Endocrine: Thyroid
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- Describe T3: what is its half-life? Affinity for receptor?
- T3 has a short half-life, a high affinity for the receptor, and is thought to be the biologically active form of the hormone.
- Describe T4: what's its half-life? Affinity for receptor?
- T4 has a short half life, low affinity for receptor, and is thought to be a "reserve".
- Is the structure of T3/T4 closer to the steroids or peptides?
- The steroids.
- What are the symptoms of hyperthyroidism?
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*muscular fatigue
*increased appetite w/wt loss
*heat intolerance
*agitation and anxiety
*increased output and amenorrhea
*increased heart rate, dyspnea
*increased sweating, hair loss - What are some symptoms of hypothyroidism?
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*fatigue, lethargy
*cold intolerance
*decreased appetite w/wt gain
*decreased sweating, hair loss, dry skin
*increased mentrual flow
*decreased cardiac output - During what periods are T3/T4 critical for CNS development? What role do they play? What does deficiency at this time cause?
- During the final 6 prenatal mos, and the first 6 postnatal mos. Signal neuroblasts to differentiate into neurons to form pathways. Cretinism (dwarfism + MR) occurs with deficiency.
- What role does iodine play in the synthesis of T3/T4?
- It is taken up by follicular cells by a Na/I pump, and then covalently bonded to Tyr residues. This is used to form thyroglobulin.
- What is thyroglobulin?
- A large protein precursor that forms the colloid center of each follicle. Each molecule yields 3-4 molecules of T3/T4.
- How is thyroglobulin converted to T3/T4?
- It is taken up by follicular cells by pinocytosis and then split into T3/T4 in follicular lysosomes. It is then secreted into the bloodstream.
- How is T3/T4 synthesis stimulated?
- TRH is released by the hypothalamus, this causes the ant pituitary to release TSH which then stimulates the thyroid follicles.
- How is T3/T4 synthesis inhibited?
- T3 exhibits negative feedback on the release of TSH and to a small degree TRH.
- How is thyroid hormone transported in the plasma?
- 70% is bound to a specific protein carrier; T4 has a greater affinity for this molecule.
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T/F:
The thyroid gland is routinely palpated during the PE and nodules can be found in ~25% of women. - False: The gland is palpated, but nodules appear in only 4% of women.
- What happens in Graves disease? What kinds of symptoms are seen? What is the typical treatment?
- AutoAb's mimic TSH and stimulate follicular cells to release T3/T4 w/o regulation. Shows sx of hyperthyroidism. Tx is surgical.
- What happens in Hashimoto's disease? What kinds of symptoms are seen? What is the likely treatment?
- AutoAb's attack and destroy thyroid tissue. Sx of hypothyroidism are seen. Tx is hormone replacement.
- What are the 3 main organs involved with Ca++ and what do they do?
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1.Intestine: change rate of absorption of Ca from diet
2.Kidney: able to resorb or excrete Ca++ in urine.
3.Bone: resorb or form new bone. - What are the 3 forms of Ca in the body? Which is most important biologically?
- Ca may be in the ionic form, part of a salt, or bound to protein. The ionic form is most impt.
- Where is PTH synthesized? Is it a peptide, steroid, or amino acid hormone?
- PTH is synth by the chief cells of the parathyroid gland. It is a peptide hormone.
- What is the function (not action) of PTH?
- To elevate [Ca++] and lower [phosphate].
- Why is [phosphate] important in determining [Ca++]?
- Because phosphate is able to form a salt with Ca++ and thus reduce the amt in the ionic form.
- How is the synthesis of PTH stimulated?
- PTH is synthesized constantly but stored until the chief cells sense a drop in [Ca++]. The sensing receptor is in their plasma membranes.
- What 3 actions does PTH have on the kidney?
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*resorption of Ca++ is increased
*resorption of phosphate is decreased
*synthesis of Vit D is stim - What are the actions of PTH on bone? (there are 3)
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*osteoclasts are stim to resorb bone
*immature osteoclasts are stim to mature
*formation of new matrix is inhibited - What is PTH-related peptide? With what condition is it associated.
- A peptide that shares the first 13 AA residues with PTH and can stimulate PTH receptors. It causes humoral hypercalcemia of malignancy.
- What are the 2 sources of Vit D for humans?
- From the diet and synthesized in the skin upon exposure to UV light.
- What happens to Vit D in the liver?
- It is converted to the 25-OH form which can then be stored or enter circulation.
- What happens to Vit D in the kidney?
- PTH stimulates the conversion of the 25-OH form to the biologically active form.
- What symptoms are seen with Vit D deficiency?
- Poor mineralization of the bones, a.k.a. "rickets"
- Where is calcitonin synthesized?
- C (parafollicular) cells in the thyroid gland.
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T/F:
Calcitonin is an essential player in CA metabolism and is important in reversing the action of PTH. - False: Calcitonin does oppose PTH action, but it is fairly unimportant in humans.
- Calcitonin is being explored as a tx for a common medical condition - what is it?
- Osteoporosis
- What is the action of PTH in the small intestine?
- It stimulates absorption of Ca++ from the luminal contents.