Diagnosis, treatment, laboratory tests.
Pathology of the thyroid gland
The thyroid gland is located on the front surface of the neck, below the cricoid cartilage, consists of 2 lobes, interconnected by an isthmus. The follicular cells of the gland produce two major hormones: tetraiodothyronine (thyroxin, T) and triiodothyronine (T). These hormones affect the cells of virtually all body tissues, affecting nuclear receptors and changing the expression of a wide range of genes. Thyroid hormones determine the normal development of the brain and somatic tissues in the fetus and newborn and regulate the metabolism of proteins, carbohydrates and fats at any age.
T has only minimal hormonal activity. Nevertheless, T has a longer duration of action, can be converted to T (in most tissues) and, thus, is saved as a reserve for the formation of T. The third form of the hormone, reversible T (pT), does not have metabolic activity, its level increases with certain diseases.
In addition, parafollicular cells (C-cells) secrete the hormone calcitonin, which realizes its action against hypercalcemia and low levels of serum calcium.
Synthesis and secretion of thyroid hormones
For the synthesis of thyroid hormones need iodine. Iodine is contained in food and water in the form of iodide, is actively accumulated by the thyroid gland and is converted into organic iodine (organization) inside the follicular cells with thyroid peroxidase. Follicular cells surround specific fields filled with a colloid, which consists of thyroglobulin, a glycoprotein containing tyrosine inside the matrix. When tyrosine comes into contact with the follicular cell membrane, it is iodinated to 1 (monoiodotyrosine) or 2 (diiodine-tyrosine) - atomic compounds, which are then combined into pairs to form two forms of thyroid hormone (diiodotyrosine + diiodotyrosine; diiodotyrosine + myoiodine accumulate in the composition of thyroglobulin follicle until the epithelium of the follicular cells absorbs thyroglobulin as a component of the colloid. Once inside the follicular epithelium, T and T are released from thyroglobulin.Then, free T and T enter the bloodstream, from where they are transported by serum globulins, the most important of which is thyroxin-binding globulin (TBG - thyroxin-binding globulin), which has a high affinity for T and T, but cannot tolerate large quantities of them. TBG normally transports about 75% of the total thyroid hormone. Other binding proteins are tyroc-synso-binding prealbumin (tranti-retin), which has a high affinity for T, but has the ability to tolerate only a small amount of it, and thyroxine-binding albumin, which has a low affinity for T and T, but is able to tolerate a large number of them. About 0.3% of total serum T and 0.03% of total serum T are free and equally bound to hormones. Only free T and T are able to interact with peripheral tissues.
All the processes described above, which are necessary for the synthesis and biological effect of T and T, are controlled by a thyroid-stimulating hormone (TSH), which is secreted by pituitary thyroid-like cells. TSH secretion is controlled by a negative feedback mechanism: an increased level of T and T inhibits the synthesis and secretion of TSH, and a reduced level of these hormones increases the synthesis and secretion of TSH by the pituitary gland.Thyrotropin-releasing hormone (TRH), which is synthesized in the hypothalamus, also affects the secretion of TSH. The regulation of the mechanism of synthesis and realization of the biological effect of TRG is not completely clear, but it is believed that a negative feedback mechanism with thyroid hormones plays a certain role here.
Most of the amount of circulating T in the blood is produced outside the thyroid gland through the process of monodeiodination T. Only1D Part of the circulating T is secreted directly by the thyroid gland.
Laboratory tests for the study of thyroid function
Determining the level of TSH is the best way to diagnose thyroid function disorders. The deviation of the indicator from the norm speaks of hyper-or hypothyroid function, with the exception of a number of patients who have pituitary resistance to thyroid hormones, or those with central hypothyroidism resulting from a disease of the hypothalamic-pituitary zone. Serum TSH can be paranormal in patients with severe non-thyroid pathology. The level of serum TSH also determines the syndromes of subclinical hyperthyroidism (low TSH in serum) and subclinical hypothyroidism (elevated TSH in serum),in both cases, normal levels of serum T 4b are observed. serum T3svoblo
When determining total T in serum, bound and free hormone is measured. Changes in the levels of thyroid-dependent serum proteins cause the corresponding changes in the level of total T even when physiologically T activity4slovenot changed. Thus, the patient may be physiologically euthyroid, but have an abnormal level of total serum T. Perhaps an independent change in the level of T4sloveserum, excluding situations that are due to the interpretation of the values of the level of total T.
The index of free thyroxin (index4slove) is a calculated value that adjusts the total T for the effects of varying amounts of thyroid hormone-binding whey proteins and, thus, allows you to evaluate T in the study of level I total T. The ratio of hormone-binding thyroid function, or the absorption of T by solid resins, is used to evaluate protein binding. The T index most reasonably reflects the true values, which is comparable with the results of direct measurement of Tfree. The level of total serum T can also be measured.Since it has a greater affinity for thyroxin-binding globulin (TSH) (albeit 10 times less than T), the level of total serum T is influenced by the change in the level of serum TBG and substances combined to affect TSH. T levels3freeserum is also measured using direct and indirect methods (T index3svoblo), well described above for T, and are mainly used to assess the severity of thyrotoxicosis. The level of TSH can also be measured; it increases during pregnancy, with estrogen therapy or taking oral contraceptives and in the acute phase of infectious hepatitis. The level of TSH may also increase with pathology associated with X-chromosoma. The most frequent decrease in TSH levels is due to the use of anabolic steroids and intensive therapy with glucocorticoids (overdose). Large doses of certain drugs, such as phenytoin and aspirin (and their derivatives), promote the release of T from the state associated with TSH, which leads to a false low level of total serum T.
Thyroid peroxidase antibodies are present in almost all patients.with Hashimoto's thyroiditis (some of them also have antibodies to thyroglobulin) and in the majority of patients with Graves disease. Antibodies indicate the presence of autoimmune pathology, but are not the cause. However, the presence of antibodies directly to the TSH receptor on the follicular cells of the thyroid gland is a sign of a hyperthyroid state in Graves' disease. Antibodies against T and T can be detected in patients with autoimmune thyroiditis and can affect the result of measuring T and T, but this does not have any significant clinical significance.
The thyroid gland is the only source of thyroglobulin, which is easily detected in the blood serum of healthy patients and is usually enlarged in patients with non-toxic or toxic goiter. The principal use of measuring serum thyroglobulin is absolutely necessary in patients after subtotal and total thyroidectomy (with or without1311 ablation) for the differential diagnosis of the presence of progression of thyroid cancer. Normal or elevated serum thyroglobulin in these cases means the presence of carcinogenically altered thyroid tissue in patients receiving TSH-suppressive doses of levothyroxine,or after the abolition of le-voiroxin. It should be borne in mind that antibodies to thyroglobulin can distort the adequacy of the result of measuring serum thyroglobulin level.
The accumulation of radioactive iodine by the thyroid gland can be determined. The estimated dose of radioiodine is administered per os or intravenously, then the patient is sent to a scanner, which calculates the amount of radioiodine absorbed by the thyroid gland. It is preferable for the patient's health to use the iodine isotope31, which has minimal radioactivity (much less than I). Absorption by the thyroid gland31 varies widely and depends on iodine supply and is low in patients receiving a lot of iodine. The test is indispensable for the differential diagnosis of the hyperthyroid state (high accumulation in Graves' disease, low in the case of thyroiditis. The test can also help in calculating the dose of radioactive I required for the treatment of hyperthyroidism.
A scintigraphic camera can pick up the injected radioisotope (radio-dioiod, technetium-pertechnetat) and give a graphic representation of the distribution of isotope accumulation.Local areas of increased accumulation (hot nodule) or low accumulation (cold nodule) help identify areas of possible carcinogenic thyroid changes (the presence of thyroid cancer in less than 1% of “hot nodules” compared to 10–20% of detectable cancer in “cold nodules ").
Examination of a patient with thyroid nodes
Hyperplastic colloid goiter, cysts, thyroiditis and adenomas can be the causes of the formation of benign nodes in the thyroid gland. Malignant nodulation includes thyroid cancer.
Many sites are found by chance during examinations of the thyroid gland and examination for other diseases. The frequency of detection of thyroid nodules increases with age. Using ultrasound sonography, nodes can be detected in 10-67% of middle-aged and elderly people.
Anamnesis of the disease. The pain suggests thyroiditis or hemorrhage in the cyst. An asymptomatic site may be thyroid cancer, but radioisotope scanning. If the size of the node is less than 1 cm in the sonographic study, the method TAB is not applied.
The choice of treatment method depends on the identified cause of the disease. TSH-blue suppression of TSH, used for small nodes, is effective only in half of the cases.
can occur and with other diseases listed above. Symptoms of hyperthyroidism can be a manifestation of hyperfunction of the thyroid gland in the case of hormonally active adenoma or thyroiditis, and the clinical symptoms of hypothyroidism are in favor of Hashimoto thyroiditis. Risk factors for malignant neoplasms of the thyroid gland are a history of thyroid gland exposure, especially in infancy; age less than 20 years; male; family history of thyroid cancer; solitary nodules; increase the size of nodes.
Clinical examination.The characteristic signs of cancer are a dense, firm consistency of the gland during palpation or the presence of cohesion with the surrounding tissues, cervical lymphadenopathy and hoarseness of the voice resulting from paralysis of the recurrent laryngeal nerve.
Diagnostics.The initial examination for detection of nodulation in the thyroid gland includes the determination of the level of TSH, T3svobloand AT to thyroid peroxidase. Ultrasound examination helps to determine the size and nature of the site and is a mandatory method in the diagnosis of thyroid cancer. In sonographic or radiographic studies, various forms of thyroid cancer can be identified: in the form of granular psammomatous calcification (papillary carcinoma) or dense homogeneous calcification of the node (medullary carcinoma). Radioisotope scanning of the thyroid gland is used in case of a decrease in the level of TSH. Nodes with an increased accumulation of radionuclides (hot) are less often malignant. Fine needle aspiration biopsy (TAB) from the node in this case is the best method of diagnosis and is performed if at the initial examination there was no hyperthyroidism or signs of thyroiditis of Hashimoto. Early use of the TAB technique is more cost-effective than a routine ultrasound scan.
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