The Thyroid Gland

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Created by:

morgansherritt  on April 1, 2012

Subjects:

physiology

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The Thyroid Gland

thyroid structure
bi-lobed structure suspended from trachea consisting of sacs known as follicles which are filled with a proteinaceous fluid called colloid
the size of the follicles can vary depending on thyroid activity or during pathogenesis; follicles become larger and inside area of colloid becomes smaller when stimulated
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thyroid structurebi-lobed structure suspended from trachea consisting of sacs known as follicles which are filled with a proteinaceous fluid called colloid
the size of the follicles can vary depending on thyroid activity or during pathogenesis; follicles become larger and inside area of colloid becomes smaller when stimulated
thyroid vascularization vascularity exceeds that of the kidney
huge amount of vascularity to the tissue because it is anatomically favored and because the thryoid is important so blood supply is needed for a constant supply of T3 and T4
thyroid growth large endocrine gland that has a large potential for growth (goiter) under pathological conditions (i.e. iodine deficiency)
TSH from the anterior pituitary can induce growth as well as biosynthesis of T3 and T4
thyroid productsthyroxine (T4) and triiodothyronine (T3) are the major products of the thyroid gland; iodine-containing derivatives of tyrosine
normal production of T3 and T4 depends on adequate supply of dietary iodine which is stored in the body as organic iodine (thyroglobulin)
only about 1/5 iodine ingested is used while the rest is excreted
thyroid hormone biosynthesisspecialized transporter traps iodine in and it is oxidized by thyroperoxidase as it exits the cell
oxidized iodine is coupled with thyroglobulin
peroxidase helps to add on mono- and diiodotyrosine (MIT and DIT)
complex is brought back into the cell via pinocytosis as a colloid droplet and then proteases cleave T3 and T4 from it; T3 and T4 then leave the cell and are secreted
transport in blood less than 1% of thyroid hormones are present in the blood as free, unbound (biologically active) hormones; majority are bound to carrier proteins because the carrier proteins stabilize the hormones and increase their half-lives
carrier proteins act as a circulating storage unit until the hormone is needed for a later use
three carrier proteins are TBG, TBPA, and albumin; albumin is the most common carrier protein
majority of T3 and T4 are bound to TBG
T3 only has two carrier proteins and T4 has three
T4 conversionmore T4 is released because it has a longer half-life so it can circulate around, but also because it can be converted to T3 on need to have basis
more T4 released because it is less potent than T3
if we don't need T3, body will naturally convert T4 to reverse T3 which is biologically inactive
liver and kidney convert the most, but the brain, CNS, and placenta can also convert
growth and developmentthyroid hormone plays a crucial role in development of CNS as well as generalized tissue growth by regulating protein synthesis synergistically with GH
thyroid hormone can act permissively in a number of growth processes; doesn't have a direct effect on growth but its presence is needed in order for growth to occur
metabolic actions classic effect of thyroid hormone is to increase energy metabolism and O2 consumption (calorigenesis)
can increase cardiac output by decreasing vascular resistance
can cause an increase in intermediary metabolism (carbs, fats, proteins) as well as sensitizing the CNS to catacholamines
T3 vs. T4 T3 is much more biologically potent than T4; a very low dose of T3 will cause a great cause in metabolism while a high dose of T4 will barely reach the same effects as the small dose of T3
T4 has a slow onset and sustained response
T4 can be considered a prohormone since it is converted to T3
mechanism of actionT3 and T4 follow mobile receptor model
T3 enters cell, finds its receptor, and binds to gene to have its effect
T4 is converted to T3 which enters the cell, finds its receptor, and binds to gene to have its effect; T4 can bind to the receptor on its own, but it does so more slowly than T3 because it isn't as potent which is why T3 is preferred
thyroid stimulating hormoneanterior pituitary secretes TSH which acts as the principal physiological regulator of the thyroid gland and stimulates thyroid hormone synthesis via GPCR binding and activation of Gs/AC/cAMP signaling pathway
when TSH reaches the thyroid hormone, signalling is kicked on in order for thyroid hormone synthesis to occur
regulators of TSH secretionnegative feedback inhibition by T3 and T4 occurs mainly at anterior pituitary with some feedback on hypothalamus
circadian neural rhythms; peak TSH levels at night controlled by hypothalamic pulse generator
environmental stimuli i.e. temperature and stress; sympathetic stimulation generally inhibits TSH
thyroid autoregulation autoregulatory mechanisms exist within the thyroid that help maintain constant levels of hormonal stores with dietary iodine being key
iodine deficiencythyroid compensates by reducing hormone production until sufficient iodine is available
TSH levels increase and hypertrophy of the follicular cells occurs sometimes leading to an iodine-deficiency goiter
T3/T4 ratio may increase as a compensatory mechanism because the body will want more T3 to regulate iodine deficiency and maximize effects
iodine excess increase in dietary iodine will initially enhance hormone synthesis, but the thyroid then escapes from the iodine effect (Wolff-Chaikoff effect)
thyroid adjusts by reduced blood flow and sensitivity to TSH; useful for surgical procedures
goitrogensnumber of chemical substances inhibit thyroid hormone synthesis and can cause goiter in sufficient doses
chemical goitrogens are often used for hyperthyroid therapy; thiocyanate decreases iodine trapping, perchloride inhibits iodine transport, propylthiouracil blocks oxidation and coupling
natural-occurring goitrogens only work in great excess; turnips, cabbage, broccoli
hyperthyroidism excessive thyroid hormone production (thyrotoxicosis) results in numerous symptoms related to metabolic actions
Grave's disease (autoimmune)
Grave's disease immune system produces antibodies that bind to and activate the TSH receptor on thyroid cells
strong familial link and about 5 times more prevalent in women
nervousness, increased appetite, increased sweating, and eye complaints (huge eyes) are some of the symptoms
hypothyroidismthyroid hormone deficiency results in decline of energy metabolism and heat production
symptoms include decreased appetite, weight gain, somnolence, fatigue, and lethargy
skin may be infiltrated with gelatinous fluid (mucopolysaccharides) causing a puffy appearance of the face, hands, and feet (myxedema)
Hashimoto's disease (autoimmune) and cretinism
Hashimoto's disease foremost cause of hypothyroidism
caused by attack from cytotoxic CD8+ lymphocytes on the thyroid along with autoimmune antibody effects that inhibit thyroid peroxidase
cretinism disease caused by inadequate production of thyroid hormone during infancy that can cause deficits in CNS and skeletal development
can result in growth and mental retardation
testing thyroid levels soon after birth can greatly reduce developmental abnormalities

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morgansherritt