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Thyroid gland diseases. The diagnosis, the differential diagnosis, preventive maintenance and craw treatment. The thyroid is a firm vascular organ lying in the neck, caudal to cricoid cartilage. It is composed of two nearly equal lobes connected by a thin isthmus and weights approximately 20 gr. Rests of thyroid tissue are occasionally presents in sublingual or retrosternal areas. Thyroid secrets: T3, T4,thyrocalcitonin. The thyroid hormones, thyroxine (T4) and triiodothyronine (T3) are secreted under the stimulatory influence of pituitary thyrotropin (thyroidstimulating hormone or TSH). TSH secretion is primary regulated by a dual mechanism: - thyrotropin-releasing hormone (TRH); thyroid hormone. Thyroid hormones exits in circulation in both free and bound forma. The thyroid gland is the sole source of T4 and only 20% of T3 is secreted in the thyroid. Approximately 80% of T3 in blood is derived from peripheral tissue (mainly hepatic or renal) deiodinatoin of T4 to T3. Iodide, ingested in food or water, is actively concentrated by the thyroid gland, converted organic iodine by peroxidase, and incorporated (by the thyroid gland) into tyrosine in intrafollicular thyroglobulin. The thyrosines are iodinated at either one (monoiodotyrosine, MIT) or two (diodotyrosine, DIT) sites and then coupled to form the active hormones (diiodotyrosine + diiodotyrosine → tetraiodothyronine (thyroxine, T4); diiodotyrosine + monoiodotyrosine → triiodotyronine (T3). Thyroglobuline, a glycoprotein, containing T3 and T4 within its matrix, is taken up from the follicle as colloid droplets by the thyroid cells. Lysosomes containing proteases cleave T3 and T4 from thyroglobulin, resulting in release of free T3 and T4. The iodotyrosines (MIT and DIT) are also released from thyroglobulin but do not normally reach the bloodstream. They are deiodinated by intracellular deiodinases, and their iodine is neutralized by the thyroid gland. Although some of free T3 and T4 is deiodinated in the thyroid gland with the iodine reentering the thyroid iodine pool, most diffuses into the bloodstream where it is bound to certain serum proteins for transport. The major thyroid transport protein is thyroxine binding globulin (TBG), which normally accounts for about 80% of the bound thyroid hormones. Other thyroid binding proteins, including thyroxine-binding prealbumin (TBPA) and albumin, account for the remainder of the bound serum thyroid hormone (20 %). About 0,05 % of the total serum T4 and 0,5 % of the total serum T3 remain free but in equilibrium with the bound hormone. About 15 - 20 % of the circulating T3 is produced by the thyroid. The remainder is produced by monodeiodination of the auter ring of T4, mainly in the liver. Monodeiodination of the inner ring of T4 also occurs in hepatic and extrahepatic sites, including kidney, to yield 3,3/, 5/-T3 (reverse T3 or rT3). This compound has minimal metabolic activity but is present in normal human serum or globulin. Observations pertaining to rT3 metabolism in fetal life are of great importance. Total amniotic T4 and T3 are low, in contrast to levels in maternal serum. Fetal rT3 levels in amniotic fluid are much higher than the corresponding values in maternal serum throughout pregnancy (15 to 42 wk). These data imply that rT3 derives primarily from the fetus and that it may be possible to diagnose fetal hypothyroidism as early as 15 wk of pregnancy, utilizing radioimmunoassay for rT3. These levels appear to decrease after 30 wk gestation and may be serve as a useful index of pregnancies of < 30 wk duration. Physiologic effects of thyroid hormones . Thyroid hormones have a major physiologic effects: 1) they increase protein synthesis in virtually every body tissue 2) they increase O2 consumption by increasing the activity of Na+ H+ ATPase (Na pump), primarily in tissues responsible for basal O2 consumption (i.e., liver, kidney, heart and skeletal muscle).) Hyperthyroidism (thyrotoxicosis) Toxic diffuse goiter. Grave’s diseaseis the condition resulting from the effect of excessive amounts of thyroid hormones on body tissues. Thyrotoxicosis is a main syndrome. Sometimes the term hyperthyroidism can be used in a narrower sense to denote this state when the thyroid gland is producing too much thyroid hormones in contrast with excessive ingestion of thyroid hormone medication. At one time or another, approximately 0,5 % of the population suffers from hyperthyroidism. Graves disease is the most common cause of hyperthyroidism and is fairly common in the population. It is responsible for over 80 % of hyperthyroid cases. It occurs most often in young women, but it may occur in men and at any age. Cause: Autoimmune disorders, which can be provoked by: - insolation; - acute infections; - hormone disbalance (pregnancy and others). Pathogenesis. Insufficiency of T suppressors excessive level of T helpers increasing function of B lymphocyte secretion of thyroid – stimulating immunoglobulin (TSI) blood the thyroid. TSI works as an antibody to the thyrotropin receptor on the thyroid follicular all resulting in stimulation of this receptor secretion of T4, T3. Pathogenesis Insufficiency of T suppressors Increasing function of B lymphocyte Toxic influence of lymfocytes Secretion of thyroid – stimulating immunoglobulin (TSI) The thyroid Secretion of T4, T3 Thyrotoxicosis Pathologic changes in different organs and systems Clinical manifestations The clinical presentation may be dramatic or subtle. Cardiovascular system Dysfunction of the cardiovascular system is common, and in some instances, the only manifestation of hyperthyroidism. Heart rate and cardiac output are increased, and peripheral resistance is decreased. These changes result in: - permanent palpitation; -sinus tachycardia or atrial fibrillation; -heart failure. Examination reveals: - tachycardia; - widened pulse pressure; - a prominent apical impulse; - bounding arterial pulsation; - accentuated heart sounds; - systolic ejection murmurs; - occasionally cardiac enlargement.. Other than arrhythmia, electrocardiographic changes are limited to nonspecific ST and T wave abnormalities. Psychological symptoms: - nervousness; - physical hyperactivity; - emotional lability; - anxiety; - distractibility; - insomnia. These changes occur commonly and often result in impairment of work or school performance and disturbances in home and family life. Neuromuscular symptoms: - a fine tremor is often evident in the hands and fingers; - performance of skills requiring fine coordination becomes difficult; - deep tendon reflexes are hyperactive; - some evidence of myopathy is common; - weakness lit usually develops gradually, is progressive, and may be accompanied by muscle wasting. Skin. The skin is warm, fine, moist and its texture is smooth or velvety erythema and pruritus may be present. Increased sweating is common complaint . Hair may become thin and fine, and alopecia occurs. Infiltrative dermopathy, also known as pretibial mixedema (a confusing term, since mixedeme suggests hypothyroidism), is characterized by nonpitting infiltration of proteinaceous ground substance, usually in the pretibial area. The lesion is very pruritic and erythematous in its early stages and subsequently becomes browny it may appear years before or after the hyperthyroidism. TSIS are invariably present. The dermopathy usually remits spontaneously after months or years. Eyes. Eye sings include: - stare (Schtelvag’s symptom); - lid lag; - lid retraction (symptoms of Dalrympl; Greffe; Koher), which results in “apparent” proptosis, but not eye and is often accompanied by symptoms of: - conjunctival irritation. These eye signs are largely due to excessive adrenergic stimulation and zemit promptly after upon successful treatment of thyrotoxicosis - infiltrative ophthalmopathy is present in 20 to 40% of patients with Graves’ disease. It is characterized by increased retro-orbital tissue, producing exophthalmos and by lymphocyte infiltration of the extraocular muscles, producing a spectrum of ocular muscle weakness frequently leading to blurred and double vision. The pathogenesis of infiltrative ophthalmopatny is poorly understood. It may occur before the onset of hyperthyroidism or as 15 to 20 years afterward and frequently worseness or improves independent of the clinical course of hyperthyroidism. Infiltrative ophthalmopathy results from immunoglobulins directed to the extraocular muscles and specific antibodies that cause retro – orbital inflammation and subsequent edema (it is not because of TSH or LATS). The antibodies are distinct from those initiating Graves’ type hyperthyroidism. The symptoms include: - pain in the eyes; - lacrimation; - photophobia; - diplopia; - blurring or loss of vision. The major signs are: - proptosis (exophthalmos); - periorbital and conjunctival congestion and edema (chemosis); - limitation of ocular mobility. Thyroid gland Enlargement of thyroid gland is very common. Both thyroid lobes are usually moderately symmetrically enlarged, but thyroid enlargement may be absent. Degrees of thyroid gland enlargement. 0- we can’t see or palpate thyroid gland; I- we can palpate but can’t see; II – we can palpate and see thyroid gland in any position of the head. Respiratory function Abnormalities of respiration include: - decreased vital capacity; - decreased pulmonary compliance. They result in dyspnea and hyperventilation during exercise and sometimes rest. Gastrointestinal system Increased caloric utilization is almost always present. It results in increased appetite and food intake, but compensation is usually inadequate, and modest loss occurs. Increased gastrointestinal motility may result in increased frequency of bowel movements and even frank diarrhea. Minor abnormalities in hepatic function are often found. Hematopoetic system Some patients have a modest anemia, caused by mild deficiency in one or more hematopoetic nutrients or increased plasma volume. Mild granulocytopenia and thrombocytopenia may be present. Energy and intermediary metabolism because of increased energy expenditure, energy production must be augmented, this is accompanied by increased oxygen consumption and heat production. In patients with diabetes mellitus, requirement for exogenous insulin catabolism. Endocrine system In women, hypomenorrhea or amenorrhea may occur, although no changes are noted. In men, there may be loss of libido and impotence hypercalcemia is found occasionally; it is caused by increased bone resorption, but clinical osteopenia is rare. In patients mild adrenal insufficiency may occur. It is present by low diastolic blood pressure and darkness of upper lid (Elynecks symptom). Degrees of severity I. mild degree: work capacity is normal; heart beat – is under 100/min; weight loss is less than 10 %. II. moderate degree: work capacity is decreased; heart beat – is 100 to 120/min; weight loss is 10 to 20 %. III. severe degree: patients cant work; heart beat – is over 120/min and arrhythmia is present; weight loss is more than 20%. Diagnosis of toxic diffuse goiter. I. Clinical manifestations (were discussed). II. Laboratory findings. (The diagnosis of hyperthyroidism is usually straightforward and depends on careful clinical history and physical examination, a high index of suspection, and routine thyroid hormone determination). 1. In most patients serum total T3 and T4 concentrations, are increased (however, these changes, also can be caused by increased thyroxine – binding globulin production, e.g. as a result of estrogen therapy). 2. Elevation of T3 - resin uptake. (T3 - resin uptake is not a measurement of circulating T3. In normal patients, 25 to 35% of TBG binding sites are occupied by thyroid hormone. When 131I-T3 is added to the patients serum, in vitro, a portion binds to unoccupied TBG sites. After equilibration, a resin is added that binds the remaining unbound 125/-T3). Thus in hyperthyroidism, characterized by increased levels of circulating thyroid hormone, there are more occupied and less unoccupied TBG binding sites. Less 131I-T3 is bound to TBG, resulting in more uptake of 131I-T3 by the resin. 3. TSN (serum thyroid stimulating hormone) may be decreased, but it is not very sensitive assay in the assessment of thyroid hyperfunction. 4. If the diagnosis of hyperthyroidism remains unclear after these initial tests, more expensive, sophisticated and time – consuming tests may be required, e.g. A TRH test (thyrotropin releasing hormone). Serum TSN is determined before and after an i/v injection of 500 mkg of synthetic TRH. Normally, there is a rapid rise in TSH of 5 to25 mkU/ml, reaching a peak in 30 min and returning to normal by 120 min. In patients with hyperthyroidism TSH release remains suppressed, even in response to injected TRH, because of the inhibitory effects of the elevated free T4 and T3 on the pituitary thyrotroph cells. The diagnosis of infiltrative ophthalmopathy when hyperthyroidism is or recently was present is not difficult. The diagnosis is less certain if the patient is not or never was hyperthyroid orbital ultrasonography or computed tomography is the best procedure to confirm the diagnosis of ophtalmopathy such as orbital pseudotumor and orbital tumors. Other forms of hyperthyroidism. Toxic adenoma and toxic multinodular goiter (Plummer’s disease) One or more thyroid nodules occasionally hyperfunction autonomously for unknown reasons. The excess T3 and T4 inhibit the hypothalamic – pituitary axis, stopping TSH production and decreasing production of hormone in the rest of the thyroid. RAI uptake in the hyperfunctioning nodule is increased while in the rest of the gland, it is decreased. Multinodular goiter with or without hyperthyroidism is more common in older people. Neither toxic multinodular goiter nor toxic adenoma is associated with LATS, exophthalmos, or the pretibial myxedema found in Grave’s disease. Since nodules often produce selective increases in T3 levels, determination of the serum total T3 should be included in the thyroid function tests selected for evaluation of nodular goiter. Toxic adenoma and multinodular goiter are treated surgically or with radioiodine. T3 toxicosis. Both T3 and T4 are regularly increased in patients with hyperthyroidism. Increases in serum T3 are usually somewhat greater proportionally compared to T4, probably because of both increased thyroidal secretion of T3 and increased peripheral conversion of T4 to T3. In some thyrotoxic patients, only T3 is elevated; this condition is called “T3 toxicosis”. It is difficult to diagnose because T3 is not measured by the ordinary thyroid function tests, but requires a specific RIA. The criteria to establish the diagnosis are: 1) symptoms and signs of hyperthyroidism; 2) normalT4 and 131I uptake; 3) nonsuppressible 131I uptake; 4) failure to release TSH in response to TRH; 5) elevated serum T3. T3 toxicosis may be seen in any of the natural disorders producing hyperthyroidism, including Graves’ disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. If T3 toxicosis continues untreated, the patient eventually develops the typical laboratory abnormalities of hyperthyroidism; i.e., elevated T4 and 131I uptake. This suggests that T3 toxicosis is an early manifestation of ordinary hyperthyroidism and should be treated as such. Thyrotoxicosis fastitia. This syndrome of hyperthyroidism results from self-administration of thyroid hormone; patients (commonly medical or paramedical personnel) may be surreptitiously taking T4 or T3. Laboratory evaluation will vary accoringly. If the disorder is caused by ingestion of preparations containing T4, the serum T4 will be elevated. When ingestion of T3 is the cause, serum T4 will be below normal. In either case, serum T3 levels will be increased, particularly when preparations containing T3 are the causative agnts; there will be no goiter. Excess TSH produced by a pituitary tumor can cause secondary hyperthyroidism through overproduction of thyroid hormone. Hyperthyroidism secondary to metastatic embryonal carcinoma or choriocarcinoma is due to the TSH-like properties of human chorionic gonadotropin (HCG). Struma ovarii is generally benign ovarian teratoma containing predominantly thyroid tissue. Approximately 5 % of the patients with struma ovarii develop hyperthyroidism. Treatment involves removal of teratoma. Treatment. I. 1. Antithyroid drugs. 2. Drugs to ameliorate thiroid hormone effects . 131 II. I- therapy III. Surgery. I. 1. Antithyroid drugs Propylthiouracil (PTU) and methimazole (MML) are effective inhibitors of thyroid hormone biosynthesis. PTU also inhibits extrathyroidal conversation of T4 to T3. The usual starting dosage is 100 to 150 mg orally g 8h and for MML 10 to 15 mg when the patient becomes eythyroid the dosage is decreased to the lowest effective amount, usually 100 to 150 mg PPU in 2 or 3 divided doses or 10 to 15 mg MML daily. In general control can be achieved within 6 wk to 3 month. More rapid control can be achieved by increasing the dose of PPU to 400 to 600 mg /day , the risk of increasing the incidence of side effects, maintenance doses can be continued for one year or many years depending on the clinical circumstances. Carbinazole (merkazolile ) is rapidly converts in vivo to MML. The usual starting dosage is 10 to 15 mg orally q 8h, maintenance dosage is 10 to 15 mg/ daily. The incidence of agranulocytosis appears to be higher for carbimazole than for eighter PPU or MML. Adverse effects include: - allergic reactions; - nausea; - loss of weight; - fever; - arthritis, hepatitis; - anemia, thrombocytopenia; - agranulocytosis (in < 1% of patients). If the patient allergic to one agent, it is acceptable to go to other, but there is a chance of cross sensitivity. In case of agranulocytosis, it is unacceptable to go to another agent, and more definitive therapy should be invoked, such as radioiodine or surgery. 2. Some manifestations of hyperthyroidism are ameliorated by adrenergic antagonists - β – adrenergic blocking drugs. Propranolol has had the greatest use phenomena that can be improved: tachycardia, tremor, mental symptoms, heat intolerance and sweating (occasional), diarrhea (occasional), proximal myopathy (occasional). II. Radioactive sodium iodine (131I) It can be used in patients > 40 yr. of age, because 131I might cause thyroidal or other neoplasm or gonadal damage. There are only two important untoward effects of 131I therapy: persistent hyperthyroidism and hypothyroidism. III. Surgery is used: - in patient <21 yr. who should not receive radioiodine; - in persons who can not tolerate other agents because of hypersensitivity or other problems; - in patient with very large goiters (100 to 400 gm) (normal thyroid weights 20gm); - in some patients with toxic adenoma and multinodular goiter; - hyperthyroidism during pregnancy; - recurrent hyperthyroidism after course of antithyroid treatment. Precautions: - patient must be euthyroid before operation. Results of the surgery: - normalization of thyroid gland function; - postoperative recurrences (2-9 %); - hypothyroidism (in about 3 % of patient the first years and in about 2 % with each succeeding year); - vocal cord paralysis; - hypoparathyroidism. Iodine is used in preparing the patient for surgery. Surgical procedures are more difficult in patients who previously have undergone thyroidectomy or radioiodine therapy. Treatment endocrine ophthalmopathy include: - steroid therapy: prednisolone 20 – 40 mg daily; - electrophoresis with glucocorticoids or KI; - aloe, FIBS; - dehydration therapy; - cavinton, piracetam; - lateral tarsorrhaphy: when there is corneal ulcer due to inability to close the lids; - extra – ocular muscle surgery: to correct persistent diplopia. Thyroid storm. Thyroid storm is a life- threatening emergency requiring prompt and specific treatment. In is characterized by abrupt onset of more severe symptoms of thyrotoxicosis, with some exacerbated symptoms and signs atypical of uncomplicated Graves disease: - fever; - marked weakness and muscle wasting; - extreme restlessness with wide emotional swings; - confusion; - psychosis or even coma; - hepatomegaly with mild jaundice; - the patient may present with cardiovascular collapse or shock. Thyroid storm results from:- untreated or inadequately treated thyrotoxicosis It may be precipitated by: - infection; - trauma - surgery; - embolism; - diabetic acidosis; - fright; - toxemia of pregnancy; - labor; - discontinuance of antithyroid medication; - radiation thyroiditis. Treatment of thyroid storm; Iodine-30 drops Lugol’s solution/day orally in 30g 4 divided doses; or 1 to 2 gr. sodium iodide slowly by i/v drip. Propylthiouracil (merkazolil) - 900 to 1200 mg/day orally or by gastric tube. Propranolol - 160mg/day orally in 4 divided doses; or 1mg slowly i/v g 4h under careful monitoring; a rate of administration should not exceed 1mg/min; a repeat 1mg dose may be given after 2 min i/v glucose solutions . Correction of dehydration and electrolyte imbalance cooling blanket for hypertermia. Digitalis if necessary. Treatment of underlying disease such as infection. Corticosteroids-100 to 300mg hydrocortisone/day i/v. Iodine in pharmacological doses inhibits the release of T3 to T4 within hours and inhibits the organification of iodine, a transitory effect lasting from a few days to a week (”escape phenomenon”.) Indications (it is used for) - the emergency management of thyroid storm; - thyrotoxic patients undergoing emergency surgery; - preoperative preparation of thyrotoxic patients selected for subtotal thyroidectomy /since it also decreases the vascularity of the thyroid gland. It is not used for routine treatment of hyperthyroidism. The usual dosage is 2 to 3 drops of satured potassium iodide solution orally tid or dig 1300 to 600 mg/day; or 0,5gr sodium iodide in 0,9% sodium chloride solution given i/v slowly g 12h. Complication of iodine therapy include: - inflammation of the salivary glands; - conjunctivitis; - skin rashes; - a transient hyperthyroidism (iod-BASEDOW phenomenon) (it can be observed in patients with nontoxic goiters after administration of iodine-contrast agents). Antithyroid drugs Doses of PPU of 450-600 mg/day or greater 800 to 1200mg/day are generally reserved for the patient with thyroid storm, because such doses block the peripheral conversation of T4 to T3. β-adrenergic blocking drugs. Propranolol rapidly decreases heart rate, usually within 2 to 3 h when given orally and within minutes when given i/v. Hypothyroidism (myxedema) It is the characteristic reaction to thyroid hormone deficiency. The spectrum of hormone ranges from a few non – specific symptoms to overt hormone, to myxedema coma. Hypothyroidism occurs in 3 to 6 for the adult population, but is symptomatic only in a minor of them. It occurs 8 to 10 times more often in woman than in men and usually develops after the age of 30. Classification 1.Congetial. 2. Acquired: 1. Primary (thyroid gland disturbances). 2. Secondary (due to pituitary disease). 3.Tertiary (due to hypothalamic disease). 4.Peripheral. Etiology A cause is usually evident from the history and physical examination. 1.Primary (thyroidal) hypothyroidism. 1) surgical removal, total thyroidectomy of thyroid carcinoma, subtotal thyroidectomy (hypothyroidism occurs from 25 to 75 of patients in different series); 2) irradiation (hypothyroidism results from external neck irradiation therapy in doses 2000 rads or more such as are used in the treatment of malignant lymphoma and laryngeal carcinoma); I131 therapy for hyperthyroidism (it results in hyperthyroidism in 20 % to 60 % of patients within the first year after therapy and in 1 % to2 % each year there after); 3) during or after therapy with propylthyouracil, methimazole, iodides or beta-blockers; 4) autoimmune processes (hypothyroidism usually occurring as a sequel to Hashimoto’s thyroiditis and results in shrunken fibroid thyroid gland with a little or no function and infiltrative diseases (tuberculosis, actynomycosis); 5) trauma; 6) iodine deficiency. 2.Secondary and tertiary hypothyroidism It occurs due to either deficient secretion of TSH from the pituitary or lack of secretion of TRH from the hypothalamus. Tumor; Infarction; Infiltrative process; Trauma; Drugs (reserpin, parlodel). 3. Peripheral hypothyroidism: - peripheral tissue resistance to thyroid hormones; - decreasing of T4 peripheral transformation into T3 (in liver or in kidneys) ; - production of antibodies to thyroid hormones. Congenital: - Maldevelopment –hypoplasia or aplasia; - Inborn deficiencies of biosynthesis or action of thyroid hormone; - Atypical localization of thyroid gland Classification (cont.) B. 1. Laboratory (subclinical) hypothyroidism. 2. Clinical hypothyroidism, which can be divided on stages of severity: mild, moderate, severe. C. 1. Compensation. 2. Subcompensation. 3. Decomposition. D. 1. Without complications. 2. With complications (myopathy, polyneuropathy, encephalopathy, coma). Clinical features The major symptoms and signs of hypothyroidism reflect showing of physiologic function. Virtually every organ system can be affected. The onset of symptoms may be rapid or gradual, severity varies considerably and correlates poorly with biochemical changes. Because many manifestations of hypothyroidism are non-specific, the diagnosis is particularly likely to be overlooked in patients with other chronic illnesses and elderly. Nervous system Most of hypothyroid patients complain of fatigue, loss of energy, lethargy, forgetfulness, reduced memory. Their level of physical activity decreases, and they may speak and move slowly. Mental activity declines and there is inattentiveness, decreased intellectual function, and sometimes may be depression. Neurological symptoms include also hearing loss, parasthesias, objective neuropathy, particularly the carpal tunnel syndrome, ataxia. Tendon reflex shows slowed or hung-up relaxation. Skin and hair. Hypothyroidism results in dry, thick and silk skin, which is often cool and pale. Glycosoamynoglicanes, mainly hyaluronic acid accumulate in skin and subcutaneous tissues retaining sodium and water. So, there is nonpitting edema of the hands, feet and periorbital regions (myxedema). Pitting edema also may be present. The faces are puffy and features are coarse. Skin may be orange due to accumulation of carotene. Hair may become course and brittle, hair growth slows and hair loss may occur. Lateral eyebrows thin out and body hair is scanty. Cardiovascular system. There may be bradycardia, reduced cardiac output, quiet heart sounds, a flabby myocardium, pericardial effusion, cardiac wall is thick, it is increased by interstitial edema. (These findings, along with peripheral edema, may simulate congestive heart failure). Increased peripheral resistance may result in hypertension. The ECG may show low voltage and/or non-specific ST segment and T wave changes. Hypercholesterolaemia is common. Whether or not these is an increased prevalence of ischemic heart disease is controversial. Angina symptoms, when present, characteristically occur less often after the onset of hypothyroidism, probably because of decreased activity. Gastrointestinal system. Hypothyroidism does not cause obesity, but modest weight gain from fluid retention and fat deposition often occurs. Gastrointestinal motility is decreased loading to constipation and abdominal distension. Abdominal distension may be caused by ascities as well. Ascitic fluid, like other serous effusions in myxedema, has high protein content. Achlorhydria occurs, often associated with pernicious anemia. Renal system. Reduced excretion of a water load may be associated with hyponatriemia. Renal blood flow and glomerular filtration rate are reduced, but serum creatinine is normal. May be mild proteinuria and infections of urinary tract. Respiratory system. Dyspnea of effort is common. This complaint may be caused by enlargement of the tongue and larynx, causing upper airway obstruction, or by respiratory muscle weakness, interstitial edema of the lungs, and for plural effusions which have high protein content. Hoarseness from vocal curt enlargement often occurs. Musculoskeletal system. Muscle and joint aches, pains and stiffness are common. Objective myopathy and joint swelling or effusions are less often present. The relaxation phase of the tendon reflexes is prolonged. Serum creatine phosphokinase and alanine aminotransferase activities are often increased, probably as much to slowed enzyme degradation as to increased release from muscle. Hemopoetic system. Anemia, usually normocytic, caused by decreased red blood cell production, may occur. It is probably from decreased need of peripheral oxygen delivery rather than hematopoetic defect. Megaloblastic anemia suggests coexistent pernicious anemia. Most patients have no evidence iron, folic acid or cyancobalamin deficiency. Endocrine system. There may be menorrhagia (from anovulatory cycles), secondary amenorrhea, infertility and rarely galactorrhea. Hyperprolactinemia occurs because of the absence of the inhibitory effect of thyroid hormone on prolactine secretion (and causes galactorrhea and amenorrhea or Van – Vik – Cheness – Ross’s syndrome). Pituitary-adrenal function is usually normal. Pituitary enlargement from hyperplasia of the thyrotropes occurs rarely in patients with primary hypothyroidism –such enlargement also may be caused by a primary pituitary tumor, which resulting TSH deficiency. Enlargement of thyroid gland in young children with hypothyroidism suggests a biosynthetic defect. Hypothyroidism in adults is caused by Hashimoto thyroiditis. Secretion of growth hormone is deficient because thyroid hormone is necessary for synthesis of growth hormone. Growth and development of children are retarded. Epiphyses remain open. Metabolic system. Hypothermia is common. Hyperlipidemia with increase of serum cholesterol and trigliceride occurs because of reduced lipoprotein lipase activity. Subclinical (laboratory) hypothyroidism. It is a state in which we cant find clinical features of hypothyroidism and euthyroidism is reached by compensatory increasing of TSH secretion and that’s why synthesis and secretion of such level of thyroid hormone that will be enough for organism. It is an asymptomatic state in which serum T4 and free T4 are normal, but serum TSH is elevated. The therapy may provide the patient with more energy, a feeling of well being, desirable weight reduction, improved bowel function or other signs of better health even though the patient is not aware of these symptoms before therapy. Diagnostic of hypothyroidism is based on: 1) history; 2) clinical features; 3) blood analysis: anemia; hypercholesterolemia; 4) levels of thyroid hormone: both serum T4 and T3 are decreased (but in 25% of patients with primary hypothyroidism may be normal circulating levels of T3); 5) ECG; 6) examination of tendon reflexes; 7) ultrasonic examination; Differential diagnosis of primary and secondary hypothyroidism: 1) clinical features: Secondary hypothyroidism is not common, but it often involves other endocrine organs affected by the hypothalamic – pituitary axis. The clue to secondary hypothyroidism is a history of amenorrhea rather than menorrhagia in a woman with known hypothyroidism. In secondary hypothyroidism, the skin and hair are dry but not as coarse; skin depigmentation is often noted; macroglossia is not prominent; breasts are atrophic; the heart is small without accumulation of the serous effusions in the pericardial sac; blood pressure is low, and hypoglycemia is often found because of concomitant adrenal insufficiency or growth hormone deficiency. 2) laboratory evaluation: shows a low level of circulating TSH in secondary hypothyroidism, whereas in primary hypothyroidism there is no feedback inhibition of the intact pituitary and serum levels of TSH are very high. The serum TSH is the most simple and sensitive test for the diagnosis of pituitary hypothyroidism. Serum cholesterol is generally low in secondary hypothyroidism, but high in pituitary hypothyroidism. Other pituitary hormones and their corresponding target tissue hormones may be low in secondary hypothyroidism. The TSH test is useful in distinguishing between secondary and tertiary hypothyroidism in the former; TSH is not released in response to TRH; whereas in the later, TSH is released. Treatment of hypothyroidism Diet №10. Regimen is not restricted etiologic Therapy of the cause Pathogenetic replacement therapy Thyroid hormones symptomatic Treatment of complications 1. Diet №10. 2. Regimen is not restricted. 3. 1) replacement therapy: - desiccated animal thyroid (this is an extract of pig and cattle thyroid glands, which standardized based on its iodine content but they are too variable in potency to be reliable and should be avoided); - synthetic preparations of : T4 (l-thyroxine) - T4 is preparation of choice, because it produces stable serum levels of both T4 and T3. Absorption is fairly constant 90 to 95% of the dose. T3 is generated from T4 by the liver. The initial dosage can be 1.6 mkg/kg of ideal weight or 12.5-25 mkg in older patients and 25-50 mkg in young adult. - The dosage can be increased in 25-50 mkg increments at 4 to 6 week intervals until clinical and biochemical euthyroidism is achieved. In older patients more gradual increments are indicated. Cautious replacement is particularly warranted in patients with ischemic heart disease, because angina pectoris or cardiac arrhythmia may be precipitated by T4 therapy. - The average maintenance dosage is 100 to 150 mkg/day orally, only rarely is a larger dosage required. In general, the maintenance dose may decrease in the elderly and may increase in pregnancy. - The dosage should be minimum that restores TSH levels to normal (though this criterion cannot be used in patients with secondary hypothyroidism). - Patient takes the whole dose of T4 once a day (in the morning), in the summer the dose may be decreased and in the winter should be increased. T3 (liothyronine sodium) should not be used alone for long-term replacement because its rapid turnover requires that it be taken. T3 is occasionally used mainly in starting therapy because the rapid excretion is useful in the initial titration of a patient with longstanding hypothyroidism in whom cardiac arrhythmia may occur early in replacement therapy. The risk of jatrogenic hyperthyroidism is therefore greater in patients receiving these preparations. In addition, administering standard replacement amounts of T3 (25 to 50 mkg/day) results in rapidly increasing serum T3 levels to between 300 and 1000 mkg within 2 to 4 h, these levels return to normal by 24 h. Therefore, when assessing serum T3 levels in patients on this particular regimen, it is important for the physician to be aware of the time of prior administration of the hormone. Additionally, patients receiving T3 are chemically hyperthyroid for at least several hours a day and thus are exposed to greater cardiac risks. Similar patterns of serum T3 concentrations are seen when mixtures of T3 and T4 are taken orally, although the peak levels of T3 are somewhat lower. Replacement regimes with synthetic preparations of T4 reflect a different pattern of serum T3 response increases in serum T3 occur gradually over weeks, finally reaching a normal value about 8 wk. after starting therapy. Synthetic T3 and T4 combinations (liotrix, thyreocomb). These preparations were developed before it was appreciated that T4 is converted to T3 outside of the thyroid. These preparations should not be used. 2) Symptomatic therapy: - beta-blockers (should be used in patients with tachycardia and hypertension) in the dose of 20 – 40 - 60 mg/day; - hypolypidemic agents; - vitamins (A, B, E); - diuretics and others. Subclinical hypothyroidism Many endocrinologists would treat such patients with T4, especially if hypercholesterolemia were present. Even in the absence of hyperlipidemia, a trial of therapy might be varianted to determine if the patient experiences improvement presumably the normal serum T4 concentrations before therapy did not reflect adequate tissue effects of thyroid hormones in such patients. Unfortunately, it is also reasonable to follow these patients without T4 therapy by surveying thyroid function at 4-to 6 months intervals to determine whether thyroid failure has occurred, as indicated by the serum T4 falling to subnormal levels along with a greater increase in serum TSH and the appearance of clear symptoms. Myxedema coma. It is a life-threatening complication of hypothyroidism, which is extremely rare in warm climates but not uncommon in cold areas. Precipitating factors include: - exposure to cold; - infection; - trauma; - drugs that suppress the CNS. Myxedema coma characteristics include a background of long-standing hypothyroidism with extreme hypothermia (temperatures 24 to 32), areflexia, seizures, CO2 retention, and respiratory depression caused by decreased cerebral blood flow. Severe hypothermia may be missed unless special low reading thermometers are used. Rapid diagnosis (based on clinical judgement, history, and physical examination) is imperative because early death is likely. Treatment of myxedema coma. It is treated with large doses of T4 (250-500 mkg I/v bolus 3 – 4 times a day) or T3 if available (40 – 100 mkg I/v bolus 3 times a day), because TBG must be saturated before any free hormone is available for response. The maintenance dose for T4 is 50 mkg/day I/v and for T3 10 20 mkg/day I/v until the hormone can be given orally. The patient should not be rewarmed rapidly because of the threat of cardiac arrhythmia. Hypoxemia is common, so PaO2 should be measured at the outset of treatment. If alveolar ventilation is compromised, immediate mechanical ventilatory assistance is required. Thyroiditis The various types of thyroiditis encompass a heterogeneous group of inflammatory disorders of diverse etiologies and clinical features. With all forms of thyroiditis, destruction of the normal architecture of the thyroid follicular occurs, yet each disorder has distinctive histologic characteristics. For the purposes of understanding the clinical manifestations, thyroiditis is classified according to either the severity or duration of illness using the following scheme: 1. Acute thyroiditis. 2. Subacute thyroiditis: - subacute granulamatous thyroiditis; - subacute lymphocytous thyroiditis. 3. Chronic thyroiditis: - Hashimoto thyroiditis; - Ridel struma. 4. Specific thyroiditis. 5. Thyroiditis caused by mechanical or physical factors. Acute thyroiditis Etiology Acute thyroiditis it is an acute bacterial inflammation due to a bacterial pathogen, most commonly staphylococcus aureus, streptococcus hemolytica,streptococcus pneumonie, of anaerobic streptococcal organisms. Infection due to other bacterial pathogens, such as salmonella and escherichia coli have been reported, as well as fungal infections such as coccidiodomycosis. Infection occurs either secondary to hematogenous or lymphatic spread, or as a result of direct introduction of an infective agent by trauma. Persistent thyroglossal duct abnormalities have also been associated with acute thyroiditis. Clinical features Fever, chills and other systemic signs or symptoms of abscess formation are present. Anterior neck pain and swelling are usual, with pain occasionally radiating to the ear or mandible. The physical examination suggests the presence of an abscess, with erythema of the skin, marked tenderness to palpation, and at times fluctuance. Laboratory tests Leucocytosis with a left shift, increased ESR are usually present. Thyroid hormone concentrations in blood are normal, although hyperthyroxinemia has been reported. Treatment Patient should be treated at surgical department. Parental antibiotics should be administered according to the specific pathogen identified. If fluctuance is present, incision and drainage might be required. Bacterial thyroiditis must be treated early and aggressively, since abscess formation can occasionally dissect downward into the mediastinum. Recurrences of the disorder are very rare. (Duration of the treatment must be nearly 1,5-2 month). Subacute thyroiditis It is an acute inflammatory disease of the thyroid probably caused by a virus. Subacute granulomatous thyroiditis (giant cell thyroiditis) SAT. Etiology SAT is most likely viral in origin .The specific agent responsible for the disorders is not known, although coxsackie virus, adenovirus and the mumps, echovirus, influenza and Epstein-Barr viruses have been implicated in the etiology. A genetic predisposition is likely because of the association of HLA-BW 35 histocompatibility antigens. Clinical features The most common symptom is unilateral anterior neck pain, often associated with unilateral radiation of pain to the ear or mandible. Pain is often proceeded by a few weeks prodrome of myalgias, low-grade fever, malaise and sore throat. Dysphagia is also common. Symptoms of hyperthyroidism (such as tachycardia, weight loss, nervousness, and diaphoresis occur in up to 50% of patients as the disorder processes, pain can migrate to the contralateral side. Physical examination discloses an exquisitely tender, very hard, nodular enlargement, which is most often unilateral. Tenderness is often so extreme that palpation is limited. Bilateral tenderness and goiter can occur as well. Tachycardia, a widened pulse pressure, warm skin and diaphoresis are also observed when hyperthyroidism is present. Laboratory findings. Early in the disease we can find an increase in T4, a decrease in RAI uptake (often 0), leucocytosis and a high ESR. After a several weeks, the T4, is decreased and the RAI uptake remains low. Full recovery is the rule; rarely, patients may become hypothyroid. Treatment An acute phase lasts from 4-8 weeks, during which treatment is symptomatic (aspirin 600 mg q 3-4 h, prednisolone 10-20 mg orally tid; after 1 week prednisolone can be tapered by 5 mg every 2-3 days; thus glucocorticoids are usually not required for longer than several weeks. Symptoms of hyperthyroidism are effectively controlled by the use of beta-blockers). Following the acute phase euthyroidism is restored, and the thyroid becomes depleted of stored hormone. Patients can either remain euthyroid or progress to hypothyroid phase. It rarely lasts longer than 2-3 months, and during this phase thyroid hormone replacement in the form of levothyroxine 0,10-0,15 mg/day should be given. After several months of treatment T4 can be discontinued. Following the hypothyroid phase recovery occurs, and the normal histologic features and secretory capacity of the thyroid are restored. Subacute lymphocytic thyroiditis (silent thyroiditis) A subacute disorder occurring most commonly in women , often in the postpartum period, characterized by a variable, but mild degree of thyroid enlargement, absence of thyroid tenderness, and self-limited hyperthyroid phase of several weeks to several months, often followed by transient hypothyroidism but with eventual recovery to the euthyroid state. Etiology Recent evidence suggests on: 1) autoimmune component (because of autoantibodies observed); 2) genetic predisposition (this is a significant prevalence of HLA-DRW3 and HLA-DRW5 histocompatibility agents); 3) viral etiology (viral antibody titers are rarely elevated); Clinical features. Hyperthyroid symptoms are frequent and vary from mild to normal. (Postpartum thyroiditis occur 6 weeks to 3 months after delivery). Physical examination usually discloses a mildly enlarged, diffuse, firm, nontender goiter it has been reported that up to 50 % of patients do not have goiter. Laboratory findings Serum total and free T4 and T3 are elevated. Biopsies reveal lymphocytic infiltration as seen in Hashimotos thyroiditis. Thyroid autoantibodies are positive in greater than 50 % of patients. Treatment Hyperthyroid phase lasts from 6 weeks to 3 month. Treatment is conservative, usually requiring only B-adrenergic blockers with propranolol. Euthyroid interval lasts for 3-6 weeks. During hypothyroid period (it usually lasts no longer than 2-3 months thyroid hormone supplementation with T4 0,10-0,15 mg/day may be required. Following the hypothyroid phase patients usually remain clinically euthyroid.) Chronic thyroiditis. Hashimoto thyroiditis (chronic lymphocytic thyroiditis) HT Etiology HT is an organ - specific autoimmune disorder, a chronic inflammation of the thyroid with lymphocytic infiltration of the gland generally though to be caused by autoimmune factors. It is mire prevalent (8:1) in woman than men and is most frequent between the ages of 30 and 50 . A family history of thyroid disorders is common, and incidence is increased in patients with chromosomal disorders, including Turners, Down and Klinefelters syndromes. Histologic studies reveal extensive infiltration of lymphocytes in the thyroid. The basic defect underlying this disease suggests an abnormality in suppressor T lymphocytes that allows helper T lymphocytes to interact with specific antigens directed against the thyroid cell. A genetic predisposition is suggested because of the frequent occurrence of the HLA- DR5 histocompatibility antigen in patients with HT. Clinical features HT is characterized by a wide spectrum of clinical features, ranging from no symptoms and the presence of small goiter to frank myxedema. Occasionally patients complain of a vague sensation of tightness in the area of the anterior neck or mild dysphagia. In general, however, thyroid enlargement is insidious and asymptomatic. Symptoms of hypothyroidism may or may not be present, depending on the presence or absence of biochemical hypothyroidism. Physical examination usually discloses a symmetrically enlarged, very firm goiter, a smooth or knobby consistency is common. Occasionally patients present with a single thyroid nodule. A small group of patients have a form of HT termed primary idiopathic hypothyroidism, goiter is usually absent in this group.(atrophic form of HT). Yet a small subset of patients(probably 2-4%) present with hyperthyroidism and have socalled hashitoxicosis (hypertrophy from of HT). Laboratory findings 1) early in the disease a normal T and high titers of antithyroid (antimicrosomal) antibodies can be detected. Late in the disease, the patient develops hypothyroidism with a decreased in T and antibodies in this stage are usually no longer detectable; 2) the thyroid scan typically shows a irregular pattern of iodine uptake; 3) fine-needle biopsy of the nodule or enlarging area should be done to rule out a coexistent neoplasm. Treatment 1) treatment of HT requires lifelong replacement with thyroid hormone to correct and prevent hypothyroidism. The average oral replacement dose with l-thyroxine is 100 to 150 mkg/day; 2) glucocorticoids have been reported to be effective in HT when true is a rapidly enlarging goiter associating with pressure symptoms; 3) symptomatic therapy Ridel thyroiditis Etiology This extremely rare inflammatory disorder is of uncertain etiology, and earlier suggestions that it might be a fibroid variant of HT have not been substained. Clinical features Clinically, Ridel thyroiditis presents with pressure symptoms, and on examination an extremely hard , immobile thyroid gland is palpated The thyroid can be uniformly enlarged, or only one lobe might be affected. The disorder can be associated with other focal sclerosing symptoms, including retroperitoneal and mediastenal fibrosis and ascending cholecystitis. Laboratory findings 1. Thyroid function tests show hypothyroidism in approximately 25 % of patients. 2. Thyroid antibodies are usually negative. 3. The thyroid scan shows decreased uptake in involved areas. Treatment - is surgical for those patients in whom symptoms of obstruction occur. - Thyroid hormone is required for treatment of hypothyroidism, but thyroid hormone alone will not result in goiter shrinkage. Iodine-defcit disease of thyroid gland: – a diffuse euthyroidic (nontoxic) goiter is the diffuse enlargement ofthyroid gland without its disfunction; – nodular euthyroid (colloid) goiter; – functional autonomy of thyroid gland and thyrotoxic adenoma; – iodine-defcit hypothyrodism (at the sharply expressed iodine defcit). Day’s necessity in an iodine (WHO, 2005) Age group or physiological state Necessity in iodine, mkg per day Neonates (from 0 to 1 year) 50 Children of young age (from 1 to 5 years) 90 Children of school age (from 6 to 12 years) 120 Adults 150 Pregnant and breast-feeding women 200 A goiter is the pathological enlargement of thyroid gland without clari-fcation of its functional state. The size of thyroid gland is determined by its examining, palpation and measuring a volume by ultrasonic investigation (USI). By international norms, in the case of using of USI in adults (over 18 years) a goiter is diagnosed, if volume of gland is more than 18 ml in women, and more than 25 ml in men. Classifcation of goiter (WHO, 2001) 0 There is no goiter (the sizes of parts do not exceed the sizes of distal phalanx of large fnger of the inspected person) 1 A goiter is palpated, but is not visible at normal head position. Nodular formations which do not cause the enlargement of the gland belong to this class 2 A goiter is palpated and is visible at normal head position Formula for the calculation of thyroid gland volume by the data of USI Volume = [(Tl × Wl × Ll) + (Td × Wd × Ld)] × 0,479 The volume of every part is counted up by multiplying of thickness (Т), width (W) and length (L) with the coeffcient of correction on the ellipse structure of part (0,479). The volume of all gland consists of volumes of its parts; the volume of the isthmus is disregarded usually. The normal thyroid gland volume in children and teenagers (97-percentil; from data of USI) [WHO, 2001] ABS (m2) 0,8 Girl 3,4 Boys 3,3 0,9 4,2 3,8 1,0 5,0 4,2 1,1 5,9 5,0 1,2 6,7 5,7 1,3 7,6 6,6 1,4 8,4 7,6 1,5 9,3 8,6 1,6 1,7 10,2 11,1 9,9 11,2 ABS is the area of body surface which is calculated by the nomogram or by a formula (M is body mass in kilograms, H is height in centimetres): ABS = М0,425 × H0,725 × 71,84 × 10 - 4 Epidemiological criteria of estimation (assessment) of iodine-defcit degree Criteria Population Easy Frequency of goiter (%) by the data of palpation Frequency of goiter (%) increase of volume of gland from data of USI Concentration of iodine in urine (median, mkg/l) Frequency of the TSH level > 5 mIU/ml at neonatal screenning Level of thyroglobulinum in a blood (median, ng/ml) Degree of iodine-defcit Middle Heavy schoolboys 5,0–19,9 % 20,0–29,9 % > 30,0 % schoolboys 5,0–19,9 % 20,0–29,9 % > 30,0 % schoolboys 50–99 20–49 < 20 babies 3,0–19,9 % 20,0–39,9 % > 40,0 % children adult 10,0–19,9 20,0–39,9 % > 40,0 Spectrum of iodine-deficiency pathology (WHO, 2001) Age periods Inwardly-uterine period New-born Children and teenagers Adults For any age Iodine-defcit pathology • Abortions • Stillborn • Innate anomalies • Increasing of perynatal death rate • Increasing of child’s death rate • Neurological cretinism: mental backwardness deaf-and-dumb squint • Mixedemic cretinism: mental backwardness undersized (low height) hypothyroidism • hypothyroidism neonatal psycho-motor violations • Violation of mental and physical development • Goiter and its complication • Iodine-inducted thyrotoxicosis • Goiter • hypothyroidism • Cognitive function disorders • Increase of absorption of radio-active iodine at nuclear catastrophes Methods of prophylaxis of iodine-defcit diseases – a mass iodine prophylaxis is a prophylaxis in the scale of population; it is carried out by addition of iodine in the most widespread food stuff (kitchen salt); – a group iodine prophylaxis is a prophylaxis in the scale of certain groups of the high risk of the IDD development: children, teenagers, pregnant and breast-feeding women. It is carried out by the regular prolonged reception of medicaments which contain the physiological doses of iodine; – an individual iodine prophylaxis is the prophylaxis of individuals by the prolonged reception of medicaments which contain the physiological doses of iodine. Histological classifcation of thyroid gland tumors (WHO, 1988) 1. Epithelial tumors 1.1. Benign tumors 1.1.1 Follicular adenoma: • normofollicullar • macrofollicular • microfollicullar • trabecullar solid 1.1.2 Others 1.2 Malignant 1.2.1 Follicular carcinoma: • minimum invasive • wide invasive oxyfphilic cellular variant light cellular variant 1.2.2. Papillary carcinoma: papillar microcarcinoma encapsulated variant follicular variant diffusesclerosis variant oxyphilic cellular variant 1.2.3. Medullary carcinoma: mixed medullar-follicular carcinoma 1.2.4. Undifferentiated (anaplastic) carcinoma 1.2.5. Other carcinomas 2. Unepithelial tumors: thyroid sarcoma malignant hemangiothelioma 3. Malignant lymphoma 4. Mixed tumors 5. Secondary tumors 6. Unclassifed tumors List of diseases with the single nodules of thyroid gland which is necessary to differentiate Primary thyroid gland damage Adenoma Carcinoma Cyst Thyroiditis autoimmune Lymphoma Previous hemithyroidectomy Cyst of thyroid-tongue duct Thyroid hemiagenesy Non thyroidic damage Lymphadenopathy Adenoma or prothyreoid cyst Cyst-like hygroma Carotid aneurism Metastases Clinical classifcation of thyroid gland cancer TNM – classifcation of differentiated thyroid gland cancer (actual since 01.01.2003) T – primary tumor Тх – conclusion about a primary tumor is impossible; T0- primary tumor is not found; Т1 – tumor size is to 2 cm, localized in a gland; Т2 – tumor size is more than 2 cm and to 4 cm, limited by the gland capsule; Т3 – tumor size over 4 cm, localized only in a thyroid gland, or tumor of any size with minimum extrathyroid spreading (by an invasion in M. sternohyoіdales or in parathyroid muscles and cellular tissue); Т4а – tumor spreads outside the thyroid gland capsule with the invasion in one or a few of such anatomic structures: hypodermic cellular tissue, trachea, throat, gullet, recurrence nerve T4b – tumor infltrate paravertebral fascia, vessels of mediastinum and surrounds a carotid artery * multifocal tumors not depending on their histological analysis must be marked by the letter of “m”, thus the gradation “Т” is determined by the tumor of most size. N – regional lymphatic nodules (lymphatic nodules of neck and mediastinum) (LN) Nх – conclusion about the regional LN damage is impossible; N0 – metastases in regional LN is not found; N1 – metastases in regional LN; N1а – damage of pretracheal, paratracheal, laryngeal LN; N1b – damage of other neck LN uni- or bilateral, contralateral on both sides or only on opposite and/or superior LN of mediastinum. ** pT, pN, pM categories which specify on morphological confrmation of the Т, N, M factors. *** pN0 – is proposed after conducting of selective lymphadenectomy and histological investigation usually from 6 LN and more. In case if in investigated LN is not determined metastatic process, but their amount does not arrive at 6, pN0-stage have to be appropriated. М – distant metastases Мх – conclusion about distant metastases is impossible; М0 – distant metastases are not determined; М1 – there are distant metastases. Ultrasonic signs of nodular formation in thyroid gland True cyst Clear limited, spherical, echo-negative, non-echogenic formation of regular shape with even and thin walls, with homogeneous incorporations, has a capsule Nodes with focal There is a node in thyroid lobule with presence of hypoecho-cystic changes genic areas, in which blood fow is absent at coloured echodo-plerography. Has a clear capsule Colloid node Nodes formation in thyroid gland with expressed hypoecho-genic, has a clear capsule, on periphery hydrophillic halo-rim can be determined (rim is low echogenic, width 1–2 mm, located around the formation) Adenoma Nodes formation of round form with clear contours, encapsulated, of decreased echogenic Adenocarcino Thyroid gland formation with unclear contours, dense structure, of decreased ma echogenic with the presence of microcal-cinats in formation and (or) absence or unclear capsule. A suspicious node does not change during pressure on it by an ultrasonic sensor. Enlarged regional lymphatic nodes as hypoechogenic formations of round or oval form are often determined References Main literature 1. Endocrinology. Textbook/Study Guide for the Practical Classes. Ed. By Petro M. Bodnar: Vinnytsya: Nova Knyha Publishers, 2008.-496 p. 2. Basіc & Clіnіcal Endocrіnology. Seventh edіtіon. Edіted by Francіs S. Greenspan, Davіd G. Gardner. – Mc Grew – Hіll Companіes, USA, 2004. – 976p. 3. Harrison‘s Endocrinology. Edited J.Larry Jameson. Mc Grew – Hill, USA,2006. – 563p. 4. Endocrinology. 6th edition by Mac Hadley, Jon E. Levine Benjamin Cummings.2006. – 608p. 5. Oxford Handbook of Endocrinology and Diabetes. Edited by Helen E. Turner, John A. H. Wass. Oxford, University press,2006. – 1005p. Additional literature 6. Endocrinology (A Logical Approach for Clinicians (Second Edition)). William Jubiz.-New York: WC Graw-Hill Book, 1985. - P. 232-236. Pediatric Endocrinology. 5th edition. – 2006. – 536p. 7. Thyroid Disordes (Aclevelend Clinic Guide) by Mario Skugor, Jesse Bryant Wilder Clevelend Press,2006. – 224p. Lecture prepared assistant, c.m.s. Chernobrova O.I. It is discussed and confirm on endocrinology department meeting " 31 " august 2012 y. Protocol № 1.