or apathy, vomiting, signs of acute heart failure, and coma occur.

Diagnosis of diffuse toxic goiter

Diagnosis is based on clinical data and determination of the content of thyroid hormones in the blood. The following changes are noted:

• T 3 and T 4 in the blood serum are increased, and TSH is decreased in 70% of patients;
• T 3 is increased, T 4 is normal, TSH is decreased - in 30% of patients;
• antibodies to TSH receptors in blood serum;
• the content of cholesterol and beta-lipoproteins in the blood serum is reduced;
• relative lymphocytosis in a clinical blood test;
• increased content of ionized calcium in blood serum;
• ECG - tachycardia, increased wave voltage.

Differential diagnosis

Differential diagnosis should be carried out with vegetative-vascular dystonia, in which tachycardia and emotional arousal are inconsistent.

Hyperthyroidism can also develop with other thyroid diseases. These include acute purulent and subacute thyroiditis, autoimmune thyroiditis, functionally active thyroid nodules.

Treatment of diffuse toxic goiter

The goal of treatment is to eliminate the manifestations of hyperthyroidism and normalize the levels of thyroid hormones. Medicinal and surgical treatment methods are used. Initial therapy is based on the use of drugs that have a thyreostatic effect. Thiamazole is prescribed for 1.5-2.5 years. The starting dose of thiamazole is 0.5-0.7 mg/kg per day, depending on the severity of thyrotoxicosis, in three doses. Every 10-14 days the dose is reduced to maintenance. The maintenance dose is 50% of the initial dose. In most patients, inhibition of thyroxine secretion by thiamazole leads to hypothyroidism and an increase in the level of TSH in the blood. In this regard, after 6-8 weeks from the start of treatment, it is advisable to combine the use of thyreostatics with the administration of levothyroxine sodium to maintain euthyroidism and prevent the goitrogenic effect of TSH.

In cases of intolerance to thyreostatics, ineffectiveness of conservative treatment, and in the presence of nodes in the thyroid gland, subtotal strumectomy is indicated.

Prognosis for diffuse toxic goiter

After drug treatment lasting more than 1.5 years, remission occurs in 50% of patients. In half of patients with remission, thyrotoxicosis recurs. Evidence of achieving remission is the disappearance of thyroid-stimulating autoantibodies in the blood. The individual prognosis in patients with diffuse toxic goiter depends on the severity of the autoimmune lesion of the thyroid gland and does not depend on the antithyroid drug used. Combined treatment with thiamazole and levothyroxine for a long time and continuation of levothyroxine therapy after discontinuation of thionamides reduces the likelihood of relapse of thyrotoxicosis.

Important to know!

Determination of antibodies to the microsomal fraction of the thyroid gland is used to diagnose autoimmune thyroiditis and hypothyroidism, in which the level of antibodies in the blood increases. Antibodies to thyroid microsomes form immune complexes on the surface of cells, activate complement and cytotoxic lymphocytes, which leads to cell destruction and the formation of an inflammatory process in the thyroid gland.

Diffuse toxic goiter (Graves-Bazedow disease)- a disease characterized by hyperplasia and hyperfunction of the thyroid gland.

Code according to the international classification of diseases ICD-10:

• E05.0

Reasons

Etiology, pathogenesis. Hereditary factors, infections, intoxications, and mental trauma are important. The pathogenesis is based on disturbances in immune “surveillance”, leading to the formation of autoantibodies that have a stimulating effect, leading to hyperfunction, hyperplasia and hypertrophy of the gland. Changes in tissue sensitivity to thyroid hormones and disruption of their metabolism are important. Clinical manifestations are caused by the effect of excess thyroid hormones on various types of metabolism, organs and tissues,

Symptoms, course . Patients complain of irritability, tearfulness, increased excitability, sleep disturbance, weakness, fatigue, sweating, hand tremors and trembling of the whole body. Weight loss progresses with preserved or even increased appetite. In young patients, on the contrary, an increase in body weight may be observed - “fat Bazedov”. The thyroid gland is diffusely enlarged; There is no relationship between the degree of its increase and the severity of thyrotoxicosis. Changes in the eyes: exophthalmos, usually bilateral, without trophic disorders and limitation of movement of the eyeballs, Graefe's symptoms (lag of the upper eyelid from the movement of the eyeball when looking down), Dalrymple's (wide opening of the palpebral fissures), Mobius (convergence weakness), Kocher (retraction of the upper eyelid during rapid gaze shifting). The leading manifestations of thyrotoxicosis include changes in the cardiovascular system - thyrotoxic cardiomyopathy: tachycardia of varying intensity, tachysystolic form of atrial fibrillation (paroxysmal or constant), in severe cases leading to the development of heart failure. In rare cases, more often in men, paroxysms of atrial fibrillation may be the only symptom of thyrotoxicosis. Characterized by high pulse pressure due to increased systolic and decreased diastolic pressure, expansion of the borders of the heart to the left, increased sounds, functional systolic murmurs over the apex and pulmonary artery, pulsation of blood vessels in the neck and abdomen. Dyspeptic symptoms, abdominal pain, and, in severe cases, increased size and dysfunction of the liver and stomach are also noted. Often there is a violation of carbohydrate tolerance. With severe thyrotoxicosis or its prolonged course, symptoms of adrenal insufficiency appear: severe adynamia, hypotension, hyperpigmentation of the skin. A common symptom of toxic goiter is muscle weakness, accompanied by muscle atrophy, and sometimes paralysis of the proximal muscles of the limbs develops. Neurological examination reveals hyperreflexia, anisoreflexia, and instability in the Romberg position. In some cases, thickening of the skin on the front of the legs and dorsum of the feet may occur (pretibial myxedema). Women often develop menstrual irregularities, men - decreased potency, sometimes bi- or unilateral gynecomastia, which disappears after treatment of thyrotoxicosis. In old age, the development of thyrotoxicosis causes weight loss, weakness, atrial fibrillation, rapid development of heart failure, and worsening of coronary artery disease. Mental changes are common - apathy, depression, proximal myopathy may develop. There are mild, moderate and severe forms of the disease. In mild cases, the symptoms of thyrotoxicosis are not clearly expressed, the pulse rate does not exceed 100 per minute, the loss of body weight is no more than 3 - 5 kg. A moderately severe disease is characterized by clearly defined symptoms of thyrotoxicosis, tachycardia 100 - 120 per minute, weight loss of 8 - 10 kg. In severe cases, the pulse rate exceeds 120 - 140 per minute, sudden weight loss and secondary changes in the internal organs are noted. The level of cholesterol in the blood is reduced, the content of protein-bound iodine, the level of thyroxine and triiodothyreonine are increased; thyroid-stimulating hormone levels are low. The absorption of 131I and 99T by the thyroid gland is high. With reflexometry, the duration of the Achilles reflex is shortened. In doubtful cases, tests with thyrotropin-releasing hormone are carried out. The absence of an increase in the level of thyroid-stimulating hormone with the administration of thyroliberin confirms the diagnosis of diffuse toxic goiter.

Treatment

Treatment. Medicinal (thyreostatic agents, radioactive iodine) and surgical methods are used. The main thyreostatic drug is Mercazolil (30 - 60 mg depending on the severity of the disease with a gradual transition to maintenance doses of the drug - 2.5 - 5 mg per day, every other day or every 3 days; course of treatment is 1 - 1.5 years) .

Complications- allergic reactions (itching, urticaria), leukopenia, agranulocytosis, goitrogenic effect. In case of intolerance, the drug is discontinued; in case of leukopenia, prednisolone, leukogen, pentoxyl, sodium nucleinate are prescribed. In the complex treatment of thyrotoxicosis, beta blockers [anaprilin (obzidan), trazicor] from 40 to 200 mg/day are also used; corticosteroids (hydrocortisone, prednisolone), tranquilizers (Relanium, Rudotel, phenazepam), peritol. In case of significant exhaustion, anabolic steroids are prescribed (retabolil, phenobolin, silabolin, methandrostenolone), and in some cases insulin (4-6 units before lunch). In case of circulatory failure - cardiac glycosides (strophanthin, korglykon, digoxin, isolanide), diuretics (triampur, veroshpiron, furosemide), potassium preparations (chloride, potassium acetate). For liver complications - Essentiale, Corsil. Multivitamins, ascorbic acid, and cocarboxylase are also prescribed. In the absence of a lasting effect of drug therapy, the development of complications (allergic reactions, leukopenia, agranulocytosis with the administration of Mercazolil), as well as in severe thyrotoxicosis, the presence of atrial fibrillation, after appropriate preparation, they are referred for surgical treatment or radioiodine therapy.

Diagnosis code according to ICD-10. E05.0