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Diffuse toxic goiter etiology clinic treatment. Goiter: classification, etiology, pathogenesis, morphological characteristics, outcomes Goiter etiology

Introduction………………………………………………………………………………...3
1. Diseases of the thyroid gland…………………………………………………….4
2. Diffuse toxic goiter, etiology and pathogenesis…………………..5
3. Clinic…………………………………………………………………………………6
4. Diagnostics……………………………………………………………………………….8
5. Treatment………………………………………………………………………………....10
6. Nursing process……………………………………………………….11
Conclusion……………………………………………………………………………….12
Literature………………………………………………………………………………..13

Introduction
The endocrine system is a system of glands that produce hormones and release them directly into the blood. These glands, called endocrine or endocrine glands, do not have excretory ducts; they are located in different parts of the body, but are functionally closely interconnected.
There are two inwardly secreting specialized structures:
a - endocrine glands,
b - single endocrine cells.
Endocrine glands: central, peripheral.
The central ones include the pituitary gland, pineal gland, and neurosecretory nuclei of the hypothalamus. All the rest are peripheral:
1. Adenopituitary-dependent - thyroid gland, adrenal cortex, gonads
2. Adenopituitary-independent - parathyroid glands, islet apparatus of the pancreas, single endocrine cells.
All glands produce hormones. Hormones are biological active substances that have a strictly specific and selective effect, capable of increasing or decreasing the level of vital activity of the body.
The most common pathological conditions of the thyroid gland are: diffuse toxic goiter, hypothyroidism, endemic goiter, autoimmune thyroiditis.

1. Thyroid diseases
Diseases of the thyroid gland are very diverse.
1. With an increase in thyroid function - thyrotoxicosis, hyperthyroidism.
2. With a decrease in thyroid function - hypothyroidism.
3. With normal function - thyroiditis, endemic goiter, sporadic goiter, nodular formations.
Thyroid hormones are triiodothyronine T3 and tetraiodothyronine (thyroxine) T4.
Insulin is formed from a precursor, proinsulin, which breaks down into two molecules - C-peptide and insulin. A healthy person secretes 40-50 units per day. insulin.
The main natural stimulator of insulin secretion is blood glucose: when it rises above the fasting level, insulin secretion is stimulated and vice versa, it falls when glycemia decreases. However, even at low glycemic values ​​between meals, insulin secretion remains, although at a minimal level (basal secretion), which is of physiological significance.
The main physiological function of insulin is to deposit energy substrates supplied with food in insulin-dependent tissues (liver, muscle and adipose tissue).
In a normal state, there is a harmonious balance between the activity of the endocrine glands, the state of the nervous system and the response of target tissues (tissues that are targeted).
Any violation in each of these links quickly leads to deviations from the norm. Excessive or insufficient production of hormones causes various diseases, accompanied by profound chemical changes in the body.

2. Diffuse toxic goiter, etiology and pathogenesis
Diffuse toxic goiter is a disease accompanied by overproduction of thyroid hormones and, in connection with this, a change in the functional state of various organs and systems. The normal weight of the thyroid gland is 20 g. On average, the weight can increase to 600-800 g.
It ranks second in prevalence among thyroid diseases after endemic goiter. The variety of clinical manifestations causes certain difficulties in diagnosing the disease.
In this regard, it is especially important to be able to promptly identify the symptoms of thyrotoxicosis, conduct a differential diagnosis of its main manifestations, assess the characteristics of the course of the disease, and prescribe adequate pathogenetic and symptomatic treatment.
The pathogenesis of the disease is based on a violation of immune control by genetically defective T-suppressors, leading to the formation of autoantibodies to thyroid tissue.
A feature of autoimmune processes in diffuse toxic goiter is that autoantibodies have a stimulating effect on thyroid cells. Among them, the most studied immunoglobulins are LATS (long-acting thyroid stimulant), which are found in the blood of patients in ¾ of all cases. LATS binds to thyroid-stimulating hormone (TSH) receptors on the cell membranes of thyrocytes, which leads to increased production of thyroid hormones by the cells.
Excessive synthesis of hormones leads to an increase in the uptake of iodine by iron, the release of large quantities of thyroxine and triiodothyronine into the blood, and an increase in their action at the cellular and subcellular level (thyrotoxicosis). Protein synthesis is disrupted, tissue degeneration develops, which leads to progressive disruption of the activity of the heart, liver, kidneys and other organs.
Diffuse toxic goiter occurs at any age, women suffer about 10 times more often.

3. Clinic
The onset of the disease can be sudden or gradual.
Toxic goiter develops after mental trauma, infection, insolation, or overheating. Often a hereditary factor plays a role.
Triad of symptoms:
Goiter;
Eye symptoms;
Tachycardia.
1. Complaints from patients: - Decreased tolerance to heat. They are always hot. This is because the body produces a lot of thermal energy. Peripheral vasodilation - adaptation to heat - sweating. The skin is hot and damp.
- A feeling of internal trembling and trembling of the hands (characteristic is a fine tremor of outstretched arms, eyelids with closed eyes).
Manifestations from the muscular system: Severe weakness leads to thyrotoxic myopathy.
From the cardiovascular system: 1. Tachycardia in 99% of patients. Patients feel palpitations. Heart rate from 90 to 150 beats per minute. This tachycardia is constant and persists even during sleep. 2. Change in blood pressure: increase in systolic and decrease in diastolic - 160/60 and 140/50. 3. Left ventricular hypertrophy - manifested by increased apical impulse. The heart size is normal. 4. On auscultation, there is a loud 1 tone (popping). The systolic murmur is intense and rough. The reason is an increase in blood flow speed. Thyrotoxic heart leads to thyrotoxic cardiopathy. Lack of vitamin B1, cocarboxylase is not formed, in such patients the heart is similar to the heart of patients with beri-beri syndrome.
This is secondary cardiopathy. More often right ventricular heart failure. In young people, thyrotoxicosis is more often manifested by the heart: 1. Atrial fibrillation. 2. Left ventricular heart failure - shortness of breath at rest or on exertion, cough, hemoptysis, cyanosis, moist rales. A symptom of sinus node weakness in the elderly is atherosclerosis of the artery supplying the sinus node.
This symptom may be delayed in case of thyrotoxicosis, if there is no tachycardia, and even a tendency to bradycardia is noted. Thyrotoxicosis is the second reason that provokes weakness of the sinus node.
Manifestations from the gastrointestinal tract: 1. A decrease in body weight in 95 - 98% is associated with lipolysis and increased activity of catecholamines. 2. Appetite is good. 3. Frequent stools (from 2 to 10 - 15 times a day) without tenesmus and mucus.
Manifestations from the eyes: Thyrotoxic exophthalmos. Usually it is bilateral, without disturbances of trophism and restriction of movements of the eyeball. wide opening of the palpebral fissures (Dalrymple's sign), increased shine of the eyes (Graefe's sign), weakness of convergence (Moebius' sign), lag of the upper eyelid when looking down with the appearance of a white strip of the sclera (Kocher's sign), infiltrative ophthalmopathy - it is judged by its appearance: swelling of the upper eyelid
Lymphatic system: lymphadenopathy as a manifestation of an autoimmune disease.
Skin: There may be areas of skin depigmentation on the eyelids, face, and neck. At the beginning of the disease, hair growth is increased; as the disease progresses, hair loss is observed.
Endocrine system: increased need for cortisil. Relative insufficiency of the adrenal cortex develops, characterized by severe weakness, fatigue, and weight loss.

4. Diagnostics
Objective research. The general condition of the patient is assessed, attention is paid to the expression of fear on the face, fussiness, tearfulness, verbosity, irrational movements, trembling of outstretched arms. Height, weight and body temperature are noted. The skin of patients with toxic goiter is warm, moist, with normal turgor. Sometimes hyperpigmentation of the skin, thickening on the front surface of the leg, brittle hair, and baldness are observed. Subcutaneous fatty tissue is moderately developed, and significant weight loss is often noted.
When examining the neck area, attention is drawn to an enlarged thyroid gland. Goiter can be diffuse, mixed and nodular, of varying density and degree of enlargement.
There are several degrees of magnification:
Grade 0 – no goiter
Grade 1 – a palpable goiter the size of the distal phalanx of the thumb
Grade 2 - the gland is palpable and visible to the eye.
First, the thyroid examination is performed standing, facing the patient. On palpation, the iron is of moderate density, not fused with the surrounding tissues, and pulsates.
The isthmus is palpable when swallowing. If the sternocleidomastoid muscle is strongly developed, the patient should be asked to lean forward. When the muscle relaxes, both lobes are palpated. If the thyroid gland is low, it is examined while swallowing or with the patient lying on his back with his neck extended. It should be borne in mind that the degree of enlargement of the thyroid gland does not determine the severity of toxic goiter.
Then the eye symptoms are assessed, the time of onset of exophthalmos is specified and compared with the development of other symptoms of the disease.
During the examination of the circulatory system, attention is paid to the pulsation of blood vessels in the neck, the frequency and rhythm of heart contractions. The pulse condition is assessed in different positions of the patient.
An important indicator of the functional state of the thyroid gland is blood pressure. It should be measured two to three times, paying attention to the value of arterial pulse pressure, which, as a rule, in thyrotoxicosis is significantly increased, both due to an increase in systolic and a decrease in diastolic. Attention is also paid to the sonority of heart sounds, the presence of murmurs and the location of their listening, as well as the nature of the conduction, which is important for the differential diagnosis of the disease.
When examining the respiratory organs, the nature of breathing is noted, the presence of shortness of breath, the digestive organs - pain on palpation of the abdomen and liver.
During the study of neuropsychic activity, attention is paid to fussiness and trembling of the fingers of outstretched arms, which does not go away when attention is distracted. Sometimes you can detect paresis of the facial muscles and increased knee reflexes.
Additional research. In patients with diffuse toxic goiter, iron deficiency anemia, leukopenia, lymphocytosis, and a slight increase in ESR are determined. At the same time, hypoalbuminemia, hypergammaglobulinemia, hypocholesterolemia, hypokalemia, hypernatremia, and hypomagnesemia are observed.
The most important diagnostic significance is the increase in iodine accumulation function of the thyroid gland, the content of total thyroxine in the blood, as well as the state of the basal metabolism.

5. Treatment
First of all, it is necessary to eliminate unfavorable factors: emotional overload, professional hazards.
Treatment of diffuse toxic goiter can be conservative (medication or radioactive iodine) or surgical.
Drug therapy is effective only when the thyroid gland is enlarged no more than grade 3.
The leading place is occupied by drugs with cytostatic action. First of all, Mercazolil is used at a dose of 30-60 mg per day 2-3 times a day after meals, depending on the severity of the disease, with a further transition to a maintenance dose of 2.5-5 mg per day for 1-1.5 years.
Treatment with iodine preparations is currently strictly limited; their prescription is possible only on an individual basis.
Beta-blockers (anaprilin, obzidan) are widely used in complex treatment. Indications for their use are persistent tachycardia, extrasystole, and atrial fibrillation. Dosages are selected individually - from 40 to 160 mg per day under ECG monitoring. With the correct dose, the effect occurs within 5-7 days.
Corticosteroid drugs are also widely used. Their effectiveness is especially high with concomitant ophthalmopathy. In severe cases, they switch to parenteral administration of hydrocortisone 50-75 mg intravenously or intramuscularly. If patients are significantly exhausted, anabolic steroids and restorative therapy are used
Therapeutic nutrition: enhanced, fortified nutrition is indicated. A diet of increased energy value (20-30% more than the physiological norm) is recommended due to a uniform increase in proteins, fats, and carbohydrates. Foods and dishes that stimulate the cardiovascular and nervous systems are excluded from the diet: strong broths, chocolate, spices, strong tea, coffee. Eating 5 times a day.

6. Nursing process

Problem What the nurse does

Increased excitability and irritability Monitor compliance with the medical and protective regime (separate room, elimination of irritating factors, silence, adherence to deontological principles.
Excessive sweating Careful skin care. Frequent change of underwear and bed linen

Lack of information about the disease Conduct a conversation with the patient about his disease, preventing possible complications. Provide the patient with the necessary popular scientific literature.
Difficulty accepting diet changes due to previously established habits. Explain to the patient the importance of following a diet. Encourage the patient to follow the diet. Monitor transfers to relatives.
The need to constantly take medications. Have a conversation about the need to take medications on a regular basis. Explain the mechanism of action of prescribed medications. Explain the possibility of side effects of the medications used and the need for timely information about them to medical staff. Monitor the timely intake of medications.

Reduced ability to work due to weakness Explain to the patient the importance of timely and systematic taking of medications, adherence to diet, work and rest schedule.

Poor heat tolerance Monitor cleaning and ventilation of the room. Recommend wearing light clothing.

Sleep disturbance Create conditions for proper rest (bed comfort, cleanliness, silence, fresh air). Offer milk with honey and soothing herbal teas at night. Have a conversation with relatives about the need for psychological support for a loved one. Consult a doctor.

Headache, heart pain, palpitations due to increased blood pressure. Teach the patient and his family members how to measure blood pressure and pulse. Convince the patient of the need to systematically take medications.

Conclusion
The endocrine system is, along with the nervous system, the main regulator of the vital functions of the entire organism. Hormones released into the blood react with almost any cell, but the effect appears only when interacting with “target” cells that have specific receptors.
Diffuse toxic goiter belongs to the group of psychoendocrine pathology, develops on a genetically altered background with the presence of autoaggression of immunocompetent cells to antigens of thyroid tissue. Mostly urban residents are affected, most often women aged 20 to 50 years.
In severe forms of thyrotoxicosis with severe neuropsychic disorders, the patient needs constant supervision by nursing staff.
The disease is usually preceded by long-term or short-term, but extremely intense stress factors, difficult experiences due to the loss of loved ones, conflicts in the family and at work.
There are also familial forms of the disease, when relatives are found to have not only diffuse toxic goiter, but also other autoimmune diseases.

Literature

1. Algorithms for the diagnosis and treatment of diseases of the endocrine system, ed. I. I. Dedova. - M., 2005 – 253 p.
2. Balabolkin M. I. Endocrinology. – M.: Medicine, 2004 – 418 p.
3. Directory of general practitioners. In 2 volumes. / Ed. Vorobyova N.S. –M.: Eksmo Publishing House, 2005- 320 p.
4. Smoleva E.V. Nursing in therapy. – Rostov n/a: Phoenix, 2007 – 473 p.

Few people know what diffuse nontoxic goiter is, so patients, upon hearing this diagnosis, often find themselves in a difficult situation. The doctor cannot always clearly explain to the patient the features of the disease, but understanding your diagnosis facilitates the treatment process.

What is non-toxic diffuse goiter

Diffuse non-toxic goiter is characterized by swelling of the thyroid gland while maintaining its ability to produce hormones. The pathology that occurs in areas of iodine deficiency is called endemic goiter, in areas with sufficient content - sporadic. More often, diffuse non-toxic goiter is diagnosed in women of fertile age, during gestation and lactation, and during menopause. In medical publications, nontoxic goiter is also called diffuse euthyroid goiter.

At the initial stage of development of pathology, hyperplasia and hypertrophy of the epithelial cells of the organ occurs. In the later stages of non-toxic damage, due to untimely and insufficient treatment, structural changes begin - the walls of the organ become denser, the follicles are filled with colloidal tissues.

Reasons for the development of non-toxic diffuse goiter:

  • lack of iodine leads to increased production of hormones by the thyroid gland and its expansion;
  • interruptions in the activity of the enzyme system responsible for the production of thyroid hormones;
  • lesions of the pituitary gland, where thyroid-stimulating hormone (TSH) is synthesized, which regulates the activity of the thyroid gland;
  • infectious diseases;
  • lack of certain vitamins and microelements (retinol, cobalt, copper, zinc, molybdenum);
  • bad habits and psycho-emotional overload;
  • taking medications;
  • heredity;
  • protein deficiency;
  • consumption of vegetables containing thiocyanates, which interfere with the normal development of the thyroid gland;
  • chemical poisoning with pesticides, cyanides, nitrogen oxides.

Non-toxic goiter in the initial stages is not associated with pathological or inflammatory processes in the body; it is expressed only in an increase in the size of the organ.

Nontoxic lesions are diffuse and nodular. In the first case, all cells of the gland are affected. In the presence of a small number of healthy cells against the background of changes in a large area of ​​the gland, the pathology is called diffuse nodular; if single areas of the organ are affected, then this is a toxic nodular goiter.

Diffuse nontoxic goiter is diagnosed in half of the cases in adolescents under 20 years of age, after 30 years of age - in 20% of cases. Women get sick several times more often than men.

Symptoms

A feature of non-toxic diffuse changes is unexpressed symptoms:

  • Swelling in the cervical area.
  • Increased fatigue, headaches, tightness around the neck, cough, difficulty breathing when lying down.
  • Insufficiency of the hormone thyronine, leading to lethargy, dry skin, and bradycardia.
  • Difficulty swallowing food.
  • Adolescents show signs of disturbances in the functioning of the endocrine system - instability of behavior, psycho-emotional breakdowns. Children are diagnosed with euthyroidism (when the enlarged gland functions normally), but speech is impaired, and there is mental and physical underdevelopment.
  • In later complicated stages of nontoxic goiter, pathological changes in the heart (dilatation of the right ventricle), hemorrhages in the thyroid tissue, inflammation (strumitis), and the development of malignant tumors are possible.
  • Violation of the concentration of TSH causes an enlargement of the thyroid gland, as a result, strangulation of the trachea and esophagus occurs.

Diagnostics

The primary diagnosis of diffuse non-toxic goiter is carried out through visual examination and palpation of the gland for swelling and the presence of nodular seals. Normally, its volume in women does not exceed 18 ml, in men - 25 ml.

With non-toxic goiter in the initial stage, the iron increases slightly, feels soft or moderately dense to the touch, and mobility during swallowing movements is good. Changes in organ volumes are rather diffuse in nature. Laboratory blood tests are necessary to check the production of hormones (TSH, T3, T4) and the presence of antibodies to exclude autoimmune thyroiditis.

Instrumental examinations:

  • Ultrasound, sonography and elastography of the gland to determine its size, structure and the presence of nodes;
  • radiograph;
  • ECG of the heart;
  • a biopsy may be prescribed;
  • scintigraphy - examination of an organ with radioisotope particles;
  • radiography with the introduction of contrast agents into the body.

Non-toxic damage is characterized by diffuse expansion, mild or moderate organ density, and unimpaired functionality.

Classification

According to the classifier, non-toxic diffuse goiter is divided into the following stages:

  • Grade 1 - slight enlargement of the thyroid gland.
  • 2nd degree - the gland is determined by palpation and is also visible when swallowing or throwing back the head.
  • 3rd degree - the organ is clearly visible. Characteristic symptoms occur: shortness of breath and frequent migraines.
  • 4th degree - obvious deformation of the cervical spine, the gland makes swallowing and breathing difficult, and speech impairment is possible.
  • Grade 5 - the thyroid gland grows to a large size, its weight can reach 2 kg.

Treatment of diffuse non-toxic goiter

Treatment methods depend on the stage of development of the pathology. A slight enlargement of the gland caused by iodine deficiency is cured by prescribing iodine preparations (Antistrumin, Iodomarin, Iodine Balance, etc.).

Treatment of non-toxic diffuse goiter of a higher degree is carried out in 2 stages using a combined method:

  • Stage 1 lasts 1-2 years until the goiter decreases or completely disappears. Levotrexin, Euthyrox, L-Thyroxine are used.
  • Stage 2 is aimed at restoring the size of the thyroid gland by taking potassium iodide preparations.

For general strengthening of the body, vitamin therapy is prescribed (complexes containing vitamins A, B12, E, D). For hormonal deficiency, medications containing the hormones T3 and T4 are prescribed. Hormonal treatment takes a long time; in most cases, lifelong use of hormones is indicated.

In advanced forms of nontoxic goiter and malignant neoplasms, surgery or treatment with radioactive iodine is required. If the operation is impossible for some reason, ethanol or laser destruction is used.

Non-drug treatment

To increase the level of iodine in the body, seafood is useful - fish, mussels, shrimp, crabs, etc. To compensate for vitamin deficiency, use butter, fish oil, red carrots, liver (beef, pork).

However, you need to know that some products slow down the process of iodine absorption and suppress the functions of the thyroid gland in adults, and remove their own iodine from the body of children. Such products include cabbage, broccoli, turnips, turnips, radish, horseradish. They should be excluded from daily nutrition. Thus, a competent combination of vitamins and diet is a fundamental factor in the favorable outcome of treatment of non-toxic goiter.

It is useful to drink dissolved sea salt (5 g dissolved in 250 ml of boiled water, drink once a day). You can also drink iodine solution (3 drops per 200 ml of water). It is recommended to place an open bottle of iodine on the closet in the patient's bedroom.

Forecast

With qualified and timely treatment of non-toxic goiter, the prognosis is favorable. The development of diffuse non-toxic damage stops or decreases.

However, one should not forget about an annual preventive examination by an endocrinologist. The healing process depends on many factors - age, degree of neglect of the disease and the individual characteristics of the body. In childhood, recovery occurs faster.

Prevention

Preventive measures include regular consumption of foods containing iodine (seaweed, persimmon, sea fish), adding iodized salt to food. It is recommended to adhere to a healthy lifestyle (proper nutrition, adequate sleep, physical activity), and avoid emotional overload.

A sanatorium-resort holiday on the seashore, where the air contains iodine particles, will be useful.

It is also necessary to pay attention to improving living conditions; it is advisable to change the place of residence if the patient is in an area where chemical waste is released. Women of fertile age should undergo regular examination by an endocrinologist. During menopause, hormonal medications are prescribed.

Diagnosis and treatment of diffuse toxic goiter

Diffuse toxic goiter is an autoimmune disease of the thyroid gland. This disorder is caused by antibodies that produce excess hormones that damage the gland. In the international classification, the disease is coded ICD 10.

Symptoms of diffuse toxic goiter are most often observed in young women; men are less likely to get sick. Diffuse toxic goiter in children is also a fairly common occurrence, which poses a serious danger if there is insufficient attention and improper treatment. The disease causes problems with the central nervous system, digestive system organs, and joint destruction.

  • Causes of the disease
  • Classification of the disease, its signs and manifestations
  • Pathogenesis of toxic goiter of the thyroid gland
  • Diagnosis of the disease

Causes of the disease

The etiology of diffuse goiter has been sufficiently studied; the problematic condition of the thyroid gland causes a state of the immune system that produces antibodies that destroy gland tissue. The etiology of goiter is also influenced by the following factors:

  • Tonsillitis, sinusitis and other bacterial and viral diseases.
  • A genetic factor, toxic goiter often affects several generations in the same family.
  • Depression, stress, negative emotions.
  • Drinking alcoholic beverages and smoking.

The etiology and development of Graves' disease is influenced by autoimmune diseases:

  • diabetes, mainly diabetes;
  • vitiligo;
  • problems with the adrenal glands;
  • arthritis.

Classification of the disease, its signs and manifestations

Experts classify Graves' disease (ICD 10) depending on the form of the pathology:

  • Mild degree, in which the shape of the thyroid gland is not disturbed, the work of the heart and its rhythm are within normal limits. A mild degree is manifested by hot temper and excessive emotionality.
  • With moderate severity of DTD, problems begin in the cardiovascular system, weight decreases sharply, and tachycardia occurs.

Classification allows you to choose the right therapy and prevent complications.

Pathogenesis of toxic goiter of the thyroid gland

DTD manifests itself in different ways, usually as a disorder of the cardiovascular system and ophthalmopathy. ICD 10 causes tachycardia, sudden increases in pulse and blood pressure. Long-term, untreated DTD leads to the development of complications such as edema, myocardial disorders, and rapid breathing.

Toxic goiter changes the condition of the eyes, visually noticeable ophthalmopathy, protrusion of the eyes, strange shine, constant blinking. The cause of these complications is high intraocular pressure. Without treatment, blindness gradually develops.

When the central nervous system is affected by DTS, the following signs are observed:

  • aggressiveness;
  • Bad mood;
  • irritability;
  • insomnia;
  • tremor;
  • poor memory;
  • speech disorders;
  • difficulties with movement.

The pathogenesis of diffuse toxic goiter is not fully understood; endocrinologists assign the main role in the development of thyroid disease to the nervous system. The evidence is the connection between diffuse goiter and vegetative-vascular dystonia that precedes DTD. The pre-stage of the disease is considered to be a violation of the absorption of iodine by the thyroid gland.

Increased functionality of the thyroid gland plays an important role in the pathogenesis of the disease. Excessive intake of hormones into the blood changes the functioning of internal organs. The offender is mainly thyrotropin, which accumulates in the thymus gland. Thyroid hormones in the muscles, kidneys and liver change the ionic composition of the blood, and calcium and protein metabolism are disrupted. Phosphorus, ammonia, nitrogen, potassium and amino acids accumulate in the blood and urine. A violation of fat metabolism is also possible. All of these factors weaken the muscles and lead to an increase in temperature.

Diagnosis of the disease

Differential diagnosis of diffuse toxic goiter is based on laboratory test data and general clinical studies. Pronounced symptoms are confirmed by test data. DTD is characterized by a decrease in TSH and high levels of T3 and T4. Often T3 titers are higher than T4.

Some forms of thyroid disease produce high T3 but normal free thyroxine. If T3 and T4 are slightly elevated and symptoms of thyrotoxicosis are observed, a rifathiroin test is performed. A low TSH confirms a toxic thyroid goiter. Very rarely, a high level of TSH is detected, confirming a pituitary adenoma; in this disease, T4 and T3 will also be elevated.

For the diagnosis of toxic goiter of the thyroid gland, the status of antibodies is important. To determine the level of antibodies to thyroglobulin, an immunofluorescent method is used, which makes it possible to isolate antibodies to thyroglobulin, nuclear antigens, colloidal antigen, and microsomal antigen in the blood serum. The detected antibodies are indicators of thyroid pathology.

To identify complications associated with toxic goiter, patients are referred for cAMP sections of the thyroid gland. The most reliable information can be obtained by combining the biological method of cAMP sections with determining the level of hormones in the blood. The percentage of hormones serves as a criterion for the duration of treatment, but does not help in determining the degree of toxic thyroid goiter. Unauthorized cessation of treatment at a thirty percent level of thyroid-stimulating immunoglobulin leads to serious complications.

Patients receiving thyreostatics are referred for determination of the TSI titer at the beginning of treatment and before its discontinuation. A persistently high level of TSI is a decisive factor for referral for thyroid resection surgery.

Adequate therapy with radioactive iodine or thyreostatics leads to a decrease in TSI levels, and patients experience a decrease in symptoms of the disease. After resection, TSI titers decrease in eighty percent of patients.

Changes in the functioning of the thyroid gland occur mainly in the first trimester of pregnancy, when the fetal thyroid gland is not yet functioning and its development is stimulated by the mother’s endocrine gland. Normally, the level of thyroid hormones in pregnant women increases by fifty percent. A low TSH level indicates a dysfunction of the thyroid gland. Developing toxic goiter complicates pregnancy and leads to miscarriage, and the threat of miscarriage most often threatens women in early pregnancy, which is associated with increased production of thyroid hormones.

Pregnant patients diagnosed with DTD develop early toxicosis; this condition is associated with the acute period of the disease, metabolic disorders and problems with the central nervous system. Severe early toxicosis in women with toxic goiter is very difficult, in some cases the pregnancy is terminated.

Clinic of disorders in pregnant women:

  • enlarged thyroid gland;
  • tachycardia;
  • tremor;
  • weakness;
  • weight loss;
  • emotional instability;
  • sweating;
  • ophthalmopathy.

Ophthalmopathy does not affect all women; sometimes the disease manifests itself as hyperemia of the conjunctiva and sclera, swelling of the eyelids and impaired eye mobility.

In the second and third trimester of pregnancy, remission may occur, the symptoms of thyrotoxicosis disappear, this is facilitated by physiological immunosuppression.

Clinical manifestations of thyrotoxicosis at an early stage can easily be confused with the symptoms of bearing a child. Pregnant women often experience tachycardia, shortness of breath, increased appetite, insomnia, and emotional instability. Thyrotoxicosis adds to this ophthalmopathy and goiter.

Diffuse toxic goiter in children is treated in a hospital. Children are prescribed bed rest and a diet high in protein, vitamins and microelements. Drug therapy with Mercazolil is carried out, which inhibits the function of the thyroid gland, as a result of which the synthesis of hormones slows down. The optimal dose of the drug is from 10 to 30 mg per kilogram of body weight. Therapy with Mercazol continues for at least seven weeks, under the supervision of the attending physician.

Starting from the third week of treatment, patients are prescribed additional thyroidin, the dose of which is selected individually.

Toxic goiter in children is classified the same as in adults. Mild, moderate and severe degree of impairment.

Children with severe forms of the disease are prescribed Reserpine, a drug that has a sedative effect, and in special cases they are treated with tranquilizers.

Diagnosis of Graves' disease in children is not difficult with clearly manifested symptoms:

  • ophthalmopathy;
  • increased fatigue;
  • tachycardia;
  • weakness;
  • sweating;
  • emotional instability.

When diagnosing toxic goiter, it is taken into account that the disease has symptoms partially similar to adolescent disorders of the autonomic vascular system. Vegetative-vascular dystonia is characterized by: sweating, high blood pressure, tachycardia. However, with adolescent vegetative-vascular dystonia, weight loss and rheumatic carditis are not observed.

Thyroid goiter - what is it? This question can be heard in different parts of the world due to the fairly wide distribution of the phenomenon. 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.

Goiters of various types appear 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 violation of the secretory function of the gland:

  • Hypothyroidism: decreased secretory function, leading to a decrease in the release of hormones, which causes consequences such as attenuation of metabolic processes, swelling, obesity, and 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 of the necessary hormones and with its acute deficiency it is necessary to pump much more blood through itself, and the iron 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 fibrous tissue is formed at the site of cell death. This type of disease mainly has hereditary causes, but can sometimes be initiated by injury, infection, cervical inflammation, chronic pharyngitis, iodine abnormality and toxic air pollution.
  • 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 nodule as a result of excessive secretion of thyrotropin, as well as disruption of the functioning 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 of an autoimmune pathology of an inflammatory nature, through the growth of connective tissue from fibrin fibers.

Degrees of enlargement of the thyroid gland

During the development of the disease, varying degrees of enlargement of the gland are observed. 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: A huge goiter that puts pressure on the neck, causing problems with breathing and swallowing.

Causes, symptoms, diagnosis and treatment of nodular goiter

Nodular goiter is a local proliferation of glandular tissue, which can be of a 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: malignant tumor 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 of nerve endings in any part of the gland; polluted habitat (increased background radiation, nitrite pollution, oversaturation of soil with calcium, etc.); psychological stress; head injuries; hormonal changes; decreased immune defense after illness.

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 apparent 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 also have a general manifestation, depending on the nature of the pathology. With hypothyroidism, the following symptoms can be identified, such as 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.

With thyrotoxicosis, the symptoms are as follows: fever and fever; increased heart rate; irritability; losing weight with a good appetite; feeling of hotness on the 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 a general blood test (for hormones). More accurate results are obtained after ultrasound of the thyroid gland, biochemical blood test, and 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); female 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 of a foreign body in the throat. Additionally, it can be noted: with hypothyroidism - slow reaction, weakness, constipation, slow heart rate, low temperature; with hyperthyroidism - excitability, insomnia, increased heart rate, increased temperature.

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

Thyroid nodules. Reasons

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. The following reasons lead to such diseases: iodine deficiency, hereditary pathologies; uncontrolled use of drugs containing iodine; female hormonal changes; diseases affecting the immune system (diabetes, arthritis, scleroderma); age factor; prolonged stress or nervous shock; surgical operations on the thyroid gland.

Specific symptoms of diffuse goiter 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 is carried out when a severe form of thyrotoxicosis develops, the goiter is too large, or complications arise in the form of atrial fibrillation.

Regardless of its functional state and morphological changes in it. Goiter should be regarded only as a symptom that can be caused by many pathological processes. The diagnosis of goiter cannot be considered sufficient; it always requires further clarification.

A simple goiter is understood as an enlargement of the thyroid gland of a non-inflammatory, non-malignant nature with clinical euthyroid function. Traditionally there is a distinction endemic goiter(in a certain area more than 5% of school-age children are affected) and sporadic(in other cases).

Endemic goiter is one of the common endocrine diseases. According to WHO, about 15 billion people live in regions with iodine deficiency, of which more than 300 million suffer from goiter. The most ancient endemic regions include the plateaus of the Alps, Andes, Himalayas, Pamirs, Carpathians, etc. Endemic foci of different sizes and severity of goiter are found in most countries. Thus, this disease is global in nature.

Today, endemic goiter is usually considered within the framework of a much broader problem - iodine deficiency disorders, which can manifest themselves at different periods of a person’s life (Table 1).

Table 1. Clinical manifestations of iodine deficiency disorders

Life period Clinical manifestations
AnyGoiter, hypothyroidism (manifest or subclinical)
NewbornsHigh perinatal mortality, congenital hypothyroidism, cretinism, congenital malformations
Children's, teenagersDelayed mental and physical development, decreased performance, susceptibility to chronic diseases, impaired sexual development
MaturityDecreased physical and mental performance, accelerated development of atherosclerosis
Reproductive period in womenInfertility, spontaneous miscarriages, stillbirths, anemia

Etiology, pathogenesis.

Numerous studies have confirmed the role of exogenous iodine deficiency as the main etiological factor of endemic goiter. If iodine intake into the body does not exceed 100 mcg per day, the thyroid gland increases compensatoryly.

Effect of iodine deficiency may be enhanced by other factors: unsatisfactory sanitary and hygienic conditions, unbalanced nutrition (deficiency of cobalt, zinc, molybdenum and, possibly, selenium), excess calcium and fluorine in water, and in some cases, genetic predisposition, natural and synthetic gormogenic substances.

The level of iodine deficiency in a particular region is assessed by determining urinary iodine excretion in a limited (randomly selected) population of individuals. At the same time, according to WHO recommendations, the following are distinguished: forms of iodine deficiency:

  • weak(median iodine excretion - 50 -99 mcg/l, goiter frequency in schoolchildren - up to 20%);
  • moderate(irodine excretion rates - 20-49 mcg/l, goiter frequency - up to 30%);
  • heavy(iodine excretion - up to 20 mcg/l, goiter frequency - more than 30%).

Additional criterion The distribution of endemic goiter can be measured by the Lenz-Bauer index - the ratio of men and women with goiter. If with mild endemicity it averages 1/6, then with severe endemicity it can approach 1/1.

Enlargement of the thyroid gland in endemic goiteris happeningdue to two mechanisms:

  • hypertrophy, depends on the hypersecretion of thyrogropin in response to a decrease in the synthesis of thyroid hormones;

hyperplasia, which depends on iodine deficiency in the gland itself and the associated activation of local factors regulating cell growth.

Initial diffuse hyperplasia Over time, it changes to uneven, focal with cell atrophy in other parts of the organ. This affects the progress of enlargement of the thyroid gland and the formation of nodes, often multiple, as well as the attachment of secondary regressive changes (hemorrhages, fibrosis, hyalinosis, cysts, etc.). So, although at the beginning the process can be regarded as compensatory, it should be considered physiological.

Classification.

There are the following forms of iodine deficiency:

  • Thyroid diseases associated with iodine deficiency and similar conditions;
  • Diffuse (endemic) goiter associated with iodine deficiency;
  • Multinodular (endemic) goiter associated with iodine deficiency;
  • Goiter (endemic), associated with iodine deficiency, unspecified;
  • Other thyroid diseases associated with iodine deficiency and similar conditions.

Clinic.

Manifestations of the disease depend on the functional state of the thyroid gland, the size and location of the goiter. In the vast majority of patients, the goiter is euthyroid, therefore, with insignificant sizes, complaints are either absent or non-specific. Often, an enlarged thyroid gland is diagnosed accidentally. With a large goiter, patients complain of discomfort and swelling of the anterior surface of the neck, difficulty swallowing, sometimes hoarseness of the voice, lack of air, indicating local mechanical complications (compression of the trachea, esophagus or blood vessels), especially characteristic of a retrosternal goiter.

According to the form, they distinguish between diffuse, nodular (mono-, polynodose) and mixed goiter. It is advisable to determine the degree of enlargement of the thyroid gland in accordance with WHO recommendations:

Degree 0- absence of goiter.

Degree 1- the goiter is determined only by palpation and is not visualized when the head is abandoned.

Degree 2- the goiter is palpated and visualized only with the head thrown back.

Degree 3- goiter is visualized with a normal neck position; Palpation is not necessary to make a diagnosis.

Degree 4- a very large goiter that can be recognized remotely.

Endemic goiter can occur in isolation or in combination with other iodine deficiency disorders (see Table 1). Some of them (manifest hypothyroidism, cretinism, congenital goiter) are observed rarely - only in regions with extreme iodine deficiency. At the same time, as studies in recent years have shown, it is quite often possible to diagnose subclinical hypothyroidism (SH), which directly or indirectly causes the development of most of the above pathological conditions.

Mostly not difficult, especially if you use the following guidelines:

  1. In all cases, anamnesis is collected, conducts an objective clinical examination and ultrasonography of the thyroid gland, including determination of its volume. Ultrasonography (ultrasound) makes it possible to diagnose goiter if the volume of the thyroid gland exceeds the upper limit of the age norm. With diffuse enlargement of the gland, there are no characteristic changes in its echo structure. With nodular goiter, round or oval-shaped formations with varying echogenicity and predominantly clear contours are visualized, in some places with echo-negative inclusions.
  2. If clarification is necessary The following measures are used for diagnosis or differential diagnosis:
  • if hypo- or hyperthyroidism is suspected, the content of thyroid hormones in the blood is determined quantitatively, and sometimes scintigraphy is performed:
  • if autoimmune thyroiditis is suspected, the level of antithyroid antibodies in the blood is determined;
  • for nodular goiter, scintigraphy and fine-head biopsy are performed;
  • in case of local mechanical complications, conducts X-ray examinations and, if necessary, CT scans.
  1. It should be especially emphasized that oncological vigilance is mandatory for nodular forms of goiter: a complex of available examination methods is used.

Treatment.

Treatment of endemic goiter can be medicinal and/or surgical.

Drug treatment carried out most often in order to reduce the volume of the thyroid gland by an average of 30-40%.

Indications for drug therapy:

  • juvenile goiter of any stage, mostly diffuse; an attempt is possible with multinodular forms, the exception is the solitary node;
  • diffuse and multinodular primary and recurrent goiter of stages I and II in adults,
  • Stage III goiter: an attempt is acceptable, but ineffective;
  • goiter in pregnant women.

Treatment with thyroid hormones. The goal is suppression (inhibition) of thyrotropin secretion and its dependent hypertrophy of thyrocytes. Most often, L-thyroxine is used at a dose of 50-150 mcg per day. It is possible to use triiodothyronine or combined drugs (thyroidome). Iatrogenic thyrotoxicosis associated with overdose develops as a complication, which does not require discontinuation of therapy, but only dose adjustment.

Treatment with iodine preparations. The goal is to eliminate intrathyroidal iodine deficiency and associated hyperplasia of thyrocytes. Especially recommended for use on children and adolescents. The daily dose of iodine is:

  • for preschool children - 100 mcg
  • for schoolchildren and adults - 200-300 mcg.

Potassium iodide tablets are prescribed (antistrumin, iodide-100, iodide-200). The main danger of this technique is the development of iodine-induced hyperthyroidism, mainly in elderly patients, in whom areas of autonomously functional thyroid tissue are often detected.

Goal of combination treatment L-thyroxine and iodine preparations- impact on both links of pathogenesis. Today this method is considered optimal. The combination of two drugs is selected individually (for example, 50-150 mcg per day of L-thyroxine + 100-200 mcg per day of potassium iodide) or some ready-made drugs are used ( thyrocomb, iodothyrox).

The duration of drug treatment is 6-18 months. The size of the gland is monitored every 3 months by palpation and ultrasound. After completing a course of drug therapy, patients are recommended to take long-term individual iodine prophylaxis to prevent relapse.

Surgical treatment.

Indications:

  • Stage III goiter, especially in the presence of manifestations of compression of the respiratory tract, esophagus or blood vessels;
  • reasonable suspicion of cancer - nodular goiter in children, men, with rapid growth, dense consistency or limited mobility, based on ultrasound or cytological examination;
  • goiter resistant to drug therapy, especially with regressive changes or a tendency to further growth;
  • persistent expression of the patient's will;
  • recurrent goiter (remember the high incidence of postoperative complications).

Surgical treatment of endemic goiter, like other diseases of the thyroid gland, it is advisable to carry out in specialized departments, which minimizes the incidence of early and late postoperative complications.

Prevention.

Despite its significant prevalence, endemic goiter is one of the diseases that will require effective primary prevention aimed at neutralizing main etiological factor- iodine deficiency.

Very important that adequate iodine prophylaxis makes it possible to prevent the occurrence of not only endemic goiter, but also the entire spectrum of iodine deficiency pathology. At the same time, they take into account the recommendations of the International Council for the Control of Iodine Deficiency Disorders regarding the optimal supply of iodine to the body, according to which its daily dose (mg) should be:

  • children under 1 year old — 50,1-6 years — 90, 7-10 years — 120;
  • children over 10 years old and adults — 150, pregnant women and mothers — 200.

It is advisable to distinguish between the following forms of goiter prevention:

  • general (mass) targeting all residents of a certain endemic region must be carried out constantly. In this case, the method of adding potassium iodide to kitchen salt, first introduced in 1922 in Switzerland, has proven itself to be the best;
  • individual (additional administration of iodine preparations to certain populations, primarily):

— Children and adolescents (especially during puberty);

— Pregnant women and mothers;

— Persons with a positive family history;

— Persons temporarily residing in an endemic region;

— Patients after drug or surgical treatment of endemic goiter (secondary prevention).

Methodology for individual prevention:

  • children of preschool age - 100 mcg per day;
  • school-age children and adults - 150-200 mcg per day of potassium iodide or iodomarin, or 1 tablet (during pregnancy and breastfeeding - 2 tablets) of antistrumin per week.

Endemic goiter - symptoms and treatment (video)


Based on materials:

Nodular goiter of the thyroid gland implies the presence of neoplasms (nodules) of various nature and morphology in the thickness of the organ. Now almost every second adult suffers from this disease, and statistics indicate a higher prevalence among women. A certain relationship has also been identified between goiter and neoplasms in the female genital organs. These diseases are often combined with each other. During an objective medical examination, a node is detected only if its size exceeds 1 cm. Otherwise, pathology can be detected only with ultrasound examination. When several nodes are identified during examination, we are talking about a multinodular goiter.

The advisability of early detection of the disease is dictated by several factors: the need to exclude malignant neoplasms and prevent hormonal disorders, aesthetic defects and compression of surrounding organs due to a possible increase in the size of the node.

Etiology of the disease

The causes of nodular goiter have not been fully studied by official medicine. They vary depending on the histological picture. Thus, toxic goiter develops as a result of a mutation in the thyroid-stimulating hormone receptor gene and G protein, which normally inhibits the production of adenylate cyclase. The altered protein uncontrollably stimulates this enzyme, which leads to increased cell proliferation. Mutations are also responsible for the development of medullary cancer.

The occurrence of colloid goiter is associated with age-related changes in the organ. A predisposing factor to the development of this disease is a lack of iodine in the body. Lack of a microelement also causes thyrotoxic multinodular goiter. We should not forget about predisposing hereditary factors, genomic pathologies, negative environmental influences (ionizing radiation), side effects from taking certain medications, smoking, lack of vitamins and minerals, psycho-emotional stress, chronic infectious and inflammatory diseases (for example, chronic tonsillitis) . All of the above factors can serve as a trigger for the development of nodular pathology of the thyroid gland.

Classification of the disease

Depending on the morphological picture they differentiate:

  • nodular colloid proliferating goiter;
  • diffuse nodular goiter;
  • benign node;
  • malignant tumor.

Colloid goiter is the most common pathology, occurring in 90% of the population in the structure of general thyroid disease. The second place is occupied by benign tumors (5-8%), and the last place in this line belongs to malignant tumors (2-5%).

Sometimes pathological foci similar to nodes are detected in the thyroid gland. This is often facilitated by inflammatory processes, including those of an autoimmune nature, as well as other diseases. For example, cysts are also frequent “companions” of nodular pathology.

Based on the number of nodules, they are distinguished:

  • solitary goiter, when there is one node in the thyroid gland;
  • multinodular goiter - two or more;
  • conglomerate goiter - several encapsulated nodes soldered to each other.

Depending on the degree of enlargement of the endocrine organ, different degrees of nodular goiter are determined. In practical medicine, two classification options are used - according to O. V. Nikolaev and according to WHO recommendations.

In the classification of goiter according to Nikolaev O.V. six degrees offered:

  • 0 - the organ is not identified upon examination and palpation;
  • 1 - organ enlargement is recognized by palpation;
  • 2 - the gland is visible during swallowing movements;
  • 3 - during a routine examination, an enlargement of the neck is recorded;
  • 4 - the shape of the neck changes due to a significant enlargement of the thyroid gland;
  • 5 - compression of surrounding organs and tissues occurs.
  • 0 - no signs of goiter (the size of each lobe is no more than the size of the distal phalanx of the thumb);
  • 1 - the node is not detected by visual inspection, but is determined by palpation;
  • 2 - the formation is visible to the naked eye.

Symptoms of the disease

Often, provided that the thyroid gland is of normal size and its function is optimal, patients do not report any complaints. Clinical manifestations make themselves felt only if excessive enlargement of the organ leads to compression of the surrounding anatomical structures, as well as in case of dysfunction of the gland itself.

Mechanical compression of nearby organs causes various complaints depending on which organ is affected. Thus, compression of the larynx and trachea leads to breathing problems, foreign body sensation, a constant dry cough and a hoarse voice. Compression of the esophagus makes swallowing difficult. Compression of blood vessels is fraught with the appearance of general cerebral symptoms, as well as difficulty in the outflow of venous blood from the upper parts of the body. Pain may also be observed at the location of the thyroid gland due to the development of an inflammatory process in it or a rapid increase in the size of the pathological focus.

Violation of the functional activity of the organ leads to the appearance of hyper- or hypothyroidism. Hyperfunction is manifested by characteristic symptoms of thyrotoxicosis: prolonged low-grade fever, trembling at the fingertips, increased heart rate, protruding eyeballs, increased irritability, insomnia, pronounced appetite, accompanied by weight loss.

Reduced thyroid function or hypothyroidism is manifested by clinical symptoms opposite to thyrotoxicosis: decreased body temperature, bradycardia, drowsiness, and lack of appetite. Patients are concerned about dry skin, pain in the cardiac region, a decrease in blood pressure, a depressive state develops, disorders of the gastrointestinal tract, genital area, patients often become susceptible to diseases of the upper respiratory tract and acute respiratory viral infections.

Our doctors:

Diagnosis of nodular goiter

To clarify the diagnosis, it is preferable to consult an endocrinologist. First of all, the specialist will conduct an objective examination and palpate the thyroid gland. At this stage, it is already possible to determine or suspect the presence of pathology.

The further sequence of actions includes performing an ultrasound examination to verify the diagnosis and clarify the nature of the disease. The next stage of diagnosis (if a node more than 1 cm in diameter is identified) is a biopsy to assess the morphological picture of the neoplasm.

As additional laboratory tests, a blood test is performed for thyroid hormones (thyroid-stimulating hormone, free T3 and free T4). To assess the activity of thyroid tissue and nodular formations, a radiological examination is used - scintigraphy. The patency of the esophagus can be seen during X-ray examination with contrast. Spiral computed tomography is performed when a detailed study of the characteristics of the gland is necessary, as well as the condition of the lymph nodes surrounding the organ.

Treatment of nodular goiter

Nodular colloidal proliferative goiter does not always require treatment. If the nodule is small in size, without a tendency to grow rapidly, and the function of the thyroid gland is not impaired, the endocrinologist will recommend only dynamic monitoring in the form of annual ultrasound monitoring and a blood test to determine the level of thyroid hormones.

If indicated, the specialist usually prescribes medication, radioactive iodine therapy, or surgery.

The effect of medications (thyroid hormones) for hypothyroidism is to inhibit the production of thyroid-stimulating hormone, which ultimately leads to regression of nodular pathological formations.

The operation is indicated for a significant increase in the size of the endocrine organ, which compresses surrounding organs and deforms the neck, as well as for the diagnosis of toxic goiter or a malignant neoplasm. The volume of intervention is determined by the surgeon strictly individually. This can be the removal of just one node, the affected lobe of the thyroid gland with the isthmus, most of it, or the total removal of both lobes of the gland with the isthmus (thyroidectomy).

Treatment with radioactive iodine, with proper dose selection, can act as an alternative to surgery, reducing the size of the goiter by 30-80%.

Disease prognosis

The prognosis of the disease depends on the morphological picture after the biopsy. For example, nodular euthyroid colloid goiter has the most positive prognostic indicators, while thyroid cancer cannot boast of this.

It is necessary to contact an endocrinologist on time, at the very first signs of the disease. It is better to carry out screening examinations so as not to miss the initial stages of thyroid disease, when there is still the possibility of a complete cure.

CELT doctors are always happy to help: establish a diagnosis, determine the causes of the disease and correctly prescribe the necessary treatment for the identified pathology, taking into account the individual characteristics of your body. If indicated, the clinic also performs surgeries to remove thyroid tumors. CELT specialists have a huge amount of knowledge and practical skills behind them, so you can safely entrust your health to our highly qualified professionals.