THYROID DISEASES

Thyroid gland diseases

Thyroid gland diseases. The diagnosis, the differential diagnosis, preventive maintenance and treatment of goiter

Iodine deficiency diseases (IDD) are pathological states caused by reduced iodine contains in organism. About 740 million of the world population are ill with IDD.

kinds of IDD:

Ø Hypothyroidism,

Ø Diffuse euthyroid goiter or nontoxic,

Ø Nodular and multinodular euthyroid goiter,

Ø Functial autonomy of the thyroid gland.

The main phatology is Goiter – diffuse. Now we use modern classification of increasing of the thyroid gland.

Degrees of Thyroid Gland Size Abnormalities

· 0 degree - goiter is hidden and not palpable;

· I degree - goiter is palpable, but hidden; or one or more nodules are palpable in the thyroid gland;

· II degree - goiter is palpable and visible.

Factors of Etiology.

- Main factor is iodine insufficiency, f.e. in water, in food

- Goitrogenes factors, which inhibit transportation of iodides to the thyroid gland

- Low level of microelements, such as Zn, Co, Se, Mg, Cu and high level of Ca

- Ionize radiation and environment pollution with radionuclides

- Infectious diseases

- Helmintic invasion

- Lack of Vitamin A - reduction

- Hereditary factors connected with disorders of syntheses thyroid hormones

Differenceeted natural stumogenes of food products contained in tapioca, soy, peanut, turnip. Some flavonoids provoked disorders of metabolism iodine, f.e. african millet, sorghum, bobs.

What do analysis of presence of iodine deficiency? Analyses of iodine deficiency can be made according to concentration of iodine in urine. There are some degrees of iodine deficiency:

Endemic goiter severity criteria (WHO, 1994)

Indices, at children and adults	Standard	Severity degree
Indices, at children and adults	Standard	Mild	Middle	Severe
goiter rate during palpation(%)	less than 5	5-19,9	20-29,9	more than 30
Thyroid gland volume rate more than 97 percentiles (%)	less than 5	5-19,9	20-29,9	more than 30
Median of iodine excretion with urine (ug/1)	more than 1 00	50-90	20-49	less than 20
Median of thyroglobulin concentration in blood (ng/ml)	less than 10	10-19.9	20-39.9	more than 40
Median of TSH level in blood more than 5 mu/1 newborns), %	less than 3	13-19.9	20-39.9	more than 40

Pathogenesis.

The Iodine Deficiency caused the secretory ability of the thyroid gland and promotes goitrogenesis. The decrease of thyroid hormone in blood leads to increasing of TSH hormone production and to the development of iodine deficiency hypothyrosis. As a result it promotes follicles hypertrophy, strengthening of bloodstream in a gland and iodine absorption - compensatory mechanisms. After that thyroid gland hyperplasia develops. This adaptive mechanisms allow to support an euthyroidism for the long time in the conditions of insufficient iodine supply. Goiter, as the basic manifestation of iodine insufficiency, is also a display of adaptation possibilities of organism.

Thyroid hormone increases in pubertal age, during pregnancy, at the serious somatic or infectious diseases. At this situations develop hyperplasia thyroid gland acquires a nodular character. Nodules and adenomas appear in a gland. A diffuse endemic goiter grows into diffuse-nodular goiter. Adenomas and nodules are able to grow into thyrotoxic in case of sufficient iodine supply. Iodine-induced thyrotoxicosis develops following this mechanism. In these conditiones functional autonomy of the thyroid gland is developing. At iodine deficiency, number of autonomously-functioning thyrocytes is increasing, they formed into nodular and multinodular forms, often with thyrotoxicosis.

In pathogenesis of clinical displays of endemic goiter certain role is played by natural immunity inhibition.

Clinical features.

Appear increasing of thyroid gland. The degree of increasing can be different. Usually the increase is diffuse, but sometimes it is diffuse-nodular. With mild and moderate iodine deficiency the increase of the thyroid gland takes place slowly, achieving maximal sizes during 10-15 years and more. Clinically the goiter is usually euthyroid, with gradual development of the hypothyroidism.

Goiter is only the external display of iodine deficiency. Clinical features are caused by a hypothyroidism. Fatigue, deceleration of psychical reactions, dysmenorrhea, galactorrhea, abnormalities of the reproductive ability arc connected with hypothyroidism.

Characteristic signs of hypothyroidism:

• constipations,

• physical and mental fatigue,

• somnolence, chillness,

• growth of body weight,

• anemia.

In severe cases endemic cretinism develops which is manifested by disorders of the nervous system.

Diagnosis. - Thyroid hormones in blood is decreasing.

- TSH in blood plasma is increasing.

- Goiter size.

- Testing of ioduria.

- Ultrasound examination of the thyroid gland enables to determine its size and presence of nodules.

On indication: - Nodules formations are punctuated.

- Scanning with radioactive iodine.

Treatment.

1. Diffuse endemic goiter prescribe iodides in daily dose up to 200μg, in case of a big goiter (2nd degree) L-thyroxin is prescribed to decrease TSH concentration in blood. The dosage of L-thyroxin is from 25 to 100 μg per day. Patient's condition must be strictly monitored and controlled to achievement an euthyroidism.

Surgical intervention is necessary for patients with large goiters or in case of presence syndrome of compression and dysfunction.

2. Nontoxic Nodular and Multinodular goiter. There are three methods of treatment: surgical, medicamental, and active supervision of the nodule.

- Medical tactics depends on functional condition of the nodule, cellular compound, growth velocity. The medicamental treatment of nodular goiter by L - thyroxine is applied in case of hypothyrosis. The purpose of the treatment is a replacement therapy, achievement of euthyrosis, inhibition of further enlargement of nodes.

- Surgery is applied in case of node malignization, autonomic adenomas, quickly enlarged retrosternal nodes, compression of trachea or esophagus, mediastinum.

- Active supervision is applied to patients with nodes (10-30 mm in diameter) without signs of proliferation, which does not enlarge during dynamical ultrasound investigation, usually these are mature and elderly people.

Prevention.

Iodine deficiency may be prevented by realizing mass, group and individual iodine prophylaxis.

Mass prophylaxis is carried out for all inhabitants of an iodine deficient area. Iodized salt consumption is a tried and tested method. Iodination is made by using potassium iodide, 20 -40 mg/kg of salt, that provides matriculation of 150 μg of iodine every day. For mass prevention oily dine solution (lipiodol) is also used. Ingestion of this product provides a body with a sufficient amount of iodine for 6 to 12 months and intramuscular introduction - for 1 to 3 years.

For individual and group prevention iodine preparations are used, primarily antistrumin, 1 tablet 1-2 times a week, as well as iodides (Iodide-Farmak, IodBalance and Iodomarin) -10 and 200 μg in tablets.

Group prevention is an additional introduction of iodides on the back-ground of the mass prophylaxis for the categories of people with an increased iodine requirement: pregnant women, nursing mothers, adolescents.

Individual prevention is prescribed to some patients in case of an increased iodine requirement. These patients will include: women one year before a scheduled pregnancy, recovers after severe somatic or infectious diseases, after antibiotic therapy courses or sulfonamide treatment, persons with affected alimentary organs, if abnormal iodine absorption may occur.

Iodine requirement for different age categories

Children under 1 years old	50 μg/day
Children 1-6 years old	80 μg /day
Children 6-12 years old	120 μg /day
Children older than 12years old and adults	150 μg /day
Pregnant women and nursing mothers	150 to 200 μg /day

Thyrotoxicosis.

Thyrotoxicosis (synonym: Basedow's, Graves' s - diffuse toxic goiter) is a disease characterized by excessive production of thyroid hormones (hyperthyroidism) and by diffuse enlargement of the thyroid gland. Changes in other organs caused by influence of thyroid hormones and autoimmune disorders.

Graves' disease is mostly a disease of women of 20-50.

Etiology.

Thyrotoxicosis occurs in consequence of the thyroid-stimulating globulins formation, which compete with TSH receptors on a surface of thyreocytes and induce a cell growth and excessive secretion of thyroid hormones.

Factors that lead to autoimmune disorders can be:

§ excessive amount of iodine,

§ treatment by lithium,

§ infectious diseases (a flu, quinsy, chronic tonsillitis, a scarlet fever, whooping cough, rheumatism, encephalitis).

Some viruses can form complexes with thyreocytes surface proteins, changing its structure and antigenic characteristics.

As provocative moments of disease manifestation can act

• an excessive insolation,

• a mental trauma,

• pregnancy and postnatal period.

Pathogenesis.

Thyrotoxicosis is classified as a disease which develops due to the mechanism of hypersensitivity of the slow type.

Genetic defect is located in organ-specific CD-8 - lymphocytes (T-supressors). Because of the suppression of "forbidden" T-lymphocytes clones is not carried out they survive and cooperate with organ-specific antigenes of a thyroid gland.

Clones of lymphocyte that are sensibilized to the antigenes of a thyroid gland stimulate B-lymphocytes to synthesis of antibodies to thyroid-stimulating hormone receptor. Thyroid-stimulating immunoglobulins of class G cooperate with follicular epithelium receptors and induce thyreocytes to excessive production of thyroid hormones and to hypertrophy and hyperplasia.

It is impossible to explain completely a pathogenesis of diffuse toxic goiter by action of thyroid-stimulating immunoglobulins. They are also found at subacute and autoimmune thyroiditis. In these cases they do not stimulate but depress the function of a thyroid gland. In pathogenesis of a diffuse toxic goiter a major importance is given to lymphocytic infiltration of the gland which produces a tumor necrosis factor and alpha interferon.

Pathogenesis of clinical symptoms of diffuse toxic goiter is connected with increased cathabolic impact of excessive amount of thyroid hormones.

Clinical features.

Most prominent clinical symptoms of disease are:

- increasing irritability,

- nervousness,

- tachycardia,

- weight loss with normal nourishment,

- weakness,

- a tremor of all body,

- sweating,

- heat intolerance,

- diarrhea,

- tearfulness.

The skin is wet and warm. In some patients an uneven hyperpigmentation of all body is observe. In some patients a pretibial swelling (thyroid acropathy, pretibial myxedema) is observed. The skin is characterized by swelling of pretibial areas, brownish in color.On feet the leather skin is horned, crawls over phalanxes of fingers.

The eyes signs are characteristic to the majority of patients with a diffuse toxic goiter – Ophtalmopathia.

v Palpebral fissures are widely opened with expression of surprise - Delremplin's symptom.

v The exophtalmus is determined, more often on both eyes. Exophotalmus can affect one eye, for instance a rare winking - Shtelwag's symptom;

v Retraction of upper lid, owing to what during the movement of an eyeball downwards between upper lid and an iris appears a white strip of sclera - Gref's symptom or during the movement of an eyeball upwards - Coher's symptom.

v Disorders of convergence of eyeballs is called - Moebius's symptom.

The most typical clinical symptoms of thyreotoxicosis are changes in cardiovascular system. The most common is sinus tachycardia. The pulse rate reaches 100 beats per a minute and more. May be: - extresystole,

- atrial fibrillation.

Symptoms of thyrotoxicosis and their frequency

Symptom	Frequency (%)
Goiter	85-100
Tachycardia	85-100
Sweating	70-90
Heat intolerance	70-80
Tremor	70-90
Increased systolic blood pressure	60-80
Weight loss	60-80
Hyperkinesia	60-80
Muscle weakness	60-80
Eye signs	50-70
Diarrhea	20-10
Ophtalmopathia	30-50
Increased appetite	40-60
Atrial fibrillation	10-30
Pretibial myxedema	2-3
Dysmenorrhea	3-5
Vitiligo	1-2

The systolic blood pressure increased and diastholic blood pressure is reduced. It is connected with increase cardiac output (systolic blood pressure) and peripheral vasodilatation (diastolic blood pressure). Borders of relative heart dullness are displaced to the left, heart tones are loud and strengthened. A systolic murmur may be often heard. The origin of murmur is connected with enlargment of atrioventricular ostiums and bloodstream acceleration. The gemodinamic changes includes increased stroke and minute volumes of bloodstream, volume of circulating blood, bloodstream. Heart insufficiency develops in 15-20 % of cases, mainly in patients with atrial fibrillation. Thyreotoxic cardiomiopathy develops under influence of excessive amount of thyroid hormones and catecholamines, which received a clinical name «hyperthyroid heart».

Electrocardiographic examination shows the signs of a left ventriclar hypertrophy. High waves R, S and T, shortening of interval S-T, sinus tachycardia are fixed. As soon as heaviness of «hyperthyroid heart» increases the waves size decreases and wave T becomes twophase or negative, the depression of S-T segment and atrial fibrillation are observed.

Changes of muscular system are shown by thyrotoxic miopathy. Significant muscular.

Half of patients suffer from changes of digestive system. Defecation becomes more frequent, it can be up to 20 times a day. Weight loss is one of the most typical symptom of thyrotoxicosis. It is caused by increased catabolism due to high amount of thyroid hormones.

Characterize presents of psychic and nervous symptoms in clinical picture, f.e. a nervous hysteria. Patients appear to be nervous, anxious, irritate with no reason, start crying. Changes of mood are often. Tremor of fingers of the extended hands (Mari's symptom) is typical. Tremor is constant. In case of serious clinical course of thyrotoxicosis depression, delirious conditions and delirium are possible.

On the part of skeletal system an intensification of osteoporosis is possible as a result of stimulating impact of thyroid hormones on osteoclasts.

Dysfunction of other glands of internal secretion, in particular, reproductive glands is frequently observed during thyrotoxicosis. Half of women with thyrotoxicosis have deranged menstrual cycle and dysmenorrhea. In case of mild forms of thyrotoxicosis menorrhea. The menstrual cycle becomes single-phase with insufficiency of lutein phase.

Males has atrophic changes in testis, prostate gland, reduced libido and potency. These specified symptoms are temporal, reverse development occurs after the liquidation of thyrotoxicosis.

Function of adrenal glands is intensified, as a result - hypocorticoidism develops, and chronic suprarenal insufficiency (Addison's desease).

Patients with thyrotoxicosis may have reduce tolerance to carbohydrates even to development of a diabetes.

The thyrotoxic crisis develops within several hours to one day.

Symptomatology:

· Excitation increases

· Tachycardia - 200 beats per a minute

· Extrasystole

· Atrial fibrillation

· Systolic arterial blood pressure increases

· Diastolic arterial blood pressure decreases.

· Sweating is increased

· The skin is warm and wet to touch

· The body temperature increases and can arise up to 40 °C

· Psychical and emotional excitation

· Psychical excitation - acute psychosis with a disorientation, delirium, hallucinations

· The diarrhea

· Vomiting

· Muscular weakness up to adynamia

· Patients can lose consciousness - Thyreotoxic coma

· Other complectation - acetone appears, ketonurine

· Acute hepatic insufficiency

· Reduction of diuresis up to anury

· The systemic alkalosis, hypokaliopenia

Diagnosis is based on the establishment of excessive production of thyroid hormones (hyperthyroidism) and on diffuse enlargement of the thyroid gland.

The most typical clinical signs are:

- excitability,

- irritability,

- weight loss,

- weakness,

- tachycardia,

- atrial fibrillation,

- sweating,

- tremor of all body.

A goiter in a patient diffuse hyperplasia

Functional activity of a thyroid gland

1. Level of thyroid hormones increased.

2. Depression of TSH.

Thyroid gland volume is determined by ultrasound studies. In case of toxic goiter a thyroid gland is diffusely enlarged.

Treatment.

Thyrotoxicosis can be treated by medications, surgery or by using a radioiodine.

Antithyroid drugs is always used - mercasolile, thyrosol, thiamazole, metisole. These medicaments block formation of organic iodine in a thyroid gland, they inhibit the process of condensation of iodotyrosines into triiodothyronine and thyroxine.

In case of intolerance to mercasolil, other medicaments with thyrostatic actions are prescribed,

a) iodides,

b) Lughole’s iodine solution is prescribed up to 50 drops a day.

Beta-blockers are prescribed with antithyroid medicaments.

· propranolol is 120 mg per day

· atenolol (50-100 mg per 24 day),

· metoprolol (100-200 mg per day),

· bysoprolol (5-10 mg per day).

Glucocorticoids can be also used in case of relative suprarenal insufficiency. The prednisolonum is prescribed in an initial dose of 20-30 mg, reducing each five days to 5 mg or other glucocorticoids in an adequate dose.

Treatment of a thyrotropic crisis includes:

-Elimination of provoking factors (whenever it is possible);

-Blockade of thyroid hormones synthesis;

-Blockade of peripheral action of hormones;

-Maintenance of vital functions of an organism;

-Removing thyroid hormones and thyroidstimulating immunoglob-ulines from an organism.

Blockade of thyroid hormones synthesis is reached by oral introduction of mercasolil or through nasogastral probe. Initial dose of mercasolil is 60 mg, further dose is 30 mg each 4 hours. Preparations of iodine are prescribed in 2 hours after introduction of mercasolil. It excludes use of iodides for thyroid hormones synthesis.

Intravenous drip-feed of 1000 ml of 5 % solution of glucose with 1 ml of Lughole’s iodine solution is prescribed. 10 % natrium iodides solution is injected, by 1 ml intravenously each 3 hours. Lughole’s iodine solution can be given by oral introduction or through nasogastral probe by 30—40 drops each 3 hours.

Peripheral action of hormones is blocked by B-blockers, that is why a pro-pranolol is injected intravenously from 1 up to 3 mg each 3 hours. Glucocorticoids are also intravenously dropwise injected. Hydrocortison is prescribed up to 500 mg per day or prednisolonum - 200 mg per day, dexamethazon up to 20 mg per day. Strengthening of thyroid hormones excretion from an organism is reached by assignment of phenobarbital, in dose up to 200 mg per day.

Body temperature of patients is reduced by covering them with bubbles of ice, cold blowing, by assignment of acetoamiphenum (paracetamol).

Excessive amount of thyroid hormones released from an organism with the help of plasmapharesis, hemadsorbtion. The water regimen of an organism is supported by introduction of a 5 % solution of glucose and 0.9 % solution of natrium chloridis.

Hypothyroidism

Hypothyroidism is a disease, caused by a persistent reduction of thyroid hormone impact on a target organs.

Classification.

Nowadays the following forms of hypothyroidism are distinguished:

1. Primary hypothyroidism – as a result pathology in a thyroid gland.

2. Central hypothyroidism (hypothalamic-pituitary). Hypothyroidism develops due to a defeat of a pituitary gland (secondary hypothyroidism) or hypothalamus (tertiary hypothyroidism).

3. Peripheral hypothyroidism, caused by resistance of tissues to thyroid hormones action

4. Subclinical hypothyroidism is a syndrome, which is characterized by increasing plasma level of TSH on a background of a normal level of thyroxine and triiodothyronine.

5. Transient hypothyroidism. Hypothyroidism, which developed on a background of some diseases (conditions) or reception of medical preparations and inclined to spontaneous disappearance of its displays after elimination of etiological factors.

Etiology.

It is known that primary hypothyroidism makes approximately 95 % of all cases of hypothyroidism. Often it is an outcome of autoimmune thyroiditis, it may be a display of congenital defects of thyoroid hormones biosynthesis, the heaviest iodine deficiency, medicamentous or toxic effects.

Pathogenesis.

The pathogenetic basis of hypothyroidism is an disorder of metabolism. Metabolism is reduced, especially in organs and tissues, which quickly grow and updated:

• erythropoesis is slowed down and anemia occurs

• Free fatty acids, triglyceridis, cholesterol are collected in organism because of lipids metabolism delay

• Proteins metabolism - accumulation of glycosaminglycans - a mucinous swelling.

Clinical features.

The disease develops slowly and gradually. Weakness, drowsiness, sluggishness, memory impairment, chill, constipations are typical complaints of patients. Frequently patients with anemias.

Clinical symptoms	Frequency %
Weakness	90-70
Dryness of the skin	90-70
Drowsiness	90-70
Speech delay	90-70
Chill	90-70
Face puffiness	90-70
Increased tongue	90-70
Hair loss	90-70
Increased borders of relative heart dullness	90-70
Bradycardia	70-50
Memory impairment	70-50
Pallor of a skin	70-50
Yellowish discoloration of the skin	70-50
Weight increase	70-50
Lack of breathe	70-50
Hoarseness of the voice	70-50
Hearing impairment	30-20

Cardiovascular system. Abradycardia in case of a significant anemia tachycardia occurs. The borders of relative heart dullness are displaced due to dystrophic changes in myocardium and accumulation of liquid in a pericardium. The diastolic pressure increases. On electrocardiography the interval R-R is increased, voltage of waves is reduced, there can be a depression of S-T segment, inversion of T wave.

Significant changes in gastrointestinal system are observed. A decreased motility of the. The tongue is increased. The secretion is decreased, the absorption of vitamin B₁₂ is disturbed, this process aggravates anemia.

Essential changes are revealed in nervous system, both in peripheral and in central. A hypothyroid patient is slow in thought, they less able to concentrate and memorize. The mental potential of a person decreases. Some of patients feel fears, disturbing-depressive syndrome is formed.

Changes in peripheral nervous system –as a result tunnel syndrome.

The bronchitis and prolonged pneumonias are.

The changes of muscles and joints - edema of synovial structures and capsules of joints of hands and legs – as a result pseudomyopathic syndrome occurs.

Anemia – decrease of hemoglobin synthesis, reduction of iron absorbtion in digestive system, vitamin B_p and folic acid deficiency.

Myxedema coma.

The reason of its development is untreated hypothyroidism.

Reasons: - cold exposures,

- respiratory diseases,

- surgical interventions,

- narcosis,

- food and medicamental intoxications,

- medical drugs, that oppress central nervous function (neuroleptics, tranquilizers, sedatives).

In patogenesis : - hypercapnia,

- hypoxia,

- water and electrolytic imbalance,

- hypothermia.

Hypoxia is caused by pulmonary hypoventilation. Adiposity, edema of body, hydrothorax, ascites, mucinous swelling of alveoluscs promote hypoxia development. Decreas of kidney’s bloodstream - hypercapnia - coma develops gradually.

Clinic features.

· Weakness,

· Apathy,

· Drowsiness occurs,

· Movements become slower.

Appearance of patients with hypothyroidism is rather specific: puffy face with specially strongly pronounced swelling lips, ears and eyelids. The skin is dry, pale, rough with scales and it feels cold. The skin practically can not be taken in folds because of significant mucinous swelling.

The body temperature is reduced. Bradycardia. Boundaricss of heart dullness arc displaced.

Diagnosis and the differential diagnosis.

Ø Hypothyroidism is diagnosed on its clinical symptoms and laboratories results of hormones in plasma of blood.

Ø Reduction of triiodothyronine

Ø Thyroxine and increasing of TSH.

Instrumental diagnostics.

Ø Increased time of Achilles tendom reflex - the limits of 270 ± 30 Msec.

Ø An atrophy of a thyroid gland - ultrosound.

Treatment.

Hypothyroidism is treated by synthetic analogues of thyroid hormones: Levothyroxine and Liothyronin. There are also combined preparations of Levothyroxine with Liothyronine and a potassium iodide (Thyrocomb, Thyrotom, Novothyral e.a.)

Thyrocomb (70 ug of the Levothyroxine, 10 ug of the Liothyronine, 160 ug of the potassium iodide).

Thyrotom (40 ug of the Levothyroxine, 19 ug of the Liothyronine).

Thyrotomorte (120 ug of the L-thyroxine, 30 ug of the L-triiodothyronin).

Novothyral (120 ug of the Levothyroxine, 20 ug of the Liothyronine).

Euthyrox with 25, 50, 75, 100, 125, 150, 175, 200 ug of levothyroxine.

Levothyroxine is the most used preparation - for adults is 1.6-2.2 ug /kg/ per day. The treatment begins with 1/4 of a day.

Calculated dose increasing each 2 weeks twice and gradually leading up to a necessary effective therapeutic dose. The treatment begins from 25 ug of the Levothyroxine per day leading up to 100-150 ug per day. All the dose is taken in the morning after a breakfast. The efficiency of the treatment is estimated by a regress of clinical symptoms regression and normalization of the TSH.

Sunday, 3 November 2013

THYROID DISEASES

Hypothyroidism