Diffuse toxic goiter (synonym: Graves disease, thyrotoxicosis) is a disease caused by increased thyroid function with excessive intake of thyroid hormones, thyroxine and triiodothyronine into the blood.
In the etiology of diffuse toxic goiter, the following are important: 1) mental trauma, 2) organic damage to the central nervous system (trauma, encephalitis , etc.), 3) acute or chronic infection (influenza, angina , etc.), 4) pituitary gland, etc. Hereditary factors have definite value.
Increased production of thyroid hormones occurs most often due to the stimulation of the thyroid gland by the thyroid-stimulating hormone of the pituitary gland. Excessive supply of thyroid hormones into the blood leads to an increase in the basal metabolism, the expansion of peripheral vessels, the disturbance of hemodynamics, the reduction in the body of energy reserves that ensure the normal functioning of cells of various organs.
The diffuse hyperplasia of the parenchymal gland elements and vasodilation are determined pathologically; in nodular goiter - multiple nodular proliferation of the parenchyma of the gland.The
Complaints: palpitation , irritability, tearfulness, bad sleep , severe general weakness, weight loss, hand trembling , menstrual irregularity , decreased sexual function, sometimes diarrhea . At objective research - a food is lowered (the appetite is usually raised), a skin of the raised or increased humidity, a body temperature subfebrile.
The clinical picture is characterized by a triad of symptoms: eyelashes, goiter, palpitations. The dilated ocular gap, protruding eyes (eyelashes, or exophthalmus , as a rule, is bilateral) and a rare flashing give the face an expression of fright. The degree of enlargement of the thyroid gland can be different and classified according to the international scale (see Goiter ). It should be remembered about the possibility of zagrudinogo location of goiter. Changes in the cardiovascular system : tachycardia , extrasystole, atrial fibrillation , the heart is enlarged due to the left ventricle; the clapping I tone is heard above the top, as well as the systolic noise .
Eye signs of thyrotoxicosis . With thyrotoxicosis, there are a number of changes associated with the organ of vision. When examining the patient, in most cases it is possible to find a frightened gaze, a glitter of the eyes, a bugger. Bilateral eyelash occurs in 50-80% of patients. Exophthalmos sometimes accompanied by lacrimation, photophobia, conjunctival hyperemia of the eyelids and sclera and edema of them, sometimes ulcerative keratitis, as well as other neurodistrophic phenomena that can lead to blindness. In this case, iodine, strumectomy and other methods of treatment of thyrotoxicosis sometimes do not have such positive effects. Often, lag of the eyelids from the eyeball (Gref symptom) is detected, while a white band of the sclera is visible between the cornea and the upper eyelid. When, in translating the gaze downward, the upper eyelid only slightly lags behind first, and then it catches up with the eyeball, it is a symptom of Boston. During the study, blinking sometimes increases. The sign of Kocher is revealed in the case of a short, jerky movement of the upper eyelid in the upward direction preceding the movement of the eyeball.
Symptom Dalrymple is in the wide opening of the eye slits.
Under the symptom of Geoffrey, it is known that the forehead does not wrinkle when viewed upward.
Under the symptom of Stelvag, a rare blinking of the eyelids is known.
With Brown's symptom during laughter, the eyes remain wide open.
The inability to wrinkle the forehead is called the sign of Jaffe.
Owing to the paresis of the rectus inner muscle of the eye, convergence is disrupted, manifested by the deviation of one of the eyeballs in the lateral direction when the object approaches the bridge to the bridge of the nose and fixes it with the patient's gaze (Mobius sign).The
If the eyeball, which is in the stage of the extreme lead, begins to move toward the center, then the eyeball stops (Wilder's symptom).
It is often impossible to twist the upper eyelid (Gilford's symptom).
The eyelids are hyperpigmented (Jellinek's symptom). When the eyelids are interlaced, a small tremor is noted (a symptom of Rosenbach).
There is swelling of the eyelids.
The cornea can be injected like a red cross ((Stasinsky's symptom).
When an acute object approaches the eye, the patient recoils and can fall back if not supported (Breitman's symptom).
Decoloration of the iris is also noted.
The course can be slow progressing or sharp, turbulent. The severity of the clinical picture is light, medium and heavy forms.
Complications - defeat of the heart, liver, gastrointestinal tract, thyrotoxic coma (see).
Diagnosis in cases of severe clinical picture (diffuse goiter, persistent tachycardia, weight loss with increased appetite, eyelashes, small trembling of fingers) is not difficult. In difficult cases for diagnostics, the main metabolism is studied, a test is performed with thyroid absorption of the radioactive isotope iodine-I 131 (see Thyroid gland ).
Prognosis - timely started treatment leads to recovery; infection, mental trauma can dramatically worsen the course of the disease.
Types of treatment: antithyroid drugs and surgical intervention. With mild forms of the disease, iodine preparations are prescribed in small doses, which inhibit the thyrotropic activity of the pituitary gland and the synthesis of thyroid hormones. Diiodotyrosine, 0.05 g 2-3 times a day, is prescribed in the form of courses for 10-20 days at intervals of 5-10 days. Sometimes a Lugolev solution is used in a dose of 15 drops (start with 1 drop and add 1 drop every day, bring up to 15 drops) 3 times a day after meals as 3-6 courses at intervals of 10-20 days. Iodine preparations have a weak thyreostatic effect. At the present time, thyreostatic preparations - derivatives of thiourea (methylthiouracil), imidazole (mercazolyl), blocking the synthesis of thyroid hormones - have become widespread. The most effective is Mercazolil. The estimated dose for a mild form of the disease is 10-20 mg per day, with moderate and severe illness - 20-40 mg per day, sometimes more. Treatment with antithyroid drugs is individual and should be done under weekly control of white blood. The course of treatment 6-12 months. and more. If antithyroid drugs do not have a positive effect, use radioactive iodine (I 131 ) or surgical treatment. Surgical treatment is indicated if the conservative treatment is unsuccessful, there is a nodular or triggered diffuse toxic goiter. In the complex treatment of patients with diffuse toxic goiter, bromides, reserpine , cardiac agents, vitamins, anabolic steroids (see) are used. Treatment of thyrotoxic coma - see Coma.
Nutrition of patients with diffuse toxic goiter should be high-calorie, diverse, rich in carbohydrates and vitamins. The number of proteins in the diet should be somewhat limited. Treatment in the resorts of the Crimea and the Caucasus is allowed in the cool season after the elimination of the main symptoms of the disease.
In children, diffuse toxic goiter is more common in girls aged 11-15 years. The etiology is unclear. Of definite importance are hereditary factors, infections (angina, rheumatism , influenza), mental trauma. The symptomatology of the disease is the same as in adults.
Treatment with mild and moderate forms is usually first conservative. Assign microdoses of iodine (Iodi puri 0,01, Kalii iodati 0,1, Extr. Valerianae 2,0, Extr. Et pulv. Liquiritiae qs ut f. Pil. No. 40) no 1 pills 2 times a day for 20 days with interruptions for 10 days. Diiodotyrosine is prescribed in a dose of 0.05 g 2 times a day for 20 days. For children aged 5-7 years, diiodotyrosine is given in a half dose. It is shown the simultaneous administration of reserpine to 0.0001 g 2-3 times a day. It is necessary to free the child from additional loads and provide adequate nutrition. With indications - removal of tonsils. With ineffectiveness of conservative treatment - surgical intervention.
Thyrotoxicosis (synonyms: Graves' disease, diffuse toxic goiter, Graves disease, Flagjani disease) is a disease caused by an increase in thyroid function, is more common in women, often affects them during puberty and menopause.
Etiological factors are infections (especially the upper respiratory tract, in particular chronic tonsillitis), intoxication, mental trauma. At the heart of the development of thyrotoxicosis is an increased delivery of blood to the tissues of thyroid hormones.
To the development of thyrotoxicosis in the normal formation of thyroxin in the thyroid gland, a lesser strength of the bond of the gland hormones to serum globulins may result. Thyrotoxicosis can develop in those cases if iodination of thyroxine is disrupted or the formation of the second hormone of the gland, triiodothyronine, is increased.
The disease most often develops gradually. Patients complain of fatigue, weakness, shortness of breath, palpitation, increased n irritability, sweating, weight loss with good appetite, diarrhea, poor heat tolerance. Vegetative disorders are manifested in the form of vasomotor lability, a violation of thermoregulation and peripheral vasodilation with subsequent swelling, trembling of limbs, affective lability, insomnia, confusion, etc. Patients are noted for the speed of speech and action, increased emotion. Developing motor anxiety. Diffusively the thyroid gland increases (with toxic adenoma it increases by the type of node). There are violations of the organ of vision: eyelashes, stretch of the upper eyelid, immobility of the eyes, violation of convergence, etc. (see Eye signs of thyrotoxicosis).
There are violations of various endocrine glands: amenorrhea or oligomenorrhea, sometimes menorrhagia, testicular hypotrophy and decreased spermatogenesis, initially increased sexual desire and potency, later a sharp drop in them, hypertrophy of the thymus gland, hypofunction of the adrenal cortex, often the insufficiency of the islets of Langerhans, which leads to development of diabetes mellitus. Probably, due to the hypofunction of the adrenal cortex, the darkening of the skin is noted. During the growth of the body, long tubular bones grow faster than usual.
Tachycardia develops, the size of the relative dullness of the heart, systolic murmur over the apex of the heart. The maximum blood pressure rises, the minimum decreases. There is also a shortening in the electrocardiogram of the PR interval, an increase in the systolic and minute volumes of the heart, often there is a functional liver failure, intestinal hyperkinesia, accompanied by diarrhea. Trophy disorders are revealed in the form of thinning of the nails, early hair loss, etc.
Increases the release of creatine in the urine. In the study of blood often neutropenia and relative lymphocytosis. All kinds of exchange are affected. There is increased excretion of calcium, phosphorus, magnesium with subsequent osteoporosis, as well as nitrogen, hyperglycemia and glycosuria, hypocholesterolemia, increased water release with dehydration, increased oxygen consumption of tissues, which leads to an increase in basal metabolism. The volume of muscles and subcutaneous fat layer decreases.
With toxic adenoma developing as a solitary thyroid gland with the entire clinical symptom-complex of thyrotoxicosis, there are no psychotraumas in anamnesis, adenoma develops against the background of an increase in the thyroid or goitre, clinical signs do not have pathological eye symptoms of thyrotoxicosis, mixed or nodular goiter.
If the disease develops before the end of the period of growth, there is an acceleration of growth. Usually increasing the accumulation of iodine in the thyroid gland and removing it from the gland. However, it should be remembered that the increase in basal metabolism and the acceleration of the accumulation of radioactive iodine in the thyroid gland are not pathognomonic for the disease. The level of protein associated with iodine increases.
Distinguish the following forms of thyrotoxicosis: mild, moderate and severe. Sh. Milku proposes to divide the stages of the disease into neurogenic, neurohormonal, visceral and cacetic. The division of the disease into forms: cardiovascular, gastrointestinal, neuropsychiatric, mystical and other is irrational, for changes on the part of various systems are usually combined.
Differential diagnostics . With neurocirculatory asthenia, in contrast to thyrotoxicosis, there is no progression of the disease, there are no pathological eye signs of thyrotoxicosis, severe cardiovascular disorders and liver function do not occur. Tachycardia with this disease is normalized during sleep.
Hyperthyroid status can be an integral part of the syndromes of acromegaly, diabetes mellitus, Troel-Junet syndrome, in which other symptoms characteristic of these symptom complexes are noted.
Function of the thyroid gland can increase in the initial stages of hypertensive disease, with rheumatic carditis. However, in these cases there are no characteristic for thyrotoxicosis tremor of the fingers of the hands, pathological eye signs, a sharp drop in weight, sweating. The nature of the trembling of the fingers of the hands in Parkinsonism differs from the thyrotoxic tremor by its roughness and decrease in volitional movements.
Treatment . The use of non-radioactive iodine for the treatment of the disease is currently limited. Avoid prolonged and continuous use of this drug. Iodine is used in the form of Lugol solution for 5-15 drops 3 times a day with a decrease in dose per drop every time until a minimum daily dose is reached. The reception lasts 20-30 days, and the break is 10 days.
It is also recommended that diiodotyrosine or betazine be taken 0.2-0.3 per day for six months. Interruptions do not necessarily.
For mild to moderate forms of thyrotoxicosis, prolonged use of potassium perchlorate is used at 0.6-1.0 per day (in 3-5 sessions) until the intensity of the disease decreases (4-8 weeks), after which the doses are somewhat reduced. The use of the drug is incompatible with iodine, since iodine inhibits the thyreostatic effect of potassium perchlorate.
6-Methylthiouracil also has a beneficial effect on the course of thyrotoxicosis. With maintenance treatment, 0.1-0.2 drugs are prescribed per day in two divided doses.
Less toxic drug 1-methyl-2-mercaptoimidazole (mercazolil or metotirin), in its thyreostatic activity, it is 16-20 times higher than 6-methylthiouracil. With a mild form of thyrotoxicosis, it is prescribed in an amount of up to 0.03 per day (in three divided doses), with an average severity and severe forms of the disease, at 0.040-0.060 per day (in 4 divided doses). With a decrease in thyrotoxicosis, the dosage is reduced to 0.010-0.020 per day. Treatment lasts up to 2-3 months.
1-Methyl-2-mercaptoimidazole is recommended to be combined with reserpine (to 0.00025 1-3 times a day).
A good treatment for thyrotoxicosis is radioactive iodine (J131). Enter into the body 4-8 millicuries J131, if necessary, after 8-10 weeks give a second dose of the drug. Radioactive iodine in the form of a solution of radioactive iodide potassium or sodium is administered in an empty stomach in a mixture with 50-75 g of water. The clinical effect is manifested after 4-6 weeks. 3-4 weeks before treatment with the drug should be canceled taking iodine and bromine.
Indication for the use of radioactive iodine: recurrence of thyrotoxicosis after subtotal strukemectomy, lack of a stable effect after conservative treatment; intolerance to methylthiouracil and mercazolil and their toxic effect on the body; severe forms of thyrotoxicosis; combination of thyrotoxicosis with cardiovascular complications, psychoses, tuberculosis.
Contraindications to the reception of radioactive iodine: children's age, ejnuhoidizm, lactation, pregnancy, squeezing goiter, toxic adenoma, diseases of the blood system with leukopenia, euthyroid goiter.
Complications of treatment include hypothyroidism, leukopenia. During treatment, the leukocytes of the patient are checked.
Treatment of thyrotoxicosis with x-rays is currently used extremely rarely and only when other methods of treatment are impossible. In this case, 2000-4000 r are prescribed with a single irradiation of 150 r, irradiating the side fields alternately. Relief of the condition comes only after the end of the course of treatment.
A good adjuvant is insulin, which is administered at 8-12 units per day under the skin before meals; apply also vitamins B1, B3, B12, C, barbiturates, valerian, bromine.
The patient's food should be high-calorie (4000-6000 calories), with sufficient protein and carbohydrates, dairy and plant products.
Surgical intervention is indicated in case of a wild-type craw, toxic adenoma, and also in those forms of thyrotoxicosis, in which other means are not effective enough. The operation is indicated in cases with irreversible changes in internal organs.