Diffuse goiter ICD code 10. Diffuse toxic goiter - description, causes, treatment. Diffuse non-toxic appearance

For diffuse toxic goiter, in most cases, a relatively short history is characteristic: the first symptoms usually appear 4-6 months before going to the doctor and making a diagnosis. As a rule, 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 sensations of palpitations. Patients can feel heartbeats not only in the chest, but also in the head, arms, and abdomen. Heart rate at rest with sinus tachycardia due to 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 arrhythmias, namely atrial fibrillation (fibrillation). 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, a catabolic syndrome is expressed, manifested by progressive weight loss (sometimes by 10-15 kg or more, especially in individuals with initial excess weight) against the background of increasing weakness and increased appetite. The skin of patients is hot, sometimes there is a pronounced hyperhidrosis. A feeling of heat is characteristic, patients do not freeze at a sufficiently low temperature in the room. In some patients (especially in the elderly) evening subfebrile condition may be detected.
Changes in the nervous system are characterized by mental lability: episodes of aggressiveness, excitement, chaotic unproductive activity are replaced by tearfulness, asthenia (irritable weakness). Many patients are not critical to 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 psyche and personality of the patient. A frequent but nonspecific symptom of thyrotoxicosis is a fine tremor: a fine tremor of the fingers of outstretched hands is detected in most patients. In severe thyrotoxicosis, tremor can be determined 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 recurrent sharp attacks of muscle weakness. In a laboratory study, hypokalemia and an increase in the level of CPK are detected. It is more common in representatives of the Asian race.
Intensification of bone resorption leads to the development of osteopenia syndrome, and thyrotoxicosis itself is considered as one of the most important risk factors for osteoporosis. Frequent complaints of patients are hair loss, brittle nails.
Changes in the gastrointestinal tract develop quite rarely. Elderly patients in some cases may have diarrhea. With long-term severe thyrotoxicosis, dystrophic changes in the liver (thyrotoxic hepatosis) may develop.
Menstrual irregularities are 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 have symptoms of thyroid (relative) adrenal insufficiency, which must be differentiated from the true one. To the already listed symptoms are added hyperpigmentation of the skin, exposed parts of the body (Jellinek's symptom), arterial hypotension.
In most cases, with diffuse toxic goiter, there is an increase in the size of the thyroid gland, which, as a rule, has a diffuse character. Often, the gland is enlarged significantly. In some cases, a systolic murmur can be heard above the thyroid gland. Nevertheless, 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 unequivocally indicates precisely 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 already obvious when examining the patient.
The clinical picture of thyrotoxicosis may have deviations from the classical variant. So, 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 (cardiac arrhythmia, subfebrile condition). In the "apathetic" variant of the course of diffuse toxic goiter, which occurs in elderly patients, clinical manifestations include loss of appetite, depression, 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 a prohibitive increase in the level of thyroid hormones in the blood. The cause of a thyrotoxic crisis may be acute infectious diseases associated with diffuse toxic goiter, surgical intervention or radioactive iodine therapy against the background of severe thyrotoxicosis, cancellation of thyrostatic therapy, administration of a contrast iodine-containing drug to the patient.
Clinical manifestations of a thyrotoxic crisis include a sharp increase in the symptoms of thyrotoxicosis, hyperthermia, confusion, nausea, vomiting, and sometimes diarrhea. Sinus tachycardia over 120 beats / min is recorded. Often there is atrial fibrillation, high pulse pressure, followed by severe hypotension. The clinical picture may be dominated by heart failure, respiratory distress syndrome. Often expressed manifestations of relative adrenal insufficiency in the form of hyperpigmentation of the skin. The skin may be icteric due to the development of toxic hepatosis. In a laboratory study, leukocytosis (even in the absence of concomitant infection), moderate hypercalcemia, and an increase in the level of alkaline phosphatase can be detected. Mortality in thyrotoxic crisis reaches 30-50%.

The International Statistical Classification of Diseases and Related Health Problems is a document developed under the leadership of WHO to provide a unified approach to the methods and principles of treating diseases.

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

Principles of classification of endocrine diseases

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

• Congenital iodine deficiency syndrome (E00 - E00.9)
• Diseases of the thyroid gland 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 number of pathological conditions that have their own characteristics - both in the causes of occurrence and in diagnostic methods. Therefore, the treatment protocol is determined by the totality of all factors and taking into account the severity of the condition.

The disease, its causes and classic symptoms

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

Despite the fact that thyroid diseases are diverse, often the causes of their occurrence are similar. And in some cases, it is not possible to establish it exactly, 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, the 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 trend:

• discomfort in the neck, tightness, difficulty swallowing;
• weight loss without changing the diet;
• violation of the sweat glands - excessive sweating or dryness of the skin can be observed;
• sudden mood swings, susceptibility to depression or excessive nervousness;
• decrease in the sharpness of thinking, memory impairment;
• complaints about the work of the digestive tract (constipation, diarrhea);
• malfunctions of the cardiovascular system - tachycardia, arrhythmia.

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

Some thyroid diseases are less common than others due to various objective and subjective reasons. Consider 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. Anything below this limit is an expansion of the follicle.

It is a mature, benign tumor that 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 the 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 such a failure, the body produces antibodies that begin to "attack" their own thyroid cells, saturate them with leukocytes, which causes inflammation. Over time, your own cells are destroyed, stop producing the right amount of hormones and a pathological condition called hypothyroidism occurs.

eutheria

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, such a condition can be asymptomatic and last a lifetime, and a person will not even be aware of 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) - a neoplasm in the thickness of the thyroid gland, which can be either abdominal or epithelial. A single node is rarely formed and indicates the beginning of the process of neoplasms in the form of multiple nodes.

Goiter multinodular

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

diffuse goiter

It is characterized by a 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 (an increase in the size of an organ without affecting hormonal function), hypothyroid (a decrease in hormone production), hyperthyroid (an increase in 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 that is characterized by underdevelopment of the organ. If this disease occurs during life, then it is called thyroid atrophy.

thyroid cancer

One of the rare pathologies that is detected only by 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 with very large sizes and untimely treatment.

For diagnostics, the following methods are used:

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

In some cases, treatment may not be required at all if the size of the neoplasms is very small. The specialist simply observes the condition of the patient. 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-treatment is unacceptable, since the pathological process requires the control and correction of a specialist.

If there are clear indications, surgical measures are taken when the part of the organ that is subject to the pathological process is removed, or the entire organ.

Treatment of autoimmune diseases of the thyroid gland has several differences:

• medication - aimed at destroying excess hormones;
• radioactive iodine treatment or surgery - leads to the destruction of the gland, which entails hypothyroidism;
• computer reflexology is designed to restore the functioning of the gland.

Thyroid disease, especially in the modern world, is a fairly common phenomenon. If you turn to a specialist in time and carry out all the necessary therapeutic measures, you can significantly improve the quality of life, and in some cases completely get rid of the disease.

The concept of nodular goiter in ICD 10 revision

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

Speaking of nodular goiter, it is important to remember that this concept summarizes 10 different forms of thyroid diseases in microbial units, 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-site depending on the quantity. At the same time, this disease can cause a visible cosmetic defect, which is 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, the ICD 10 revision nevertheless laid the basis for the classification not only morphology, but also the causes of occurrence, highlighting:

• Endemic goiter due to iodine deficiency
• non-toxic goiter
• thyretoxicosis

Endemic goiter with iodine deficiency

According to microbial 10, this nosological unit belongs to the 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. You 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, with the only difference being at what stage the body lacks this element. If the deficiency is caused by a violation of the 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. An absolute deficiency occurs in endemic areas where water, soil and food are critically low in iodine.

Pathogenesis

With iodine deficiency, the synthesis of T3 and T4 hormones decreases and, according to the type of 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 may become isolated, that is, with the formation of a nodular goiter or diffuse. However, a mixed type is not excluded.

sporadic forms

In ICD 10, under the code E04, non-toxic forms of goiter are considered. Scientists are still talking about the conditionality of dividing this term into the concept of endemic and sporadic, since the pathogenesis and causes of the latter have not been fully elucidated. In microbial 10 revision, the non-toxic form is divided into single-nodular, multi-nodular and diffuse.

Etiology

Genetic factors in the development of the sporadic form play an important role. 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 the X chromosome are more prone to it. As a result, the body may change the sensitivity threshold to iodine deficiency, as well as to thyroid-stimulating stimulation. The classical reasons include the lack of the amino acid tyrosine, which is necessary for the synthesis of thyroxine. Taking medications containing perchlorates, lithium salts, thiourea.

Under the code E05 in microbial 10, thyrotoxicosis syndrome is separately indicated. This clinical syndrome is due to 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, the concept of the forms of this severe pathology is given. It also lists and characterizes the degree of development of the disease with visual photos and videos.

Severe chronic endocrine disease - diffuse goiter of the thyroid gland, the symptoms of which come from almost all systems of the human body, has 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 growth 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.

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

1. Psychic trauma.
2. Diseases of an infectious-toxic nature.
3. Organic lesions of brain structures (trauma, encephalitis).
4. autoimmune pathologies.
5. Smoking (see Thyroid gland and smoking: dangers lie in wait).
6. Endocrine disorders and so on.

Further, thyroid hormones produced with a significant excess of the norms accelerate metabolic reactions, which leads to a rapid depletion of energy resources, both the tissues of individual organs and the entire human body in general. First of all, the structural elements of the central nervous and cardiovascular systems suffer. A detailed description of all stages of the development of pathology describes the video in this article.

Classification

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

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

1. Zero - no goiter.
2. The first - 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. The second - Goiter is determined both by palpation and visually.

Goiter, depending on the form, it happens:

1. diffuse.
2. Nodal.
3. Diffuse-nodular (mixed).

According to the severity of the process:

1. Easy degree.
2. Average.
3. Heavy.

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

1. Euthyroid.
2. Hypothyroid.

According to localization, it can be:

1. Ordinary.
2. Partially chesty.
3. Koltsev.
4. Dystopirovannym from the bookmarks of the embryo.

The symptomatology of the disease depends on all the characteristics mentioned in the classification.

Manifestations of the disease, depending on the severity of the course 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. With a mild form, 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 is added, reaching 10 kg within a month.
3. The severe form is characterized by progressive weight loss, up to cachexia. In addition, the first signs of impaired functioning of the heart, as well as the liver and kidneys, appear.

A severe form of the development 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 proper knowledge try to cope with this disease on their own.

Features of the manifestation of the euthyroid state

Since the thyroid gland functions normally with euthyroid goiter, the clinical picture depends entirely on the degree of enlargement of the gland. The zero degree against the background of maintaining the normal working capacity of the organ is absolutely not manifested. As the size of the thyroid gland increases, its influence on other body systems appears and gradually increases.

For example, euthyroid goiter, diffuse 1st degree, the symptoms are not yet very obvious:

1. General weakness.
2. Increased fatigue.
3. Headache.
4. Behind the sternum, in the projection of the heart, unpleasant sensations appear.

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

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

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 increase in the thyroid gland, provided there are no local seals 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 gland pathologies in terms of frequency of occurrence.

The first stages of the disease can give meager symptoms or not give it at all. But the 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 WHO international classification or in five according to the Russian one:

• Zero degree (I according to WHO). No symptoms, discovered incidentally during examination of other organs
• First degree (I according to WHO). It is manifested by a slight increase in the patient's weight, an unreasonable decrease in body temperature, chronic fatigue, hypotension.
• Second degree (II according to WHO). It is manifested by problems with swallowing, pain in the head and neck when performing torso and head tilts. Since diffuse nodular goiter, the symptoms of which gradually increase, continues to grow and increase hormone production, manifestations of hyperthyroidism begin to join, blood pressure rises, edema, exophthalmos, pathological psychomotor reactions, and tremor appear. Also, due to compression of the trachea by the tissues of the thyroid gland, shortness of breath develops.
• Third degree (II according to WHO). At this stage of its development, diffuse nodular goiter of the thyroid gland demonstrates symptoms even more pronounced. The cardiovascular, endocrine and nervous systems suffer. The shape of the neck has been greatly changed. The skin is either dry or waterlogged due to excess production of iodine-containing hormones, it develops a reddish tint. From the gastrointestinal tract - diarrhea alternates with constipation. The patient is concerned about severe tremor, hypotension, bradycardia up to 40 beats/min or tachycardia over 100 beats/min. Despite increased appetite, patients lose weight. Changing the position of the head 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). The extreme severity of the course of the disease is characterized, in which many systems of the human body suffer: endocrine, nervous, digestive, cardiovascular. Sometimes death is possible. The size of the goiter is huge, which decorously changes the appearance of the patient. His voice becomes hoarse or completely disappears. Decreased intelligence, memory, reproductive functions.

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.

Cretinism is one of the strongest manifestations of the depletion of thyroid gland resources - hypothyroidism, which developed in childhood. It is characterized by a pronounced lag in physical, mental, mental and intellectual development, short stature, tongue-tied tongue, slow maturation of the bones, and in some cases deaf-mutism.

Separate 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 that are characteristic of this disease in hyperthyroidism.

The cardiovascular system

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

1. Tachycardia at rest (up to 130 beats / min), in which the pulsation is felt in various parts of the body, such as the arms, abdomen, head, chest.
2. Rise in systolic blood pressure and fall in diastolic.
3. Severe myocardial dystrophy (especially in the elderly).
4. Cardiosclerosis.

Violations of the cardiovascular system are a direct threat to the life of the patient. The fight against them should be carried out jointly by endocrinologists and cardiologists, and patients should clearly follow the treatment instructions developed by these specialists.

catabolic syndrome

It is characterized by the following manifestations:

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

The latter manifestation is characterized by a constant sensation of heat, due to which patients do not freeze even at a noticeably low ambient temperature.

organs of vision

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

1. Expansion of the eye slits.
2. Incomplete closure of the eyelids, leading to "sand in the eyes", dryness of the mucous membrane of the eyes, chronic conjunctivitis.
3. bug-eyed.
4. Glitter of 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 the 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. Tremor of varying severity.
4. Muscle weakness with a decrease in the volume of the muscles of the limbs.
5. Increased tendon reflexes.

In severe forms of thyrotoxicosis, patients may develop stable mental disorders of the patient and his personality.

Skeleton bones

The 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 and density.
3. Pain in the bones.

The fingers on the hands 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 degeneration of the liver and cirrhosis.

Endocrine glands

Since all the components of the endocrine system are interconnected, thyroid disorders lead 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 open areas).
2. Hypotension.

Disruption of the ovaries due to thyrotoxicosis is a rather rare phenomenon in which such 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

In patients with thyrotoxicosis, there is an increase in 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 acropachia.

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.

In order for diffuse goiter not to reach its late stages and not endanger not only health, but also the life of the patient, when the first signs of the disease appear, you should immediately contact a therapist or endocrinologist.

The human body is a reasonable and fairly balanced mechanism.

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There are no people in the world who have never had ARVI (acute respiratory viral diseases) ...

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Thyroid gland code for microbial code 10

Nodular goiter code according to ICD 10: how is it indicated and what is the classifier for?

The International Classification of Diseases in the tenth revision or ICD 10 is designed to group information about diseases depending on the type and stage of progression. A special coding has been created from numbers and uppercase Latin letters to indicate pathologies. Thyroid ailments assigned section IV. Nodular goiter has its own ICD 10 codes as a type of endocrinological disease.

Types of illness according to the classifier

The normative volume of the thyroid gland is 18 cm in women and 25 in men. Exceeding the size usually indicates the development of a goiter.

The disease is a significant proliferation of thyroid cells, provoked by its dysfunction or structural deformation. In the first case, the toxic form of the disease is diagnosed, in the second, the euthyroid form. This disease often affects people living in areas with land that is not rich in iodine.

Nodular goiter is not a single ailment, but rather a clinical syndrome, which includes formations of various sizes and structures that form in the region of the thyroid gland. When diagnosing, the medical term "struma" is also used, which means an increase in the thyroid gland.

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

1. Diffuse endemic goiter;
2. Multinodular endemic goiter;
3. Goiter endemic, unspecified;
4. Non-toxic diffuse goiter;
5. Non-toxic single-nodular goiter;
6. Non-toxic multinodular goiter;
7. Other specified species;
8. Non-toxic goiter, unspecified.

The non-toxic species, unlike the toxic species, does not affect the production of hormones, and the provocateur of the growth of the thyroid gland is its morphological changes.

Even when the defect becomes visible to the naked eye, it is impossible to identify the sources and form of pathology without additional examination and laboratory tests. To establish a reliable diagnosis, an ultrasound scan and the result of a blood test for hormones are required.

Diffuse endemic goiter

The most common type of this disease is diffuse endemic goiter. E01.0 is its ICD code 10. Its root cause is acute or persistent iodine deficiency.

Main symptoms:

• prostration;
• indifference to life circumstances;
• migraine or dizziness;
• feeling of tightness in the throat;
• difficulty swallowing;
• sweating;
• disorder of the digestive system.

As the disease progresses, due to the reduced level of thyroid hormones, pain in the heart may appear. In some situations, surgery will be needed. Surgical intervention is indicated with a significant growth of cysts, when, for example, a patient has a diffuse toxic goiter of an advanced stage.

This is usually an endemic disease. As its prevention, it is necessary to expand the diet with iodine-rich foods and courses of vitamins.

Multinodular endemic species

This species has been assigned the code E01.1. The disease is characterized by the formation of several pronounced formations that increase due to a lack of iodine in a particular region.

Symptoms:

• hoarse or hoarse voice;
• pain in the throat;
• It's difficult to breathe;
• dizzy.

These signals become noticeable when the disease is already progressing. Prior to this, some patients report increased drowsiness and constant fatigue.

Unspecified endemic goiter

Its ICD 10 code is E01.2. This type of disease is provoked by a territorial deficiency of iodine.

It does not have a set of characteristic features, and the doctor cannot establish the type of disease even based on the results of a deep examination. Diagnosis is based on endemic characteristics.

Diffuse non-toxic appearance

Its code is E04.0. A distinctive feature of the disease is the growth of the thyroid gland without affecting its activity. The source of the disease is autoimmune defects in the structure of the thyroid gland.

The pathological process is evidenced by:

• headache;
• feeling of suffocation;
• typical neck distortion.

Some endocrinologists are of the opinion that the euthyroid species does not require treatment if it does not cause narrowing of the esophagus and trachea and does not provoke a spasmodic cough and pain.

Non-toxic uninodular goiter

This euthyroid goiter has the ICD10 code E04.1. This type is determined by a single neoplasm on the thyroid gland. With late-started or illiterate treatment, the knot causes significant inconvenience, and with the development of the disease, a noticeable bulge forms on the neck.

The progression of the disease leads to squeezing of nearby organs and causes severe consequences:

• violations of the functionality of the cardiovascular system;
• voice changes, breathing problems;
• difficulty swallowing leading to indigestion;
• dizziness and headaches.

Non-toxic multi-node view

This type in ICD 10 is designated by the code E04.2. It is distinguished by the presence of several clearly marked formations. The nodes are arranged asymmetrically. They usually cause less discomfort than single-nodular pathologies.

Other specified types of non-toxic goiter

By code E04.8 pass:

1. diseases characterized by diffuse proliferation of tissues and the formation of nodes. This is called the "diffuse-nodular" form of the disease.
2. pathologies characterized by the growth and adhesion of nodes - a conglomerate form.

Such neoplasms are noted in 25% of cases of the disease.

Unspecified non-toxic species

This type is assigned the code E04.9 in ICD 10. It is set when the analysis specialist rejects the toxic form of the disease, but cannot determine what specific change in the structure of the thyroid gland is present. Symptoms in such situations are versatile, and the examination does not give a complete picture.

Separate codes are assigned to thyrotoxicosis, which often causes goiter. This disease, otherwise called hyperthyroidism, according to the ICD 10 classifier is indicated as follows:

E05.0 - Thyrotoxicosis with diffuse goiter;

E05.1 - Thyrotoxicosis with toxic single-nodular goiter;

E05.2 - Thyrotoxicosis with toxic multinodular goiter

E05.3 - Thyrotoxicosis with ectopic thyroid tissue

E05.4 - Artificial thyrotoxicosis;

E05.5 Thyroid crisis or coma

What is ICD 10 for?

This classification was created to take into account and analyze the clinical picture of diseases, for a statistical study of the causes of death in various regions.

The classifier makes it possible to quickly establish a diagnosis and choose the most effective treatment regimen.

myzhelezy.ru

ICD-10: types of goiter

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

To designate diseases, a special encoding has been developed, in which capital letters of the Latin alphabet and numbers are used.

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 - a clearly defined increase in thyroid tissue that occurs due to 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 poor iodine soils - these are mountainous areas, areas far from the sea.

An 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-site;
6. Other specified species;
7. Endemic, unspecified;
8. Non-toxic, unspecified.

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

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

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

For accurate diagnosis, all patients need to undergo ultrasound examinations, donate blood for hormones.

Diffuse endemic process

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

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

Patients experience:

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

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

In severe cases, surgical intervention and removal of the goiter are indicated.

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

Multinodal endemic process

This species has the 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 with the progression of the disease, the symptoms become pronounced.

At the initial stage, fatigue, 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 area of ​​the thyroid gland with no change in functionality.

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

• headache;
• suffocation;
• characteristic deformity of the neck.

Complications in the form of hemorrhages are possible.

Some doctors believe that a euthyroid goiter can be left untreated until it narrows the esophagus and trachea and causes pain and a 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 node brings discomfort with improper or untimely treatment.

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

When the node grows, the nearby organs are squeezed, which leads to serious problems:

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

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

Goiter, unspecified, endemic

It has an ICD 10 code - E01.2.

This type is due to territorial iodine deficiency.

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

The disease is assigned on an endemic basis.

Non-toxic multi-site process

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

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

The centers are usually located asymmetrically.

Other types of non-toxic goiter (specified)

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

1. Pathology, in which both diffuse proliferation of tissues and the formation of nodes were revealed - 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 the examination, rejects the toxic form of the disease, but cannot determine which pathology of the thyroid gland structure is present.

The symptoms in this case are versatile, the analyzes do not represent the full picture.

How will ICD 10 help?

This classification was developed primarily for the accounting and comparison of the clinic of diseases, for the statistical analysis of mortality in certain areas.

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

proshhitovidku.ru

ICD-10: E00-E07 - Diseases of the thyroid gland

Diagnosis code E00-E07 includes 8 clarifying diagnoses (ICD-10 headings):

1. E00 - Congenital iodine deficiency syndrome Contains 4 blocks of diagnoses. Included: endemic conditions associated with iodine deficiency in the natural environment, both directly and due to iodine deficiency in the mother's body. Some of these conditions cannot be considered true hypothyroidism, but are the result of inadequate secretion of thyroid hormones in the developing fetus; there may be a connection with natural goiter factors. If necessary, to identify the accompanying mental retardation, use an additional code (F70-F79). Excludes: subclinical hypothyroidism due to iodine deficiency (E02).
2. E01 - Thyroid diseases associated with iodine deficiency and similar conditions Contains 4 blocks of diagnoses. Excludes: congenital iodine deficiency syndrome (E00.-) subclinical hypothyroidism due to iodine deficiency (E02).
3. E02 - Subclinical hypothyroidism due to iodine deficiency
4. E03 - Other forms of hypothyroidism Contains 8 blocks of diagnoses.
5. E04 - Other forms of non-toxic goiter Contains 5 blocks of diagnoses. Excludes: congenital goiter: . NOS ) . diffuse ) (E03.0) . parenchymal) goiter associated with iodine deficiency (E00-E02).
6. E05 - Thyrotoxicosis [hyperthyroidism] Contains 8 blocks of diagnoses. Excludes: chronic thyroiditis with transient thyrotoxicosis (E06.2) neonatal thyrotoxicosis (P72.1).
7. E06 - Thyroiditis Contains 7 blocks of diagnoses. Excludes: postpartum thyroiditis (O90.5).
8. E07 - Other diseases of the thyroid gland Contains 4 blocks of diagnoses.

Additional information about the diagnosis E00-E07 is not available in the ICD-10 classifier.

mkb10.su

Diffuse nodular goiter or hyperplasia of the thyroid gland - microbial code 10

In order to figure out which diffuse nodular goiter has a code for microbial 10 and what it means, you need to figure out what the designation "microbial 10" is. It stands for "International Classification of Diseases" and is a regulatory document whose task is to combine 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.

Classification

If we talk about diffuse nodular goiter, it should be remembered that the classification according to microbial 10 combines into a group various pathologies of the thyroid gland, which differ both in the causes of appearance and in morphology. These are nodular neoplasms in the tissues of the thyroid gland (single-nodular and multi-nodular), and pathological growth 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 be felt only during palpation, others, in general, are determined only when using ultrasound.

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

Class IV. Diseases of the endocrine system, eating disorders and metabolic disorders (E00-E90)

Note. All neoplasms (both functionally active and inactive) are included in class II. Appropriate codes in this class (for example, E05.8, E07.0, E16-E31, E34.-) can be used as additional codes, if necessary, to identify functionally active neoplasms and ectopic endocrine tissue, as well as hyperfunction and hypofunction of the endocrine glands, associated with neoplasms and other disorders classified elsewhere.
Excludes: complications of pregnancy, childbirth and the puerperium (O00-O99), symptoms, signs and abnormal findings from clinical and laboratory investigations, not elsewhere classified (R00-R99), transient endocrine and metabolic disorders, specific for fetus and newborn (P70-P74)

This class contains the following blocks:
E00-E07 Diseases of the thyroid gland
E10-E14 Diabetes mellitus
E15-E16 Other disorders of glucose regulation and pancreatic endocrine secretion
E20-E35 Disorders of other endocrine glands
E40-E46 Malnutrition
E50-E64 Other types of malnutrition
E65-E68 Obesity and other types of malnutrition
E70-E90 Metabolic disorders

The following categories are marked with an asterisk:
E35 Disorders of the endocrine glands in diseases classified elsewhere
E90 Nutritional and metabolic disorders in diseases classified elsewhere

THYROID DISEASES (E00-E07)

E00 Congenital iodine deficiency syndrome

Includes: endemic conditions associated with iodine deficiency in the natural environment, both directly and
and due to iodine deficiency in the mother's body. Some of these conditions cannot be considered true hypothyroidism, but are the result of inadequate secretion of thyroid hormones in the developing fetus; there may be a connection with natural goiter factors. If necessary, to identify the accompanying mental retardation, use an additional code (F70-F79).
Excludes: subclinical hypothyroidism due to iodine deficiency (E02)

E00.0 Syndrome of congenital iodine deficiency, neurological form. Endemic cretinism, neurological form
E00.1 Syndrome of congenital iodine deficiency, myxedematous form.
Endemic cretinism:
. hypothyroid
. myxedematous form
E00.2 Syndrome of congenital iodine deficiency, mixed form.
Endemic cretinism, mixed form
E00.9 Congenital iodine deficiency syndrome, unspecified.
Congenital hypothyroidism due to iodine deficiency NOS. Endemic cretinism NOS

E01 Thyroid disorders associated with iodine deficiency and related conditions

Excludes: congenital iodine deficiency syndrome (E00.-)
subclinical hypothyroidism due to iodine deficiency (E02)

E01.0 Diffuse (endemic) goiter associated with iodine deficiency
E01.1 Multinodular (endemic) goiter associated with iodine deficiency. Nodular goiter associated with iodine deficiency
E01.2 Goiter (endemic) associated with iodine deficiency, unspecified. Endemic goiter NOS
E01.8 Other thyroid diseases associated with iodine deficiency and related conditions.
Acquired hypothyroidism due to iodine deficiency NOS

E02 Subclinical hypothyroidism due to iodine deficiency

E03 Other forms of hypothyroidism

Excludes: hypothyroidism associated with iodine deficiency (E00-E02)
hypothyroidism following medical procedures (E89.0)

E03.0 Congenital hypothyroidism with diffuse goiter.
Goiter (non-toxic) congenital:
. NOS
. parenchymal
E03.1 Congenital hypothyroidism without goiter. Aplasia of the thyroid gland (with myxedema).
Congenital:
. atrophy of the thyroid gland
. hypothyroidism NOS
E03.2 Hypothyroidism caused by drugs and other exogenous substances.
If it is necessary to identify the cause, use an additional external cause code (class XX).
E03.3 Post-infectious hypothyroidism
E03.4 Thyroid atrophy (acquired).
Excludes: congenital atrophy of thyroid gland (E03.1)
E03.5 Myxedema coma
E03.8 Other specified hypothyroidisms
E03.9 Hypothyroidism, unspecified. Myxedema NOS

E04 Other forms of non-toxic goiter

Excludes: congenital goiter:
. NOS )
. diffuse ) (E03.0)
. parenchymal)
goiter associated with iodine deficiency (E00-E02)

E04.0 Non-toxic diffuse goiter.
Goiter non-toxic:
. diffuse (colloidal)
. simple
E04.1 Non-toxic single nodular goiter. Colloidal node (cystic) (thyroid).
Non-toxic mononodous goiter. Thyroid (cystic) nodule NOS
E04.2 Non-toxic multinodular goiter. Cystic goiter NOS. Polynodous (cystic) goiter NOS
E04.8 Other specified forms of non-toxic goiter
E04.9 Nontoxic goiter, unspecified. Goiter NOS. Nodular goiter (nontoxic) NOS

E05 Thyrotoxicosis [hyperthyroidism]

Excludes: chronic thyroiditis with transient thyrotoxicosis (E06.2)
neonatal thyrotoxicosis (P72.1)

E05.0 Thyrotoxicosis with diffuse goiter. Exophthalmic or toxic call NOS. Graves' disease. Diffuse toxic goiter
E05.1 Thyrotoxicosis with toxic single-nodular goiter. Thyrotoxicosis with toxic mononodous goiter
E05.2 Thyrotoxicosis with toxic multinodular goiter. Toxic nodular goiter NOS
E05.3 Thyrotoxicosis with ectopic thyroid tissue
E05.4 Thyrotoxicosis artificial
E05.5 Thyroid crisis or coma
E05.8 Other forms of thyrotoxicosis. Hypersecretion of thyroid-stimulating hormone.

E05.9 Thyrotoxicosis, unspecified. Hyperthyroidism NOS. Thyrotoxic heart disease (I43.8)

E06 Thyroiditis

Excludes: postpartum thyroiditis (O90.5)

E06.0 Acute thyroiditis. Thyroid abscess.
Thyroiditis:
. pyogenic
. purulent
If necessary, an additional code (B95-B97) is used to identify the infectious agent.
E06.1 Subacute thyroiditis.
Thyroiditis:
. de Quervain
. giant cell
. granulomatous
. nonpurulent
Excludes: autoimmune thyroiditis (E06.3)
E06.2 Chronic thyroiditis with transient thyrotoxicosis.
Excludes: autoimmune thyroiditis (E06.3)
E06.3 Autoimmune thyroiditis. Hashimoto's thyroiditis. Chasitoxicosis (transient). Lymphoadenomatous goiter.
Lymphocytic thyroiditis. Lymphomatous struma
E06.4 Medical thyroiditis
E06.5 Thyroiditis:
. chronic:
. NOS
. fibrous
. woody
. Riedel
E06.9 Thyroiditis, unspecified

E07 Other thyroid disorders

E07.0 hypersecretion of calcitonin. C-cell hyperplasia of the thyroid gland.
Hypersecretion of thyrocalcitonin
E07.1 Dishormonal goiter. Family dyshormonal goiter. Syndrome Pendred.
Excludes: transient congenital goiter with normal function (P72.0)
E07.8 Other specified diseases of the thyroid gland. Tyrosine-binding globulin defect.
hemorrhage)
Heart attack) (in) the thyroid gland (s)
Syndrome of impaired euthyroidism
E07.9 Thyroid disease, unspecified

DIABETES (E10-E14)

If necessary, to identify the drug that caused diabetes, use an additional external cause code (class XX).

The following fourth characters are used with categories E10-E14:
.0 Coma
Diabetic:
. coma with or without ketoacidosis (ketoacidotic)
. hypermolar coma
. hypoglycemic coma
Hyperglycemic coma NOS

1 With ketoacidosis
Diabetic:
. acidosis)
. ketoacidosis) with no mention of coma

2 With kidney damage
Diabetic nephropathy (N08.3)
Intracapillary glomerulonephrosis (N08.3)
Kimmelstiel-Wilson syndrome (N08.3)

3 With ocular lesions
Diabetic:
. cataract (H28.0)
. retinopathy (H36.0)

4 With neurological complications
Diabetic:
. amyotrophy (G73.0)
. autonomic neuropathy (G99.0)
. mononeuropathy (G59.0)
. polyneuropathy (G63.2)
. autonomous (G99.0)

5 With peripheral circulatory disorders
Diabetic:
. gangrene
. peripheral angiopathy (I79.2)
. ulcer

6 With other specified complications
Diabetic arthropathy (M14.2)
. neuropathic (M14.6)

7 With multiple complications

8 With unspecified complications

9 No complications

E10 Insulin-dependent diabetes mellitus

[cm. the above headings]
Includes: diabetes (diabetes):
. labile
. with onset at a young age
. prone to ketosis
. type I
Excludes: diabetes mellitus:
. newborns (P70.2)
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)

E11 Non-insulin dependent diabetes mellitus

Includes: diabetes (diabetes) (non-obese) (obese):
. with onset in adulthood
. not prone to ketosis
. stable
. type II
Excludes: diabetes mellitus:
. associated with malnutrition (E12. -)
. neonates (P70.2)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

E12 Diabetes mellitus associated with malnutrition

[cm. above subheadings]
Includes: diabetes mellitus associated with malnutrition:
. insulin dependent
. non-insulin dependent
Excludes: diabetes mellitus during pregnancy, during childbirth
and in the puerperium (O24.-)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
neonatal diabetes mellitus (P70.2)
postoperative hypoinsulinemia (E89.1)

E13 Other specified forms of diabetes mellitus

[cm. above subheadings]
Excludes: diabetes mellitus:
. insulin dependent (E10.-)
. associated with malnutrition (E12. -)
. neonatal (P70.2)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

E14 Diabetes mellitus, unspecified

[cm. above subheadings]
Includes: diabetes NOS
Excludes: diabetes mellitus:
. insulin dependent (E10.-)
. associated with malnutrition (E12. -)
. neonates (P70.2)
. non-insulin dependent (E11.-)
. during pregnancy, during childbirth and postpartum
period (O24. -)
glycosuria:
. NOS (R81)
. renal (E74.8)
impaired glucose tolerance (R73.0)
postoperative hypoinsulinemia (E89.1)

OTHER DISORDERS OF GLUCOSE AND INTERNAL SECRETION REGULATION

PANCREAS (E15-E16)

E15 Non-diabetic hypoglycemic coma. Non-diabetic insulin coma caused by drugs
means. Hyperinsulinism with hypoglycemic coma. Hypoglycemic coma NOS.
If necessary, to identify the drug that caused non-diabetic hypoglycemic coma, use an additional external cause code (class XX).

E16 Other disorders of internal secretion of the pancreas

E16.0 Medical hypoglycemia without coma.
If it is necessary to identify the medicinal product, use an additional code for external causes (class XX).
E16.1 Other forms of hypoglycemia. Functional non-hyperinsulinemic hypoglycemia.
Hyperinsulinism:
. NOS
. functional
Hyperplasia of pancreatic islet beta cells NOS. Encephalopathy after hypoglycemic coma
E16.2 Hypoglycemia, unspecified
E16.3 Increased secretion of glucagon.
Pancreatic islet cell hyperplasia with glucagon hypersecretion
E16.8 Other specified disorders of the internal secretion of the pancreas. Hypergastrinemia.
Hypersecretion:
. growth hormone releasing hormone
. pancreatic polypeptide
. somatostatin
. vasoactive intestinal polypeptide
Zollinger-Ellison Syndrome
E16.9 Violation of the internal secretion of the pancreas, unspecified. Islet cell hyperplasia NOS.
Hyperplasia of pancreatic endocrine cells NOS

DISORDERS OF OTHER ENDOCRINE GLANDS (E20-E35)

Excludes: galactorrhea (N64.3)
gynecomastia (N62)

E20 Hypoparathyroidism

Excludes: Di George syndrome (D82.1)
hypoparathyroidism following medical procedures (E89.2)
tetany NOS (R29.0)
transient hypoparathyroidism of the newborn (P71.4)

E20.0 Idiopathic hypoparathyroidism
E20.1 Pseudohypoparathyroidism
E20.8 Other forms of hypoparathyroidism
E20.9 Hypoparathyroidism, unspecified. Parathyroid tetagy

E21 Hyperparathyroidism and other disorders of the parathyroid [parathyroid] gland

Excludes: osteomalacia:
. in adults (M83.-)
. in childhood and adolescence (E55.0)

E21.0 Primary hyperparathyroidism. Hyperplasia of the parathyroid glands.
Generalized fibrous osteodystrophy [Recklinghausen's bone disease]
E21.1 Secondary hyperparathyroidism, not elsewhere classified.
Excludes: secondary hyperparathyroidism of renal origin (N25.8)
E21.2 Other forms of hyperparathyroidism.
Excludes: familial hypocalciuric hypercalcemia (E83.5)
E21.3 Hyperparathyroidism, unspecified
E21.4 Other specified parathyroid disorders
E21.5 Disease of the parathyroid glands, unspecified

E22 Hyperfunction of the pituitary gland

Excludes: Itsenko-Cushing's syndrome (E24.-)
Nelson's syndrome (E24.1)
hypersecretion:
. adrenocorticotropic hormone [ACTH], unrelated
with Itsenko-Cushing's syndrome (E27.0)
. pituitary ACTH (E24.0)
. thyroid-stimulating hormone (E05.8)

E22.0 Acromegaly and pituitary gigantism.
Arthropathy associated with acromegaly (M14.5).
Hypersecretion of growth hormone.
Excluded: constitutional:
. gigantism (E34.4)
. tall (E34.4)
hypersecretion of growth hormone-releasing hormone (E16.8)
E22.1 Hyperprolactinemia. If necessary, to identify the drug that caused hyperprolactinemia, use an additional code of external causes (class XX).
E22.2 Syndrome of inappropriate secretion of antidiuretic hormone
E22.8 Other states of hyperfunction of the pituitary gland. Precocious puberty of central origin
E22.9 Hyperfunction of the pituitary gland, unspecified

E23 Hypofunction and other disorders of the pituitary gland

Includes: listed conditions due to diseases of the pituitary and hypothalamus
Excludes: hypopituitarism following medical procedures (E89.3)

E23.0 Hypopituitarism. Fertile eunuchoid syndrome. Hypogonadotropic hypogonadism.
Idiopathic growth hormone deficiency.
Isolated deficiency:
. gonadotropin
. growth hormone
. other pituitary hormones
Kalmann syndrome
Short stature [dwarfism] Loreina-Levi
Pituitary necrosis (postpartum)
Panhypopituitarism
Pituitary :
. cachexia
. insufficiency NOS
. short stature [dwarfism]
Sheehan's syndrome. Simmonds disease
E23.1 Medical hypopituitarism.
E23.2 Diabetes insipidus.
Excludes: nephrogenic diabetes insipidus (N25.1)
E23.3 Hypothalamic dysfunction, not elsewhere classified.
Excludes: Prader-Willi syndrome (Q87.1), Russell-Silver syndrome (Q87.1)
E23.6 Other diseases of the pituitary gland. Abscess of the pituitary gland. Adiposogenital dystrophy
E23.7 Pituitary disease, unspecified

E24 Itsenko-Cushing's syndrome

E24.0 Itsenko-Cushing's disease of pituitary origin. Hypersecretion of ACTH by the pituitary.
Hyperadrenocorticism of pituitary origin
E24.1 Nelson syndrome
E24.2 Drug Itsenko-Cushing's syndrome.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E24.3 Ectopic ACTH syndrome
E24.4 Cushingoid syndrome caused by alcohol
E24.8 Other Conditions Characterized by Cushingoid Syndrome
E24.9 Itsenko-Cushing syndrome, unspecified

E25 Adrenogenital disorders

Includes: adrenogenital syndromes, virilization or feminization acquired or due to hyperplasia
adrenal glands, which is a consequence of congenital enzyme defects in the synthesis of hormones
female(s):
. adrenal false hermaphroditism
. heterosexual precocious false genitalia
maturity
male(s):
. isosexual precocious false genitalia
maturity
. early macrogenitosomia
. precocious puberty with hyperplasia
adrenal glands
. virilization (female)

E25.0 Congenital adrenogenital disorders associated with enzyme deficiency. Congenital adrenal hyperplasia. Deficiency of 21-hydroxylase. Congenital adrenal hyperplasia causing salt loss
E25.8 Other adrenogenital disorders. Idiopathic adrenogenital disorder.
If necessary, to identify the drug that caused the adrenogenital disorder, use an additional code of external causes (class XX).
E25.9 Adrenogenital disorder, unspecified. Adrenogenital syndrome NOS

E26 Hyperaldosteronism

E26.0 Primary hyperaldosteronism. Conn's syndrome. Primary aldosteronism due to hyperplasia of the supra-
kidney (bilateral)
E26.1 Secondary hyperaldosteronism
E26.8 Other forms of hyperaldosteronism. Barter syndrome
E26.9 Hyperaldosteronism, unspecified

E27 Other adrenal disorders

E27.0 Other types of hypersecretion of the adrenal cortex.
Hypersecretion of adrenocorticotropic hormone [ACTH] not associated with Itsenko-Cushing's disease.
Excludes: Itsenko-Cushing's syndrome (E24.-)
E27.1 Primary adrenal insufficiency. Addison's disease. Autoimmune inflammation of the adrenal glands.
Excludes: amyloidosis (E85.-), Addison's disease of tuberculous origin (A18.7), Waterhouse-Friderichsen syndrome (A39.1)
E27.2 Addisonian crisis. Adrenal crisis. adrenocortical crisis
E27.3 Drug insufficiency of the adrenal cortex. If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E27.4 Other and unspecified insufficiency of the adrenal cortex.
Adrenal(th):
. bleeding
. heart attack
Adrenocortical sufficiency NOS. Hypoaldosteronism.
Excludes: adrenoleukodystrophy [Addison-Schilder] (E71.3), Waterhouse-Friderichsen syndrome (A39.1)
E27.5 Hyperfunction of the adrenal medulla. Hyperplasia of the adrenal medulla.
Catecholamine hypersecretion
E27.8 Other specified disorders of the adrenal glands. Impaired cortisol-binding globulin
E27.9 Adrenal gland disease, unspecified

E28 Ovarian dysfunction

Excludes: isolated gonadotropic insufficiency (E23.0)
ovarian failure following medical procedures (E89.4)

E28.0 Excess estrogen. If necessary, to identify the drug that caused the excess estrogens, use an additional code of external causes (class XX).
E28.1 An excess of androgens. Hypersecretion of ovarian androgens. If necessary, to identify the drug that caused the androgen excess, use an additional code of external causes (class XX).
E28.2 Polycystic ovarian syndrome. Sclerocystic ovarian syndrome. Stein-Leventhal syndrome
E28.3 Primary ovarian failure. Low estrogen content. Premature menopause NOS.
Persistent ovarian syndrome.
Excl.: menopause and female climacteric status (N95.1)
pure gonadal dysgenesis (Q99.1)
Turner's syndrome (Q96.-)
E28.8 Other types of ovarian dysfunction. Ovarian hyperfunction NOS
E28.9 Ovarian dysfunction, unspecified

E29 Testicular dysfunction

azoospermia or oligospermia NOS (N46)
isolated gonadotropic insufficiency (E23.0)
Klinefelter's syndrome (Q98.0-Q98.2, Q98.4)
testicular hypofunction following medical procedures (E89.5)
testicular feminization (syndrome) (E34.5)

E29.0 Testicular hyperfunction. Hypersecretion of testicular hormones
E29.1 Testicular hypofunction. Impaired biosynthesis of testicular androgen NOS
5-alpha reductase deficiency (with male pseudohermaphroditism). Testicular hypogonadism NOS.
If necessary, to identify the drug that caused testicular hypofunction, use an additional
external cause code (class XX).
E29.8 Other types of testicular dysfunction
E29.9 Testicular dysfunction, unspecified

E30 Disorders of puberty, not elsewhere classified

E30.0 Delayed puberty. Constitutional delay in puberty.
Delayed puberty
E30.1 Precocious puberty. Premature menstruation.
Excludes: Albright(-McCune)(-Sternberg) syndrome (Q78.1)
precocious puberty of central origin (E22.8)
female heterosexual precocious false puberty (E25.-)
male isosexual precocious false puberty (E25.-)
E30.8 Other disorders of puberty. Premature thelarche
E30.9 Disorder of puberty, unspecified

E31 Polyglandular dysfunction

Excludes: telangiectatic ataxia [Louis Bar] (G11.3)
myotonic dystrophy [Steinert] (G71.1)
pseudohypoparathyroidism (E20.1)

E31.0 Autoimmune polyglandular insufficiency. Schmidt syndrome
E31.1 Polyglandular hyperfunction.
Excludes: multiple endocrine adenomatosis (D44.8)
E31.8 Other polyglandular dysfunction
E31.9 Polyglandular dysfunction, unspecified

E32 Diseases of the thymus

Excludes: aplasia or hypoplasia with immunodeficiency (D82.1), myasthenia gravis (G70.0)

E32.0 Persistent hyperplasia of the thymus. Hypertrophy of the thymus
E32.1 Abscess of the thymus
E32.8 Other diseases of the thymus
E32.9 Thymus disease, unspecified

E34 Other endocrine disorders

Excludes: pseudohypoparathyroidism (E20.1)

E34.0 carcinoid syndrome.
Note. If necessary, to identify the functional activity associated with a carcinoid tumor, you can use an additional code.
E34.1 Other conditions of hypersecretion of intestinal hormones
E34.2 Ectopic hormonal secretion, not elsewhere classified
E34.3 Short stature [dwarfism], not elsewhere classified.
Short stature:
. NOS
. constitutional
. laron type
. psychosocial
Excludes: progeria (E34.8)
Russell-Silver syndrome (Q87.1)
limb shortening with immunodeficiency (D82.2)
short stature:
. achondroplasty (Q77.4)
. hypochondroplastic (Q77.4)
. with specific dysmorphic syndromes
(code these syndromes; see index)
. alimentary (E45)
. pituitary (E23.0)
. renal (N25.0)
E34.4 Constitutional tallness. Constitutional gigantism
E34.5 Syndrome of androgen resistance. Male pseudohermaphroditism with androgen resistance.
Violation of peripheral hormonal reception. Reifenstein syndrome. Testicular feminization (syndrome)
E34.8 Other specified endocrine disorders. Dysfunction of the pineal gland. Progeria
E34.9 Endocrine disorder, unspecified.
Violation:
. endocrine NOS
. hormonal NOS

E35 Disorders of endocrine glands in diseases classified elsewhere

E35.0 Thyroid disorders in diseases classified elsewhere.
Thyroid tuberculosis (A18.8)
E35.1 Adrenal disorders in diseases classified elsewhere.
Addison's disease of tuberculous etiology (A18.7). Waterhouse-Friderichsen syndrome (meningococcal) (A39.1)
E35.8 Disorders of other endocrine glands in diseases classified elsewhere

malnutrition (E40-E46)

Note. The degree of malnutrition is usually assessed in terms of body weight, expressed in standard deviations from the mean value for the reference population. Lack of weight gain in children or evidence of decreased
A decrease in body weight in children or adults with one or more previous body weight measurements is usually an indicator of malnutrition. If there is evidence from only a single measurement of body weight, the diagnosis is based on assumptions and is not considered definitive unless other clinical and laboratory studies are performed. In exceptional cases, when there is no information about body weight, clinical data are taken as the basis. If an individual's body weight is below the mean for the reference population, then severe malnutrition is highly likely when the observed value is 3 or more standard deviations below the mean for the reference group; moderate malnutrition if the observed value is 2 or more but less than 3 standard deviations below the mean, and mild malnutrition if the observed body weight is 1 or more but less than 2 standard deviations below the mean for the reference group.

Excludes: intestinal malabsorption (K90.-)
nutritional anemia (D50-D53)
consequences of protein-energy malnutrition (E64.0)
wasting disease (B22.2)
starvation (T73.0)

E40 Kwashiorkor

Severe malnutrition accompanied by alimentary edema and pigmentation disorders of the skin and hair

E41 Alimentary insanity

Severe malnutrition accompanied by insanity
Excluded: senile kwashiorkor (E42)

E42 Marasmic kwashiorkor

Severe protein-energy malnutrition [as in E43]:
. intermediate form
. with symptoms of kwashiorkor and marasmus

E43 Severe protein-energy malnutrition, unspecified

Severe weight loss in a child or adult or no weight gain in a child that results in detectable weight being at least 3 standard deviations below the mean for the reference group (or similar weight loss reflected by other statistical methods) . If only a single measurement of body weight is available, severe wasting is highly likely when the detected body weight is 3 or more standard deviations below the mean for the reference population. hungry edema

E44 Moderate and mild protein-energy malnutrition

E44.0 Moderate protein-energy insufficiency. Weight loss in children or adults or lack of weight gain in a child that results in detectable body weight below the mean
for a reference population by 2 standard deviations or more but less than 3 standard deviations (or
similar weight loss reflected by other statistical methods). If only a single measurement of body weight is available, then moderate protein-energy malnutrition is highly likely when the detected body weight is 2 or more standard deviations below the mean for the reference population.

E44.1 Mild protein-energy malnutrition. Weight loss in children or adults or lack of weight gain in a child that results in detectable body weight below the mean
for a reference population by 1 or more but less than 2 standard deviations (or similar weight loss reflected by other statistical methods). If data from only a single measurement of body weight are available, then mild protein-energy malnutrition is highly likely when the detected body weight is 1 or more, but less than 2 standard deviations, below the mean for the reference population.

E45 Developmental delay due to protein-energy malnutrition

Alimentary:
. short stature (dwarfism)
. growth retardation
Delayed physical development due to malnutrition

E46 Protein-energy malnutrition, unspecified

Malnutrition NOS
Protein-energy imbalance NOS

OTHER MALNUTRITIONS (E50-E64)

Excludes: nutritional anemia (D50-D53)

E50 Vitamin A deficiency

Excludes: consequences of vitamin A deficiency (E64.1)

E50.0 Vitamin A deficiency with conjunctival xerosis
E50.1 Vitamin A deficiency with Byto's plaques and conjunctival xerosis. Bitot's plaque in a young child
E50.2 Vitamin A deficiency with corneal xerosis
E50.3 Vitamin A deficiency with corneal ulceration and xerosis
E50.4 Vitamin A deficiency with keratomalacia
E50.5 Vitamin A deficiency with night blindness
E50.6 Vitamin A deficiency with xerophthalmic corneal scars
E50.7 Other ocular manifestations of vitamin A deficiency. Xerophthalmia NOS
E50.8 Other manifestations of vitamin A deficiency.
Follicular keratosis) due to insufficiency
Xeoderma) vitamin A (L86)
E50.9 Vitamin A deficiency, unspecified. Hypovitaminosis A NOS

E51 Thiamine deficiency

Excludes: consequences of thiamine deficiency (E64.8)

E51.1 Take it.
Take take:
. dry form
. wet form (I98.8)
E51.2 Wernicke's encephalopathy
E51.8 Other manifestations of thiamine deficiency
E51.9 Thiamine deficiency, unspecified

E52 Nicotinic acid deficiency [pellagra]

Failure:
. niacin (-tryptophan)
. nicotinamide
Pellagra (alcoholic)
Excludes: consequences of nicotinic acid deficiency (E64.8)

E53 Deficiency of other B vitamins

Excludes: consequences of vitamin B deficiency (E64.8)
vitamin B12 deficiency anemia (D51.-)

E53.0 Riboflavin deficiency. Ariboflavinosis
E53.1 Pyridoxine deficiency. Vitamin B6 deficiency.
Excludes: pyridoxine-responsive sideroblastic anemia (D64.3)
E53.8 Deficiency of other specified B vitamins.
Failure:
. biotin
. cyanocobalamin
. folate
. folic acid
. pantothenic acid
. vitamin B12
E53.9 B vitamin deficiency, unspecified

E54 Ascorbic acid deficiency

Vitamin C deficiency. Scurvy.
Excludes: anemia due to scurvy (D53.2)
consequences of vitamin C deficiency (E64.2)

E55 Vitamin D deficiency

osteoporosis (M80-M81)
effects of rickets (E64.3)

E55.0 Rickets is active.
Osteomalacia:
. children's
. youthful
Excludes: rickets:
. intestinal (K90.0)
. Crown (K50.-)
. inactive (E64.3)
. renal (N25.0)
. vitamin D-resistant (E83.3)
E55.9 Vitamin D deficiency, unspecified. Avitaminosis D

E56 Deficiency of other vitamins

Excludes: consequences of other vitamin deficiencies (E64.8)

E56.0 Vitamin E deficiency
E56.1 Vitamin K deficiency.
Excludes: clotting factor deficiency due to vitamin K deficiency (D68.4)
vitamin K deficiency in newborn (P53)
E56.8 Deficiency of other vitamins
E56.9 Vitamin deficiency, unspecified

E58 Nutritional calcium deficiency

Excludes: disorders of calcium metabolism (E83.5)
consequences of calcium deficiency (E64.8)

E59 Alimentary deficiency of selenium

Keshan disease
Excludes: sequelae of selenium deficiency (E64.8)

E60 Nutritional zinc deficiency

E61 Insufficiency of other batteries

If necessary, to identify the medicinal product that caused the failure, use an additional external cause code (class XX).
Excludes: disorders of mineral metabolism (E83.-)
thyroid dysfunction associated with iodine deficiency (E00-E02)

E61.0 copper deficiency
E61.1 iron deficiency.
Excludes: iron deficiency anemia (D50.-)
E61.2 Magnesium deficiency
E61.3 Manganese deficiency
E61.4 Chromium deficiency
E61.5 Molybdenum deficiency
E61.6 Vanadium deficiency
E61.7 Deficiency of many nutrients
E61.8 Deficiency of other specified nutritional elements
E61.9 Deficiency of batteries, unspecified

E63 Other malnutrition

Excludes: dehydration (E86)
growth disorders (R62.8)
feeding problems of the newborn (P92. -)
consequences of malnutrition and other nutritional deficiencies (E64. -)

E63.0 Deficiency of essential fatty acids
E63.1 Unbalanced intake of food elements
E63.8 Other specified malnutrition
E63.9 Malnutrition, unspecified. Cardiomyopathy due to malnutrition NOS+ (I43.2)

E64 Sequelae of malnutrition and deficiencies of other nutrients

E64.0 Consequences of protein-energy insufficiency.
Excludes: developmental delay due to protein-energy malnutrition (E45)
E64.1 Consequences of vitamin A deficiency
E64.2 Consequences of vitamin C deficiency
E64.3 Consequences of rickets
E64.8 Consequences of other vitamin deficiencies
E64.9 Sequelae of nutritional deficiencies, unspecified

OBESITY AND OTHER OVERNUTRITION (E65-E68)

E65 Localized fat deposition

Fat pads

E66 Obesity

Excludes: adiposogenital dystrophy (E23.6)
lipomatosis:
. NOS (E88.2)
. painful [Dercum's disease] (E88.2)
Prader-Willi syndrome (Q87.1)

E66.0 Obesity due to excess intake of energy resources
E66.1 Obesity caused by medication.
If necessary, to identify the medicinal product, use an additional external cause code (class XX).
E66.2 Extreme obesity accompanied by alveolar hypoventilation. pickwick syndrome
E66.8 Other forms of obesity. Morbid obesity
E66.9 Obesity, unspecified. Simple obesity NOS

E67 Other types of power redundancy

Excludes: overeating NOS (R63.2)
consequences of overnutrition (E68)

E67.0 Hypervitaminosis A
E67.1 Hypercarotenemia
E67.2 Syndrome of megadoses of vitamin B6
E67.3 Hypervitaminosis D
E67.8 Other specified forms of overnutrition

E68 Consequences of oversupply

METABOLIC DISORDERS (E70-E90)

Excludes: androgen resistance syndrome (E34.5)
congenital adrenal hyperplasia (E25.0)
Ehlers-Danlos syndrome (Q79.6)
hemolytic anemias due to enzyme disorders (D55.-)
Marfan syndrome (Q87.4)
5-alpha-reductase deficiency (E29.1)

E70 Disorders of aromatic amino acid metabolism

E70.0 Classic phenylketonuria
E70.1 Other types of hyperphenylalaninemia
E70.2 Tyrosine metabolism disorders. Alkaptonuria. Hypertyrosinemia. Ochronosis. Tyrosinemia. Tyrosinosis
E70.3 Albinism.
Albinism:
. ophthalmic
. dermo-ocular
Syndrome:
. Chediaka (-Steinbrink) -Higashi
. cross
. Hermanski-Pudlaka
E70.8 Other metabolic disorders of aromatic amino acids.
Violations:
. histidine metabolism
. tryptophan metabolism
E70.9 Disorders of aromatic amino acid metabolism, unspecified

E71 Disorders of branched-chain amino acid metabolism and fatty acid metabolism

E71.0 Maple Syrup Disease
E71.1 Other types of metabolic disorders of branched chain amino acids. Hyperleucine isoleucinemia. Hypervalinemia.
Isovaleric acidemia. Methylmalonic acidemia. propionic acidemia
E71.2 Disorders of branched-chain amino acid metabolism, unspecified
E71.3 Fatty acid metabolism disorders. Adrenoleukodystrophy [Addison-Schilder].
Deficiency of muscle carnitine palmityltransferase.
Excludes: Refsum's disease (G60.1)
Schilder's disease (G37.0)
Zellweger syndrome (Q87.8)

E72 Other disorders of amino acid metabolism

Excludes: abnormal without evidence of disease (R70-R89)
violations:
. aromatic amino acid metabolism (E70. -)
. branched-chain amino acid metabolism (E71.0-E71.2)
. fatty acid metabolism (E71.3)
. metabolism of purines and pyrimidines (E79. -)
gout (M10.-)

E72.0 Amino acid transport disorders. cystinosis. Cystinuria.
Fanconi syndrome (-de Toni) (-Debre). Hartnap's disease. Low's syndrome.
Excludes: disorders of tryptophan metabolism (E70.8)
E72.1 Metabolic disorders of sulfur-containing amino acids. Cystationinuria.
Homocystinuria. Methioninemia. Deficiency of sulfite oxidase.
Excludes: transcobalamin II deficiency (D51.2)
E72.2 Urea cycle metabolic disorders. Argininemia. Argininosuccinic aciduria. Citrullinemia. Hyperammonemia.
Excludes: disorders of ornithine metabolism (E72.4)
E72.3 Metabolic disorders of lysine and hydroxylysine. Glutaric aciduria. Hydroxylysinemia. Hyperlysinemia
E72.4 Ornithine metabolism disorders. Ornithinaemia (types I, II)
E72.5 Glycine metabolism disorders. Hyperhydroxyprolinemia. Hyperprolinemia (types I, II). Non-ketone hyperglycinemia.
Sarcosinemia
E72.8 Other specified disorders of amino acid metabolism.
Violations:
. beta amino acid metabolism
. gamma-glutamyl cycle
E72.9 Amino acid metabolism disorders, unspecified

E73 Lactose intolerance

E73.0 Congenital lactase deficiency
E73.1 Secondary lactase deficiency
E73.8 Other types of lactose intolerance
E73.9 Lactose intolerance, unspecified

E74 Other disorders of carbohydrate metabolism

Excludes: increased secretion of glucagon (E16.3)
diabetes mellitus (E10-E14)
hypoglycemia NOS (E16.2)
mucopolysaccharidosis (E76.0-E76.3)

E74.0 Diseases of glycogen storage. Cardiac glycogenosis.
Disease:
. Andersen
. Corey
. Forbes
. Gersa
. McArdle
. pompe
. Tauri
. Gierke
Liver phosphorylase deficiency
E74.1 Fructose metabolism disorders. Essential fructosuria.
Fructose-1,6-diphosphatase deficiency. hereditary fructose intolerance
E74.2 Disorders of galactose metabolism. Galactokinase deficiency. Galactosemia
E74.3 Other disorders of absorption of carbohydrates in the intestine. Malabsorption of glucose-galactose.
Deficiency of sucrose.
Excludes: lactose intolerance (E73.-)
E74.4 Disorders of pyruvate metabolism and gluconeogenesis.
Failure:
. phosphoenolpyruvate carboxykinase
. pyruvate:
. carboxylase
. dehydrogenases
Excludes: with anemia (D55.-)
E74.8 Other specified disorders of carbohydrate metabolism. Essential pentosuria. Oxalosis. Oxaluria.
Renal glucosuria
E74.9 Disorder of carbohydrate metabolism, unspecified

E75 Disorders of sphingolipid metabolism and other lipid storage diseases

Excludes: mucolipidosis types I-III (E77.0-E77.1)
Refsum's disease (G60.1)

E75.0 Gangliosidosis-GM2.
Disease:
. Sendhoff
. Thea-Saxa
GM2 gangliosidosis:
. NOS
. adults
. juvenile
E75.1 Other gangliosidoses.
Gangliosidosis:
. NOS
. GM1
. GM3
Mucolipidosis IV
E75.2 Other sphingolipidoses.
Disease:
. Fabri(-Anderson)
. Gaucher
. Crabbe
. Niman-Peak
Faber syndrome. Metachromatic leukodystrophy. sulfatase deficiency.
Excludes: adrenoleukodystrophy (Addison-Schilder) (E71.3)
E75.3 Sphingolipidosis, unspecified
E75.4 Lipofuscinosis of neurons.
Disease:
. Batten
. Bilshovsky-Yansky
. Kufsa
. Spielmeier-Vogt
E75.5 Other disorders of lipid accumulation. Cerebrotendinous cholesterosis [Van Bogart-Scherer-Epstein]. Volman disease
E75.6 Lipid storage disease, unspecified

E76 Disorders of metabolism of glucosaminoglycans

E76.0 Mucopolysaccharidosis, type I.
Syndromes:
. Gurler
. Gurler-Sheie
. Sheye
E76.1 Mucopolysaccharidosis, type II. Gunther's syndrome
E76.2 Other mucopolysaccharidoses. Deficiency of beta-glucuronidase. Mucopolysaccharidoses types III, IV, VI, VII
Syndrome:
. Maroto-Lami (light) (heavy)
. Morchio (-similar) (classic)
. Sanfilippo (type B) (type C) (type D)
E76.3 Mucopolysaccharidosis, unspecified
E76.8 Other disorders of glycosaminoglycan metabolism
E76.9 Disorder of glycosaminoglycan metabolism, unspecified

E77 Disorders of glycoprotein metabolism

E77.0 Defects in post-translational modification of lysosomal enzymes. Mucolipidosis II.
Mucolipidosis III [Hurler pseudopolydystrophy]
E77.1 Defects in the degradation of glycoproteins. Aspartyl glucosaminuria. Fucosidosis. Mannosidosis. Sialidosis [mucolipidosis I]
E77.8 Other disorders of glycoprotein metabolism
E77.9 Disorders of glycoprotein metabolism, unspecified

E78 Disorders of lipoprotein metabolism and other lipidemias

Excludes: sphingolipidosis (E75.0-E75.3)
E78.0 pure hypercholesterolemia. Familial hypercholesterolemia. Hyperlipoporteinemia Fredrickson, type Iia.
Hyper-beta-lipoproteinemia. Hyperlipidemia, group A. Hyperlipoproteinemia with low-density lipoprotein
E78.1 pure hyperglyceridemia. endogenous hyperglyceridemia. Hyperlipoporteinemia Fredrickson, type IV.
Hyperlipidemia, group B. Hyperpre-beta-lipoproteinemia. Hyperlipoproteinemia with very low lipoproteins
density
E78.2 Mixed hyperlipidemia. Extensive or floating beta-lipoproteinemia.
Hyperlipoporteinemia Fredrickson, types IIb or III. Hyperbetalipoproteinemia with pre-beta lipoproteinemia.
Hypercholesterolemia with endogenous hyperglyceridemia. Hyperlipidemia, group C. Tuboeruptive xanthoma.
Tuberous xanthoma.
Excludes: cerebrotendinous cholesterosis [Van Bogart-Scherer-Epstein] (E75.5)
E78.3 Hyperchylomicronemia. Hyperlipoporteinemia Fredrickson, types I or V.
Hyperlipidemia, group D. Mixed hyperglyceridemia
E78.4 Other hyperlipidemias. Familial combined hyperlipidemia
E78.5 Hyperlipidemia, unspecified
E78.6 Lack of lipoproteins. A-beta-lipoproteinemia. Deficiency of high density lipoproteins.
Hypo-alpha-lipoproteinemia. Hypo-beta-lipoproteinemia (familial). Deficiency of lecithincholesterol acyltransferase. Tangier disease
E78.8 Other disorders of lipoprotein metabolism
E78.9 Disorders of lipoprotein metabolism, unspecified

E79 Disorders of purine and pyrimidine metabolism

Excludes: kidney stone (N20.0)
combined immunodeficiencies (D81.-)
gout (M10.-)
orotaciduric anemia (D53.0)
xeroderma pigmentosum (Q82.1)

E79.0 Hyperuricemia without signs of inflammatory arthritis and gouty nodes. Asymptomatic hyperuricemia
E79.1 Lesch-Nychen syndrome
E79.8 Other metabolic disorders of purines and pyrimidines. hereditary xanthinuria
E79.9 Disturbance of purine and pyrimidine metabolism, unspecified

E80 Disorders of porphyrin and bilirubin metabolism

Includes: catalase and peroxidase defects

E80.0 Hereditary erythropoietic porphyria. Congenital erythropoietic porphyria.
Erythropoietic protoporphyria
E80.1 Porphyria cutaneous slow
E80.2 Other porphyrias. hereditary coproporphyria
Porfiria:
. NOS
. acute intermittent (hepatic)
If it is necessary to identify the cause, use an additional external cause code (class XX).
E80.3 Catalase and peroxidase defects. Acatalasia [Takahara]
E80.4 Gilbert's syndrome
E80.5 Crigler-Najjar Syndrome
E80.6 Other disorders of bilirubin metabolism. Dubin-Johnson Syndrome. Rotor syndrome
E80.7 Disorder of bilirubin metabolism, unspecified

E83 Disorders of mineral metabolism

Excludes: malnutrition (E58-E61)
parathyroid disorders (E20-E21)
vitamin D deficiency (E55.-)

E83.0 Copper metabolism disorders. Menkes disease [curly hair disease] [steel hair]. Wilson's disease
E83.1 Iron metabolism disorders. Hemochromatosis.
Excludes: anemia:
. iron deficiency (D50. -)
. sideroblastic (D64.0-D64.3)
E83.2 Disorders of zinc metabolism. Enteropathic acrodermatitis
E83.3 Phosphorus metabolism disorders. Acid phosphatase deficiency. Familial hypophosphatemia. Hypophosphatasia.
Vitamin D resistant:
. osteomalacia
. rickets
Excl.: adult osteomalacia (M83.-)
osteoporosis (M80-M81)
E83.4 Magnesium metabolism disorders. Hypermagnesemia. Hypomagnesemia
E83.5 Calcium metabolism disorders. Familial hypocalciuric hypercalcemia. Idiopathic hypercalciuria.
Excludes: chondrocalcinosis (M11.1-M11.2)
hyperparathyroidism (E21.0-E21.3)
E83.8 Other disorders of mineral metabolism
E83.9 Mineral metabolism disorder, unspecified

E84 Cystic fibrosis

Includes: cystic fibrosis

E84.0 Cystic fibrosis with pulmonary manifestations
E84.1 Cystic fibrosis with intestinal manifestations. Meconium ileus(P75)
E84.8 Cystic fibrosis with other manifestations. Cystic fibrosis with combined manifestations
E84.9 Cystic fibrosis, unspecified

E85 Amyloidosis

Excludes: Alzheimer's disease (G30.-)

E85.0 Hereditary familial amyloidosis without neuropathy. Familial Mediterranean fever.
hereditary amyloid nephropathy
E85.1 Neuropathic hereditary familial amyloidosis. Amyloid polyneuropathy (Portuguese)
E85.2 Hereditary familial amyloidosis, unspecified
E85.3 Secondary systemic amyloidosis. Amyloidosis associated with hemodialysis
E85.4 limited amyloidosis. Localized amyloidosis
E85.8 Other forms of amyloidosis
E85.9 Amyloidosis, unspecified

E86 Reducing the volume of liquid

Dehydration. Decreased volume of plasma or extracellular fluid. hypovolemia
Excludes: dehydration of newborn (P74.1)
hypovolemic shock:
. NOS (R57.1)
. postoperative (T81.1)
. traumatic (T79.4)

E87 Other disorders of water-salt metabolism or acid-base balance

E87.0 Hyperosmolarity and hypernatremia. Excess sodium. Sodium overload
E87.1 Hypoosmolarity and hyponatremia. Sodium deficiency.
Excludes: syndrome of impaired secretion of antidiuretic hormone (E22.2)
E87.2 Acidosis.
Acidosis:
. NOS
. lactic acid
. metabolic
. respiratory
Excludes: diabetic acidosis (E10-E14 with common fourth character.1)
E87.3 Alkalosis.
Alkalosis:
. NOS
. metabolic
. respiratory
E87.4 Mixed acid-base imbalance
E87.5 Hyperkalemia. Excess potassium [K]. Potassium overload [K]
E87.6 Hypokalemia. Potassium deficiency [K]
E87.7 Hypervolemia.
Excludes: edema (R60.-)
E87.8 Other disorders of water-salt balance, not elsewhere classified.
Electrolyte imbalance NOS. Hyperchloremia. Hypochloremia

E88 Other metabolic disorders

Excludes: histiocidosis X (chronic) (D76.0)
If necessary, to identify the drug that caused the metabolic disorder, use an additional code of external causes (class XX).

E88.0 Disorders of plasma protein metabolism, not elsewhere classified. Alpha-1 antitrypsin deficiency.
Bis-albuminemia.
Excludes: disorders of lipoprotein metabolism (E78.-)
monoclonal gammopathy (D47.2)
polyclonal hyper-gamma globulinemia (D89.0)
Waldenström's macroglobulinemia (C88.0)
E88.1 Lipodystrophy, not elsewhere classified. Lipodystrophy NOS.
Excludes: Whipple's disease (K90.8)
E88.2 Lipomatosis, not elsewhere classified.
Lipomatosis:
. NOS
. painful [Derkum's disease]
E88.8 Other specified metabolic disorders. Adenolipomatosis Lonua-Bansod. Trimethylaminuria
E88.9 Metabolic disorder, unspecified

E89 Endocrine and metabolic disorders following medical procedures, not elsewhere classified

E89.0 Hypothyroidism following medical procedures.
Radiation-induced hypothyroidism. Postoperative hypothyroidism
E89.1 Hypoinsulinemia after medical procedures. Hyperglycemia after removal of the pancreas.
Hypoinsulinemia postoperative
E89.2 Hypoparathyroidism following medical procedures. Parathyroid tetany
E89.3 Hypopituitarism after medical procedures. Radiation-induced hypopituitarism
E89.4 Ovarian dysfunction following medical procedures
E89.5 Testicular hypofunction following medical procedures
E89.6 Hypofunction of the adrenal cortex (medulla) after medical procedures
E89.8 Other endocrine and metabolic disorders resulting from medical procedures
E89.9 Endocrine and metabolic disorder occurring after medical procedures, unspecified

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, and the process normally triggered by TSH is activated - the synthesis of thyroid hormones. The autonomous activity of the thyroid gland begins, which is not amenable to central regulation.

The disease is considered genetically determined. It is known that the production of thyroid-stimulating antibodies is due to an antigen-specific defect in cell suppression. A provoking factor in the formation of thyroid-stimulating immunoglobulins can be an infectious disease or stress. At the same time, a long-acting thyroid stimulator is found in most patients.

The 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 progressively increases, thyroid hormones in the blood do not exceed normal values.
• III. The hyperthyroid stage is morphologically accompanied 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 hyperproduction of thyroid hormones;
• symptoms associated with concomitant autoimmune diseases. The thyroid gland is significantly enlarged, as a rule, the increase is noticeable on examination. On palpation, a dense consistency is determined, vascular noises are heard over the gland.

Symptoms due to thyrotoxicosis increase gradually over several months. The child becomes whiny, emotionally unstable, irritable, sleep is disturbed. On examination, attention is drawn to smooth velvety skin, there is pigmentation, especially in the eyelids. Sweating is increased, muscle weakness is often noted. Appetite is increased, but the child progressively loses weight. There are tremors of the fingers, increased motor activity. Characterized by tachycardia at rest and increased pulse arterial pressure. Frequent stools are noted, sometimes hepatomegaly is detected. Girls have amenorrhea.

Sympathicotonia provokes the appearance of eye symptoms: Graefe's symptom - exposure of the sclera area above the iris when looking down, Möbius's 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 more often observed with diffuse toxic goiter. It is caused by the formation of antibodies to the membrane of the oculomotor muscles and their lymphocytic infiltration, which also extends to the retrobulbar tissue. This results in edema, hyperpigmentation of the eyelids, exophthalmos.

Complications of diffuse toxic goiter

If untreated, the patient may develop a thyrotoxic crisis. At the same time, the temperature rises, motor anxiety or apathy, vomiting, signs of acute heart failure, 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 reduced - in 70% of patients;
• T 3 is increased, T 4 is normal, TSH is reduced - in 30% of patients;
• antibodies to TSH receptors in the 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 the blood serum;
• ECG - tachycardia, increased voltage of the teeth.

Differential Diagnosis

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

Hyperthyroidism can also develop with other thyroid disorders. These include - acute purulent and subacute thyroiditis, autoimmune thyroiditis, functionally active nodes of the thyroid gland.

Treatment of diffuse toxic goiter

The goal of treatment is to eliminate the manifestations of hyperthyroidism and normalize the levels of thyroid hormones. Medical and surgical treatments 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 divided 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 thyreostatics with the appointment of sodium levothyroxine to maintain euthyroidism and prevent the goiter effect of TSH.

In case of intolerance to thyreostatics, ineffectiveness of conservative treatment, 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. Thyrotoxicosis recurs in half of patients with remission. Evidence of the achievement of 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 agent used. Combined treatment with thiamazole and levothyroxine for a long time and continued therapy with levothyroxine after discontinuation of thionamides reduces the likelihood of recurrence of thyrotoxicosis.

It's important to know!

The 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 rises. Antibodies to microsomes of the thyroid gland 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.