What is the pathogenesis of non-concave mucinous edema

  Non-concave mucinous edema is the characteristic clinical response to thyroid hormone deficiency in adults. Primary hypothyroidism (hypothyroidism) is the most common type and is probably an autoimmune disease. It usually occurs as a result of Hashimoto’s thyroiditis and is often accompanied by a firm enlarged thyroid gland, which later develops as the disease progresses to a shrunken, fibrous thyroid with no or little function. The second most common type is post-treatment hypothyroidism, especially due to hyperthyroidism with radioactive iodine and surgical treatment, propylthiouracil, tabazol and iodine overtreatment of hypothyroidism, which often recovers after termination of treatment, and mild hypothyroidism commonly seen in older women. So what is the pathogenesis of non-concave mucinous edema? Here’s what we can tell you.  1, mucinous edema The fluid containing hyaluronic acid, mucin, mucopolysaccharide infiltrates in the tissue, infiltrates under the skin resulting in skin swelling, epidermal atrophy, keratinization; infiltration of muscle fibers causes degenerative changes in skeletal muscle and cardiac muscle, resulting in necrosis.  The thyroid gland can be atrophied or enlarged depending on the cause. In the case of a shrunken thyroid gland, the thyroid follicles and glial material partially or completely disappear, and dense, transparent fibrous tissue appears; in the case of an enlarged thyroid gland, the thyroid follicular cells are hyperplastic and enlarged in the early stages, and the glial material is reduced or disappears; in the case of a long-standing disease, the thyroid gland is nodular, the follicular epithelial cells are flattened, and the follicles are filled with glial material.  In primary hypothyroidism, due to the decrease of thyroid hormone secretion, the feedback inhibition of pituitary TSH cells is weakened, and TSH cells proliferate to enlarge the pituitary gland, even in the form of nodular hyperplasia.