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 a contrast iodine-containing 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%.

The International Statistical Classification of Diseases and Related Health Problems is a document developed under the guidance of WHO to provide a uniform approach to the methods and principles of disease treatment.

Once every 10 years it is reviewed, changes and amendments are made. Today there is ICD-10, a classifier that makes it possible to determine an international protocol for the treatment of a particular disease.

Principles of classification of endocrine diseases

Class IV. E00 - E90. Diseases of the endocrine system, nutritional disorders and metabolic disorders also include diseases and pathological conditions of the thyroid gland. Nosology code according to ICD-10 - from E00 to E07.9.

• Congenital iodine deficiency syndrome (E00 – E00.9)
• Thyroid diseases associated with iodine deficiency and similar conditions (E01 – E01.8).
• Subclinical hypothyroidism due to iodine deficiency (E02).
• Other forms of hypothyroidism (E03 – E03.9).
• Other forms of non-toxic goiter (E04 – E04.9).
• Thyrotoxicosis (hyperthyroidism) (E05 – E05.9).
• Thyroiditis (E06 – E06.9).
• Other diseases of the thyroid gland (E07 – E07.9).

All these nosological units are not one disease, but a whole series of pathological conditions that have their own characteristics - both in the causes of occurrence and in diagnostic methods. Consequently, the treatment protocol is determined based on the totality of all factors and taking into account the severity of the condition.

The disease, its causes and classic symptoms

First, let us remember that the thyroid gland has a special structure. It consists of follicular cells, which are microscopic balls filled with a specific liquid - keloid. Due to pathological processes, these balls begin to grow in size. The developing disease will depend on the nature of this growth, whether it has an effect on the production of hormones by the gland.

Despite the fact that thyroid diseases are varied, their causes are often similar. And in some cases it is not possible to establish it precisely, since the mechanism of action of this gland is still not fully understood.

• Heredity is called a fundamental factor in the development of pathologies of the endocrine glands.
• Environmental impact - unfavorable environmental conditions, radiological background, iodine deficiency in water and food, use of food chemicals, additives and GMOs.
• Diseases of the immune system, metabolic disorders.
• Stress, psycho-emotional instability, chronic fatigue syndrome.
• Age-related changes associated with hormonal changes in the body.

Often, the symptoms of thyroid diseases also have a general tendency:

• feeling of discomfort in the neck, tightness, difficulty swallowing;
• losing weight without changing your diet;
• disruption of the sweat glands - excessive sweating or dry skin may occur;
• sudden mood swings, susceptibility to depression or excessive nervousness;
• decreased thinking acuity, memory impairment;
• complaints about the gastrointestinal tract (constipation, diarrhea);
• disruptions in the functioning of the cardiovascular system - tachycardia, arrhythmia.

All these symptoms should suggest that you need to see a doctor - at least a primary care physician. And after conducting initial research, he will, if necessary, refer you to an endocrinologist.

Some thyroid diseases are less common than others due to various objective and subjective reasons. Let's look at those that are statistically the most common.

Types of thyroid pathologies

Thyroid cyst

A small benign tumor. It is generally accepted that a cyst can be called a formation that exceeds 15 mm. in diameter. Everything below this border is an expansion of the follicle.

This is a mature benign tumor, which many endocrinologists classify as a cyst. But the difference is that the cavity of the cystic formation is filled with keloid, and the adenoma is made up of epithelial cells of the thyroid gland.

Autoimmune thyroiditis (AIT)

A disease of the thyroid gland, characterized by inflammation of its tissue caused by a malfunction of the immune system. As a result of this failure, the body produces antibodies that begin to “attack” its own thyroid cells, saturate them with leukocytes, which causes inflammatory processes. Over time, your own cells are destroyed, they stop producing the required amount of hormones, and a pathological condition called hypothyroidism occurs.

Eutheriosis

This is an almost normal state of the thyroid gland, in which the function of producing hormones (TSH, T3 and T4) is not impaired, but there are already changes in the morphological state of the organ. Very often, this condition can be asymptomatic and last a lifetime, and the person will not even suspect the presence of the disease. This pathology does not require specific treatment and is often detected by chance.

Nodular goiter

Nodular goiter code according to ICD 10 - E04.1 (with a single node) is a neoplasm in the thickness of the thyroid gland, which can be either cavitary or epithelial. A single node is rarely formed and indicates the beginning of the process of neoplasms in the form of multiple nodes.

Multinodular goiter

Multinodular goiter ICD 10 - E04.2 is an uneven enlargement of the thyroid gland with the formation of several nodes, which can be either cystic or epithelial. As a rule, this type of goiter is characterized by increased activity of the internal secretion organ.

Diffuse goiter

It is characterized by uniform growth of the thyroid gland, which affects the decrease in the secretory function of the organ.

Diffuse toxic goiter is an autoimmune disease characterized by diffuse enlargement of the thyroid gland and persistent pathological production of excessive amounts of thyroid hormones (thyrotoxicosis).

This is an increase in the size of the thyroid gland, which does not affect the production of normal amounts of thyroid hormones and is not a consequence of inflammation or neoplastic formations.

Thyroid disease caused by iodine deficiency in the body. There are euthyroid (increase in organ size without affecting hormonal function), hypothyroid (decreased hormone production), hyperthyroid (increased hormone production) endemic goiter.

An increase in the size of the organ, which can be observed both in a sick person and in a healthy one. The neoplasm is benign and is not considered a tumor. It does not require specific treatment until changes in the organ or an increase in the size of the formation begin.

Separately, it is necessary to mention such a rare disease as hypoplasia of the thyroid gland. This is a congenital disease, which is characterized by underdevelopment of the organ. If this disease occurs during life, it is called atrophy of the thyroid gland.

Thyroid cancer

One of the less common pathologies, which is detected only through specific diagnostic methods, since the symptoms are similar to all other thyroid diseases.

Diagnostic methods

Almost all pathological neoplasms rarely develop into a malignant form (thyroid cancer), only if they are very large in size and untimely treatment.

The following methods are used for diagnosis:

• medical examination, palpation;
• analysis of antibody titer to thyroid tissue
• ultrasound examination of the thyroid gland;
• hormone analysis;
• if necessary, fine-needle biopsy.

In some cases, treatment may not be required at all if the tumors are very small. The specialist simply monitors the patient's condition. Sometimes neoplasms spontaneously resolve, and sometimes they rapidly begin to increase in size.

The most effective treatments

Treatment can be conservative, that is, medication. Drugs are prescribed in strict accordance with laboratory tests. Self-medication is unacceptable, since the pathological process requires monitoring and correction by a specialist.

If there are clear indications, surgical measures are carried out when a part of an organ that is susceptible to a pathological process, or the entire organ, is removed.

Treatment of autoimmune thyroid diseases has several differences:

• medicinal – aimed at destroying excess hormones;
• treatment with radioactive iodine or surgery leads to destruction of the gland, which leads to hypothyroidism;
• Computer reflexology is designed to restore the functioning of the gland.

Thyroid diseases, especially in the modern world, are quite common. If you consult a specialist in time and carry out all the necessary therapeutic measures, you can significantly improve your quality of life, and in some cases completely get rid of the disease.

The concept of nodular goiter in the ICD 10 revision

This nosological unit belongs to the class of diseases of the endocrine system, nutritional disorders and metabolic disorders (E00-E90), and the block of thyroid diseases (E00-E07).

When speaking of nodular goiter, it is important to remember that this concept generalizes according to ICD 10 different forms of thyroid diseases, differing in the cause of occurrence and morphological characteristics. In other words, these are nodes or neoplasms located in the gland and having their own capsule. The process can be single or multi-node depending on the quantity. Moreover, this disease can cause a visible cosmetic defect, determined by palpation, or even be confirmed only with the help of ultrasound diagnostics. Thus, the following morphological types of goiter are distinguished:

• Nodal
• Diffuse
• Diffuse nodular

Classification

However, ICD 10 revision nevertheless based the classification not only on morphology, but also on the causes of occurrence, highlighting:

• Endemic goiter due to iodine deficiency
• Non-toxic goiter
• Thyretoxicosis

Endemic goiter with iodine deficiency

According to ICD 10, this nosological unit belongs to code E01. This pathology is characterized by hyperthyroidism. That is, the activity of the thyroid gland without clinical manifestations of the toxic effects of thyroid hormones. We can talk about thyrotoxicosis syndrome when pronounced symptoms of intoxication with thyroid hormones appear.

Etiology

As the name implies, the cause of this disease is iodine deficiency in the body, the only difference being at what stage the body experiences a lack of this element. If the deficiency is caused by impaired absorption of iodine in the intestine, or by congenital pathologies of the thyroid gland, in which the production of the hormone is disrupted, this is a variant of relative deficiency. Absolute deficiency occurs in endemic areas where water, soil and food are critically low in iodine.

Pathogenesis

With iodine deficiency, the synthesis of the hormones T3 and T4 decreases and, by feedback in the pituitary gland, the production of thyroid-stimulating hormone increases, which stimulates a hyperplastic reaction in the tissues of the thyroid gland. In the future, the process can become isolated, that is, with the formation of a nodular goiter or diffuse. However, a mixed type cannot be ruled out.

Sporadic forms

In ICD 10, code E04 deals with non-toxic forms of goiter. Scientists still talk about the convention of dividing this term into the concepts endemic and sporadic, since the pathogenesis and causes of the latter are not fully understood. In ICD 10 revision, the non-toxic form is divided into single-nodular, multi-nodular and diffuse.

Etiology

Genetic factors play an important role in the development of the sporadic form. It is an established fact that not all residents of endemic areas develop hyperthyroidism, but families with congenital genetic diseases associated with a defect in chromosome X are more prone to it. As a result, the body may change the threshold of sensitivity to iodine deficiency, as well as to thyroid-stimulating stimulation. Classic reasons include a lack of the amino acid tyrosine, which is necessary for the synthesis of thyroxine. Taking medications containing perchlorates, lithium salts, thiourea.

Under code E05 in ICD 10, thyrotoxicosis syndrome is separately indicated. This clinical syndrome is caused by the negative influence of excess TSH. Thyrotoxicosis is a consequence of diseases of the thyroid gland, namely:

• diffuse toxic goiter
• autoimmune thyroiditis
• excessive intake of iodine preparations or thyroid hormones into the body
• toxic adenoma
• pituitary adenomas
• increased sensitivity to thyroid hormones

Diffuse goiter of the thyroid gland: symptoms and manifestations of the disease

The article describes the symptoms of diffuse toxic goiter, all the variety of its manifestations, and gives an idea of ​​the forms of this severe pathology. Also here the degrees of development of the disease are listed and characterized with visual photos and video materials.

A severe chronic endocrine disease, diffuse goiter of the thyroid gland, the symptoms of which come from almost all systems of the human body, is of an autoimmune nature. Its development is associated with the appearance of a defect in the immune system, manifested in the production of antibodies directed against TSH receptors that stimulate the thyroid gland.

The consequence of this is:

1. Uniform proliferation of thyroid tissue.
2. Hyperfunction of the gland.
3. An increase in the concentration of hormones produced by the thyroid gland - thyroxine (T4) and triiodothyronine (T3).

The hypertrophied thyroid gland has its own name - goiter.

Etiology and pathogenesis of the disease

This pathology most often affects women in the age group of 20–50 years. In children and the elderly, diffuse goiter occurs very rarely. As for the causes of the disease and the mechanisms that trigger the autoimmune process, they currently remain a task for endocrinology that has yet to be solved.

For now we can only talk about hereditary predisposition, which is realized under the influence of a complex of factors, both internal and external:

1. Mental trauma.
2. Diseases of an infectious-toxic nature.
3. Organic damage to brain structures (trauma, encephalitis).
4. Autoimmune pathologies.
5. Smoking (see Thyroid and smoking: dangers lurk).
6. Endocrine disorders and so on.

Further, thyroid hormones produced significantly in excess of norms accelerate metabolic reactions, which leads to rapid depletion of energy resources, both in the tissues of individual organs and in the entire human body in general. The structural elements of the central nervous and cardiovascular systems are primarily affected. A detailed description of all stages of the development of pathology is described in the video in this article.

Classification

For a disease such as diffuse goiter, the symptoms largely depend on its form and degree of manifestation. Pathology has several classifications.

Depending on the enlargement of the thyroid gland, the following degrees of the disease are distinguished:

1. Zero - no goiter.
2. The first is that the goiter is determined by palpation, but is not visually distinguishable. The size of the lobes does not exceed the length of the distal phalanx of the first finger.
3. Second - Goiter is determined both by palpation and visually.

Goiter, depending on its shape, can be:

1. Diffuse.
2. Uzlov.
3. Diffuse-nodular (mixed).

According to the severity of the process:

1. Mild degree.
2. Average.
3. Heavy.

Depending on the functional state of the thyroid gland, goiter can be:

1. Euthyroid.
2. Hypothyroid.

By localization it can be:

1. Ordinary.
2. Partially substernal.
3. Koltsev.
4. Digested from the embryonic anlage.

The symptoms of the disease depend on all the characteristics mentioned in the classification.

Manifestations of the disease, depending on the severity of the pathological process

Diffuse toxic goiter, the symptoms of which are very diverse, depending on the severity of the process, has the following manifestations:

1. In mild forms, neurotic complaints predominate. Tachycardia is observed, but the heart rate does not exceed 100 beats/min, without rhythm disturbances. Other endocrine glands are not included in the pathological process.
2. With moderate severity, the diffuse thyroid gland has slightly different symptoms - in addition to tachycardia exceeding 110 beats/min, weight loss reaches 10 kg within a month.
3. The severe form is characterized by progressive weight loss, up to cachexia. In addition, the first signs of dysfunction of the heart, as well as the liver and kidneys, appear.

A severe form of the disease, as a rule, is observed in the absence of treatment for diffuse toxic goiter for a long time, and also when people without the proper knowledge try to cope with this disease with their own hands.

Features of the manifestation of the euthyroid state

Since the thyroid gland functions normally in euthyroid goiter, the clinical picture depends entirely on the degree of enlargement of the gland. The zero degree does not manifest itself at all against the background of maintaining the normal functioning of the organ. As the size of the thyroid gland increases, its influence on other systems of the body appears and gradually increases.

For example, euthyroid goiter, diffuse grade 1, has symptoms that are not yet very obvious:

1. General weakness.
2. Increased fatigue.
3. Headaches.
4. Unpleasant sensations appear behind the sternum, in the projection of the heart.

1. Difficulty breathing.
2. Sensation of pressure in the neck.
3. Difficulty swallowing.
4. Compression of the trachea, leading to attacks of suffocation and dry cough.

In order to prevent the condition from worsening, you should seek medical help in a timely manner and not self-medicate. In addition, it should be remembered that the more advanced the disease, the higher the cost of treatment.

Features of manifestations of diffuse nodular goiter

In addition to diffuse goiter, there are also mixed (diffuse-nodular) and nodular forms. Diffuse goiter is a uniform enlargement of the thyroid gland, provided there are no local compactions in the tissues. In the nodular form, pathological nodular growths appear in normal structures.

Mixed goiter is a complex of nodular formations and diffuse growth. It occupies one of the first places in the structure of thyroid pathologies in terms of frequency of occurrence.

The first stages of the disease may produce scant symptoms or no symptoms at all. But further progression of the pathological process makes the manifestation of the disease more vivid.

The development of diffuse nodular goiter occurs in three degrees according to the international WHO classification or five according to the Russian one:

• Zero degree (I according to WHO). Has no symptoms, discovered by chance during examination of other organs
• First degree (I according to WHO). It manifests itself as a slight increase in the patient’s weight, an unreasonable decrease in body temperature, chronic fatigue, and hypotension.
• Second degree (II according to WHO). It manifests itself as problems with swallowing, pain in the head and neck when bending the torso and head. Since diffuse nodular goiter, the symptoms of which gradually intensify, continues to grow and increase the production of hormones, manifestations of hyperthyroidism begin to appear - blood pressure rises, edema, exophthalmos, pathological psychomotor reactions, and tremor appear. Also, due to compression of the trachea by the thyroid tissue, shortness of breath develops.
• Third degree (II according to WHO). At this stage of its development, diffuse nodular goiter of the thyroid gland shows even more pronounced symptoms. The cardiovascular, endocrine and nervous systems are affected. The shape of the neck is greatly changed. The skin is either dry or over-moisturized, due to the excessive production of iodine-containing hormones, it appears reddish. From the gastrointestinal tract - diarrhea alternates with constipation. The patient is concerned about severe tremor, hypotension, bradycardia up to 40 beats/min or tachycardia more than 100 beats/min. Despite the increased appetite, patients lose weight. When changing the position of the head, they feel a sharp attack of suffocation. They suffer from constant shortness of breath.
• Fourth degree (III according to WHO). It differs from the previous one only in the shape and size of the goiter, which completely changes the configuration of the neck.
• Fifth degree (III according to WHO). It is characterized by the extreme severity of the disease, in which many systems of the human body suffer: endocrine, nervous, digestive, cardiovascular. Sometimes death is possible. The size of the goiter is enormous, which dramatically changes the appearance of the patient. His voice becomes hoarse or disappears completely. Intelligence, memory, and reproductive functions decrease.

Doctors use both types of classification, but the Russian one is more valuable, since with its help the course of goiter is described in much more detail.

One of the most powerful manifestations of depletion of thyroid resources, hypothyroidism, which developed in childhood, is cretinism. It is characterized by severe retardation of physical, mental, mental and intellectual development, short stature, tongue-tiedness, slow bone maturation, and in some cases deaf-muteness.

Selected syndromes characteristic of diffuse goiter

The defeat of each body system leads to the appearance of specific complaints, in addition, there are a number of individual syndromes characteristic of this disease in hyperthyroidism.

Cardiovascular system

Disruption of the normal functioning of the heart and blood vessels is manifested by:

1. Tachycardia at rest (up to 130 beats/min), in which pulsation is felt in various parts of the body, such as arms, stomach, head, chest.
2. An increase in systolic blood pressure and a decrease in diastolic.
3. Severe myocardial dystrophy (especially in older people).
4. Cardiosclerosis.

Disorders of the cardiovascular system pose a direct threat to the patient’s life. The fight against them should be carried out through the joint efforts of endocrinologists and cardiologists, and patients should strictly follow the treatment instructions developed by these specialists.

Catabolic syndrome

It is characterized by the following manifestations:

1. Sudden weight loss (up to 15 kg) with increased appetite.
2. General weakness.
3. Hyperhidrosis.
4. Low-grade fever in the evenings (occurs in a limited number of elderly patients).
5. Thermoregulation disorder.

The latter manifestation is characterized by a constant feeling of heat, thanks to which patients do not freeze even at noticeably low ambient temperatures.

Organs of vision

Thyrotoxicosis leads to endocrine ophthalmopathy, characterized by the following symptoms:

1. Widening of the palpebral fissures.
2. Incomplete closure of the eyelids, leading to “sand in the eyes,” dry eye mucosa, chronic conjunctivitis.
3. Bug-eyed.
4. The sparkle of the eyes.
5. Periorbital edema in combination with proliferation of periorbital tissues.

The last symptom is perhaps the most threatening, since it leads to compression of the optic nerve and eyeball, increased intraocular pressure, pain in the eyes, and even complete blindness.

Nervous system

Thyrotoxicosis primarily leads to mental instability from mild excitability and tearfulness to aggressiveness and difficulty concentrating.

The disease also leads to other disorders:

1. Depression.
2. Sleep disorders.
3. Tremors of varying severity.
4. Muscle weakness with decreased muscle volume in the limbs.
5. Increased tendon reflexes.

In severe forms of thyrotoxicosis, patients may develop persistent disturbances in the patient’s psyche and personality.

Skeleton bones

A prolonged course of thyrotoxicosis, with an excess of thyroxine, leads to the leaching of phosphorus and calcium ions from the bones, which causes:

1. Destruction of bone tissue.
2. Decreased bone mass as well as bone density.
3. Bone pain.

The fingers gradually become like “drumsticks”.

Gastrointestinal tract

Digestive disorders are expressed in pain, stool instability up to diarrhea, sometimes nausea and vomiting. A severe form of the disease leads to thyrotoxic hapatosis, fatty liver degeneration and cirrhosis.

Endocrine glands

Since all the components of the endocrine system are interconnected, disruption of the thyroid gland leads to malfunctions of many other glands.

The adrenal glands may suffer from relative thyroid insufficiency, the symptoms of which are:

1. Skin hyperpigmentation (especially in exposed areas).
2. Hypotension.

Malfunction of the ovaries due to thyrotoxicosis is a rather rare phenomenon in which the following changes occur:

1. The frequency and intensity of menstruation decreases.
2. Fibrocystic mastopathy develops.

Moderate thyrotoxicosis may not affect a woman’s reproductive function. The threat here is different - antibodies that stimulate the thyroid gland are able to pass the transplacental barrier, leading in some cases to the manifestation of transient neonotal thyrotoxicosis in newborns.

The sexual sphere of men suffers quite often and is expressed in gynecomastia and erectile dysfunction.

Respiratory system

Patients with thyrotoxicosis experience increased breathing, as well as a tendency to develop pneumonia.

Skin

Thyrotoxicosis affects the condition of the skin. It becomes soft, warm and moist. Sometimes vitiligo develops, the skin folds darken, which is especially noticeable in the area of ​​the elbows, neck, and lower back. Hair falls out, nails are affected by onychomycosis and thyroid acropachy.

A small number of patients suffer from pretibial myxedema, which is expressed in swelling, induration, and erythema of the skin on the feet and legs, which also itch.

To ensure that diffuse goiter does not reach its later stages and does not put at risk not only the health, but also the life of the patient, when the first signs of the disease appear, you should immediately contact a therapist or endocrinologist.

A cyst, being a benign neoplasm, is a cavity with fluid inside. Statistics show that about 5% of the world's population suffer from this disease, and most of them are female. Despite the fact that the cyst is initially benign, its presence in the thyroid gland is not normal and requires the use of therapeutic measures.

Types of pathology

According to the international classification of this disease, code D 34 is assigned. Cysts can be:

• single;
• multiple;
• toxic;
• non-toxic.

According to the possible nature of the course, they are divided into benign and malignant. Therefore, for a thyroid cyst, the ICD 10 code is determined depending on the type of endocrine pathology.

A cyst is considered to be a formation whose diameter exceeds 15 mm. In other cases, there is a simple expansion of the follicle. The thyroid gland consists of many follicles that are filled with a kind of helium fluid. If the outflow is disrupted, it can accumulate in its cavity and eventually form a cyst.

There are the following types of cysts:

• Follicular. This formation consists of many follicles that have a dense structure, but do not have a capsule. At the initial stage of its development it has no clinical manifestations and can be visually detected only with a significant increase in size. As it develops, it begins to acquire pronounced symptoms. This type of neoplasm has the ability to undergo malignant degeneration with significant deformations.
• Colloidal. It has the shape of a node that contains a protein liquid inside. Most often it develops with non-toxic goiter. This type of cyst leads to the formation of a diffuse nodular goiter.

The colloid type of neoplasm generally has a benign course (more than 90%). In other cases, it can transform into a cancerous tumor. Its development is primarily caused by a lack of iodine, and secondly by a hereditary predisposition.

When the size of such a formation is less than 1 cm, it has no symptoms and does not pose a health hazard. Concern arises when the cyst begins to increase in size. The follicular type has a less favorable course. This is explained by the fact that the cyst more often turns into a malignant formation if left untreated.

Causes and symptoms

The formation of a cyst in the thyroid tissue is caused by various factors. The most common and significant, according to endocrinologists, are the following reasons:

• hereditary predisposition;
• lack of iodine in the body;
• diffuse toxic goiter;
• exposure to toxic substances;
• radiation therapy;
• radiation exposure.

Often, hormonal imbalance becomes a factor that affects the thyroid gland, causing the formation of cystic cavities in it. Both hypertrophy and degeneration of thyroid tissue can be a kind of impetus for the formation of cysts.

It should be noted that such formations do not affect the functioning of the thyroid gland. The addition of characteristic symptoms occurs with concomitant organ lesions. The reason for contacting an endocrinologist is a significant increase in the size of the formation, which deforms the neck. As this pathology progresses, patients experience the following symptoms:

• feeling of a lump in the throat;
• breathing problems;
• hoarseness and loss of voice;
• difficulty swallowing;
• neck pain;
• sore throat;
• enlarged lymph nodes.

Clinical manifestations depend on the type of pathology that appears. So, with a colloid cyst, the following is added to the general symptoms:

• tachycardia;
• excessive sweating;
• increased body temperature;
• chills;
• headache.

A follicular cyst has distinctive symptoms:

• difficulty breathing;
• neck discomfort;
• frequent coughing;
• increased irritability;
• fatigue;
• sudden weight loss.

In addition, such a hollow formation, when large, is visually noticeable and easily palpated, but there is no pain.

Diagnosis and treatment

Diagnosis of neoplasms in the thyroid gland is carried out using various methods. It could be:

• visual inspection;
• palpation;
• ultrasound examination.

They are often discovered accidentally during examination for other diseases. In order to clarify the nature of the formation, puncture of the cyst may be prescribed. As additional measures for examining the patient, a blood test is prescribed to determine thyroid hormones - TSH, T3 and T4. For differential diagnosis the following are carried out:

• radioactive scintigraphy;
• computed tomography;
• angiography.

Treatment of this pathology is individual and depends on the symptoms and nature of the tumor (type, size). If the detected cyst does not exceed 1 cm in size, then the patient is indicated for dynamic observation, which includes an ultrasound examination once every 2–3 months. This is necessary in order to monitor whether it is increasing in size.

Treatment can be conservative and surgical. If the sheets are small in size and do not affect the functioning of the organs, then thyroid hormone medications are prescribed. In addition, you can influence the cyst with an iodine-containing diet.

Most often, sclerotherapy is used to treat large cysts. This procedure involves emptying the cyst cavity using a special thin needle. Surgical treatment is used if the cyst is large. In this case, it can provoke suffocation, and there is also a tendency to suppurate, and therefore, in order to avoid more serious complications, it must be removed.

Since in most cases such pathology has a benign course, the prognosis will be favorable. But this does not exclude the possibility of a relapse. Therefore, after successful treatment, it is necessary to conduct a control ultrasound of the thyroid gland every year. If a cyst becomes malignant, the success of treatment depends on its location and the presence of metastases. If the latter are detected, the thyroid gland is completely removed along with the lymph nodes.

How safe is surgery to remove thyroid cancer?

Symptoms of hyperthyroidism

What to do if nodules form in the thyroid gland

Reasons for the development of adenoma in the thyroid gland

First aid for thyrotoxic crisis

Treatment of hyperandrogenism

ICD-10: types of goiter

ICD 10 - International Classification of Diseases, 10th revision, was created to systematize data on diseases according to their type and development.

To designate diseases, a special encoding has been developed, which uses capital Latin letters and numbers.

Thyroid diseases are classified as class IV.

Goiter, as a type of thyroid disease, is also included in ICD 10 and has several types.

Types of goiter according to ICD 10

Goiter is a clearly defined enlargement of the thyroid gland tissue, resulting from dysfunction (toxic form) or due to changes in the structure of the organ (euthyroid form).

The ICD 10 classification provides for territorial foci of iodine deficiency (endemic), due to which the development of pathologies is possible.

This disease most often affects residents of regions with iodine-poor soils - these are mountainous areas, areas far from the sea.

The endemic type of goiter can seriously affect thyroid function.

The classification of goiter according to ICD 10 is as follows:

1. Diffuse endemic;
2. Multinodular endemic;
3. Non-toxic diffuse;
4. Non-toxic single-node;
5. Non-toxic multi-node;
6. Other specified species;
7. Endemic, unspecified;
8. Non-toxic, unspecified.

A non-toxic form is one that, unlike the toxic one, does not affect the normal production of hormones; the reasons for the enlargement of the thyroid gland lie in the morphological changes of the organ.

An increase in volume most often indicates the development of a goiter.

Even with visual defects, it is impossible to immediately determine the cause and type of disease without additional tests and studies.

For an accurate diagnosis, all patients must undergo ultrasound examinations and donate blood for hormones.

Diffuse endemic process

Diffuse endemic goiter has an ICD 10 code - E01.0, and is the most common form of the disease.

In this case, the entire parenchyma of the organ is enlarged due to acute or chronic iodine deficiency.

Patients experience:

• weakness;
• apathy;
• headaches, dizziness;
• suffocation;
• difficulty swallowing;
• Digestive problems.

Later, pain in the heart area may develop due to a reduced concentration of thyroid hormones in the blood.

In severe cases, surgery and goiter removal are indicated.

Residents of iodine-deficient areas are advised to regularly take iodine-containing foods, vitamins, and undergo regular examinations.

Multinodular endemic process

This species has code E01.1.

With pathology, several well-defined neoplasms appear on the tissues of the organ.

Goiter grows due to iodine deficiency, characteristic of a particular area. The symptoms are as follows:

• hoarse, hoarse voice;
• sore throat;
• breathing is difficult;
• dizziness.

It should be noted that only as the disease progresses do the symptoms become pronounced.

At the initial stage, fatigue and drowsiness are possible; such signs can be attributed to overwork or a number of other diseases.

Non-toxic diffusion process

The code in ICD 10 is E04.0.

Enlargement of the entire thyroid gland area with no changes in functionality.

This happens due to autoimmune disorders in the structure of the organ. Signs of the disease:

• headaches;
• suffocation;
• characteristic neck deformity.

Complications in the form of hemorrhages are possible.

A number of doctors believe that euthyroid goiter can not be treated until it narrows the esophagus and trachea and does not cause pain and spasmodic cough.

Non-toxic single-node process

Has code E04.1.

This type of goiter is characterized by the appearance of one clear neoplasm on the thyroid gland.

The knot causes discomfort if it is treated incorrectly or untimely.

As the disease progresses, a pronounced bulge appears on the neck.

As the node grows, nearby organs are compressed, which leads to serious problems:

• voice and breathing disorders;
• difficulty swallowing, digestive problems;
• dizziness, headaches;
• improper functioning of the cardiovascular system.

The area of ​​the node can be very painful, this is due to the inflammatory process and swelling.

Endemic goiter, unspecified

It has a code according to ICD 10 - E01.2.

This type is caused by territorial iodine deficiency.

It does not have certain pronounced symptoms; the doctor cannot determine the type of disease even after the required tests.

The disease is assigned based on endemic characteristics.

Non-toxic multi-node process

The non-toxic multi-node type has code E04.2. in ICD 10.

Pathology of the structure of the thyroid gland. in which there are several clearly defined nodular neoplasms.

The lesions are usually located asymmetrically.

Other types of non-toxic goiter (specified)

Other specified forms of non-toxic goiter of the disease, which are assigned code E04.8, include:

1. A pathology in which both diffuse tissue proliferation and the formation of nodes are detected - diffuse-nodular form.
2. The growth and adhesion of several nodes is a conglomerate form.

Such formations occur in 25% of cases of the disease.

Unspecified nontoxic goiter

For this type of goiter, code E04.9 is provided in ICD 10.

It is used in cases where the doctor, as a result of an examination, rejects the toxic form of the disease, but cannot determine what kind of pathology of the thyroid gland structure is present.

The symptoms in this case are varied; tests do not provide the full picture.

How will ICD 10 help?

This classification was developed primarily for recording and comparing the clinical picture of diseases and for statistical analysis of mortality in individual territories.

The classifier benefits the doctor and the patient, helps to quickly make an accurate diagnosis and choose the most advantageous treatment strategy.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017

Thyrotoxicosis [hyperthyroidism] (E05), Unspecified thyrotoxicosis (E05.9), Chronic thyroiditis with transient thyrotoxicosis (E06.2)

Endocrinology

General information

Brief description

Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated August 18, 2017
Protocol No. 26

Thyrotoxicosis(hyperthyroidism) is a clinical syndrome caused by an excess of thyroid hormones (TG) in the blood and their toxic effect on various organs and tissues.

"Thyrotoxicosis with diffuse goiter (diffuse toxic goiter, disease Graves, Bazedov)" is an autoimmune disease that develops as a result of the production of antibodies to rTSH, clinically manifested by damage to the thyroid gland with the development of thyrotoxicosis syndrome in combination with extrathyroidal pathology (endocrine ophthalmopathy (EOP), pretibial myxedema, acropathy). The simultaneous combination of all components of the systemic autoimmune process occurs relatively rare and not necessary for diagnosis (level A). In most cases, the greatest clinical significance in thyrotoxicosis with diffuse goiter is the thyroid lesion.
Thyrotoxicosis in patients with node/multi-node goiter occurs due to the development of functional autonomy of the thyroid node. Autonomy can be defined as the functioning of thyroid follicular cells in the absence of the main physiological stimulator - pituitary TSH. With functional autonomy, thyroid cells escape the control of the pituitary gland and synthesize TG in excess quantities. If the production of TG by autonomous formations exceeds the physiological need, the patient develops thyrotoxicosis. Such an event can occur as a result of the natural course of nodular goiter or after additional amounts of iodine enter the body with iodine supplements or as part of iodine-containing pharmacological agents. The process of development of functional autonomy lasts for years and leads to clinical manifestations of functional autonomy, mainly in people of the older age group (after 45 years) (level B).

INTRODUCTORY PART

ICD-10 code(s):

ICD-10
Code	Name
E05	Thyrotoxicosis [hyperthyroidism]
E 05.0	Thyrotoxicosis with diffuse goiter
E 05.1	Thyrotoxicosis with toxic uninodular goiter
E 05.2	Thyrotoxicosis with toxic multinodular goiter
E 05.3	Thyrotoxicosis with ectopia of thyroid tissue
E 05.4	Artificial thyretoxicosis
E 05.5	Thyroid crisis or coma
E 05.8	Other forms of thyrotoxicosis
E 05.9	Thyrotoxicosis, unspecified
E 06.2	Chronic thyroiditis with transient thyrotoxicosis

Date of protocol development/revision: 2013 (revised 2017).

Abbreviations used in the protocol:

AIT	-	autoimmune thyroiditis
BG	-	Graves' disease
TG	-	thyroid hormones
TSH	-	thyroid-stimulating hormone
MUTZ	-	multinodular toxic goiter
TA	-	thyrotoxic adenoma
T3	-	triiodothyronine
T4	-	thyroxine
thyroid gland	-	thyroid gland
TAB	-	fine-angle aspiration biopsy of the thyroid gland
PTG	-	parathgorgomon
hCG	-	human chorionic gonadotropin
AT to TPO	-	antibodies to thyroperoxidase
AT to TG	-	antibodies to thyroglobulin
AT to rTSH		antibodies to TSH receptor
I 131	-	radioactive iodine
image intensifier	-	endocrine ophthalmopathy

Protocol users: emergency doctors, general practitioners, therapists, endocrinologists.

Level of evidence scale:

A	A high-quality meta-analysis, systematic review of RCTs, or large RCTs with a very low probability (++) of bias, the results of which can be generalized to an appropriate population.
IN	High-quality (++) systematic review of cohort or case-control studies or High-quality (++) cohort or case-control studies with very low risk of bias or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population .
WITH	Cohort or case-control study or controlled trial without randomization with a low risk of bias (+), the results of which can be generalized to the relevant population or RCT with a very low or low risk of bias (++ or +), the results of which cannot be directly distributed to the relevant population.
D	Case series or uncontrolled study or expert opinion.
GPP	Best clinical practice. Recommended good clinical practice is based on the clinical experience of the members of the CP working group.

Classification

TOclassification:
1) Thyrotoxicosis caused by increased production of thyroid hormones:
Graves' disease (GD);
· toxic adenoma (TA);
iodine-induced hyperthyroidism;
· hyperthyroid phase of autoimmune thyroiditis (AIT);
· TSH - conditioned hyperthyroidism.
− TSH-producing pituitary adenoma;
− syndrome of inadequate secretion of TSH (resistance of thyrotrophs to thyroid hormones).
· trophoblastic hyperthyroidism.

2) Hyperthyroidism caused by the production of thyroid hormones outside the thyroid gland:
· metastases of thyroid cancer producing thyroid hormones;
Chorinonepithelioma.

3) Thyrotoxicosis not associated with hyperproduction of thyroid hormones:
· drug-induced thyrotoxicosis (overdose of thyroid hormones);
· thyrotoxicosis, as a stage of subacute de Quervain's thyroiditis, postpartum thyroiditis.

Table 2. Classification of goiter sizes :

Table 3. Classification and pathogenesis of thyrotoxicosis:

Form of thyrotoxicosis	Pathogenesis of thyrotoxicosis
Graves' disease	Thyroid stimulating antibodies
Thyrotoxic thyroid adenoma	Autonomous secretion of thyroid hormones
TSH-secreting pituitary adenoma	Autonomous secretion of TSH
Iodine-induced thyrotoxicosis	Excess iodine
AIT (hasitoxicosis)	Thyroid stimulating antibodies
	Destruction of follicles and passive entry of thyroid hormones into the blood (calloidorrhagia)
Drug-induced thyrotoxicosis	Overdose of thyroid drugs
T4 and T3-secreting ovarian teratoma	Autonomous secretion of thyroid hormones by tumor cells
Tumors that secrete hCG	TSH-like action of hCG
TSH receptor mutations
McCune-Albright-Britsev syndrome	Autonomous secretion of thyroid hormones by thyrocytes
Thyroid hormone resistance syndrome	Stimulating effect of TSH on thyrocytes due to the lack of feedback

Diagnostics

DIAGNOSTIC METHODS, APPROACHES AND PROCEDURES

Diagnostic criteria

Complaints and anamnesis:
Complaints to:
· nervousness;
· sweating;
· heartbeat;
· increased fatigue;
· increased appetite and, despite this, weight loss;
· general weakness;
· emotional lability;
shortness of breath;
· sleep disturbance, sometimes insomnia;
· poor tolerance to elevated ambient temperatures;
· diarrhea;
· discomfort from the eyes - unpleasant sensations in the area of ​​the eyeballs, trembling of the eyelids;
· menstrual cycle disorders.

IN medical history:
· presence of relatives suffering from thyroid diseases;
· frequent acute respiratory diseases;
· local infectious processes (chronic tonsillitis).

Physical examination:
· increase in the size of the thyroid gland;
· disturbances of cardiac activity (tachycardia, loud heart sounds, sometimes systolic murmur at the apex, increased systolic and decreased diastolic blood pressure, attacks of atrial fibrillation);
· disorders of the central and sympathetic nervous system (tremor of the fingers, tongue, entire body, sweating, irritability, feelings of anxiety and fear, hyperreflexia);
· metabolic disorders (heat intolerance, weight loss, increased appetite, thirst, accelerated growth);
· disorders of the gastrointestinal tract (loose stools, abdominal pain, increased peristalsis);
ocular symptoms (wide opening of the palpebral fissures, exophthalmos, frightened or wary gaze, blurred vision, double vision, lag of the upper eyelid when looking down and the lower eyelid when looking up).

Approximately 40-50% of patients with HD develop image intensifier, which is characterized by damage to the soft tissues of the orbit: retrobulbar tissue, extraocular muscles; involving the optic nerve and auxiliary apparatus of the eye (eyelids, cornea, conjunctiva, lacrimal gland). Patients develop spontaneous retrobulbar pain, pain with eye movements, erythema of the eyelids, edema or swelling of the eyelids, conjunctival hyperemia, chemosis, proptosis, and limited mobility of the extraocular muscles. The most severe complications of EOP are: optic neuropathy, keratopathy with the formation of a cataract, corneal perforation, ophthalmoplegia, diplopia, from the muscular system (muscle weakness, atrophy, myasthenia gravis, periodic paralysis)).

Laboratory research:
Table 4. Laboratory parameters for thyrotoxicosis:

Test*	Indications
TSH	Reduced to less than 0.1 mIU/l
Free T4	Promoted
Free T3	Promoted
AT to TPO, AT to TG	Promoted
AT to TSH receptor	Promoted
ESR	Increased in subacute de Quervain's thyroiditis
Human chorionic gonadotropin	Increased in choriocarcinoma

*TSH concentration in thyrotoxicosis should be low (< 0.1 мЕ/л), содержание в сыворотке свТ4 и свТ3 повышено (уровень А).
Some patients experience a decrease in TSH levels without a simultaneous increase in the concentration of thyroid hormones in the blood (level A). This condition is regarded as subclinical thyrotoxicosis, unless it is due to other reasons (taking medications, severe non-thyroid diseases). A normal or elevated TSH level against the background of high fT4 levels may indicate a TSH-producing pituitary adenoma, or selective resistance of the pituitary gland to thyroid hormones. Antibodies to rTSH are detected in 99-100% of patients with autoimmune thyrotoxicosis (level B). During treatment or spontaneous remission of the disease, antibodies may decrease, disappear (level A) or change their functional activity, acquiring blocking properties (level D).
Antibodies to TG and TPO are detected in 40-60% of patients with autoimmune toxic goiter (level B). During inflammatory and destructive processes in the thyroid gland of a non-autoimmune nature, antibodies may be present, but in low levels (level C).
Routine determination of the level of antibodies to TPO and TG for the diagnosis of DTG is not recommended (level B). Determination of antibodies to PTO and TG is carried out only for the differential diagnosis of autoimmune and non-autoimmune thyrotoxicosis.

Instrumental studies:
Table 5. Instrumental studies for thyrotoxicosis:

Research method	Note	UD
Ultrasound	The volume and echostructure of the thyroid gland is determined. In HD: diffuse increase in thyroid volume, thyroid echogenicity is uniformly reduced, echostructure is homogeneous, blood supply is increased. With AIT: heterogeneity of echogenicity. With MUTZ: formations in the thyroid gland. In thyroid cancer: hypoechoic formations with uneven contours of the node, growth of the node beyond the capsule and calcification.	IN
Scintigraphy of the thyroid gland. The isotope used is technetium 99mTc, I 123, less commonly I 131	In HD there is an increase and uniform distribution of the isotope. With functional autonomy, the isotope accumulates in an actively functioning node, while the surrounding thyroid tissue is in a state of suppression. In case of destructive thyroiditis (subacute, postpartum), the uptake of the radiopharmaceutical is reduced. TA and MUTZ are characterized by “hot nodes”, while cancer is characterized by “cold nodes”	A
	Thyroid scintigraphy is indicated for MUTZ, if the TSH level is below normal, or for the purpose of topical diagnosis of ectopic thyroid tissue or retrosternal goiter	IN
	In iodine-deficient regions, thyroid scintigraphy for MUT is indicated even if the TSH level is in the lower limit of normal	WITH
Computed tomography	These methods help to diagnose substernal goiter, clarify the location of the goiter in relation to the surrounding tissue, determine displacement or compression of the trachea and esophagus	IN
Magnetic resonance imaging
X-ray examination with barium contrast of the esophagus
TAB cytological examination	They are carried out in the presence of nodes in the thyroid gland. A puncture biopsy is indicated for all palpable nodules; The risk of cancer is the same for solitary nodular formation and multinodular goiter. With neoplasms of the thyroid gland, cancer cells are detected. In AIT - lymphocytic infiltration.	IN

Table 6. Additional diagnostic methods for thyrotoxicosis:

Type of study	Note	Probability of appointment
ECG	Diagnosis of rhythm disturbances	100%
24-hour Holter ECG monitor	Diagnosis of heart disorders	70%
Chest X-ray/fluorography	Exclusion of a specific process during the development of CHF	100%
Ultrasound of the abdominal organs	In the presence of CHF, toxic liver damage	50%
ECHO-cardiography	In the presence of tachycardia	90%
EGDS	In the presence of concomitant pathology	50%
Densitometry	Diagnosis of osteoporosis	50%

Table 7. Indications for specialist consultation:
· consultation with a neurologist/epileptologist - differential diagnosis with epilepsy;
· consultation with a cardiologist - in case of development of “thyrotoxic heart”, CHF, arrhythmia;
· consultation with an ophthalmologist - in combination with an image intensifier to assess the function of the optic nerve, assess the degree of exophthalmos, identify disturbances in the functioning of the extraocular muscles;
· consultation with a surgeon - to resolve the issue of surgical treatment;
· consultation with an oncologist - in the presence of a malignant process;
· consultation with an allergist - if side effects develop in the form of skin manifestations when taking thyreostatics;
· consultation with a gastroenterologist - if side effects develop when taking thyreostatics, in the presence of pretibial myxedema;
· consultation with an obstetrician-gynecologist - during pregnancy;
· consultation with a hematologist - if agranulocytosis develops.

Diagnostic algorithm:

Differential diagnosis

Differential diagnosis

Table 8. Differential diagnosis of thyrotoxicosis:

Diagnosis	In favor of diagnosis
Graves' disease	Diffuse changes on the scintigram, increased levels of antibodies to TPO, the presence of an image intensifier and pretibial myxedema
Multinodular toxic goiter	Heterogeneity of the scintigraphic picture
Autonomous hot nodes	“Hot” lesion on the scanogram
Subacute de Quervain's thyroiditis	The thyroid gland is not visualized on the scanogram, elevated levels of ESR and thyroglobulin, pain syndrome
Iatrogenic thyrotoxicosis, Amiodarone-induced thyrotoxicosis	History of taking interferon, lithium, or drugs containing large amounts of iodine (amiodarone)
TSH-producing pituitary adenoma	Increased TSH level, lack of TSH response to stimulation with thyrotropin-releasing hormone
Choriocarcinoma	Increased levels of human chorionic gonadotropin
Thyroid cancer metastases	In most cases there was a previous thyroidectomy
Subclinical thyrotoxicosis	Thyroid iodine uptake may be normal
Relapse of thyrotoxicosis	After HD treatment
Struma ovarii - ovarian teratoma containing thyroid tissue, accompanied by hyperthyroidism	increased radiotracer uptake in the pelvic area during whole body scanning

In addition, differential diagnosis is carried out with conditions similar in clinical picture to thyrotoxicosis and cases of suppression of TSH levels without thyrotoxicosis:
· anxiety states;
· pheochromocytoma;
· euthyroid pathology syndrome (suppression of TSH levels in severe somatic non-thyroid pathology) does not lead to the development of thyrotoxicosis.

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Treatment

Drugs (active ingredients) used in treatment

Groups of drugs according to ATC used in treatment

Treatment (outpatient clinic)

TREATMENT TACTICS AT THE OUTPATIENT LEVEL: patients with previously diagnosed Graves' disease without decompensation of the disease, who do not require radioiodine therapy, surgical treatment, and without thyrotoxic crisis are subject to outpatient treatment .

Non-drug treatment:
· Mode: depends on the severity of the condition and the presence of complications. Avoid physical activity, because with thyrotoxicosis, muscle weakness and fatigue increase, thermoregulation is disrupted, and the load on the heart increases.
· Diet: until euthyroidism is established, it is necessary to limit the intake of iodine into the body with contrast agents, because Iodine in most cases contributes to the development of thyrotoxicosis. Caffeine should be avoided because... caffeine may increase symptoms of thyrotoxicosis.

Drug treatment:
Conservative thyreostatic therapy:
To suppress the production of thyroid hormones by the thyroid gland, it is necessary to use thiamazole. Thiamazole is used in a daily dose of 20-40 mg. In case of severe clinical and biochemical hyperthyroidism, doses can be increased by 50-100%. Dosage regimen - usually 2-3 times a day, it is permissible to take the drug once a day
Possible side effects of thyreostatic therapy: allergic reactions, liver pathology (1.3%), agranulocytosis (0.2 - 0.4%). If fever, arthralgia, ulcers on the tongue, pharyngitis or severe malaise develop, the use of thyreostatics should be immediately stopped and an expanded leukogram determined. The duration of conservative treatment with thyreostatics is 12-18 months.
* TSH remains suppressed for a long time (up to 6 months) during the treatment of thyrotoxicosis. Therefore, determining the TSH level is not used to adjust the dose of thyreostatic. The first monitoring of TSH levels is carried out no earlier than 3 months after achieving euthyroidism.

The dose of the thyreostatic agent should be adjusted depending on the level of free T4. The first control of free T4 is prescribed 3-4 weeks after the start of treatment. The dose of the thyreostatic agent is reduced to a maintenance dose (7.5-10 mg) after reaching a normal level of free T4. Then free T4 is monitored once every 4-6 weeks using the “Block” regimen and once every 2-3 months using the “Block and Replace” regimen (levothyroxine 25-50 mcg) in adequate doses.

Before discontinuing thyreostatic therapy, it is advisable to determine the level antibodies to TSH receptor, as this helps in predicting the outcome of treatment: patients with low levels of AT-rTSH have a greater chance of stable remission.

Most patients with a resting heart rate greater than 100 beats per minute or with concomitant cardiovascular disease should be treated with β-blockers for 3-4 weeks (anaprilin 40-120 mg/day, atenolol 100 mg/day, bisoprolol 2.5-10 mg/day).

When combined with EOP and the presence of symptoms of adrenal insufficiency, resort to corticosteroid therapy: prednisolone 10-15 mg or hydrocortisone 50-75 mg intramuscularly.

Treatment of thyrotoxicosis during pregnancy:
If a suppressed TSH level is detected in the first trimester (less than 0.1 mU/l), it is necessary to determine the levels of fT4 and fT3 in all patients. Differential diagnosis of GD and gestational thyrotoxicosis is based on the detection of goiter, antibodies to rTSH, EOP; detection of antibodies to TPO does not allow this to be done (level B). Thyroid scintigraphy is absolutely contraindicated. The method of choice for treating thyrotoxicosis during pregnancy is antithyroid drugs.

PTU and thiamazole freely penetrate the placental barrier, enter the fetal blood and can cause the development of hypothyroidism and goiter and the birth of a child with reduced intelligence. Therefore, thyreostatics are prescribed in the lowest possible doses, sufficient to maintain thyroid hormones at a level 1.5 times higher than the level in non-pregnant women, and TSH below the level typical for pregnant women. The dose of thiamazole should not exceed 15 mg per day, the dose of propylthiouracil* - 200 mg per day.

FT4 monitoring is carried out after 2-4 weeks. After reaching the target fT4 level, the dose of the thyreostatic agent is reduced to maintenance (thiamazole to 5-7.5 mg, propicil to 50-75 mg). FT4 levels should be monitored monthly. By the end of the second and third trimester, due to increased immunosuppression, immunological remission of GD occurs and in most pregnant women the thyreostatic drug is canceled.
Drug of choice in the first trimester there is a vocational school, in the second and third - thiamazole (level C). This is due to the fact that taking thiamazole in isolated cases can be associated with congenital anomalies that develop during the period of organogenesis in the first trimester. If PTU is unavailable and intolerable, thiamazole can be prescribed. In patients receiving thiamazole, if pregnancy is suspected, it is necessary to conduct a pregnancy test as early as possible and, if pregnancy occurs, transfer them to taking PTU, and at the beginning of the second trimester, return to taking thiamazole again.
If the patient initially received PTU, it is similarly recommended to switch her to thiamazole at the beginning of the second trimester.
Using a block-and-replace scheme contraindicated during pregnancy(level A). The “block and replace” regimen involves the use of higher doses of thyroid hormones, which can lead to the development of hypothyroidism and goiter in the fetus.
In case of severe thyrotoxicosis and the need to take high doses of antithyroid drugs, as well as intolerance to thyreostatics (allergic reactions or severe leukopenia) or refusal of the pregnant woman to take thyreostatics, surgical treatment is indicated, which can be performed in the second trimester (level C).

Table 9. Treatment of Graves' disease in pregnant women:

Diagnosis time	Features of the situation	Recommendations
GD diagnosed during pregnancy	GD diagnosed in the first trimester	Start taking Propylthiouracil*.
	GD diagnosed after the first trimester	Start taking thiamazole. Measure the antibody titer to rTSH; if it is elevated, repeat at 18-22 weeks and 30-34 weeks. If thyroidectomy is necessary, the optimal time is the second trimester.
HD diagnosed before pregnancy	Taking thiamazole	Switch to Propylthiouracil* or discontinue thyreostatics as soon as the pregnancy test is confirmed. Measure the antibody titer to rTSH; if it is elevated, repeat at 18-22 weeks and 30-34 weeks.
	In remission after discontinuation of thyreostatics.	Determine thyroid function to confirm euthyroidism. Do not measure the AT titer to rTSH.
	Received radioiodine therapy or had a thyroidectomy	Measure the antibody titer to rTSH in the first trimester; if it is elevated, repeat at 18-22 weeks

After thyroidectomy or extremely subtotal resection of the thyroid gland, replacement therapy with levothyroxine is prescribed at a rate of 2.3 mcg/kg body weight.

Carrying out radioiodine therapy pregnant women contraindicated. If I 131 is inadvertently prescribed to a pregnant woman, she should be informed of the radiation risks, including the risk of fetal thyroid destruction if I 131 I is taken after 12 weeks of pregnancy. There are no recommendations for or against terminating a pregnancy during which a woman received 131 I.

With a transient hCG-induced decrease in TSH levels in early pregnancy, thyreostatics are not prescribed.
When thyrotoxicosis is detected in a woman in the postpartum period, it is necessary to carry out a differential diagnosis between GD and postpartum thyroiditis. For women with severe symptoms of the thyrotoxic phase of postpartum thyroiditis, β-blockers may be recommended.

Treatment of drug-induced thyrotoxicosis:
For the treatment of manifest iodine-induced For thyrotoxicosis, β-blockers are used as monotherapy or in combination with thiamazole.
In patients in whom thyrotoxicosis developed during therapy interferon-α or interleukin-2, It is necessary to carry out a differential diagnosis between GD and cytokine-induced thyroiditis.

During therapy amiodarone Assessment of thyroid function is recommended before, 1 and 3 months after the start of treatment, then at intervals of 3-6 months. The decision to stop taking amiodarone against the background of severe thyrotoxicosis should be made individually, based on consultation with a cardiologist and the presence or absence of alternative effective antiarrhythmic therapy. Thiamazole should be used for the treatment of type 1 amiodarone-induced thyrotoxicosis, and glucocorticosteroids for the treatment of type 2 amiodarone-induced thyrotoxicosis. In cases of severe amiodarone-induced thyrotoxicosis, which does not respond to monotherapy, as well as in situations where the type of disease cannot be accurately determined, a combination of thyreostatics and glucocorticoids is indicated. In patients with amiodarone-induced thyrotoxicosis who fail to respond to aggressive combination therapy with thiamazole and prednisolone, thyroidectomy should be performed.

Approaches to the treatment of HD in patients with endocrine ophthalmopathy:
Thyrostatic therapy in patients with GD and EOP is preferably carried out according to the “block and replace” scheme (level C). Surgical treatment of GD in combination with an image intensifier is recommended to be performed in the amount of total thyroidectomy in order to prevent the progression of an image intensifier in the postoperative period (level B).

All patients with GD and EOP require mandatory drug correction of postoperative hypothyroidism from the 1st day after surgery, followed by regular determination of TSH levels at least once a year.

Radioiodine therapy can be recommended as a safe method of treating thyrotoxicosis in HD in patients with EOP, which does not lead to a worsening of its course, provided that a stable euthyroid state is achieved in the post-radiation period against the background of levothyroxine replacement therapy (level C).

When planning surgical treatment or RIT of HD, it is necessary to take into account degree of activity of the image intensifier. For patients with an inactive phase of the image intensifier (CAS)<3) предварительная подготовка не требуется, назначается только симптоматическое лечение (уровень А). В активную фазу (CAS≥5) до проведения хирургического лечения или РЙТ необходимо лечение глюкокортикоидами (уровень В). При низкой активности процесса (CAS=3-4) глюкокортикоиды назначаются, в основном, после радикального лечения. Пациентам с тяжелой степенью ЭОП и угрозой потери зрения проведение RHT is contraindicated. Patients with HD and EOP need to quit smoking, as well as reduce body weight (level B).

List of essential medicines (having a 100% probability of use):
Table 9. Drugs used to treat HD:

Pharmacological group	International nonproprietary name of the drug	Directions for use	Level of evidence
Antithyroid drug	Thiamazole H03BB02	Tablets 5 and 10 mg orally, daily dose 10-40 mg (1-3 doses)	IN
	Propylthiuracil* H03BA02	Tablets 50 mg orally, daily dose 300-400 mg (for 3 doses)
β-blockers
Non-selective (β1, β2)	Propranolol C07AA05	Orally 10-40 mg 3-4 times a day	IN
Cardioselective (β1)	Atenolol C07AB03	Tablets orally, 25-100 mg 1-2 times a day	IN

List of additional medications (less than 100% probability of use):
Table 10. Drugs used for adrenal insufficiency:
* apply after registration on the territory of the Republic of Kazakhstan

Surgical intervention: No.

Further management[4-6]:
· Monitoring of patients receiving thyreostatic therapy is carried out for early detection of side effects, such as rash, liver pathology, agranulocytosis. It is necessary to study the levels of fT4 and TSH every 4 weeks for early detection of hypothyroidism and prescription of replacement therapy. Within a year after achieving euthyroidism, laboratory assessment of thyroid function is carried out once every 3-6 months, then every 6-12 months.
· In pregnant women with HD, it is necessary to use the lowest doses of thyreostatics, ensuring the achievement of thyroid hormone levels slightly above the reference range, with suppressed TSH. Thyroid function during pregnancy should be assessed monthly and the dose of thyreostatic agent adjusted as needed.

After radioactive iodine therapyI 131 Thyroid function progressively decreases. Monitoring TSH levels - every 3-6 months. Hypothyroidism usually develops 2-3 months after treatment, and when detected, levothyroxine should be prescribed immediately.

After thyroidectomy Regarding HD it is recommended:
· stop taking antithyroid drugs and ẞ-blockers;
· start taking levothyroxine in a daily dose corresponding to the patient’s body weight (1.6-1.8 mcg/kg), 6-8 weeks after starting levothyroxine, determine the TSH level and, if necessary, adjust the dose (taking levothyroxine is a lifelong replacement therapy , TSH levels should be determined at least 2-3 times a year);
· in the first days after surgery, it is necessary to determine the level of calcium (preferably free calcium) and PTH and, if necessary, prescribe calcium and vitamin D supplements.
· For hypoparathyroidism, the main method of treatment is preparations of hydroxylated vitamin D (alfacalcidol, calcitriol). The dose is selected strictly individually based on the level of calcium in the serum, which is determined once every 3 days. The starting dose of the drug depends on the level of free calcium (less than 0.8 mmol/l: 1-1.5 mcg/day; 0.8-1.0 mmol/l: 0.5-1 mcg/day).

There are no restrictions on the minimum or maximum dose of vitamin D. The criterion for an adequate dose is the level of ionized calcium not higher than 1.2 mmol/l for 10 days; after selecting an adequate dose, calcium levels are monitored continuously once every 2-4 weeks, and if necessary, the dose of the drug is adjusted. Additionally, calcium supplements are prescribed at a dose of 500-3000 mg/day to ensure sufficient calcium intake in the body.

Patients who have undergone thyroidectomy and are receiving levothyroxine replacement therapy should subsequently be monitored in the usual manner as for patients with hypothyroidism (hypoparathyroidism).
After I 131 therapy or surgical treatment, the patient should be monitored for all his life in connection with the development of hypothyroidism.

Indicators of treatment effectiveness:
· reduction or elimination of symptoms of thyrotoxicosis, allowing the patient to be transferred to outpatient treatment;
Reducing the size of the goiter;
· reducing the dose of thyreostatics required to maintain euthyroidism;
· disappearance or decrease in the content of antibodies to TSH receptors.

Treatment (inpatient)

TREATMENT TACTICS AT THE INPATIENT LEVEL: patients with newly diagnosed thyrotoxicosis, for radioiodine therapy and surgical treatment, as well as in a state of decompensation and thyrotoxic crisis, are subject to inpatient treatment .

Patient observation card, patient routing

Non-drug treatment: see outpatient level.

Radioactive iodine therapy:
Indications to radioactive iodine therapy are:
· postoperative relapse of thyrotoxicosis;
· recurrent course of thyrotoxicosis during treatment with thyreostatics;
· intolerance to thyreostatics.

In patients with GD who have not developed disease remission 1-2 years after thiamazole therapy, treatment with radioactive iodine or thyroidectomy should be considered.
In persons with severe thyrotoxicosis, when the total T4 level is > 20 μg/dl (260 nmol/l) or the fT4 level is > 5 ng/dl (60 pmol/l), thiamazole and β-blockers must be prescribed before I 131 therapy in order to normalize these indicators. Drug treatment with thyreostatics is usually stopped 10 days before the appointment of I 131 (in cases of severe thyrotoxicosis, it is possible to stop treatment 3-5 days before). Thyrostatic agents are not discontinued before radioactive iodine therapy in patients with severe thyrotoxicosis and/or large goiter to prevent thyrotoxic crisis.

Drug treatment: see outpatient level.

Thyrotoxic crisis (TC)- a rare disease characterized by multisystem involvement and mortality in 8%-25% of cases. Diagnostic criteria TC - unified diagnostic criteria (BWPS scale).

All patients with TC require observation in the intensive care unit, and all vital functions should be monitored. Treatment should be started immediately, without waiting for the results of a hormonal blood test.

Table 11. Treatment of thyrotoxic crisis:

PM

Dose

In order to figure out which one has a diffuse at evil goiter code according to ICD 10 and what it means, you need to figure out what the designation “ICD 10” represents. It stands for “international classification of diseases” and is a normative document whose task is to unite methodological approaches and compare materials among doctors around the world. That is, in simple terms, this is an international classification of all known diseases. And the number 10 indicates the version of the revision of this classification, at the moment it is the 10th. And diffuse nodular goiter as a pathology belongs to class IV, including diseases of the endocrine system, metabolic and digestive disorders, which have alphanumeric codes from E00 to E90. Diseases of the thyroid gland occupy positions from E00 to E07.

If we talk about diffuse nodular goiter, it should be remembered that the classification according to ICD 10 combines into a group various pathologies of the thyroid gland, which differ both in the reasons for their appearance and in morphology. These are nodular neoplasms in the tissues of the thyroid gland (uninodular and multinodular), and pathological proliferation of its tissues due to dysfunction, as well as mixed forms and clinical syndromes associated with diseases of the endocrine organ.

They can also be diagnosed in different ways, some pathologies visually “disfigure” the neck, some can only be felt during palpation, others, in general, are determined only using ultrasound.

The morphology of the diseases allows us to distinguish the following types: diffuse, nodular and diffuse nodular goiter.

One of the changes made by the 10th revision to the ICD was the classification of thyroid pathologies not only by morphological characteristics, but also by the reasons for their appearance.

Thus, the following types of goiter are distinguished:

• endemic origin due to iodine deficiency;
• euthyroid or non-toxic;
• thyrotoxicosis conditions.

For example, if we consider the endemic goiter ICD 10 that has arisen as a result of iodine deficiency, it is assigned the code E01. The official wording is as follows: “Thyroid diseases associated with iodine deficiency and similar conditions.” Since this group combines diffuse and nodular forms of endemic goiter, as well as their mixed forms, diffuse nodular goiter can be classified under this international classification code, but only as a type that has developed as a result of iodine deficiency.

ICD 10 E04 code implies sporadic non-toxic forms of goiter. This includes both its diffuse types and nodal types - one node or many. That is, diffuse nodular goiter, which is not caused by iodine deficiency, but, for example, by a genetic predisposition to thyroid dysfunction, can be “marked” with the alphanumeric code E04.

If you pay attention to the group of diseases under ICD code E05, the main concept of these pathologies will be thyrotoxicosis. Thyrotoxicosis is a condition in which toxic poisoning of the body occurs due to an excess of thyroid hormones in the blood, for example, thyroid adenoma. The main causes of such processes are toxic types of goiter: diffuse toxic goiter, nodular toxic goiter (single and multinodular) and their mixed form. So the toxic type of diffuse nodular goiter belongs specifically to group E05.

Thyroid diseases can be very dangerous for the body. These include diffuse nodular goiter. Therefore, their timely diagnosis and treatment is the key to a favorable prognosis.

However, it is not always possible to see one doctor. There are times when there is a need to move to another city or country. Or the opportunity arises to continue treatment in a foreign clinic with more experienced specialists. And doctors need to exchange research and laboratory test data. It is in such cases that the importance and usefulness of a document such as ICD 10 is felt. Thanks to it, the boundaries between doctors from different countries are erased, which naturally saves both time and resources. And time, as we know, is very valuable.