- Causes of acquired hypothyroidism
- What happens in the body?
- Risk groups
- The main symptoms of acquired hypothyroidism
- Diagnosis of acquired hypothyroidism
- Treatment of acquired hypothyroidism
- The main causes of congenital hypothyroidism
- What happens in the body with congenital hypothyroidism?
- Symptoms of congenital hypothyroidism
- Diagnosis and treatment of congenital hypothyroidism
Hypothyroidism is a condition of the body characterized by a deficiency of thyroid hormones. Hormonal deficiency can be primary because of thyroid or secondary disease, when there are no pathological changes in the gland itself, and hormone deficiency is caused by the action of other factors. It is believed that the primary hypothyroidism occurs in almost 99% of cases.
Congenital hypothyroidism is due to underdevelopment or the absence of the thyroid gland, when thyroid hormones are either completely absent or their production is negligible. In some situations, a genetic defect is observed in the enzymes involved in the formation of these hormones, as a result of which iodine digestion by thyroid cells is disrupted, another type of genetic change is a violation of the structure of the protein part of thyroglobulin. In these cases, the thyroid gland synthesizes inferior molecules of active thyroid hormones that are not perceived by the cells of the body.
Acquired hypothyroidism develops as a result of diseases of the thyroid gland that have arisen in the process of human life. For example:
- After removal of a part of the thyroid gland by an operative route;
- When the tissue is destroyed by ionizing radiation (treatment with radioactive iodine preparations, irradiation of the neck organs, etc.);
- After taking some medications: lithium preparations, beta-adrenoblockers, hormones of the adrenal cortex, vitamin A in large doses;
- With iodine deficiency in food and the development of some forms of endemic goiter.
The mechanism of development distinguishes hypothyroidism:
- Primary (thyreogenic),
- Secondary (pituitary),
- Tertiary (hypothalamic),
Primary hypothyroidism is when pathological changes initially develop in the thyroid gland itself, for example, its congenital hypoplasia or hypothyroidism, which appeared due to the removal of goiter.
Secondary hypothyroidism is when everything is in order with the thyroid gland, but there is a deficiency of thyrotropin, which is produced in the pituitary gland and normally should trigger the synthesis of thyroid hormones in the thyroid gland itself. The causes of secondary hypothyroidism may be hemorrhage in the pituitary gland, tumors or inflammatory processes in this area of the brain, oxygen starvation of cells due to blood loss. Also, the production of tirotropin in the pituitary gland can inhibit certain medications, for example: apomorphine, reserpine, antiparkinsonian agents.
Tertiary hypothyroidism - in this case there is a deficiency of tiroliberin, which is produced in the hypothalamus and triggers the production of thyrotropin in the pituitary gland, directly controlling the activity of the thyroid gland.
Peripheral hypothyroidism is characterized by a decrease in the sensitivity of the tissues of the body and the receptors of cells to the action of thyroid hormones. The reasons for the development of such a state have not been studied enough.
Acquired hypothyroidism is more or less the most common among thyroid diseases. Most often, it develops as a result of chronic autoimmune thyroiditis or occurs as a result of the removal of a large amount of thyroid tissue during surgery.
Causes of acquired hypothyroidism
In the overwhelming majority of cases, persistent hypothyroidism develops due to chronic autoimmune thyroiditis, removal of a portion of the thyroid gland, or treatment with radioactive iodine.
Transient (temporary, transient) hypothyroidism is observed when taking thyreostatic medications or large doses of iodine. Acquired hypothyroidism can be observed in newborns and pregnant women due to severe iodine deficiency, when this element is practically not supplied with food (these conditions are commonly called transient neonatal hyperthyrotropinemia and gestational hypothyroxinemia).
What happens in the body?
Deficiency of thyroid hormones affects the functioning of almost all organs and systems of the body:
- The consumption of oxygen by the cells decreases (in fact, cellular respiration suffers);
- Decreases the production of energy,
- There is a deficit of a number of enzymes, the development of which depends on the energy resource of the cell,
- There is a myxedema - mucinous edema (in the connective tissue hyaluronic acid accumulates, which "pulls" the liquid on itself),
- Virtually all types of metabolism are disrupted.
The following categories of the population are at risk for developing hypothyroidism:
- In the presence of diseases of the thyroid gland, including thyroiditis;
- Suffering from pernicious anemia, diabetes mellitus;
- Using some medicines (lithium salts, amiodarone, preparations of radioactive iodine, etc.);
- If changes in biochemical blood tests are detected: a high atherogenicity index, hyponatremia, elevation of CKK and LDH (lactate dehydrogenase), and an increase in prolactin.
The main symptoms of acquired hypothyroidism
Diagnosis of acquired hypothyroidism in some cases may be difficult, since some symptoms of hypothyroidism can be observed in 15% of adults who suffer from mental or physical illnesses but have a normally functioning thyroid gland.
Classical primary hypothyroidism
Classical hypothyroidism is characterized by the following symptoms and syndromes:
1. Obmenno-gipotermichesky syndrome : icterus of the skin, obesity, early development of atherosclerosis, increased blood cholesterol, chilliness, decreased body temperature.
2. Connective tissue - myxedema edema:
- Puffiness of the face, including in the periorbital region,
- Mucous membranes of the auditory tube and nose (hearing loss, difficulty breathing through the nose),
- Language (visible prints of teeth),
- Vocal cords (hoarseness of voice),
- Cerebral membranes, pleura, pericardium (polyserosite).
3. Nervous system:
- Memory loss,
- The development of secondary pituitary adenoma,
- Muscle tension and slow relaxation,
4. Cardiovascular system:
- Myxedematous heart (slow pulse, increase in heart size),
- Development of heart failure.
5. Organs of digestion:
- Enlargement of the liver,
- Propensity to develop cholelithiasis,
- Development of biliary dyskinesia.
6. Circulatory system:
- Anemia of various types (megaloblastic, iron deficiency, hypo- or normochromic).
7. Reproductive system:
- The violation of menstrual function until its complete disappearance,
- Galactorrhea (discharge of milk from the mammary glands).
8. Skin and its derivatives:
- Brittle and dull hair,
- Their increased loss and slow growth,
- Dry skin,
- Thin, exfoliating and outlined nails.
If hypothyroidism remains for a long time without appropriate treatment, then a myxedematous (hypothyroid) coma may develop. Its main manifestations are:
- Hypothermia (up to 30 0 C),
- Decrease in respiratory rate and heart rate,
- Arterial hypotension,
- Intestinal obstruction due to a sharp decrease in peristalsis,
- Change of consciousness (stupor, coma).
Without timely treatment, lethality is up to 80%.
Features of the course of secondary acquired hypothyroidism
Diagnosis of acquired hypothyroidism
In the diagnosis of hypothyroidism, there are several main points:
1. Primary and repeated examination of the doctor who identifies the complaints and symptoms characteristic of hypothyroidism, and also analyzes the results of the survey and conducts differential diagnosis of various diseases that have a similar manifestation.
2. Laboratory and instrumental examination:
- A general blood test (reduction of hemoglobin, the nature of anemia),
- Biochemical blood tests (elevated cholesterol, hypoproteinemia, etc.)
- A study of thyroid hormone levels (thyroxine, triiodothyronine), as well as pituitary tyrotropin under normal conditions and with a tiroliberin test, when 500 μg of tiroroliberin is administered intravenously,
- Ultrasound of the thyroid gland,
- The definition of bone age (for children).
Treatment of acquired hypothyroidism
The endocrinologist is engaged in the treatment of hypothyroidism, which, if necessary, can involve other specialists. Self-treatment of hypothyroidism is unacceptable in connection with possible deterioration of health.
If possible, it is necessary to eliminate the cause that caused the development of hypothyroidism, for example:
- To cancel drugs that cause a decrease in the activity of thyroid hormones,
- To treat thyroiditis,
- Normalize the supply of iodine for food.
The deficiency of thyroid hormones is compensated by means of substitution therapy with levothyroxine and similar drugs. Lifetime thyroid hormones are prescribed in the case of hypothyroidism due to its removal, irradiation, or if it is impossible to restore its function for other reasons. Also, symptomatic treatment is performed depending on the prevalence of certain disorders (eg, the administration of drugs that reduce cholesterol).
Treatment for hypothyroid coma is often carried out in intensive care settings and includes intensive measures aimed at correcting and providing vital functions and eliminating the thyroid hormone deficiency.
The prognosis under the condition of daily reception of thyroid hormones is favorable: patients lead a usual way of life. In those cases when treatment of hypothyroidism is absent, clinical manifestations can worsen until the onset of meksedematoznoy coma.
The main causes of congenital hypothyroidism
The main reasons for the development of congenital hypothyroidism are:
- Absence or underdevelopment of thyroid tissue (its agenesis, hypoplasia, dystopia).
- Influence on the thyroid gland of a child of maternal antibodies that circulate in the blood of women suffering from autoimmune thyroiditis.
- Hereditary defects of T4 synthesis (defects of thyroid peroxidase, thyroglobulin, etc.).
- Hypothalamic-hypophyseal congenital hypothyroidism.
What happens in the body with congenital hypothyroidism?
While the fetus is in the mother's body, the lack of thyroid hormones is compensated by the action of the mother, but immediately after birth, their level in the baby's body begins to drop sharply.
If during the neonatal period the deficiency of these hormones is not compensated, then irreversible changes occur in the brain and other parts of the nervous system leading to dementia of varying degrees. If treatment with thyroid hormones is started during the first week of a child's life, then the neuropsychic development is practically not affected.
Symptoms of congenital hypothyroidism
Symptoms of congenital hypothyroidism do not contribute to early diagnosis of the disease and fully manifest from the 3rd month of life. Nevertheless, an experienced specialist at an early stage can be identified the following signs of hypothyroidism:
- Late terms of birth (from 40 weeks or more),
- Prolonged jaundice (more than 7 days),
- Heavy weight (at birth),
- An increase in the tongue (half-open mouth with a "flattened" tongue) and the thyroid gland,
- Later departure of meconium,
- Low voice at crying, crying,
- Puffiness in the form of cushions-seals on the rear surfaces of feet, brushes, as well as in subclavian pits,
- Swelling of the face, lips, eyelids,
- An enlarged posterior fontanelle,
- umbilical hernia.
At 3-4 months without adequate treatment appear:
- Bad weight gain,
- Hypothermia (brushes and feet cold to the touch),
- Decreased appetite,
- Dry skin,
- Increased brittleness and dryness of hair,
- Difficulty in swallowing,
- Muscle hypotension.
After 5-6 months of life:
- Signs of disproportional growth (late closure of fontanelles, broad and sunken bridge of nose),
- Delay of physical and psychomotor development.
Diagnosis and treatment of congenital hypothyroidism
Since the clinical picture at first can be erased, then neonatal screening is performed to diagnose congenital hypothyroidism. To do this, in the dried blood spots on the filter paper, which are taken from the heel of the baby on the 4-5th day of his life, determine the level of TSH (for preterm screening performed from 7 to 14th day of life). Earlier diagnosis (on the 2 nd, 3 rd day) leads to false positive results.
Substitution therapy is assigned depending on the results obtained at the level of TTG:
- Up to 20 microU / ml is the norm, no treatment measures are performed;
- 20-50 microU / ml is a doubtful result requiring a re-study, which includes the determination of TSH and T4: L-thyroxine is prescribed at T4 of less than 120 nmol / L, and TSH is more than 20 μU / ml;
- 50-100 microU / ml - suspicion of hypothyroidism, the treatment is prescribed immediately and can be canceled if the result is positive for a second examination;
- More than 100 microU / ml - a high probability of hypothyroidism, replacement therapy is prescribed even in the absence of clinical manifestations of the disease.
After 2 weeks, as well as 1-1,5 months from the start of therapy, a control study of TSH and T4 is carried out, and at the age of 1 year the diagnosis is clarified by abolishing L-thyroxine for 2 weeks and then measuring the level of TSH and T4. If the result is normal, the treatment is stopped.
With timely treatment started (in the first and second week of life), the prognosis is favorable, but without signs of delay, the signs of delayed neuropsychiatric development, including severe forms of dementia, are progressing.