General characteristics of the thyroid gland.
The thyroid gland secretes basal metabolic regulators – iodine-containing hormones – triiodothyronine (T3) and thyroxine (T4), as well as calcitonin, one of the endocrine regulators of calcium metabolism. Two pairs of parathyroid glands (upper and lower), secreting a calcitonin antagonist, parathyrocrine (PTH), are almost always anatomically closely associated with the thyroid gland. In the thymus, antigen-independent differentiation of T-lymphocytes occurs, as well as the synthesis of peptide hormones (thymosins and typopoietin).

Fascia of the neck
1. The first fascia of the neck (superficial) (fascia colli superficialis) in the anterolateral parts of the neck is split into two sheets, between which is the subcutaneous muscle of the neck (m.platysma). Under the superficial fascia of the necks is a layer of fiber, in which the branches of the superficial jugular vein pass.
2. The second (own) fascia of the neck (fascia colli propria) covers the neck in the form of a case. In the area of ​​the sternocleidomastoid and trapezepid muscles, it splits into two sheets, superficial and deep, forming fascial sheaths for these muscles.
3. The third (median) fascia (fascia colli media), forms the vagina for the sternohyoid, thyroid-lingual, sterno-thyroid muscles.
4. The fourth (intra-cervical) fascia (fascia endocervicalis), is divided into parietal and visceral sheets (similar to the peritoneum or pleura), forming capsules for the internal organs of the neck. The visceral leaf covering the thyroid gland separates it from the nearby parathyroid glands, recurrent laryngeal nerves, trachea, esophagus, neurovascular bundle. Performing resections of the thyroid gland under the visceral leaf of the fourth fascia of the neck (subfascial resections) avoids trauma to these vital organs.

Thyroid anatomy.
The blood supply to the thyroid gland is intense and comparable to the blood supply to the brain, blood perfusion through the kidneys and liver.
Arterial blood supply.
– the upper thyroid arteries (branches of the external carotid arteries) supply the upper poles of the lobes of the gland;
– the lower thyroid arteries start from the thyroid-cervical trunks (branches of the subclavian arteries) and supply the lower poles of the gland;
– the unpaired thyroid artery, which occurs in 12% of cases, originates from the aortic arch. Its branches take part in the blood supply to the isthmus of the thyroid gland.
Venous outflow.
– paired upper thyroid veins run along the same name arthriasis and flow into the internal jugular veins
– the middle veins of the thyroid gland depart from the lateral surfaces of the lobes and also flow into the internal jugular veins
– the lower thyroid veins drain from the lower poles of the lobes and the isthmus. They fall either directly into the internal or into an unnamed vein.
Lymphatic drainage.
– the outflow of lymph from the thyroid gland occurs in the lymph nodes located in the esophageal-tracheal groove, in front and on the sides of the trachea.
– The involvement of the lymph nodes of the esophageal-tracheal sulcus during metastasis of thyroid tumors promotes the spread of the tumor to the underlying recurrent nerve, trachea or esophagus
. Innervation.
Recurrent laryngeal nerve.
– location. The recurrent laryngeal nerves depart from the vagus and pass in the esophageal-tracheal sulcus, adjacent to the posterior medial surface of the thyroid gland
– on the right side, the nerve bends around the subclavian artery and ascends obliquely from the outside to the inside, crossing the lower thyroid artery at the posterior surface of the lower lobe of the thyroid gland
– on the left, the nerve begins below, at the level of the aortic arch, bends around it and lies in the left esophageal-tracheal groove.
– Branches: the nerve has an external branch that provides sensory innervation to the larynx and an internal branch that runs to the muscles of the pharynx.
– Damage to the recurrent laryngeal nerve, with the development of paralysis of the laryngeal muscles and impaired phonation, most often occurs either where it crosses the lower thyroid artery, or where it pierces the membrane between the cricoid and thyroid cartilage. Damage to a nerve during an operation requiring removal of a lobe of the gland can be prevented by first isolating it.
Superior laryngeal nerve.
– passage: the nerve is intimately intertwined with the branches of the superior thyroid artery
– branches: the superior laryngeal nerve gives a sensory external branch that innervates the larynx and a motor internal branch to the cricoid-thyroid muscle.
– Damage: the superior laryngeal nerve can be injured when the upper pole of the gland is mobilized, especially if the lobe is enlarged.
– The damage causes a weakening of the voice, which is of great importance for singers and orators
– The damage can be prevented by ligating the branches of the superior thyroid artery when the latter enters the gland tissue. Distant ligation of the artery should be avoided.
Anomalies of the anlage of the thyroid gland in the embryonic period lead to ectopic localization of the thyroid tissue in the tongue, under the hyoid bone or in the mediastinum.

Examination of the thyroid gland.
Examination:
1. Anamnesis: specify the place of birth, residence (to identify endemic foci).
2. Complaints (if any) change in voice, weakness, drowsiness, edema – in favor of hypofunction; weight loss, increased appetite, hand tremor, lability – in favor of hyperfunction.
3. Palpation:
– carried out from the side of the chest. Determine the size, consistency, soreness, displacement, areas of regional metastasis – the area inside the jugular vein.
– Palpation in the supine position with a pillow under the shoulder blades.
4. Instrumental methods:
– X-ray: goiter can be determined only in large sizes and high density due to calcification. The width and displacement of the trachea can be seen.
– Artificial contrast: pneumothyrography – was used in the 50s.
– Angiography of the thyroid gland – as the gland is rich in blood vessels. A puncture of the femoral artery is performed, a probe is inserted and brought to the thyrothyroid trunk. Contrast is introduced.
– Thyreolymphography. Superfluid oil contrast agents are introduced. Normal structure: openwork network of lymphatic vessels. If there are nodular lesions, there will be a contrast accumulation defect.
– Ultrasound: we determine the size, structure of tissues (you can determine a cyst with a size of 2-3 mm), the degree of tissue density (if a cyst, then echogenicity is reduced, if a tumor or nodes, then echogenicity is increased). More often isoechoic nodes.
– Morphology is crucial. Morphologists make the diagnosis based on morphological features. Preoperative puncture aspiration fine needle biopsy. The diagnosis is made in 80-90%.
– Trepanobiopsy – a needle with a cutter is used. Then the drug is sent for histological examination. Under local anesthesia. With small formations, the introduction of the needle is monitored using an ultrasound machine.
Assessment of thyroid function.
1. Radioimmunoassay allows you to directly measure the content of T3, T4, TSH. In this case, the ratio between free and bound forms of hormones should be taken into account.
2. The uptake of hormones by resins is a widely used indirect method for the determination of hormone-binding proteins.
3. Index of free thyroxine – an estimate of free T4, taking into account the content of hormone-binding proteins.
4. The test of stimulation of TSH by thyroliberin is determined by the secretion of thyrotropin into the blood in response to intravenous administration of thyroliberin.
5. Tests for the detection of antibodies to TSH receptors reveal a heterogeneous group of Ig that bind to the TSH receptors of the endocrine cells of the thyroid gland and change its functional activity.
6. Scanning the thyroid gland using technetium isotopes (99mTc) allows to identify areas of low accumulation of radionuclide (cold nodules), to detect ectopic foci of the thyroid gland or organ parenchyma defect, technetium accumulates only in the thyroid gland, the half-life is only 6 o’clock.
7. Study of absorption of radioactive iodine using iodine-123 (123I) and iodine -131.
8. Content of iodine in drinking water. Water iodization is carried out at waterworks.
Classification of diseases of the thyroid gland.
I Congenital anomalies of the thyroid gland: aplasia, hypoplasia, ectopia.
II Endemic goiter
By form:
– nodular
– diffuse
– mixed
By function:
– euthyroid
– hyperthyroid
– hypothyroid
III Sporadic goiter:
By form:
– nodular
– diffuse
– mixed
By function:
– euthyroid
– hyperthyroid
– hypothyroid
IV Diffuse toxic goiter
By severity thyrotoxicosis:
– mild
– medium
– severe
V Hypothyroidism
In severity:
– mild
– medium
– severe (myxedema)
VI Inflammatory diseases:
– acute thyroiditis (strumite
– goiter inflammation) – subacute thyroiditis
– chronic lymphatic thyroiditis (autoimmune, Hashimoto’s)
– Riedel (fibrous)
– rare inflammatory diseases of a specific nature: tuberculosis, syphilis
VII Thyroid damage:
– open
– closed
VII Malignant tumors

Congenital anomalies of the thyroid gland.

Pharyngeal (lingual) thyroid gland.
1. Localization. The pharyngeal localization of the gland is observed if it does not descend to the neck and retains its original position in the region of the tongue root.
2. Symptoms: enlargement of the gland in such a localization causes impaired swallowing or speech.
3. The diagnosis is established by examination or indirect laryngoscopy. Scanning with an isotope of iodine is used to identify thyroid tissue.
4. Treatment:
– suppression of TSH production by prescribing thyroxine (since in this case the function of the pharyngeal thyroid tissue is usually reduced)
– surgical removal of the gland should be performed in case of symptoms of pharyngeal obstruction, especially if hormonal therapy is ineffective.

Ectopic median location of the gland.
Localization: such an arrangement of the gland should be assumed when a volumetric formation is found below the hyoid bone.
Diagnosis: if the thyroid gland is absent in a typical place, then its ectopic tissue should be identified by radioisotope scanning. Removing the “tumor” is unacceptable without this study, since it is possible to deprive the patient of a single functioning gland.

Thyroid gland in the mediastinum.
Localization: the majority of abberant (incorrectly positioned) thyroid glands of the mediastinum lie in its antero-upper sections. They are represented either by areas of an enlarged thyroid gland of normal localization descending from the neck behind the sternum, or by ectopic unchanged glands.
– normally functioning thyroid tissue accumulates radioactive iodine, so it can be detected by radioisotope scanning of the mediastinum.
– In many cases, the retrosternal location of the gland (retrosternal goiter) is caused by adenomatous hyperplasia, in which the isotope does not accumulate in the gland tissue.
– Retrosternal goiters are usually found in older age groups
– They often cause symptoms of compression of the trachea and esophagus
– Compression syndrome does not respond to conservative therapy aimed at suppressing the production of TSH by thyroxine
Treatment: To eliminate the syndrome of compression, surgery is usually performed. Retrosternal goiter can be removed using a cervical approach, without a sternotomy.

Cysts and sinuses of the thyroid-lingual duct (median cysts of the neck). The rudiment of the gland is initially connected to the pharynx with a hollow cord that opens on the surface of the tongue root (later – foramen coecum). Normally, this strand degenerates.
Localization: cysts of the thyroid-lingual duct usually look like masses, localized along the midline of the neck between the hyoid bone and the isthmus of the thyroid gland. Crossing the center of the hyoid bone, they reach the root of the tongue.
Symptoms:
– find uniform nodes or cysts that can form fistulas that open onto the skin.
– They are found at any age, more often in children.
– A third of patients have a history of cyst infection (local inflammation of the skin and fatty tissue).
Treatment: the operation consists in complete excision of the cyst together with a part of the hyoid bone, as well as the proximal part of the duct to the root of the tongue (Systranka operation).

By the nature of the changes in the thyroid gland, it is customary to distinguish diffuse and nodular goiter.
Diffuse toxic goiter.
Diffuse toxic goiter (DTZ) is the most common disease (both among thyroid diseases and in the structure of endocrine diseases) DTZ develops at any age, more often in working age.
Etiology.
Insufficiently studied, at present, dtz is regarded as a genetic disease of an autoimmune nature, and is caused by a congenital defect in the system of immunological control. Evidence of
genetic nature of the disease is the high incidence of familial forms of blood detection in rodst-Vennikov antibodies to various elements of thyroid more often than in the population as a common co-cetanah DTZ with other diseases autoimmune diseases (rheumatoid arthritis, etc.).
The result of disorders of cell and humoral immunity is the accumulation of Ig (mainly class G) in the blood, which have the ability to interact with thyroid-stimulating hormone receptors on the plasma membrane of thyrocytes and, like TSH, stimulate the thyroid gland. These thyroid-stimulating immunoglobulins compete successfully for TSH receptors, displacing the action of TSH.
Unlike TSH, these immunoglobulins retain their activity for a long time. The complexes of these immunoglobulins are referred to as long-acting thyroid stimulants. These complexes retain their activity for more than 2 weeks. This pathological factor does not lend itself to any regulation (it is autonomous). At the same time, the thyroid gland acquires complete autonomy, regardless of any regulation. Although TSH exists, it does not participate in the regulation of the thyroid gland (its concentration may be different). Antigen to-th, causes the production of these antibodies was not identified.
The pathogenesis of the main symptoms of the disease is due to the influence of an excessive amount of hormones. An exception to this rule is eye damage (ophthalmopathy) – this symptom complex develops outside of direct connection with an excess of thyroid hormones.
Clinic is variable due to the multiple action of thyroid hormones. The most sensitive to an excess of thyroid hormones is the central nervous system (the first symptoms are symptoms from the central nervous system).
1. Complaints: mental irritability, irritability, sleep disturbance, tremors.
2. Symptoms: tachycardia, which appears early and is a consequence of increased activity of the sympathetic division of the autonomic nervous system; behavior of patients: patients are fussy, verbose, inconsistent, hasty, uncollected.
3. Symptoms caused by increased basal metabolic rate:
1. Shortness of breath at the beginning is not a manifestation of cardio-respiratory failure. This is a compensatory reaction of the body to an increase in basal metabolism (increased oxygen demand)
2. increased sweating, heat transfer. The patient feels a constant feeling of heat. Sweat has time to evaporate quickly, the skin becomes soft, elastic, velvety.
3. Strengthening excretion and catabolism, which contributes to weight loss, and increased appetite (one of the rare diseases where weight loss is accompanied by an increase in appetite) Sometimes there are cases of increased body weight – “fat graves”, more common in girls.
4. persistent tachycardia reflects an increase in basal metabolism and an increase in myocardial oxygen demand. Differential diagnostic test with neurosis: it is necessary to count the pulse day and night, with neurosis at night the pulse will be normal, with dtz the pulse rate will not change.

All organs and systems are involved in the pathological process:
SKIN COVERINGS: elastic, warm, soft, often a specific color appears – bronze (hyperpigmentation of the skin) – this is evidence of severe thyrotoxicosis and this is due to the fact that thyroid hormones increase the metabolism of many hormones, in including cortisol, and thereby increase the body’s need for it, the adrenal glands are compensated by the production of ACTH, which also has the property of increasing pigmentation. This pigmentation is diffuse more often on the upper and lower eyelids (Erenek’s symptom). Approximately 10-15% of patients have specific changes in the skin of the lower leg in the form of compaction,
hyperemia. Sometimes hyperpigmentation, while the skin of the anterior surface of the leg becomes denser, more often on the back of the foot, forming dense mucous edema – pretibial myxedema – is formed due to the accumulation of muco-polysaccharides, salts, proteins. These changes sometimes lead to diagnostic errors – these edema is attributed to primary thyroid insufficiency.
MUSCULAR SYSTEM: because Thyroid hormones in high concentrations have a catabolic effect that promotes the breakdown of muscle protein. Clinically, this is manifested by muscle weakness, sometimes reaching the degree of flaccid paralysis, which makes it possible to differentiate them from paralysis of a neural nature. Weakness can be generalized, sometimes there can be weakness of only certain muscle groups. The muscles of the lower
extremities are more often captured . The extreme severity of this symptom is paroxysmal myoplegia, which most often affects the muscles of the thigh and lower leg.
BONE TISSUE: in severe forms of thyrotoxicosis in the elderly, the phenomena of osteoporosis have been described, which is an extreme manifestation of catabolism.
CARDIOVASCULAR SYSTEM: tachycardia that appears in the early stages. Further, dystrophic changes in the muscle occur, which are manifested by a violation of the rhythm, in the future, insufficient
blood circulation. The most characteristic rhythm disturbance is atrial fibrillation, which first appears in the form of paroxysms, then becomes permanent.
BP: as a rule, systolic pressure rises and diastolic pressure decreases. Changes in blood pressure and, in particular, a drop in diastolic pressure largely reflects the severity of thyrotoxicosis, because, as a rule, a significant drop in diastolic pressure is a consequence of the relative insufficiency of the adrenal cortex – a formidable complication. Progressive circulatory failure is a frequent cause of death in patients.
BODY TEMPERATURE increased. Patients often suffer from colds (they wear clothes not for the season).
Gastrointestinal tract increased stool. A decrease in the acid-forming function of the stomach, dystrophic changes in the mucous membrane and further frequent stools are replaced by constipation. In severe cases, toxic hepatitis may occur.
BLOOD leukopenia, normochromic anemia.
ENDOCRINE ORGANS:
1. adrenal glands (relative adrenal insufficiency, under stress conditions can develop acute relative adrenal insufficiency – which poses a threat to life.
2. dysfunction of the insular apparatus: thyroid hormones are insulin antagonists. Therefore, with a long course, frequent relapses, the severity of toxicosis, especially in persons predisposed to diabetes, may develop diabetes mellitus
3. dysfunction of the sex glands: in women, menstrual irregularities, miscarriages, infertility, amenorrhea, in men: impotence, gynecomastia.

A characteristic feature of the clinical picture of DTG is the steady progression of symptoms to the development of complications, including heart failure, rhythm disturbances, acute adrenal cortex insufficiency.

SYMPTOMS OF OPHTHALMOPATHY
Eye damage in patients with DTZ is of 2 types:
1. in patients, the tone of the sympathetic nervous system increases – dilated eye slits, a surprised gaze, spontaneous bulging may appear. Appears or disappears as thyrotoxicosis is treated.
2. have qualitative differences. Pathological changes of the constant component, which is the infiltration of retro-orbital tissue with jelly-like (mucoid masses). This tissue has much in common with the pretibial myxedema. This tissue is rich in proteins, salts, mucopolysaccharides and is highly hydrophilic, prone to edema. At the same time, the bed of the eyeball decreases and it is pushed out and bulging develops (unlike bulging eyes with type 1 eye lesion, it has an organic basis).
These masses disrupt lymphodynamics, hemodynamics, the neurovascular bundle is compressed, and a violation of the blood supply develops.
If at the same time a violation of the complete closure of the eyelids joins, then there may be the development of infection (keratitis leads to scarring and loss of vision). A feature of this symptom complex is
its autonomy (it does not depend on the concentration of thyroid hormones, it can appear at different stages of the disease – long before the first symptoms of thyrotoxicosis, or during weight loss, etc.) This is the least controllable symptom complex.
CLASSIFICATION OF THE SEVERITY OF THYROTOXICOSIS
1 tbsp. light current pulse 100 beats per minute,
weight loss 3-5 kg
2 tbsp. average severity pulse 100 -120 beats per
minute, weight loss 8-10 kg
3 tbsp. severe course 120 -140 and more dramatic
weight loss .