goiter
Introduction
Introduction Thyroid tissue has a strong ability to concentrate iodine. The human thyroid gland needs 60-80 ug of iodine per day to produce physiologically active thyroid hormone. In the body, there is an interdependent and mutually restrictive feedback relationship between the thyroid hormone secreted by the thyroid gland and the thyroid stimulating hormone (TSH) secreted by the pituitary. In the absence of iodine, the thyroid cells cannot synthesize enough thyroid hormone and the concentration of thyroid hormone in the blood. Decreased, the inhibitory effect of thyroid hormone on pituitary secretion (TSH) is weakened, the secretion of pituitary TSH is increased, and the level of TSH in the blood is increased, causing hypertrophy of thyroid hypertrophy. Simple thyroid glands are commonly called "rough neck", "big neck" or "squat neck". It is a compensated thyroid with iodine deficiency, which is more common in young women. It is generally not associated with thyroid dysfunction. Sporadic goiter can have multiple causes leading to similar results, that is, the body needs increased thyroid hormone, or the thyroid gland. Hormonal dysfunction, the body is in a relative or absolute state of thyroid hormone deficiency, serum thyroid stimulating hormone (TSH) secretion increases, only thyroid tissue hypertrophy.
Cause
Cause
Cause :
I. Iodine deficiency
In ancient China, it was known to treat endemic goiter with seaweed. In modern times, the cause of endemic goiter was deeply studied. In 1895, it was proved that iodine and thyroid were closely related. After the invention of the quantitative determination of trace iodine in 1923, the relationship between thyroid disease and iodine metabolism was well understood. After analyzing the iodine content of water, soil and agricultural products in the natural environment, it is proved that the lack of iodine content in water, soil and food in the local goiter area and the resulting decrease in iodine intake in the diet are the most important determinants of the disease. factor. The current iodine deficiency theory is recognized worldwide. Domestic survey data also supports the theory of iodine deficiency. In 1960, the Shaanxi Branch of the Chinese Academy of Medical Sciences analyzed the iodine content of 60 water samples in seven areas of Shaanxi Province. The lower the iodine content of drinking water, the higher the prevalence of endemic goiter. Investigations in Hebei Province have also shown that iodine deficiency is the cause of endemic goiter.
Second, the cause of goiter
Iodine deficiency is not the only cause of endemic goiter. In some serious goiter areas, the iodine content in water, soil, food and vegetables is not low; in some wards, the prevalence rate is significantly reduced after salt iodization, but the last 10% is not easy to fall again. It is. These patients are not necessarily all patients with obvious fibrotic nodular or mixed type, and many are diffuse mild patients. This makes people think of other thyroid-causing substances. There are about a thousand such substances currently known.
1. Some vegetables such as cabbage, rapeseed and radish have the effect of causing goiter under certain conditions; only rabbits are raised with cabbage, and the thyroid is 10 times larger than normal. Because this type of vegetable has substances that inhibit the synthesis of thyroxine. The prevalence of goiter in countries such as Zaire and Malaysia in Central Africa is due to the endogenous release of thiocyanate from cyanide-containing glucose in the long-term consumption of cassava by residents.
2. Thiourea derivatives such as thiourea, thiouracil, thiosemicarbazide and methylthioimidazole, etc., which cause goiter to inhibit the concentration of iodide in the thyroid gland and promote the release of iodide from the thyroid gland. It also inhibits the binding of iodine to tyrosine. The mechanism may be that SCN "has a similar molar volume and charge to I. Under the condition that SCN-I competes with I into human thyroid cells, I is relatively excluded, causing goiter.
3. Inorganic anions such as fluoride, thiocyanide, nitrate, chlorate, perchlorate and hypochlorite can inhibit the thyroid stimulating ability of thyroid and release iodine rapidly.
4. Aromatic compounds such as resorcinol, p-hydroxypropiophenone, and orange peel are also inhibiting the thyroid gland. In addition, cobalt, molybdenum deficiency, increased manganese, calcium and water pollution can cause goiter.
Third, genetic factors or autoimmune factors
The role of genetic or autoimmune in the etiology of endemic goiter has long been suggested but has not been further confirmed. Some people in the same environment have goiter, and some do not have goiter, which makes people think of genetic factors. A large number of studies in Greece have confirmed that endemic goiter has a family predisposition. In recent years, Japanese scholars in the southern district of Japan have found that the family positive rate of goiter patients is 12%. Explain that heredity is not a major factor in endemic goiter, it is only a contributing factor.
Fourth, nutritional factors
Protein is an indispensable substance in the synthesis and transport of thyroid hormones. The decline in anterior pituitary function when food is insufficient is very similar to the reduction in anterior pituitary function after excision of the pituitary gland. Low-protein food-fed rats showed an enhanced response of TSH to TRH and a decrease in peripheral T4 to T3.
Examine
an examination
Related inspection
Total triiodothyronine thyroid 131 iodine absorption rate serum total thyroxine (TT4) thyroxine (T4) triiodothyronine inhibition test
First, medical history and clinical manifestations
In patients with endemic goiter, in addition to gland enlargement in the early stage, there is generally no symptoms. As the gland enlarges, it gradually compresses the surrounding organs and tissues, and some local symptoms may be caused in the later stage.
(1), difficulty breathing
More common, especially in patients with nodular goiter. Such as oppression of the trachea, there are symptoms of impotence. When the tumor is too large, the trachea can be displaced, bent or narrowed, causing severe breathing difficulties.
(two), difficulty swallowing
Compression of the esophagus can cause difficulty swallowing. Generally less common, only seen in the gland between the esophagus and the trachea, or when there is malignant change. Symptoms of persistent difficulty in swallowing often occur at this time.
(C), face and neck congestion
Glandular swelling often causes large blood vessels to be compressed, and the jugular vein is more common. At this time, the face and neck are congested. If the gland enlarges to the sternum, it tends to compress the large vein. If the superior vena cava is pressed, the venous return of the head and neck is blocked, which can cause facial edema, jugular varicose veins, chest skin and upper arm also edema and obvious. Varicose veins.
(four), tone change
When the recurrent laryngeal nerve is compressed, there are many irritating symptoms at first, such as hoarseness and sputum cough. When the recurrent laryngeal nerve is paralyzed, severe hoarseness and aphasia often occur.
(5) Changes in the eye
When the sympathetic nerve is compressed, the ipsilateral pupil enlarges. If it is severely oppressed and paralyzed, the eyeball will sink and sag. The pupil is reduced.
Diagnosis
Differential diagnosis
The diagnosis should be differentiated from the following symptoms:
1. Postpartum thyroid enlargement Most patients with postpartum thyroiditis appear to have goiter or increase on the original basis. Postpartum thyroiditis (PPT) is a thyroid dysfunction syndrome that occurs one year after birth and can be temporary or permanent. Its pathological basis is thyroid autoimmune inflammation, which is the most common and most characteristic postpartum autoimmune thyroiditis. The disease can also occur after abortion 5 to 20 weeks of pregnancy. Postpartum thyroiditis and postpartum thyroid syndrome are two different concepts. The latter refers to thyroid dysfunction that occurs after birth or is developing thyroid disease.
2. Goiter: Simple thyroid is commonly called "rough neck", "big neck" or "squat neck". It is a compensated thyroid with iodine deficiency, which is more common in young women. It is generally not associated with thyroid dysfunction. Sporadic goiter can have multiple causes leading to similar results, that is, the body needs increased thyroid hormone, or the thyroid gland. Hormonal dysfunction, the body is in a relative or absolute state of thyroid hormone deficiency, serum thyroid stimulating hormone (TSH) secretion increases, only thyroid tissue hypertrophy.
3. Glandular nodular nodular goiter, also known as adenoma-like goiter, actually refers to multiple nodules formed by endemic goiter and sporadic goiter. The incidence rate is very high, and it has been reported to reach 4% of the population.
Nodular goiter is caused by long-term iodine deficiency or relative iodine deficiency and thyroid-induced substances, causing diffuse thyroid enlargement. After a longer course, follicular epithelium changes from general hyperplasia to focal hyperplasia. In some areas, degenerative changes occur. Finally, due to the repeated alternation of long-term proliferative lesions and degenerative lesions, nodules of different developmental stages appear in the gland.
It is actually a late manifestation of the natural evolution of simple goiter. In patients with nodular goiter, some nodules may have functional autonomy, called toxic nodular goiter or Plummer disease. Some nodular goiter, due to excessive proliferation of epithelial cells, can form embryonic adenomas or papillary adenomas, and can also form thyroid cancer.
4. Hyperthyroidism during pregnancy: hyperthyroidism (hyperthyroidism) is a common endocrine disease caused by excessive secretion of thyroid hormone. Women with hyperthyroidism often present with menstrual disorders, reduced or amenorrhea, and low fertility. However, among the untreated women with hyperthyroidism after treatment, there are many pregnant women, and the incidence rate is about 1:1000-2500 pregnancies. Most of the hyperthyroidism during pregnancy is Graves' disease, which is mainly caused by autoimmune and mental stimulation, characterized by diffuse goiter and exophthalmos.
