Myxedema

Introduction Mucinous edema, also known as true myxedema, is caused by a deficiency of thyroid hormone caused by thyroid dysfunction and waxy edema on the face. More common in hyperthyroidism due to hyperthyroidism or excessive destruction of radiotherapy. Often accompanied by other endocrine diseases.

Cause

A characteristic clinical response to thyroid hormone deficiency in adults.

Primary hypothyroidism (hypothyroidism) is the most common type, presumably an autoimmune disease, usually due to Hashimoto's thyroiditis, often accompanied by a solid goiter, and then shrinks as the disease progresses. The fibrous thyroid has no or little function. The second most common type is hypothyroidism after treatment, especially for radioactive iodine and surgical treatment of hyperthyroidism. Propylthiouracil, tazobactam and iodine over-treatment for hypothyroidism, often recovered after termination of treatment. Mild hypothyroidism is common in older women.

Most patients with non-Hashimoto goiter have normal thyroid function or hyperthyroidism, but hypothyroidism can occur in patients with endemic goiter. Iodine deficiency can reduce thyroid hormone synthesis; TSH release, thyroid enlargement under TSH excitation, iodine absorption increases, and thyroid enlargement. If the iodine is severely deficient, the patient will become hypothyroidism, but since the emergence of iodized salt, the disease has actually been eliminated in the United States. Endemic cretinism is the most common cause of congenital hypothyroidism in iodine-deficient areas and the leading cause of mental disorders worldwide.

Rare genetic enzyme deficiency can cause thyroid hormone synthesis disorders and hypothyroidism secondary hypothyroidism occurs when the hypothalamic TRH secretion is absent, hypothalamic pituitary axis failure or pituitary lack of TSH secretion.

an examination

Related inspection

Perchlorate release test for determination of mucus-ciliary clearance in the respiratory tract

The symptoms and signs of primary hypothyroidism are significantly contrasted with the formation of hyperthyroidism, which can be concealed and elusive. Facial expression is dull, dumb, slow speech; due to the infiltration of vitreous acid and chondroitin sulfate, the face and periorbital swelling, fear of cold; due to lack of adrenal impulses, drooping eyelids; hair thin, rough and dry; skin Dry, rough, scaly peeling and thickening. Moderate weight gain is mainly due to reduced food metabolism and water retention. Patient forgetfulness and display of intelligent impairment with progressive personality changes. Some manifestations of depression, may have obvious mental illness (mucinous edema mania).

Caroteneemia is often present, especially in the palms and soles of the feet, due to the deposition of carotene in the fat-rich epithelium. Protein matrix deposition causes the tongue to become hypertrophied. Decreased thyroid hormone and adrenal glands can cause bradycardia. The heart can be enlarged, in part because of expansion, but mainly because of the high protein containing slurry exudation stored in the pericardial cavity. There may be exudation of the chest and abdominal cavity. Pericardial and thoracic exudation develops slowly, and only a few can cause respiratory distress and hemodynamic disorders. Patients generally have constipation and can be extremely serious. Hands and feet are more common, this is often due to wrist-sacral syndrome, which is caused by protein matrix deposition on the wrist and nerve compression around the ligament around the ankle. Reflection is very helpful for diagnosis because the contraction is active and the relaxation is slow. Women with hypothyroidism often have menorrhagia, and the opposite is true for menstruation. The body temperature is low. Often anemia, usually normal cells - positive pigmentation, the cause is unclear, but due to menorrhagia can be low pigmentation, sometimes due to the occurrence of pernicious anemia and folic acid absorption decreased large cell anemia. In general, anemia is rare (Hb>9g/dL). When low metabolism is corrected, anemia is improved, sometimes taking 6 to 9 months.

Myxedema coma is a complication of life-threatening hypothyroidism. Features include a long course of hypothyroidism, a coma with very low body temperature (24 to 32 °C), reflexes, seizures, CO2 retention and respiratory depression. Severe low temperatures can be ignored unless a special low reading thermometer is used. A rapid diagnosis must be made based on clinical, medical history and physical examination because of the possibility of premature death. The triggering factors include cold, disease, infection, trauma and central inhibitors.

Differential diagnosis

The most important is to identify secondary and primary hypothyroidism; secondary hypothyroidism is rare, often due to hypothalamic-pituitary axial disease affecting other endocrine organs. In women with hypothyroidism, the clues of secondary hypothyroidism are amenorrhea (rather than menorrhagia) and some signs suggest differences in physical examination. Secondary hypothyroidism The skin and hair are dry, but not rough; the skin is often pale; the tongue is not obvious; the heart is carefully packed without oozing slurry; hypotension; because it is accompanied by adrenal insufficiency and GH deficiency, so often Hypoglycemia.

Laboratory evaluations showed secondary hypothyroidism with low blood TSH levels (although radioimmunoassay TSH levels were normal, but biological activity was reduced), while primary hypothyroidism, no feedback inhibition of pituitary, and elevated serum TSH levels. Serum TSH is the simplest and most sensitive test for the diagnosis of primary hypothyroidism. Primary hypothyroidism often increases serum cholesterol, which is rarely the case with secondary hypothyroidism. Other pituitary hormones and their corresponding target gland hormones can be low.

The TRH test (see previous thyroid function laboratory tests) helps distinguish between hypothyroidism secondary to pituitary failure and secondary hypothalamic failure. The latter reaction to TRH is TSH release. The TT3 determination of hypothyroidism is noteworthy. In addition to primary and secondary hypothyroidism, other diseases have reduced blood TT3 characteristics, including decreased TBG, certain drug effects (see above), and normal thyroid function due to acute and chronic diseases, hunger, and low carbohydrates. Ill-conditioned syndrome (see discussion of normal thyroid dysfunction syndrome above).

Patients with more severe hypothyroidism have lower T3 and T4. However, many patients with primary hypothyroidism (high serum TSH, low serum T4) can have normal circulation T3, presumably because of persistent stimulating thyroid gland, leading to preferential synthesis and secretion of biologically active T3.

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