this lecture (sadly, dr. brons' last lecture during our time here) covered the thyroid anatomy and thyroid hormones release and physiological effects on the body. the thyroid hormone is situated between the thyroid cartilage and the 6th tracheal cartilage ring and is composed of functional units called follicles. these follicles are vesicles that are lined with cuboidal cells which take in iodine and secrete it, along with thyroglobulin, into the lumen of the follicles. in the lumen, iodine combines with thyroglobulin and tyrosine to form mono and di-iodotyrosine, which can be combined to form the main thyroid hormones T3 and T4, which are stored in the lumen of the follicles.
the release of T3 and T4 from the thyroid gland is mediated by the HPA axis; the hypothalamus releases TRH (thyrotropin releasing hormone) into the portal veins and anterior pituitary, which then releases TSH (thyroid stimulating hormone) into the circulation. the thyroid reacts to TSH by endocytosing T3/T4 from the lumen into follicle cells, where thryoglobulin is removed from T3/T4 via phagolysosomes. T3/T4 then enter general circulation in the approximate ratio of 10:1 T4:T3. high T3 levels allow for feedback inhibition of the hypothalamus, causing it to downregulate TRH receptor sites as well as disrupting synthesis of TSH, homeostatically lowering T3 levels.
in peripheral cells, T4 is converted to T3; T3 has a host of effects on virtually all organs and tissues in the body. on a cellular level, it functions as a modulator of cell metabolism (rather than an on-off switch, it simply amplifies existing metabolic processes) by acting as a transcription factor which can upregulate certain metabolic proteins; such as the ATP-ase Na+/K+ pump. the net effect of T3 on cells is to increase basal metabolic rate, oxidative metabolism (except in the brain, spleen, and testes) by increasing O2 consumption, facilitating hormonal actions on metabolic fuels (such as glucose, fatty acids, etc), and increasing cardiac output by upregulating beta-receptors. due to this close relationship to metabolism, the release of thyroid stimulating hormones is regulated by body temperature; higher body temperatures will inhibit release of TSH and lower body temperatures will stimulate TSH release.
hyperthyroidism is an excess production of T3/T4 and the accompanying metabolic frenzy, and is either caused by reduced feedback inhibition or an immune dysfunction where antibodies produced against the thyroid stimulates excess release of T3/T4; in this case, the high levels of T3/T4 would cause feedback inhibition and thus low levels of TSH. hyperthyroidism results in a goiter due to hyperplasia of thyroid cells, heat intolerance, weight loss, exophthalamos, nervousness, irritability, tachycardia, arrhythmia. hypothyroidism is the opposite condition of low T3/T4 levels which can be the result of autoimmune destruction of thryoid, iodine deficiency, or excess consumption of goitrogens. the symptoms include lethargy/sluggishness, colloid goiter, cold intolerance, delayed tendon reflexes, high cholesterol, hair loss, enlarged liver/kidney/tongue, and myxedema, among other things.
questions
thyroid anatomy and functional anatomy...
1. what is the endocrine axis that regulates release of thyroid hormone?
2. what is TRH? how is it released?
3. what is TSH? how is it released?
4. how does the thyroid respond to TSH?
5. where is the thyroid gland located?
6. what is the functional unit of the thyroid and what does it consist of?
T3, T3 synthesis, release, feedback...
7. describe the synthesis of T3 and T4.
8. how long can T3 and T4 be stored in the lumen of thyroid follicles?
9. describe the release of T3 and T4 from the thyroid into the blood.
10. what is the ratio of T4 to T3 at release from the thyroid?
11. in cells, what happens to T4?
12. describe the feedback inhibition of T3.
13. how does temperature affect T3/T4 release?
physiological and metabolic effects of T3...
14. which organs does T3 affect?
15. describe the role that T3 plays in regulating cellular functioning.
16. what is cretinism and what does it result in?
17. in peripheral cells, T3 enhances...
18. in which tissues does T3 not enhance oxidative metabolic functioning?
19. describe T3's effects on metabolism.
pathologies...
20. what is hyperthyroidism and what are its causes?
21. describe relative levels of T3/T4 and TSH in hyperthyroidism that results from autoimmune dysfunction.
22. what are some of the symptoms of hyperthyroidism?
23. what is hypothyroidism and what are its causes?
24. describe the relative levels of T3/T4 and TSH in hypothyroidism.
25. what are the symptoms of hypothyroidism?
answers
1. HPA axis.
2. thyrotropin releasing hormone is released from the PVN of the hypothalamus into the portal veins and anterior pituitary.
3. thryoid stimulating hormone is released from the anterior pituitary into general circulation.
4. by releasing T3 and T4 into the circulation.
5. between the thyroid cartilage to the 6th tracheal cartilage ring.
6. a follicle which is a vescicle surrounded by cuboidal cells that incorporate iodine and synthesize thyroglobulin, and a colloid interior where T3 and T4 are synthesized and stored, bound to thyroglobulin.
7. iodine is pumped into follicular cells and subsequently into the lumen of the follicles, along with thyroglobulin. in the lumen, thyroglobulin is combined with iodine and tyrosine to form mono and di-iodo tyrosine (MIT and DIT), and T3 and T4 are formed by combining MIT and DIT or two DIT's.
8. 2-3 months.
9. T3 and T4 are endocytosed back into follicle cells where the thyroglobulin is degraded into amino acids via phagolysosomes. T3 and T4 are then released into the circulation.
10. 10:1
11. it is converted to T3.
12. high T3 levels can act on the anterior pituitary to downregulate TRH receptors as well as inhibiting signal transduction in the TSH pathway, ultimately reducing the level of T3/T4 that is released from the thyroid.
13. high temperature inhibit T3/T4 release and cold temperatures stimulate T3/T4 release via hypothalamic temperature centers.
14. all organs.
15. acts as a modulator of cell function rather than an on/off switch.
16. an early thyroid deficiency; abnormal development of bones and CNS. results in stunted bones, malformation of facial bones and mental retardation.
17. basal metabolic rate, oxidative metabolism, upregulation of ATP-ase sodium/potassium pump.
18. brain, spleen, testes.
19. increases O2 consumption, facilitates hormonal actions on metabolic fuels (glucose, lipids, etc.), increases cardiac output by upregulating beta-receptors.
20. increased synthesis of T3/T4, caused by reduced feedback inhibition or autoimmune dysfunction, where antibodies to thyroid gland stimulate excess release of T3/T4.
21. high T3/T4 levels and low TSH levels due to feedback inhibition of the anterior pituitary.
22. goiter due to hyperplasia of thyroid cells, heat intolerance, weight loss, exophthalamos, nervousness, irritability, tachycardia, arrhythmia.
23. decreased synthesis of T3/T4 due to autoimmune destruction of thyroid, iodine deficiency, or goitrogens in the diet such as turnips or cabbage (but only in ridiculous, comical quantities according to dr. brons)
24. low levels of T3/T4 but high levels of TSH; results in increased colloid volume in thyroid due to synthesis and storage of T3/T4 without release.
25. colloid goiter, cold intolerance, fatigue/somnolescence, delayed tendon reflexes, bradycardia, high cholesterol, hair loss, enlarged liver/kidney/tongue, myxedema (mucopolysaccharide gel in skin osmotically holding water).
No comments:
Post a Comment