eye symptoms. Clinical signs, symptoms of thyrotoxicosis

Delrymple's symptom is a wide opening of the palpebral fissure in patients with thyrotoxicosis.

Symptom Graefe (A.Graefe) - lag of the upper eyelid and the appearance of a white strip of sclera over the iris when the eyeball moves downwards in patients with thyrotoxicosis.

Kocher's symptom (E.Th.Kocher) - the lag of the movement of the eyeball from the movement of the upper eyelid and the appearance of a white strip of sclera above the iris when the eyeball moves upward in patients with thyrotoxicosis.

Stelvag's symptom (C.Stellwag) is a rare and incomplete blinking in patients with thyrotoxicosis.

Symptom Repreva-Melikhov - an angry look in patients with thyrotoxicosis.

Symptom Moebius (P.J. Moebius) - weakness of convergence in patients with thyrotoxicosis.

Symptom Jellinek (S.Jellinek) - pigmentation of the skin on the eyelids in patients with thyrotoxicosis.

Symptom Rosenbach (O.Rosenbach) - a small rapid trembling of the lowered eyelids in patients with thyrotoxicosis.

Symptom of Stasinsky (T. Stasinski) - injection of sclera with a cruciform arrangement of dilated vessels in patients with thyrotoxicosis.

Symptoms in the pathology of the gastrointestinal tract

Symptom Courvoisier - Terrier - below the edge of the liver, an enlarged (stagnant) gallbladder is palpated, oval in shape, elastic in consistency, displaceable, painless. Described in compression of the common bile duct in cancer of the head of the pancreas, as well as in the primary lesion of the major duodenal papilla: papillitis, stenosis, cancer.

Symptom Mussi - Georgievsky - pain on palpation between the legs m. sternoclaidomastoideus on the right. A sign of damage to the gallbladder, most often with acute cholecystitis.

Murphy's symptom (J.B. Murphy) - palpation on inspiration at the site of the gallbladder projection (the patient is on the left side, sitting or standing, when either 4 fingers or 1 finger are immersed). A symptom is considered positive if, during a deep breath, the patient suddenly interrupts it due to the appearance of pain when the fingertips come into contact with a sharply sensitive gallbladder, as evidenced by the patient's reaction in the form of a cry of pain and mimic manifestation.

Symptom Ker (H.Kehr) - the appearance of pain in the area of localization of the gallbladder with deep palpation in the right hypochondrium.

Gausmann's symptom - a feeling of pain in the gallbladder area with a short blow with the edge of the palm below the right costal arch at the height of inspiration.

Symptom Lepene - Vasilenko - the appearance of pain in the area of the gallbladder when jerky blows are applied with the fingertips while inhaling below the right costal arch.

Symptom of Ortner-Grekov (N.Ortner, I.I. Grekov) - pain appears when the inflamed gallbladder is shaken when the edge of the palm is struck along the edge of the right costal arch.

Eisenberg's symptom - the patient stands up on his toes, and then quickly falls on his heels. A positive symptom is the occurrence of pain in the right hypochondrium as a result of concussion of the inflamed gallbladder.

Symptom Pekarsky - pain when pressing on the xiphoid process. The symptom is often observed in recurrent chronic cholecystitis.

Symptom Mendel (F.Mendel) - tapping fingers on the anterior abdominal wall. It is positive when pain occurs, usually coinciding with the projection site of a sufficiently deep ulcerative defect in the stomach or duodenum.

Grotta's symptom (J.W. Grotta) - atrophy of the subcutaneous tissue in the area corresponding to the projection of the pancreas on the abdominal wall.

Choledochopancreatic zone of Chauffard (A.E. Chauffard) - in the epigastrium on the right (in the right upper quadrant of the abdomen) - medially from the bisector separating the right angle formed by two intersecting lines: the anterior midline of the abdomen and a line drawn perpendicular to it through the navel.

Desjardins point (A.Desjardins) - a point on the border of the middle and upper third of the distance between the navel and the right costal arch along the line from the navel to the right armpit.

Zone Gubergritsa - Skulsky - in the epigastrium on the left, symmetrically to the zone of Chauffard.

Gubergrits point - 5-6 cm above the navel on the line connecting it with the left armpit.

Symptom Mayo-Robson (A.W. Mayo-Robson) - the appearance of pain on palpation of the left costovertebral angle, which indicates an inflammatory process of the caudal pancreas.

EYE SYMPTOMS OF DIFFUSE TOXIC GOITER arise as a result of complex neurohormonal disorders, the mechanism of which is not fully disclosed. They usually appear with diffuse toxic goiter.

Ocular symptoms of diffuse toxic goiter (GSDT3) mainly consist of exophthalmos and are associated with a violation of friendly movements of the eyeballs (Mobius sign) and muscles of the face, caused by myasthenia of the muscles of the face and oculomotor muscles, damage to the nuclei of the oculomotor nerves.

Of the numerous GS DT3 occupies a leading position exophthalmos(E).

There are a number of hypotheses explaining the reasons for its development, but none of them is able to reveal the entire mechanism of this process. It has been experimentally established that extracts of the anterior pituitary gland, in particular TSH, administered to an animal, in addition to hyperthyroidism, cause exophthalmos. However, clinical observations show that with diffuse toxic goiter, when hypersecretion of TSH occurs in almost all cases, exophthalmos is observed in a few. It is known that in hypothyroidism, TSH secretion is significantly increased, but exophthalmos does not develop. Recent studies have shown that the factor that causes exophthalmos is not the TSH itself, but the substance that is with it, called exophthalmic factor. It is assumed that this factor is not produced to the same extent in all patients with thyrotoxicosis.

In practice, it is often observed unilateral exophthalmos. This fact indicates that bulging is not completely predetermined by the exophthalmic factor. In all likelihood, the autonomic nervous system, in particular the sympathetic one, plays a certain role in this, which is confirmed experimentally: when the cervical sympathetic nerves are irritated, exophthalmos occurs in animals. The immediate cause of exophthalmos is an increase in the tone of the extensors of the oculomotor muscles, an increase in the volume of retrobulbar tissue, in particular, acid mucopolysaccharides (which increase the hydrophilicity of tissues), fat and connective tissue. This leads to a sharp increase in intraorbital pressure, to stagnation in the eyelids and their swelling.

There are a number of other theories.
For example, according to autoimmune theory, thyroglobulin can become an antigen and, by coming into contact with thyroidin together with B-lymphocytes , is fixed on the cell membranes of the extracular muscles, causing their damage with the subsequent development of edema of the retrobulbar tissues.

Exophthalmos explain and violation of lymphatic drainage in the thyroid gland, followed by lymphostasis and edema of the extraocular and retrabulbar tissues. Along with swelling of the retrabulbar and intrabulbar tissue, the tone of the oculomotor nerves and muscles is disturbed, which leads to a violation of the friendly movements of the eyeballs. It is often observed in people who do not suffer from thyrotoxicosis.

There is evidence that with the so-called euthyroid exophthalmos the content of thyroid hormones in the blood, in particular T 3 , increased, but without tachycardia and weight loss. It is assumed that exophthalmos is caused by hyperthyroidism, however, the sensitivity of peripheral receptors to them is reduced, and the receptors of the eye muscles, on the contrary, are increased.
Euthyroid exophthalmos often has a family character, and often individual family members may develop thyrotoxicosis. At the same time, thyrotoxicosis in such individuals is not necessarily accompanied by weight loss, sometimes there is even some obesity, which, in all likelihood, is due to the simultaneous defeat of diencephalic formations.

Histologically, edema and cellular infiltration of the retroorbital tissue by lymphocytes, macrophages, and plasma cells are first noted.
Later in the muscle fibers - edema, loss of transverse striation, homogenization with an increase in their size up to 10 times with an increase in their contractility.

The speed and degree of development of exophthalmos varies widely from several weeks to a year. Rarely, the development of exophthalmos is lightning fast.
Subjective symptoms of exophthalmos are lacrimation, pain behind the eyes, when moving the eyeballs, an unpleasant feeling of feeling "sand in the eyes", especially with visual strain, rarely diplopia.
Initially, the upper eyelid swells, with a pronounced degree, both the lower and the temple area, the eyebrow. Hyperemia of the mucosa causes the progress of swelling and leads to chymosis, an edematous shaft is formed around the cornea, eversion of the lower eyelid. The mucous membrane is exposed to drying and ulceration. The frequency of exophthalmos in thyrotoxicosis ranges from 10 to 40%. The degree of protrusion of the eyeballs is determined by an exophthalmometer.

According to expressibility, exophthalmos is divided into four degrees:

1st degree(mild form) - moderate exophthalmos with slight dysfunction of the oculomotor muscles. Eye protrusion 15.9+0.2 mm.
2nd degree(moderate) - moderate exophthalmos with a slight dysfunction of the oculomotor muscles and mild changes in the conjunctiva. Eye protrusion 17.9+0.2 mm.
3rd degree(severe form) - a pronounced exophthalmos with a violation of the closure of the eyelids. A pronounced change in the conjunctiva and the function of the oculomotor muscles, a mild lesion of the cornea, the initial manifestations of atrophy of the optic nerve. Eye protrusion 22.8 ± 1.1 mm.
4th degree(extremely severe form) - a pronounced manifestation of the above symptoms with a threat of loss of vision and eyes. Protrusion more than 24 mm.

In addition to exophthalmos, a number of ocular symptoms characteristic of thyrotoxicosis are described:

Abadi symptom (1842-1932, France) - spasms of the muscles that lift the eyelid.
Ballet symptom (1888) - partial or complete immobility of one or more external muscles of the eye without damage to the internal muscles.
Berke symptom - expansion and pulsation of retinal vessels.
bella symptom - deviation of the eye upward and outward with active closing of the palpebral fissure.
Boston symptom (1871 - 1931, American doctor) - jerky, uneven delay of the upper eyelid when looking down.
Botkin symptom (1850) - a fleeting expansion of the palpebral fissures during fixation of the gaze.
Brahma symptom. During laughter, the eyes remain wide open, while in healthy people, the palpebral fissures are significantly narrowed.
Govena symptom - jerky constriction of the pupil of one eye when illuminating the other.
Goldziger symptom - hyperemia of the conjunctiva.
Graefe symptom (1823-1870, German ophthalmologist). The patient is asked to follow the finger with which the examiner leads in front of the eyes (at a distance of 30 - 40 cm) from top to bottom and at the same time the doctor supports the patient's head with the other hand so that he cannot move it. With a positive symptom, the upper eyelid is late and does not keep up with the downward movement of the eyeball. As a result, a strip of conjunctiva opens between the upper eyelid and the limbus of the cornea. This symptom is the result of increased tone of the muscle that lifts the upper eyelid.
Grifft's symptom - retardation of the lower eyelid when looking closely at an object at eye level.
Dalrymple symptom (1804 - 1852, Scottish ophthalmologist). When fixing vision on an object located at the level of the pupils, the palpebral fissures open wide. At the same time, areas of the sclera are revealed, which are normally covered by the upper and lower eyelids. Caused by paresis of the circular muscles of the eyelids.
Gifford symptom (1906, Britain). Due to thickening and increased muscle tone, the upper eyelid turns out with great difficulty.
Jellinek symptom (1187, Austrian doctor) - pigmentation of the skin of the eyelids. Considered as a sign of adrenal insufficiency.
Geoffrey's symptom (1844-1908, French doctor). When looking up, wrinkles do not form on the forehead: asthenia of the frontal muscles.
Zatler symptom - weak blurring.
Zenger-Entrout symptom - cushion-like swelling of the eyelids.
Ibn Sina symptom - retroocular resistance in exophthalmos.
knysa symptom - anisocoria.
Cowan's symptom - vibration of the pupils.
Kocher symptom (1841 -1917, Swiss surgeon). The patient follows the finger of the researched, led in front of his gaze from the bottom up. With a positive symptom, the sclera, which is normally located under the upper eyelid, is exposed and becomes visible. The symptom is due to a faster displacement of the upper eyelid than the eyeball, due to an increase in its tone.
Levi symptom. Pupil dilation when exposed to the conjunctiva with a weak solution of adrenaline.
Mobius symptom (1880). When the finger moves quickly from the lateral side to the middle, the eyeball does not keep up with the movement of the finger and transient strabismus occurs. Convergence disorder is due to weakness of the rectus viscera of the eye.
Mina symptom - delay of the eyeballs behind the movement of the eyelids with a close look.
Niza symptom - uneven dilation of the pupils.
Popovasymptom (USSR) - spasmodic movement of the upper eyelid when looking down.
Reprev-Melikhov symptom (USSR) - characterized by the angry look of patients.
Rosenbach symptom (1851-1907, German, doctor) - trembling of the eyelids when they are closed.
Snellensymptom (1834-1908, Dutch ophthalmologist) - buzzing, heard with a phonendoscope over closed eyes. Characteristic of thyrotoxic exophthalmos.
Spector symptom - soreness of the points of attachment of the oblique muscles to the sclera with initial exophthalmos.
Stasinsky symptom - Injection of the cornea in the form of a red cross.
Topolyansky symptom (USSR) - conjunctival hyperemia in the form of a "red cross".
Wilder's symptom. If the eyeball is in a state of extreme abduction and begins to move towards the center, its displacement occurs in steps, with stops.
Shtelvaga symptom (1869, Austrian ophthalmologist) - retraction of the upper eyelid in combination with a rare blinking due to a decrease in the sensitivity of the cornea.
Ecrota symptom - swelling of the upper eyelid.
Jaffa symptom - the inability to wrinkle the forehead, as in Geoffroy's symptom, is due to a decrease in the tone of the frontal muscles.

Not all eye symptoms of thyrotoxic goiter are detected in the same patients with thyrotoxicosis; symptoms Gre fe, Kocher, Dalrymple, associated with dysfunction of the upper eyelid, Yaffe symptoms and Geoffroy, symptom we Rosenbach, Stelwag, associated with neurogenic factors, and, finally, Moebius, Wilder caused by impaired convergence of the eyes.

TREATMENT OF EYE SYMPTOMS OF THYROTOXICOSIS.

Treatment of eye symptoms is mainly pathogenetic.
Prevention of exophthalmos is the timely treatment of thyrotoxicosis.

If there are signs of exophthalmos, large doses of drugs should not be used from the very beginning. imidazole, which can lead to hypersecretion of TSH, an exophthalmic factor.
In the future, when the euthyroid state is reached, a long time should be prescribed thyroid hormones (T 4 , Tz) in such a way that the pulse rate does not go beyond physiological boundaries - 100 beats per minute.
During the development of exophthalmos, when mucopolysaccharides have just accumulated in the retrobulbar space, a good therapeutic effect is exerted by glucocorticosteroids and gamma therapy (6000 rad) of the hypothalamic-pituitary region from three fields, as well as retroorbital with simultaneous administration in large doses With t roid hormones up to 40-80 mg per day or by administration hydrocortisone into the orbital space for 10-12 days, 30-40 mg daily in each orbit.

Regression of exophthalmos often does not occur in cases where it has a long prescription, during which a lot of fat and connective tissue accumulate in the retroorbital space. In these cases, conservative treatment is not effective. An operation is proposed - decompression of the orbit by expanding it in three spatial directions.

Thyrotoxicosis is a pathological process in the body, which is characterized by an increased level of thyroid hormones in the body. This condition is not a separate disease, but it can become an impetus for the development of various disorders in the body, and it is completely unrelated to the thyroid gland.

In our article, we will tell you how to recognize thyrotoxicosis, the symptoms and treatment directly depend on how much the patient's hormone levels are elevated.

As we all know, the thyroid gland plays a special role in the activity of our body.

It produces several types of hormones, the main ones being:

thyroxine (T4);
triiodothyronine (T3).

The percentage of thyroxine production is 4/5 of the total number of thyroid hormones produced, and triiodothyronine is 1/5. Thyroxine has the function of converting to the hormone triiodothyronine, which is the biologically active form.

Controls the production of thyroid hormones by the pituitary gland. The pituitary gland is a small part of the brain that produces thyroid-stimulating hormone (TSH). It is its function to stimulate thyroid cells to produce thyroid hormones.

With increased productivity of thyroid hormones, the pituitary gland reduces the productive function, and vice versa, with reduced production of thyroid hormones, the TSH content exceeds the norm.

It turns out that when the level of thyroid hormones decreases, the pituitary gland begins to more actively produce thyroid-stimulating hormone. This condition is called thyrotoxicosis. There are several factors that influence the development of this pathology, which we will discuss further.

Important. Patients suffering from thyrotoxicosis differ in one feature: they constantly feel a feeling of hunger. Each time they overeat, they do not begin to gain weight, but, on the contrary, actively begin to lose it. Patients feel unquenchable thirst, which is accompanied by copious urination. In this case, the characteristic difference is the eye symptoms, with thyrotoxicosis, the eyes become bulging.

Etiology and clinical picture

If anyone is familiar with such a pathological condition as hypothyroidism, then thyrotoxicosis is the opposite condition to it. With hypothyroidism, all processes in the body begin to slow down, which is associated with a reduced level of thyroid hormones.

And with thyrotoxicosis, on the contrary, they begin to function actively, a prerequisite for this process is the increased production of thyroid hormones. There are several reasons for the development of this pathology.

Reasons for the development of thyrotoxicosis

As we have already said, there are several different factors that affect the formation of this pathology in the body.

Autoimmune pathologies. The most common disease that causes the development of thyrotoxicosis in 80% of cases is diffuse toxic goiter. With this disease, the thyroid gland increases in size, which acts as a provoking factor for the active production of thyroid hormones.
Pathologies associated with a violation of the cellular tissue of the thyroid gland. These include diseases: postpartum thyroiditis, thyroiditis without pain.
Overdose of medications containing thyroid hormones.
Multiple nodes. Nodular formations secrete a large number of hormones, which provokes the development of thyrotoxicosis.
Toxic adenoma. This pathology is called Plummer's disease, which is characterized by the presence of a single nodular formation (adenoma), which secretes a large amount of hormones.
Increased iodine intake.

The above factors are the main reasons for the development of thyrotoxicosis, but in addition to them, there are additional factors that can act as a provocateur to the development of thyrotoxicosis. For example, thyrotoxicosis in children is a rare phenomenon.

The main cause of the pathology is the disease of the mother with thyrotoxicosis during pregnancy. At the same time, the probability of the disease in girls is higher than in boys.

Important. One of the main causes of thyrotoxicosis is diffuse toxic goiter. The disease belongs to a number of hereditary autoimmune diseases. The disease can manifest itself even in the presence of at least one disease-causing gene responsible for the spread of pathology. The manifestation of symptoms of autoimmune pathology in children is a rare phenomenon; in most cases, people from 20 to 40 years old suffer.

Forms of the disease

Thyrotoxicosis has three forms of manifestation:

light;
average;
heavy.

Table number 1. Forms of thyrotoxicosis:


	With this form, the patient begins to lose weight, but within the acceptable range. At the same time, he has an increased appetite. There is an increased heartbeat, which reaches 100 beats per minute, mild tachycardia. In this situation, there is a violation of only the function of the thyroid gland, without affecting all other functions of the body.
	With this form of pathology, a high heart rate is observed (up to 120 beats per minute). Weight loss exceeds the allowable rate. Frequent tachycardia appears, which does not go away either with a change in body position or with healthy sleep. Digestion is disturbed, accompanied by diarrhea. The level of cholesterol decreases, there is a failure in carbohydrate metabolism.
	This form can manifest itself as a result of poor-quality treatment of an existing pathology of the thyroid gland, or its absence. As a result, pronounced thyrotoxicosis affects other organs and systems of the body, which is manifested by their strong dysfunction.

In addition to the above forms, another one is distinguished - this is subclinical thyrotoxicosis. This form is asymptomatic, but at the same time, hormonal disorders can already be diagnosed in the blood.

This pathology is characterized by the following symptoms:

tachycardia;
cramps of the limbs;
high irritability;
insomnia;
excitability;
thromboembolism;
flickering arrhythmia.

Symptoms

A large percentage of the development of pathology occurs in the female sex, and at a young age (from 20 to 40 years). The symptomatology of thyrotoxicosis is varied and at first glance it may seem that it is not associated with thyroid dysfunction. This is because thyroid hormones are involved in many body processes and can cause disruptions throughout the body.

Table number 2. The main symptoms of thyrotoxicosis:


	Patients have frequent unreasonable attacks of irascibility, anxiety, emotional instability. They are constantly in an excited state, start to rush somewhere, make a lot of excessive movements, constantly fiddle with some thing in their hands, etc. The main symptom of agitation is trembling of the limbs.
	Patients suffer from constant insomnia, while feeling completely tired. Even when falling into a deep sleep, they wake up abruptly and often.
	Thyrotoxicosis is characterized by disturbances towards an increase in upper systolic blood pressure and towards a decrease in diastolic pressure (lower). Heart rhythm disturbances can be of various types. For example, they may appear: sinus tachycardia (increased heart beats up to 90 per minute); atrial fibrillation (irregular contraction of the heart muscle with small or large intervals).
	Often patients feel a constant feeling of hunger, constantly overeat. But there are cases when the appetite is completely absent.
	Patients often suffer from persistent liquid diarrhea and crampy abdominal pain. In some cases, vomiting occurs. There may be a violation of the outflow of bile, which contributes to an increase in the size of the liver. And this, in turn, threatens the development of a severe form of jaundice.
	The body temperature is constantly kept at around 37.5 degrees, the patient feels hot, which is accompanied by high sweating. In hot weather, the symptoms intensify, the temperature may rise above the indicated mark.
	With increased appetite, the same level of physical activity, patients begin to actively lose weight.
	There is a feeling of weakness in the muscles, depression, fatigue. Against the background of thyrotoxicosis, thyroid myopathy develops, which is associated with a lack of nutrients in muscle tissue. In a severe form of the pathology, thyrotoxic muscle paralysis may occur.
	Under the adverse influence of hormones, fragility of bone tissue develops.
	In women, the menstrual cycle is disturbed, amenorrhea is possible. It is almost impossible to get pregnant in this situation. Menstruation passes with severe pain, nausea, vomiting, fainting, dizziness. In men, against this background, potency decreases, an increase in the mammary glands may occur.
	There is a strong swelling of the soft tissues, especially the shins are affected.
	People with thyrotoxicosis turn gray early, their hair becomes thinner, and I begin to fall out. The nail system becomes brittle.
	Victims are tormented by frequent and profuse urination, as a result of increased thirst.
	The level of glucose in the blood rises.
	According to the ultrasound examination, an increase in the size of the thyroid gland and a change in its structure are diagnosed. When probing, nodules can be seen.
	There is shortness of breath, difficulty swallowing. With an enlarged thyroid gland, a feeling of a lump in the throat appears.

Attention. The clinical picture of the disease in children differs from the symptomatic manifestations in adults. They do not have eye symptoms of thyrotoxicosis, so it is almost impossible to recognize the pathology by external signs. An accurate diagnosis can be made by a doctor after a complete examination of the body.

Eye symptoms

Separately, one can note the eye symptoms that occur in people with thyrotoxicosis. Pathology can be recognized by wide-open palpebral fissures and by some characteristic symptoms.

Delrymple's sign. There seems to be a lot of surprise or anger on the face.
Stelwag's sign. There is a strong protrusion of the eyeballs.
Symptom Zenger. Puffiness of the upper eyelids predominates.
Ellinek's sign. Dark circles appear around the eyes.
Graefe's symptom in thyrotoxicosis. When the patient's gaze is turned downwards, the upper eyelid lags behind the iris, it turns out that a white stripe of sclera forms between the iris and the upper eyelid.
Moebius sign. This symptom is characterized by a deviation of the eyeball to the side when fixing the gaze on one slowly approaching object.
Kocher's symptom in thyrotoxicosis. There is retraction of the upper eyelid, when the gaze quickly changes position. A section of the sclera is exposed when the gaze is held on the object that goes up.
Rosenbach's sign. Tremor of closed eyelids.

With thyrotoxicosis, there is increased tearing of the eyes, photophobia, a feeling of sand, decreased vision.

Possible Complications

With timely and high-quality treatment, thyrotoxicosis does not pose a serious danger, but if a person does not pay due attention to his health, serious consequences can develop.

Arterial hypertension.
Disturbances from the central nervous system.
Atrial fibrillation.

The most dangerous complication is thyrotoxic crisis, which, with its clinical picture, threatens the life of the patient.

This condition is characterized by the manifestation of such signs:

tremor of the limbs;
nausea and vomiting;
a significant increase in body temperature (up to 40 degrees);
high blood pressure;
violation of the heart rhythm;
weak urination in small amounts (possible anuria);
loss of consciousness;
coma.

Treatment of pathology is carried out in the intensive care unit under the strict supervision of doctors.

Diagnosis and treatment

Before starting treatment, it is necessary to determine the form of thyrotoxicosis and the cause of its occurrence. Treatment is carried out with the help of drug therapy and only as prescribed by the doctor after the diagnosis. At home, it is strictly forbidden to rescue the patient.

Diagnostics

The diagnosis is established by the endocrinologist after the examination of the patient. Methods of laboratory and instrumental studies are used to diagnose the disease.

Table number 3. Laboratory and instrumental research methods:

Research method	Description
	Conduct a laboratory blood test for the level of hormones (T3, T4, TSH).
	Based on the results of an ultrasound examination, the structure of the organ and its size are determined. When using a special sensor (color Doppler mapping), it is possible to assess the blood flow in the thyroid gland.
	This research method allows you to determine the work of various departments of the body, including the presence of nodes.
	It is used as an additional research method to establish the exact characteristics of thyroid dysfunction.

Treatment

Treatment of thyrotoxicosis is purely individual in nature and depends on the form of pathology, concomitant diseases and the age of the patient.

Therapies can be:

conservative;
operational.

Table number 4. The main methods of treatment of thyrotoxicosis:

Treatment method	Description
Medical therapy	It consists in taking medications that eliminate the active production of thyroid hormones. Widely known drugs such as Mercazolil and Tyrozol. Instructions for their use are prescribed by the attending physician, taking into account the individual characteristics of the patient. Drugs are taken for a long time (from 1 to 1.5 years). During the treatment period, it is important to regularly conduct biochemical blood tests (ALAT and ASAT), as well as control the level of hormones (TSH, T3, T4). After the normalization of hormone levels, maintenance therapy is prescribed. In some difficult situations, specialists prescribe preparatory drug therapy before carrying out the necessary operation.
Surgical intervention	It consists in the surgical removal of part of the thyroid gland, and in some cases the entire organ (subtotal resection). This method is used when drug treatment does not give the desired result, and the thyroid gland rapidly begins to grow in size. When the thyroid gland is removed, there is a risk of developing hypothyroidism, that is, the opposite phenomenon is a lack of thyroid hormones. They are compensated by taking artificial hormones.
Treatment with radioactive iodine	Treatment consists of a single dose of drugs based on radioactive iodine, absorbed only by thyroid cells. These cells are destroyed by radiation within a few weeks. This method of treatment is comparable to surgery, when the pathogenic cellular tissue of the thyroid gland is removed, because the process of cell destruction under the influence of radiation is also irreversible. If the first stage of radioactive therapy is ineffective, it is possible to take the drug a second time, in order to destroy the remaining cells. After the treatment, there is also a risk of developing hypothyroidism, which is eliminated with the help of replacement therapy.

Video in this article:

Attention. Thyrotoxicosis is a complex pathological process that is treated only with the help of special medications. Therefore, people who wish to carry out treatment on their own at home should think about it, because the price of the patient's life will depend on what decision will be made.

As an addition to drug therapy, it is necessary to follow a diet. The diet should include foods rich in vitamins and minerals. Fried, spicy and salty foods should be avoided. A complex of vitamins (Centrum, Vitrum) and B vitamins (Neuromultivit, Milgamma) can also be prescribed.

Appropriate treatment allows you to get rid of the pathology, and the symptoms of thyrotoxicosis will be completely eliminated. But it should be understood that recovery can be achieved if you strictly adhere to the doctor's recommendations and constantly take drugs that control hormonal levels in the blood.

Eye symptoms in thyrotoxicosis

Among the eye symptoms in thyrotoxicosis note:
protrusion of the eyeballs exophthalmos ).
wide opening of the eyes (called the "Delrymple symptom").
Stelwag's symptom - means a rare blinking.
eye glitter.
Graefe's symptom. It consists in the fact that the upper eyelid lags behind when lowering the eye. This is due to an increase in the tone of the muscle that regulates the raising and lowering of the upper eyelid. In this case, a strip of white sclera becomes noticeable.
Moebius sign. It means a disorder of convergence, that is, the loss of the ability to fix various objects at close range due to the predominance of the tone of the oblique muscles over the tone of the internal rectus muscles.
Kocher's symptom.
Jellinek's symptom.
These signs, especially exophthalmos, i.e., protrusion of the eyes, and opening of the palpebral fissures, give the patient's face a characteristic expression of frozen fear or fright.
However, the presence of eye symptoms is not at all necessary: some patients with very severe thyrotoxicosis do not have them at all. Therefore, it is erroneous to assess the severity of thyrotoxicosis on the basis of the severity of eye symptoms.

The interpretation of individual eye symptoms encounters some difficulties. So, for example, it is not easy to explain bulging eyes (exophthalmos). It has now been proven that it is due to the contracture of m. orbitalis (mullerian muscle). Previously, it was explained by the growth of retrobulbar fatty tissue, expansion of retrobulbar veins, arterial vessels of the orbit, etc. These assumptions are opposed by the absence of pronounced changes in the vessels of the fundus, and mainly by the fact that bulging eyes can appear suddenly, sometimes in a few hours. In such cases, it is associated with irritation of the cervical sympathetic nerve. Irritation of the sympathetic nerve can lead to a state of sharp contraction of m. orbitalis, which at the same time covers the back of the eyeball and thus, as it were, pushes the eye out of the orbit.
Since through m. orbitalis, veins and lymphatic vessels pass, with spastic contraction of the muscle, their compression is possible with the development of edema of the eyelids and retrobulbar space.
Exophthalmos in patients with thyrotoxicosis may be completely absent. Usually it is bilateral, less often (in about 10% of patients) unilateral exophthalmos is observed.

Rare blinking (Stelwag's symptom), wide opening of the palpebral fissures ( Delrymple's symptom), and the special brilliance of the eyes is explained by the increased tone of m. tarsalis sup. et infer.
Graefe's symptom is unstable. It is characterized by the lag of the eyelid (upper) from the iris when looking down, so that a white strip of sclera becomes visible between the eyelid and the iris. This symptom is also explained by the increased tone of m. levatoris palpebrae, as a result of which the voluntary movement of the upper eyelid is disturbed. When the eye fixes any moving object, the eyeball moves freely behind it. Graefe's symptom occurs not only with thyrotoxicosis. It is also observed in various cachexic conditions that have nothing to do with.
The Mobius symptom - weakness of convergence - is characterized by the fact that with severe thyrotoxicosis, patients begin to quickly diverge. This symptom is sometimes found in healthy people. In addition, it is far from constant.
In addition to the eye symptoms already listed, in patients with thyrotoxicosis, the so-called Kocher's symptom occurs - retraction of the eyelid (upper) with a quick change in gaze, but it is also not constant.
noteworthy and lacrimation disorders in patients with thyrotoxicosis. Sometimes it is increased, sometimes it is reduced. With long-term bulging (exophthalmos), patients develop conjunctivitis, inflammatory changes in the cornea and even panophthalmitis due to non-closure of the eyelids day and night, which, of course, is a great danger.
To eye symptoms in thyrotoxicosis can be attributed to the so-called Jellinek's symptom- darkening of the skin on the eyelids. It occurs infrequently and has no diagnostic value.

Anatomical and physiological data and symptoms of lesions of the first pair of craniocerebral insufficiency

The patient states that objects sometimes seem distorted, beveled, twisted around their axis, and sometimes too distant from the patient. Name the symptom(s).

Will the patient reject any notion that the symptoms are stress related?

Eye symptoms of thyrotoxicosis are fundamentally different from an independent disease of endocrine ophthalmopathy.

6. Endocrine ophthalmopathy (EOP)- defeat of periorbital tissues of autoimmune origin, in 95% of cases combined with autoimmune diseases of the thyroid gland (TG), clinically manifested by dystrophic changes in the oculomotor muscles (OOM) and other structures of the eye. There are 3 degrees of severity of the image intensifier:

I. Swelling of the eyelids, a feeling of "sand in the eyes", lacrimation, in the absence of diplopia.

II. Diplopia, limitation of abduction of the eyeballs, paresis of the gaze upward.

III. Vision-threatening symptoms: incomplete closure of the palpebral fissure, corneal ulceration, persistent diplopia, optic nerve atrophy.

EOP is an independent autoimmune disease, however, in 90% of cases it is combined with diffuse toxic goiter (DTG), in 5% with autoimmune thyroiditis, in 5-10% of cases there is no clinically detectable pathology of the thyroid gland. In some cases, DTZ manifests later than the EOP. The ratio of men to women is 5:1, in 10% of cases the image intensifier tube is unilateral. Anti-TSH receptor antibodies (AT-TSH) have several functionally and immunologically distinct subpopulations. Mutant variants of AT-TSH can cause immune inflammation of the retrobulbar tissue. Immune inflammation of the retrobulbar tissue leads to excessive deposition of glycosaminoglycans and a decrease in the volume of the orbital cavity with the development of exophthalmos and HDM dystrophy. The severity of EOP does not correlate with the severity of concomitant thyroiditis.

EOP begins gradually, often on one side. Chemosis, feeling of pressure behind the eyeballs, increased photosensitivity, sensation of a foreign body, "sand in the eyes". Further, the symptoms increase according to the described degrees of severity. Instrumental research methods (ultrasound, MRI of the orbits) make it possible to determine the protrusion of the eyeball, the thickness of the HDM, including in the framework of monitoring and evaluation, the effectiveness of treatment.

7. Ectodermal disorders: fragility of nails, hair loss.

8. Digestive system: abdominal pain, unstable stool with a tendency to diarrhea, thyrotoxic hepatosis.

9. Endocrine glands: ovarian dysfunction up to amenorrhea, fibrocystic mastopathy, gynecomastia, impaired carbohydrate tolerance, tyrogenic relative, that is, with a normal or elevated level of cortisol secretion, adrenal insufficiency (moderate melasma, hypotension).

10. Diseases associated with DTG: endocrine ophthalmopathy, pretibial myxedema (1-4%; swelling and thickening and hypertrophy of the skin of the anterior surface of the lower leg), acropathy (extremely rare; periosteal osteopathy of the feet and hands radiographically resembles "soap foam").

11. Thyrotoxic crisis- an urgent clinical syndrome, which is a combination of severe T. with tyrogenic adrenal insufficiency. The main reason is inadequate thyreostatic therapy. Provoking factors are: surgery, infectious and other diseases. Clinically: advanced T. syndrome, severe mental anxiety up to psychosis, motor hyperactivity, followed by apathy and disorientation, hyperthermia (up to 40 0 C), suffocation, pain in the heart, abdominal pain, nausea, vomiting, acute heart failure, hepatomegaly , thyrotoxic coma.

| | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |