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The Endocrine System
Thyroid gland
The Thyroid gland is one of the largest endocrine glands in the body. It is positioned on the neck
just below the Larynx and has two lobes with one on either side of the trachea. It is involved in the
production of the hormones T3 (triiodothyronine) and T4 (thyroxine). These hormones increase the
metabolic activity of the body‘s cells. The thyroid also produces and releases the hormone calcitonin
(thyrocalcitonin) which contributes to the regulation of blood calcium levels. Thyrocalcitonin or
calcitonin decreases the concentration of calcium in the blood. Most of the calcium removed from the
blood is stored in the bones.
The thyroid hormone consists of two components, thyroxine and iodine. This hormone increases
the metabolism of most body cells. A deficiency of iodine in the diet leads to the enlargement of the
thyroid gland, known as a simple goiter. Hypothyroidism during early development leads to cretinism.
In adults, it produces myxedema, characterized by obesity and lethargy. Hyperthyroidism leads to a
condition known as exophthalmic goiter, characterized by weight loss as well as hyperactive and
irritable behavior.
The thyroid gland is a two-lobed gland that manifests a remarkably powerful active transport
mechanism for uptaking iodide ions from the blood. As blood flows through the gland, iodide is
converted to an active form of iodine. This iodine combines with an amino acid called tyrosine. Two
molecules of iodinated tyrosine then combine to form thryroxine. Following its formation, the
thyroxine becomes bound to a polysaccharide-protein material called thyroglobulin. The normal
thyroid gland may store several weeks supply of thyroxine in this bound form. An enzymatic splitting
of the thyroxine from the thyroglobulin occurs when a specific hormone is released into the blood. This
hormone, produced by the pituitary gland, is known as thyroid-stimulating hormone (TSH). TSH
stimulates certain major rate-limiting steps in thyroxine secretion, and thereby alters its rate of release.
A variety of bodily defects, either dietary, hereditary, or disease induced, may decrease the amount of
thyroxine released into the blood. The most popular of these defects is one that results from dietary
iodine deficiency. The thyroid gland enlarges, in the continued presence of TSH from the pituitary, to
form a goiter. This a futile attempt to synthesize thyroid hormones, for iodine levels that are too low.
Normally, thyroid hormones act via a negative feedback loop on the pituitary to decrease stimulation of
the thyroid. In goiter, the feedback loop cannot be in operation - hence continual stimulation of the
thyroid and the inevitable protuberandce on the neck. Formerly, the principal source of iodine came
from seafood. As a result, goiter was prevalent amongst inland areas far removed from the sea. Today,
the incidence of goiter has been drastically reduced by adding iodine to table salt.
Thyroxine serves to stimulate oxidative metabolism in cells; it increases the oxygen consumption
and heat production of most body tissues, a notable exception being the brain. Thyroxine is also
necessary for normal growth, the most likely explanation being that thyroxine promotes the effects of
growth hormone on protein synthesis. The absence of thyroxine significantly reduces the ability of
growth hormone to stimulate amino acid uptake and RNA synthesis. Thyroxine also plays a crucial role
in the closely related area of organ development, particularly that of the central nervous system.
If there is an insufficient amount of thyroxine, a condition referred to as hypothyroidism results.
Symptoms of hypothyroidism stem from the fact that there is a reduction in the rate of oxidative
energy-releasing reactions within the body cells. Usually the patient shows puffy skin, sluggishness,
and lowered vitality. Other symptoms of hypothyroidism include weight gain, decreased libido,
inability to tolerate cold, muscle pain and spasm, insomnia and brittle dry hair. Hypothyroidism in
children, a condition known as cretinism, can result in mental retardation, dwarfism, and permanent
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