Thyroid

All vertebrates, from the most primitive fish to humans, have a pair of so-called thyroid glands located in the neck. In humans, both glands are connected into one by a narrow isthmus, running transversely in front of the trachea, just under the larynx. The thyroid gland develops as an outgrowth of the anterior side of the pharynx, but by the time the human embryo reaches about 6 mm in length, the connection with the pharynx is lost and the gland becomes an independent formation.

The thyroid gland consists of groups of cuboidal epithelial cells that form hollow spherical vesicles with walls one cell thick. The cavity of the vesicle contains a gelatinous substance called colloid secreted by these cells. The hormone released by the cells is a protein called thyroglobulin.

Its active group is the amino acids thyroxine and triiodotyrosine, the molecules of which contain 4 and 3 iodine atoms, respectively. Thyroxine was artificially synthesized in 1927, and currently patients are administered mainly a synthetic hormone.

If you remove 2 out of 4 iodine atoms, the activity of the substance will decrease significantly, and if all 4 atoms are removed, it will be completely lost. The main effect of thyroxine is to accelerate energy-producing oxidative processes in all tissues of the body. When additional amounts of thyroxine are administered, the body consumes more oxygen, produces more metabolic products and generates more heat than under normal conditions.

When thyroxine is added to a suspension of mitochondria, the permeability of their membranes decreases, the mitochondria swell, and this is what possibly leads to the uncoupling of the processes of phosphorylation and electron transfer. Whether thyroxine has the same effect on mitochondria in an intact organism is not yet clear. When the secretion of thyroxine is insufficient, the level of basal metabolism drops to 600-900 kcal per day, which is 30-50% compared to the norm.

Sections of individual tissues of an animal with insufficient thyroid function also reveal, when incubated in vitro, a lower metabolic rate than sections of tissue from a normal animal. By influencing metabolism, thyroxine thereby has a strong effect on growth and differentiation. Removal of the thyroid gland in young animals leads to delayed growth and mental development and delayed or insufficient development of the genital organs.

Insufficient secretion of thyroxine in an adult leads to a disease called myxedema; This disease is characterized by low metabolic rate and, as a consequence, reduced heat production. The body temperature may drop several degrees below normal, so that the patient feels cold all the time. In addition, the pulse is slow and the patient experiences sluggish movements and mental reactions.

However, the appetite usually remains normal, and since the food eaten is not used with normal intensity, there is a tendency towards obesity. The skin becomes dry and swollen due to the accumulation of mucous fluid in the subcutaneous tissues, and hair usually begins to fall out. Myxedema responds well to treatment with thyroxine or desiccated thyroid gland.

Since thyroxine is almost not destroyed by digestive juices, it can be administered orally. Myxedema is caused by underactivity or degeneration of the thyroid gland itself. Another form of hyperthyroidism develops when water and food contain too little iodine and there is not enough iodine for the synthesis of thyroxine.

In this case, the gland itself seeks to compensate for the deficiency by increasing in size. Such an increase, called a simple goiter, can be expressed in a small swelling, difficult to notice when feeling the neck, or in the appearance of a huge, disfiguring growth weighing more than 1 kg. The symptoms accompanying goiter resemble those of myxedema, but are much less pronounced.

This type of goiter occurs in areas where the soil is poor in iodine, or in areas where