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Nodular goiter. Degree of thyroid enlargement according to WHO

Goiter thyroid gland- what it is? This question can be heard in different parts of the world for a reason: widespread phenomena. The thyroid gland can be enlarged for various reasons, but for some areas the level of the disease is such that it is classified as a regional disease.

The question of goiter suddenly arises when a person suddenly discovers that an incomprehensible and frightening formation begins to grow on his throat. Goiter itself is not a disease, but a symptom of a disease that can indeed be very dangerous and requires serious attention and treatment.

Features of thyroid goiter

A goiter is an increase in the size of an organ, being a sign of a number of its diseases, expressed in functional disorders. This pathology may present as a small swelling in the area of the Adam's apple, but can grow so large that it deforms the neck and puts pressure on other organs.

Goiter different types It occurs much more often in women than in men, which is associated with hormonal processes.

The type of manifestation of goiter depends on the type of dysfunction of the secretory function of the gland:

Hypothyroidism: decreased secretory function leading to decreased hormone release, causing effects such as attenuation metabolic processes, swelling, obesity, slow reaction.
Hyperthyroidism: excessive activation of secretion; is accompanied by an abnormal acceleration of metabolic processes and leads to weight loss and overload of the nervous system.
Euthyroidism: normal hormone production, but goiter growth occurs due to the pathological size of the gland itself.

Main types of goiter

What a goiter is is determined by the type of thyroid disease. The following main varieties can be distinguished:

Endemic goiter: described by an increase in organ volume and a decrease in the secretion of thyroxine and triiodothyronine; has a characteristic geographical dependence, distributed in places where there is a clear lack of iodine in water and foods. The pathogenesis of the disease is due to the fact that iodine in the body is necessary for the production necessary hormones and with its acute deficiency, it is necessary to pump much more blood through itself, and the gland reflexively increases the number of cells responsible for the production of this hormone. To correct the situation, the pituitary gland produces thyrotropin, which activates cell division in the organ and increases its volume and weight.
Thyroiditis (Hashimoto's goiter): similar in etiology to diffuse goiter, but related to hypothyroidism. As a result of erroneous actions of the immune system, excess leukocytes attack the gland, and at the site of cell death, a fibrous tissue. This type of disease mainly has hereditary causes, but can sometimes be initiated by injury, infection, cervical inflammation, chronic pharyngitis, iodine anomaly and atmospheric pollution with toxic substances.
Diffuse toxic goiter: this is a disease that can be attributed to thyrotoxicosis, and excess iodine leads to poisoning of the body; provoked by pathology of the autoimmune system at the genetic level, with infections, head injuries, and nervous shocks.
Nodular goiter (thyroid adenoma): formation of a node as a result of excess secretion thyrotropin, as well as dysfunction of nerve processes. Cell proliferation leads to hormone poisoning of the body (thyrotoxicosis).
Congenital goiter: appears in children if the mother had a significant iodine deficiency during pregnancy or due to a genetic predisposition.
Fibrous thyroiditis (fibroplastic goiter): the thyroid gland grows due to the manifestation autoimmune pathology inflammatory in nature, by the growth of connective tissue from fibrin fibers.

Degrees of enlargement of the thyroid gland

During the development of the disease there are observed various degrees enlarged gland. The international classification distinguishes the following degrees:

Grade 0: the goiter is not visible or palpable.
Grade 1: Grade 1 enlargement of the thyroid gland is not noticeable, but the isthmus of the gland is palpable.
Grade 2: A grade 2 goiter is noticeable during swallowing and is easily palpable.
Grade 3: the gland is enlarged, which visually looks like the effect of a thick neck.
Degree 4: grade 4 goiter has a pronounced appearance, the configuration of the neck is disturbed, and the neck is deformed.
Grade 5: huge goiter pressing on the neck, troublesome when breathing and swallowing.

Causes, symptoms, diagnosis and treatment of nodular goiter

Nodular goiter is a local proliferation of glandular tissue, which can be single-nodular or multi-nodular (more than 2) type. It is mainly of cellular type.

Exercises for the thyroid gland will help even with nodes and hypothyroidism!

Causes of nodular goiter

Nodular goiter can be a manifestation of diseases such as:

nodular colloid goiter: the most common nodular formation in the form of an increased size of the follicle filled with a viscous colloid;
thyroid adenoma;
thyroid cancer: malignancy with the ability to metastasize;
pituitary adenoma: enlargement of the thyroid gland as a result of excess thyrotropin;
Hashimoto's thyroiditis;
cyst: goiter is associated with a dermoid cyst and is a congenital form.

These reasons are provoked by a number of internal and external factors: deficiency of iodine and some other minerals in water and diet; impaired outflow of blood and lymph from the gland associated with atherosclerosis; hereditary predisposition; dysfunction nerve endings on any part of the gland; polluted habitat (increased background radiation, nitrite pollution, oversaturation of soil with calcium, etc.); psychological stress; head injuries; hormonal changes; decrease immune defense after illnesses.

Symptoms of nodular goiter

The nodes appear when palpated in the form of compactions or visually when they reach a size of more than 10-20 mm. From stage 3 onwards, symptoms become evident causing an asymmetrical neck shape; for example, swelling of the right lobe. Thickening of the neck can occur on both sides with a multinodular type of development.

Symptoms have and general manifestation, depending on the nature of the pathology. Symptoms of hypothyroidism include: low temperature and blood pressure; swelling of the face, lips, limbs; night insomnia, but desire to sleep during the day; weight gain; depression; decreased attention and memory; dry skin; hair loss; constipation; lack of appetite.

For thyrotoxicosis, the symptoms are as follows: elevated temperature and feverish condition; increased heart rate; irritability; losing weight with a good appetite; feeling hot on skin; increased sweating; hand trembling; diarrhea. Less obvious signs appear with euthyroidism: shortness of breath when rotating the head; cough turning into bronchitis; sore throat; feeling of a lump in the throat; swallowing problems.

Diagnosis and treatment

The primary diagnosis is made by examination and general analysis blood (for hormones). More accurate results are obtained after ultrasound of the thyroid gland, biochemical analysis blood, scintigraphy. The final differentiation of the disease is carried out based on the results of radiographic studies, puncture biopsy and computed tomography.

Drug treatment includes the prescription of drugs such as antithyroid drugs (mercazolyl, propylthiouracil); thyroid medications (levothyroxine, thyroidome); combined iodine-containing substances (potassium iodide 200, iodotirox).

An effective method for treating nodular goiter is radioiodine therapy using the radioactive isotope iodine 131. During treatment, thyromegaly is controlled. If there is a risk of malignancy of the formation, progression of the disease to grade 4-5, or multinodular development, surgical treatment is performed.

Symptoms and treatment of colloid goiter

Colloid goiter of the thyroid gland is its enlargement as a result of filling the follicles with colloidal fluid in a volume of more than 18 ml (in women) and 25 ml (in men).

The main forms of colloid goiter can be distinguished.

Diffuse colloid goiter: distribution of colloid throughout the organ.
Nodular colloid goiter: local placement of filled follicles.
Cystic colloid goiter: accumulation of colloids in a cyst surrounded by an elastic membrane.

The main causes of colloid goiter: deficiency of iodine intake; age-related anomalies (after 40 years); women's hormonal surges; pathology of the endocrine system; increased background radiation; genetic predisposition; nervous stress; infectious and inflammatory diseases; hypothermia.

Symptoms of colloid goiter

Symptoms begin to appear from stage 3 of the disease. A goiter in the form of a wide roller or butterfly is noticeable visually. To the touch, the formation is an elastic growth containing many small bubbles with colloid. Signs that can be felt: pressure in the neck; problems swallowing; coughing; hoarseness; feeling foreign body in the throat. Additionally, it can be noted: with hypothyroidism - inhibition of reaction, weakness, constipation, slowdown heart rate, low temperature; with hyperthyroidism - excitability, insomnia, increased heart rate, increased temperature.

Thyroid nodules: diagnosis, puncture (biopsy), types, consequences

Thyroid nodules. Causes

Treatment of colloid goiter

Drug treatment includes the prescription of products containing iodine (iodomarin 100, potassium iodide); thyreostatics (thiamazole, propylthiouracil); drugs based on thyroid hormones (L-thyroxine, euthirox).

Causes of toxic goiter

Toxic goiter is an enlargement of the thyroid gland, in which the body is poisoned with thyroid hormones (thyrotoxicosis). The main causes of this type of disease:

heredity;
pathology of the pituitary gland;
excessive consumption of iodine-containing drugs and thyroid hormones;
psychological and hormonal changes in the female body;
infections (flu, sore throat, tuberculosis);
head injuries;
encephalitis;
psychological stress;
excessive exposure to ultraviolet radiation.

Causes and treatment of diffuse goiter

Diffuse goiter is a uniform expansion of the volume of the thyroid gland. It can have a toxic and non-toxic type of disease. Quite often there is a combination of nodular and diffuse types of the disease - mixed goiter.

Types and causes of the disease

The main diseases characterized by a diffuse nature: diffuse toxic type ( Graves' disease); diffuse colloidal type; endemic goiter. These diseases lead to following reasons: deficiency of iodine intake, hereditary pathologies; uncontrolled use of drugs containing iodine; women's hormonal changes; diseases affecting immune system(diabetes, arthritis, scleroderma); age factor; prolonged stress or nervous shock; surgical operations on the thyroid gland.

TO specific symptoms diffuse goiter may include noisy breathing; shortness of breath that appears in a lying position; dizziness. The main external manifestation is a characteristic convex formation on the front surface of the neck with uniform growth of both halves.

Treatment of diffuse goiter. For the drug treatment of diffuse goiter, iodide preparations (diiodotyrosine) are prescribed; thyreostatics and antithyroids (Mercazolil); thyroid hormones (propranolol, anaprilin); sedatives(primidone); steroid hormones- corticosteroids (prednisolone). Surgical treatment carried out with the development of severe thyrotoxicosis, too large size goiter, the occurrence of complications in the form of atrial fibrillation.

The thyroid gland takes part in many processes occurring in the body. Grade 1 enlargement of the thyroid gland can be observed in many people, even healthy ones. The degree of enlarged goiter depends on the size, shape, complaints of the patient and external manifestations of the disease. If you discover various pathologies in yourself, you should begin diagnosis and treatment.

An enlarged thyroid gland is called hyperplasia. This disease in grade 1 is most often observed in medical practice. It may not cause discomfort to a person, which makes it difficult to detect it in a timely manner.

However, grade 1 hyperplasia can quickly progress to the next stages when pathological symptoms and various disorders. Let us remind you on the website that we're talking about O benign education, which can become malignant, that is, further developments can lead to the appearance.

Changes in metabolism.
Improper development of tissues, bones, growth.
Improper functioning of the sympathetic and parasympathetic nervous systems.
Loss of energy due to lack of adequate nutrition of cells.

Types of iodine deficiency

The functioning of the thyroid gland largely depends on the amount of iodine that enters the body. However, the person himself can rarely notice the various disorders that occur with iodine deficiency. This may include hormonal disorders, loss of libido, fatigue, susceptibility to infectious diseases, sleep disturbances, even loss or speed dial weight. There are many types of iodine deficiency, which are divided depending on the disease that manifests itself:

Thyroid dysfunction, goiter.
Pain and muscle weakness.
Radiculitis lumbar or thoracic.
Anemia.
Violation of tissue formation and oxygen consumption.
Disruption internal secretion: exchange of water and salt, lipids, proteins, etc.
Disruption of the reproductive and nervous systems, mammary glands, and brain.
Negative impact on work of cardio-vascular system and liver, atherosclerosis, arrhythmia.
Changes in skin color, appearance of hair, nails due to an imbalance in the amount of calcium.
Mental retardation and physical development child: dementia, deafness, cretinism, etc.
Pathologies in reproductive function: stillbirth, miscarriages, infertility, toxicosis, premature birth, lack of milk.

Depending on the amount of iodine in the body, the thyroid gland develops various pathologies in case of deficiency of this element:

Hyperthyroidism is increased production of hormones.
Euthyroidism is the normal production of hormones during the destruction of tissue structure.
Hypothyroidism is a decrease in the amount of active substances.

Separation according to the degree of goiter enlargement

Hyperplasia has many degrees of development. Let's consider the division of goiter enlargement by degrees:

Zero degree - the enlargement of the thyroid gland is insignificant, which is not felt, externally visible or palpated. It may be discovered during a random examination or annual physical examination.
The first degree is a significant enlargement of the thyroid gland beyond normal, which is palpated by a doctor and observed on an ultrasound. Externally, it can only be detected by swallowing saliva or eating food; in other cases, the gland may not be visible. Benign cysts may appear and disappear on their own.
The second degree is marked by significant changes in the thyroid lobes and isthmus. It can also be felt by palpation and swallowing.
The third degree is noted external manifestations diseases when a protruding thyroid gland is visible on the throat. This becomes especially visible when turning the head to the sides. The neck externally takes on a full and even rounded shape.
The fourth degree is a significant enlargement of the thyroid gland, which is impossible not to notice. The patient complains of pain when breathing and swallowing.
The fifth degree is a significant enlargement of the thyroid gland, which is visible upon external examination. Discomfort is also felt by the patient himself, who feels pain not only when breathing and swallowing. On palpation, hardened, non-elastic lesions are felt, which may indicate the development of oncology.

Depending on the structure of the disease, there are different kinds goiter:

Nodular - seals are located in the tissues of the endocrine organ. Since it is difficult to detect early stages, is called “thyroid goiter degree 1”. Divided into the following types:

Endemic formation associated with iodine deficiency.
Cystic formation.
Multiple or single nodes.
Follicular adenoma.
Conglomerate of fused nodules.

Colloid goiter is the safest. Formed due to the accumulation of colloid in the thyroid gland - follicular connective tissue, containing iodine, thyroglobulin and amino acids.
Diffuse goiter is a uniform increase in the volume of the thyroid gland.
Graves' disease (diffuse toxic goiter).
Toxic goiter - when the body is intoxicated with a large amount of iodine and thyroid hormones.

Diagnosis of stage 1 enlarged thyroid gland

Examination of the thyroid gland should be done even in the absence of obvious signs of hyperplasia. It is better to undergo a diagnosis of grade 1 enlarged thyroid gland annually after the age of 30. The risk group includes women over 60 years of age. If a person has previously had diseases related to the thyroid gland, then a medical examination should be carried out regularly to early detection diseases.

Initially, a person may conduct a self-examination. To do this, stand in front of a mirror, take water into your mouth and throw your head back. We swallow the water, while paying attention to the part of the neck below the Adam's apple. If a bulge or swelling appears there, then you should urgently contact an endocrinologist.

When examining the thyroid gland to detect grade 1 enlargement, the following procedures are performed:

Palpation and external examination.
A blood test to detect thyroid hormones: thyrotropin, triiodothyronine, calcitonin and thyroxine.
Puncture biopsy in the thyroid area.
Radioisotope scanning.
Ultrasound of the thyroid gland.

Treatment of enlarged goiter

An enlarged goiter should be treated by a doctor. After receiving all the tests, the correct treatment is determined. Enlargement of the thyroid gland by 1 degree can be noted by the following treatment:

Medications. These include:

Corticosteroids and aspirin to relieve inflammation.
Preparations for replenishing iodine deficiency.
Hormonal medications to replenish the thyroid gland with the necessary elements.

Radioactive iodine to introduce the required element directly into the thyroid gland.
Laser destruction.

Already at stages 2 and 3 of the disease, more radical measures are prescribed, which include surgical intervention– partial or complete removal of the gland (thyroidectomy).

Basically, treatment of 1st degree hyperplasia is limited to drugs that replenish the body with iodine, and eating food full of this element:

Seafood.
Walnuts.
Herbs and plants: madder, licorice, dandelion, white cinquefoil, St. John's wort, soapwort roots, stems pink radio, licorice, cocklebur, rosehip, etc.
Buckwheat grain.
Aronia berries.

The patient is periodically examined by a doctor to monitor the progress of the disease. If improvements are noted, then treatment in the form of replenishing the body with iodine continues until complete recovery.

Forecast

Stage 1 enlarged thyroid gland should not be ignored, since the disease continues to develop and progress to more severe stages. The prognosis may be disappointing if a person is not treated by a doctor.

Life expectancy depends on how quickly complications develop:

Pressure on neighboring organs, which may cause loss of voice or ability to breathe.
Change in the patient's appearance.
Loosening of the nervous system, which leads to tearfulness, irritability, nervousness and imbalance.
Disruption of the cardiovascular, respiratory systems and liver functionality (leading to atherosclerosis).
Thyrotoxicosis, which develops with an increase in the amount of thyroid hormones. Life-threatening.

To avoid all possible pathological changes, you should use medical recommendations, which at the 1st stage of the disease are easy and quickly lead to recovery.

Being important body endocrine system, has the property of regulating almost all processes occurring in the body. With its help, it is carried out, responsible for hematopoiesis, digestion, and absorption of incoming nutrients.

For this reason, any deviations in its functioning cause all kinds of diseases that can provoke the development of irreversible negative consequences in the body, worsening the patient’s well-being and capable of significantly aggravating current organic changes.

Thyroid 1st degree, as well as other degrees, is a lesion of the entire endocrine system with consequences for many internal organs and their systems.

Methods for identifying thyroid pathologies

Enlargement of the thyroid gland of the 1st degree is accompanied by a slight increase in the shares of this organ; to clarify this diagnosis, it is already prescribed after an external examination and palpation.

It allows you to identify the degree of pathology, its prevalence, and determine which treatment will be the most effective. However, to obtain a more detailed picture of the disease, a number of tests should be carried out, which are carried out by drawing blood.

Enlargement of the thyroid gland of the 2nd degree differs from the first in that its identification through an external examination and analysis of the patient’s complaints gives an almost complete picture of the disease: a stronger increase in the area of the goiter, severe difficulty in swallowing movements, along with such blood test indicators as an increase in thyroxine levels and thyrotropin cause a decrease in quality Everyday life, soreness in the throat and neck area.

Stages of pathology development

Diffuse proliferation of thyroid tissue is accompanied by a gradual worsening pathological condition patient, which is expressed in the gradual transition of one stage to the next.

When answering the question, stage 1 thyroid gland - what is it, the doctor will also tell you about the characteristics of the course of the disease and its impact on the overall picture of a person’s health.

Based on information about existing parallel current diseases, an idea of necessary treatment, which will reduce the severity of the main symptoms of the disease and speed up the recovery process.

Today, there is a division of the process of thyroid pathology caused by severe iodine deficiency into five stages, each of which is accompanied by certain changes in the structure of the gland tissue and the quality of its functioning.

The generally accepted classification looks like this:

The thyroid gland may become enlarged with right side and on the left, while external changes also occur in the area where the goiter is located, and subjective unpleasant sensations are noted when swallowing and breathing.

The main therapeutic effect for thyroid pathologies

Depending on the degree of enlargement of the thyroid gland the disease has reached, the effects pathological process a therapeutic effect is prescribed on the functioning of internal organs and their systems, which eliminates iodine deficiency in the body and stabilizes the general condition of the patient.

While eliminating the most obvious manifestations of diffuse pathology of the thyroid gland, treatment should also be aimed at normalizing the process of absorption of this microelement.

The most effective way to identify thyroid pathologies is to use it in therapeutic doses, which ensure the elimination of insufficient production of this hormone.

The dosage of its administration is determined by the weight of the patient and the stage of advanced disease, as well as its tolerance. The doctor initially makes an appointment small doses thyroxine analog drugs, then, as the body gets used to it, the volume of each dose gradually increases.

By monitoring the treatment process, the endocrinologist can make the necessary changes to the treatment system by combining various drugs or changing their dosage.

Sea fish, seaweed, lean beef and lamb are a valuable source of microelements necessary for the health of the thyroid gland in both adults and children. Vitamin preparations They will support the onset of seasonal epidemics and stimulate the functioning of the immune system.

Etiology and pathogenesis.

Plays a role in the development of the disease hereditary predisposition, multifactorial (polygenic) type of inheritance:

a) autosomal recessive,

b) autosomal dominant.

The direct cause of diffuse toxic goiter can be infections, stress, and insolation. Women suffer from diffuse toxic goiter 7 to 10 times more often than men. 15% of patients with diffuse toxic goiter have relatives with this disease, and 50% of relatives have circulating antithyroid antibodies.

Over the past 20 years, it has been proven in experimental and clinical work that diffuse toxic goiter is an autoimmune disease in which an increase in the titer of antibodies to thyroid antigens is detected, in combination with other autoimmune diseases: rheumatic diseases, hepatitis, nonspecific ulcerative colitis. In monozygotic twins, if one of them is sick, the risk for the other is 60%, in dizygotic twins it is only 9%. In diffuse toxic goiter, a connection has been established with histocompatibility antigens - HLA, carriage of HLA B 8, and there is a particularly high risk of the disease in the presence of HLA DW 3, DR 3 and DQ A 1. When carrying antigens HLA B 8, DR 3, diffuse toxic goiter is often combined With endocrine ophthalmopathy.

The pathogenesis of diffuse toxic goiter (Adams and Purves, 1956) was associated with LATS-long-acting thuroid stimulator, this is an immunoglobulin that stimulated the thyroid function of white mice in an experiment long time(DDTS is a long-acting thyroid stimulant). But LATS did not correlate with the severity of thyrotoxicosis and an increase in blood LATS was found only in 50% of patients with diffuse toxic goiter. Thus, the pathogenesis of diffuse toxic goiter cannot be explained by this mechanism alone. Although it is known that the stimulating effect of LATS on thyroid gland carried out by increasing the formation of cAMP and increasing the biosynthesis and release of thyroid hormones into the blood, that is, according to the known mechanism of action of TSH itself.

Currently, in the pathogenesis of diffuse toxic goiter, the main place is occupied by thyroid-stimulating antibodies (TSI) - these are immunoglobulins of class G, they are able to complex with the TSH receptor, compete with TSH for communication with the receptor and displace TSH from the hormone receptor complex. The thyroid-stimulating effect of these antibodies is exerted both on the connection of TSH with the receptor and directly on the thyroid gland. This is the mechanism humoral immunity in the development of diffuse toxic goiter, however, the antigen to which the formation of thyroid-stimulating antibodies occurs has not yet been established. Thus, TSIs have an effect in two directions: increasing the function of the thyroid gland and the formation of goiter.

Impaired cellular immunity also plays a role in the development of diffuse toxic goiter. It is assumed that there is a congenital defect - insufficiency of T-suppressors, the survival of forbidden, phorbid clones of T-lymphocytes occurs, which either directly act on the thyroid gland cytotoxically, or through B-lymphocytes producing antibodies that have a unique thyroid-stimulating effect. In the active stage of the disease, TSI is detected in 90% of patients with diffuse toxic goiter.

Clinic of diffuse toxic goiter. A triad of symptoms was described by Karl Basedow in 1840: goiter, bulging eyes, tachycardia.

Complaints: weakness, fatigue, irritability, tearfulness, bad dream, sweating, palpitations, unstable stools, weight loss with good appetite (catabolism of proteins, fats).

The thyroid gland is enlarged, diffuse, mobile, painless, with a dense elastic consistency.

Classification according to the degree of increase in goiter (O.V. Nikolaev 1955), modified in 1966

0 – the thyroid gland is not enlarged,

I – the isthmus and one of the lobes of the thyroid gland are palpated,

II – both lobes of the thyroid gland are palpable, the isthmus is visible when swallowing,

III – the thyroid gland is visible on examination, a symptom of a “thick neck”,

IV – the thyroid gland extends beyond the m.sternocleidomastoideus,

V – goiter of enormous size with compression of surrounding tissues.

Classification of thyroid gland sizes recommended by WHO, 1994.

degree 0 – no goiter,

grade I – the size of the lobes is larger than the distal phalanx of the thumb, the goiter is palpable but not visible,

degree II - the goiter is palpable and visible to the eye.

This classification is used in a population survey of the population by sex endemic goiter. IN clinical practice: O.V. Nikolaev’s classification has advantages, since the treatment tactics for DTG are different for goiter - 2 - 3 - 4 degrees.

Over the thyroid gland, you can listen to a systolic murmur with diffuse toxic goiter, due to increased blood supply (increased minute volume of blood, blood flow velocity).

Ocular symptoms: exophthalmos, symptoms of Graefe, Kocher, Moebius, Stellwag, Delrymple, Jellinek, Krauss.

Graefe's sign is a lag of the upper eyelid from the iris, a white stripe of the sclera when fixing an object moving downwards.

Kocher's sign - a white stripe of sclera between the upper eyelid and the iris appears when the vision fixes an object moving upward.

Moebius sign is a convergence disorder, loss of the ability to fixate an object at close range.

Stellwag's sign is rare blinking.

Delrymple's sign is a wide open palpebral fissure.

Jellinek's sign is pigmentation around the eyes.

Krauss's sign is brightness in the eyes.

It is necessary to distinguish eye symptoms diffuse toxic goiter from an independent disease - endocrine or autoimmune ophthalmopathy, which can be combined with diffuse toxic goiter from 5 - 20% to 40 - 50%, with AIT - 11% and without thyroid pathology - 5%.

Endocrine ophthalmopathy is characterized by a triad of symptoms:

1) changes in the conjunctiva - lacrimation, photophobia, feeling of sand in the eyes, 2) edematous exophthalmos, 3) damage to the extraocular muscles, up to paresis of upward gaze, diplopia, lagophthalmos.

Plays a role in the pathogenesis of endocrine ophthalmopathy autoimmune mechanism: infiltration, swelling of retrobulbar tissue and orbital muscles, which is caused by the formation of antibodies to the tissues of retrobulbar tissue and extraocular muscles. The main treatment for endocrine ophthalmopathy is the administration of glucocorticoids per os: prednisolone from 30 – 40 to 60 – 100 mg/day, steam or retrobulbar: dexazone, dexamethasone, metipred, kenalog. R-therapy, plasmapheresis, surgical decompression of the orbits with removal of retrobulbar tissue in severe cases.

P retibial m i xedema occurs in 1 – 4% of patients with diffuse toxic goiter. There is swelling on the anterior surface of the leg, thickening of a purplish-cyanotic color - mucinous edema due to infiltration of mucopolyscharides, probably of autoimmune origin.

Acropathy is a thickening of the phalanges of the fingers, often combined with pretibial myxedema.

With diffuse toxic goiter, a triad of symptoms was described by Bazedov in 1840: goiter, bulging eyes, tachycardia.

Damage to the cardiovascular system - thyrotoxic heart, which is characterized by: constant sinus tachycardia, atrial fibrillation, paroxysmal or constant, extrasystole, heart failure, arterial hypertension with increased systolic pressure, decreased diastolic pressure, increased pulse pressure. The borders of the heart are normal or enlarged to the left. Heart sounds are loud, functional systolic murmur.

On the ECG - high waves R, P and T, shortening and then lengthening of the P - Q interval, inversion of the T wave - biphasic, negative.

Respiratory system- without features. There may be shortness of breath, dissatisfaction with breathing.

Digestive system - changes in appetite, unstable stools, thyrotoxic hepatosis, liver enlargement, sometimes jaundice.

The urinary system is unremarkable.

Nervous system - increased fussiness, excitability, Marie's symptom - small tremor of outstretched arms, telegraph pole syndrome - trembling of the torso.

Endocrine system– ovarian dysfunction up to amenorrhea, mastopathy, gynecomastia, impaired carbohydrate tolerance, relative adrenal insufficiency – endogenous hypocortisolism.

Thyrotoxic crisis. A severe complication of diffuse toxic goiter.

Provoking factors: stress, physical strain, infections, surgical interventions for severe undiagnosed diffuse toxic goiter. In pathogenesis, the main role is played by sudden entry into the blood large quantities thyroid hormones, an increase in adrenal insufficiency, an increase in the activity of the sympathetic-adrenal system, an increase in catecholamines in the blood and a decrease in adrenal hormones.

Basic clinical symptoms often increase quickly, less often gradually: anxiety, agitation, tremors, muscle weakness, stupor, loss of consciousness, coma.

Cardiovascular system - tachycardia from 150 to 200 beats/min, atrial fibrillation, extrasystole, increase and then decrease blood pressure, heart failure.

Digestive system - nausea, vomiting, abdominal pain, diarrhea, jaundice, acute liver failure.

Urinary system – decreased diuresis up to anuria.

1) Classification of severity and rheotoxicosis:

mild form - pulse up to 80 - 100 beats/min., weight loss 10 - 15%,

medium form – pulse up to 120 beats/min, weight loss up to 20%,

severe form - pulse more than 120 beats/min, weight loss 30 - 50%, complications: thyrotoxic heart, thyrotoxic crisis, adrenal insufficiency, thyrotoxic hepatosis (endocrine ophthalmopathy).

Diagnosis of diffusive toxic goiter:

Laboratory diagnostics: general blood test: tendency to leukopenia, relative or absolute neutropenia, relative or absolute lymphocytosis, monocytosis, tendency to thrombocytopenia, less often eosinophilia. Reducing blood cholesterol.

2) Classification of thyrotoxicosis by severity

Hormonal spectrum: subclinical mild thyrotoxicosis (decrease in TSH with normal level T4, T3), moderate severity– manifest thyrotoxicosis (decrease in TSH, increase in T4 and T3), severe thyrotoxicosis, complicated atrial fibrillation, circulatory failure, adrenal insufficiency (decrease in TSH, increase in T4 and T3).

Ultrasound of the thyroid gland allows you to examine the echostructure, volume, presence of nodes and cysts. Diffuse toxic goiter is characterized by diffuse hypoechogenicity, the thyroid gland is homogeneous, with clear contours, and an increase in the volume of the thyroid gland. Volumetric calculation: (length x width x thickness of the right lobe) + (length x width x thickness of the left lobe) x 0.5. Normally, in women the volume of the thyroid gland is up to 18 cm 3, in men up to 25 cm 3.

Radioisotope scintigraphy of the thyroid gland with iodine - 131 and technetium - 99 is shown:

1) retrosternal goiter,

2) nodular goiter,

3) recurrence of diffuse toxic goiter after surgery,

4) suspicion of thyroid cancer.

In diffuse toxic goiter, the absorption of iodine-131 is increased in the first 2–4 hours. Normally, after 2 hours - 11%, after 4 hours - 18%, after 24 hours - 31%, with diffuse toxic goiter, iodine absorption is 131 - 41% - 49% - 62%, respectively.

Radioisotope scanning of the thyroid gland after ingestion of 20 - 100 µCi after 24 hours allows us to identify the distribution of the radiopharmaceutical, the presence of hot, cold, warm nodes, retrosternal location, aberrant goiter, shape, size of the thyroid gland.

In doubtful cases, you can conduct a test with TRH, which is administered intravenously in a bolus at a dose of 200 - 500 mcg in 2 ml of isotonic NaCl solution. In healthy people, TSH increases 5 times at the 20th minute; in patients with diffuse toxic goiter, TSH does not increase.

Structure of the diagnosis:

Main: Diffuse toxic goiter (nosological form of thyroid pathology indicating the degree of increase in goiter). Thyrotoxicosis according to severity.

Complications: thyrotoxic heart, thyrotoxic crisis, etc.

Concomitant diagnosis.

Differential diagnosis diffuse toxic goiter is carried out with neuro-circulatory dystonia, subacute thyroiditis, autoimmune thyroiditis, nodular and multinodular toxic goiter. Main meaning in differential diagnosis Along with the clinic, he has a thyroid hormonal status.

METHOD OF TREATMENT OF DIFUSE TOXIC GOOTER:

1) medicinal (conservative),

2) surgical (operative),

3) treatment radioactive iodine.

I. Medication (conservative) method.

Indications for treatment with a conservative method: diffuse toxic goiter of I – II degrees, mild to moderate thyrotoxicosis.

Thyrostatic drugs:

1) imidazole group: mercazolil, thiamazole, carbimazole, methimazole, tyrosol,

2) thiouracil group: propicyl (propylthiouracil),

3) group: potassium perchlorate and lithium carbonate, have no practical use due to toxic properties and difficult dose selection.

Mechanism of action of Mercazolil (1 tablet – 5 mg):

1) suppression of the formation of the active form of iodine by influencing TPO,

2) inhibition - blocking the iodination of tyrosine or tyrosine residues of thyroglobulin,

3) blocking the conversion of iodotyrosines to iodothyronines,

4) impact on autoimmune process, decrease in thyroid-stimulating antibodies.

The selection of the initial starting dose of Mercazolil depends on the severity of thyrotoxicosis:

mild form – 20 – 30 mg, moderate – 30 – 40 mg, severe – 40 – 60 mg. After 7 - 10 days, upon reaching a euthyroid state with normalization of the pulse, stabilization and increase in body weight, improvement general condition Mercazolil is gradually reduced by 5 mg per week to a maintenance dose of 5–10 mg for up to 6 months continuously or intermittently for 1.5–2 years.

Propicil (1 tablet - 50 mg), in addition to the thyreostatic mechanism of action, has an extrathyroidal effect in the periphery by converting T4 into inactive reverse rT3. Prescribe propicil from 200 – 300 mg to 400 – 600 mg/day, when the euthyroid state is achieved, reduce to 200 mg, maintenance dose 50 – 100 mg/day. Indications: allergies, relapse of thyrotoxicosis, pregnancy with thyrotoxicosis.

Side effect thyreostatic drugs – leukopenia, goitrogenic effect. It is necessary to conduct a general blood test once every 7–10 days, with a maintenance dose once every 2 weeks–1 month.

Potassium perchlorate. The mechanism of action is to block the flow of iodine into the thyroid gland. Prescribed 0.25 g 2 – 3 times a day. Currently practically not used.

Lithium carbonate. Mechanism of action - stabilizes membranes and thus reduces the stimulating effect of TSH and thyroid-stimulating antibodies on the thyroid gland, reduces the formation of T3 and T4 and their content in the blood. Prescribed from 0.3 g - to 0.9 - 1.5 g per day, more often in preoperative preparation and in preparation for treatment with radioactive iodine, or in case of intolerance to Mercazolil.

Inorganic iodine preparations: 1% potassium iodide solution is used only in preparation for surgery, 15 - 30 drops. 3 times a day 7 – 10 days before the intended operation.

In the complex therapy of diffuse toxic goiter, b-blockers are used, which reduce the sensitivity of b-receptors to catecholamines, and also reduce the transition of T4 to active T3 due to the conversion of T4 to reverse T3. Use atenolol 25–50 mg 1–2 times/day, anaprilin 20–40 mg 2–3 times/day. IN complex therapy include sedatives, vitamins B, A, C, good nutrition. In severe forms of diffuse toxic goiter, prednisolone 5–20 mg per day or hydrocortisone 75–100 mg per day intramuscularly can be prescribed, since they inhibit, as b-blockers, the conversion of T4 to active T3. To increase appetite and sedation, you can prescribe peritol (cyproheptadine) 4 mg 3 times a day. To prevent the goitrogenic effect of Mercazolil, when a euthyroid state is achieved, L-thyroxine 50 - 100 mcg can be prescribed against the background of a maintenance dose of Mercazolil “block and replace”. Criteria for achieving a euthyroid state or clinical remission: normalization of pulse, weight, thyroid gland size with confirmation of normal TSH-T3, T4 - thyroid hormonal status.

II. Surgical method.

Indications:

Diffuse toxic goiter of grade III or higher,

Severe thyrotoxicosis and moderate severity with relapses of the disease,

Nodular, diffuse nodular and substernal goiter,

Diffuse toxic goiter of childhood and adolescence, if a stable euthyroid state is not achieved,

During pregnancy and lactation,

Diffuse toxic goiter with atrial fibrillation with moderate severity of the disease,

Allergy to thyreostatic therapy.

The operation is subtotal, subfascial resection of the thyroid gland according to O.V. Nikolaev.

III. Treatment with radioactive iodine.

Indications:

Diffuse toxic goiter of moderate severity with no effect from conservative therapy for a long time > 1.5 – 2 years ( relapses of the disease),

Severe thyrotoxicosis with pronounced changes in internal organs, especially the cardiovascular system (thyrotoxic heart, circulatory failure),

Diffuse toxic goiter in combination with severe concomitant pathology ( hypertonic disease Stage III, history of myocardial infarction),

Recurrence of diffuse toxic goiter after subtotal resection of the thyroid gland,

Diffuse toxic goiter with severe endocrine ophthalmopathy, if a stable euthyroid state is not achieved,

Thyrotoxic psychosis and combination with mental illness,

The patient's refusal to undergo surgery.

Contraindications:

Light form thyrotoxicosis,

Nodular and substernal goiter,

Pregnancy, lactation,

Diseases of the blood, kidneys, peptic ulcer,

Young age.

Principles of treatment of thyrotoxic crisis:

1% NaJ solution 1.0 ml in 1 liter of 5% glucose solution intravenously,

Through a probe, 1% KJ solution or orally, 30–40 drops. 3 – 4 times a day,

Mercazolil 40 – 60 mg every 4 hours,

Hydrocortisone 100 mg x 3 – 4 times a day IM,

B-blockers (if there are no contraindications).

Intravenous drip of glucose solution 5%, saline. solution up to 2 - 3 l,

B vitamins, ascorbic acid,

Cardiac glycosidases, antibiotics,

Phenobarbital 0.3 – 0.4 g/day,

Plasmapheresis, hemosorption.

During this therapy, a decrease in thyroid volume occurs in most patients. After this, transfer of the patient to potassium iodide monotherapy is discussed, since the advisability of long-term L-T4 suppressive therapy is questionable.

Rice. 3.28. Treatment of diffuse euthyroid goiter

Forecast

Favorable, in most cases indicated therapeutic measures allow you to normalize the volume of the thyroid gland. In regions of mild iodine deficiency, diffuse euthyroid goiter, even in the absence of treatment, very rarely reaches significant degrees and leads to compression syndrome; in some patients, nodular formations form, and in the future functional autonomy of the thyroid gland may develop (chapter 3.9.2.2).

3.9.2.2. Functional autonomy of the thyroid gland

Functional autonomy(FA) The thyroid gland is the production of thyroid hormones, independent of the regulatory influences of the pituitary gland, in the absence of external stimulants.

Etiology

The cause of the development of FA is chronic hyperstimulation of the thyroid gland, which occurs under conditions of mild to moderate iodine deficiency. The main etiological basis for the development of FA is the microheterogeneity of thyrocytes, which have significantly different proliferative potential (Table 3.27).

Table 3.27. Functional autonomy of the thyroid gland

End of table. 3.27

Pathogenesis

The stages of pathogenesis of thyroid FA are presented in Fig. 3.29. IN lung conditions and moderate iodine deficiency, the thyroid gland is in a state of chronic hyperstimulation, since it must provide the body with thyroid hormones with insufficient supply of the necessary substrate for their synthesis from the outside. As a result, at the 1st stage, mainly due to hypertrophy of thyrocytes (Fig. 3.27), a diffuse increase in the thyroid gland occurs (diffuse euthyroid goiter). Due to the fact that thyrocytes have different proliferative potential, some of them subsequently divide more actively, resulting in the formation of nodular formations (multinodular euthyroid goiter). At the next stage, part of the thyroid cells (not always constituting nodules) acquires the properties of autonomous functioning, that is, it begins to produce thyroid hormones regardless of any regulatory influences. It is believed that the reason for this is the development of activating somatic mutations in dividing cells, in the genetic apparatus of which reparative processes are delayed. Among the activating mutations, a mutation of the TSH receptor gene has been described so far, which results in a conformational change in the receptor into a stable active state, as well as a mutation that brings the α-subunit of the post-receptor adenylate cyclase cascade into an active state. The result of both mutations is persistent activation of the synthesis of thyroid hormones in altered thyrocytes. As a result