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39 Cards in this Set

  • Front
  • Back
What type of cell synthesizes thyroid hormones?
follicular epithelial cells
What is contained in the follicular lumen?
colloid (thyroid hormones bound to thyroglobulin)
Where is thyroglobulin synthesized, and where is it transported to?
synthesized on RER and Golgi of follicular epithelial cells; extruded to follicular lumen via secretory vessels
What is the "I- trap"?
I- is actively transported across basal membrane from blood into follicular epithelial cells, against chemical and electrical gradients
What factors inhibit the I- pump?
thiocyanate and perchlorate ions, and high levels of I-, thus inhibiting thyroid hormone synthesis (Wolff-Chaikoff effect); also, very low levels of I-
What factors stimulate the I- pump?
mild to moderate I- deficiency (compensatory effect)
What happens to the I- in the follicular cell?
I- gets oxidized to I2 by peroxidase as it is transported across apical membrane
What substance inhibits peroxidase, and what effect does this have?
propylthiouracil (PTU), used therapeutically to reduce thyroid hormone synthesis in hyperthyroidism
What happens to I2 in the follicular lumen?
I2 organification. just inside the lumen, I2 reacts with thyroglobulin to form MIT and DIT (which remain attached to thyroglobulin)
How are T3 and T4 produced from MIT and DIT?
Coupling reactions on TG:
DIT + DIT = T4
MIT + DIT = T3
What happens when the thyroid gland is stimulated?
TG is endocytosed, lysosomal enzymes digest TG, releasing T4/T3 into circulation, while MIT and DIT are recycled
What does thyroid deiodinase do? What happens if there is a deficiency of this enzyme?
It deiodinates MIT and DIT so the I2 can be reutilized; deficiency mimics I2 deficiency
What is the most common circulating form of T3 and T4?
bound to thyroxine binding globulin (acts as a reservoir)
What happens to TBG and free hormone levels during hepatic failure?
TBG levels decrease, thus decreased total thyroid hormone level, but normal levels of free hormone (maintained by negative feedback)
What happens to TBG and free hormone levels during pregnancy?
TBG levels increase (estrogen inhibits hepatic TBG breakdown), thus increased total thyroid hormone, but normal levels of free hormone (maintained by negative feedback)
What are the differences between T3 and T4? What enzyme catalyzes their conversion?
more T4 is produced by the thyroid gland, but T3 is more active. T4 is converted to T3 by 5'-iodinase in peripheral tissues
What are the actions of TRH?
released from hypothalamus to stimulate release of TSH from a/p
What are the actions of TSH?
released from a/p to stimulate each step of synthetic pathway and s/c of thyroid hormones ; causes hypertrophy of thyroid w/chronic elevation
What negative feedback mechanism regulates thyroid hormone secretion?
free T3 feeds back to down regulate TRH receptors in a/p
Pt w/high circulating levels of thyroid hormone but low TSH levels. What could be the cause, what is the disease?
thyroid stimulating-immunoglobulins (antibodies to TSH receptor) stimulate thyroid gland to produce T3/T4; aka Grave's disease
What is the molecular mechanism of action of thyroid hormones?
(T4 (via 5' iodinase)-> T3) T3 binds nuclear receptor -> transcription -> translation -> new proteins many physiologic effects
What are the major actions of thyroid hormones?
promote bone formation, increase BMR, heat production, and O2 consumption, alter cardio/resp fns to increase blood flow/02 delivery to tissues, maturation of CNS in perinatal period
What is the main mechanism through which thyroid hormones increase BMR and O2 consumption?
increased synthesis and activity of Na-K ATPase

*results in increase in heat production*
If thyroid hormones increase O2 consumption, what must happen to metabolism?
body needs increased substrates for oxidative metabolism: increased glucose GI absorption, gluconeogenesis, lipolysis, proteolysis
Is the overall action of thyroid hormones catabolic or anabolic? Does this cause increased or decreased lean muscle mass?
catabolic (even thought they inc both protein synthesis and degradation); decreased muscle mass
Thyroid hormones increase O2 consumption. How do thyroid hormones ensure that there is a subsequent increase in O2 delivery to tissues?
increased synthesis of beta-1 adrenergic receptors, to increase heart rate and contractility (e.g. cardiac output) (myocardium is thus more sensitive to sympathetic stimulation); also increases ventilation rate
Why would propranolol be an effective adjunct therapy for hyperthyroidism?
beta-adrenergic blocker -> blocks autonomic effects of thyroid hormones (which upregulate beta-1 adrenergic receptors in heart)
What are the effects of thyroid hormones on the CNS during the perinatal period?
CNS maturation depends on thyroid hormones; deficiency causes irreversible MR (this is why screening for neonatal hypothyroidism is mandatory)
What are the effects of hyperthyroidism on the CNS in adulthood?
hyperexcitability and irritability
What are the effects of hypothyroidism on the CNS in adulthood?
listlessness, slowed speech, somnolence, impaired memory, decreased mental capacity
What are some possible causes of hyperthyroidism?
Graves disease (antibodies to TSH receptor), excessive exogenous thyroid hormones, thyroid neoplasm, excessive s/c of TSH or TRH
Under what conditions would you see elevated T3/T4 levels, but low TSH levels?
Graves disease, thyroid neoplasm, exogenous administraion
What are the common symptoms of hyperthyroidism?
weight loss w/inc food intake, inc metabolic rate, sweating, inc HR, breathlessness on exertion, tremor, nervousness, weakness, goiter
What are some common treatments for hyperthyroidism?
propylthiouracil (PTU) - inhibits thyroid hormone synthesis by blocking peroxidase

thyroidectomy, or radioactive ablation w/(131)

beta-blockers (adjunct therapy)
What are some possible causes of hypothyroidism?
autoimmune destruction (thyroiditis), surgical removal, hypothal/pit failure (dec TRH/TSH), I- deficiency, cretinism (aka congenital myxedema)
Where would the primary defect be if pt had low T3/T4 levels but increased TSH levels?
defect in thyroid/thyroid hormones themselves
Where would the primary defect be if pt had low T3/T4 levels and low TSH levels?
defect in hypothalamus or a/p
What are the common sx of hypothyroidism?
dec metabolic rate, weight gain, cold sensitivity, dec HR, slowed mental activity, lethargy, somnolence, periorbital puffiness (drooped eyelids), constipation, hair loss, menstrual dysfn, hypoventilation, sometimes myxedema, goiter (from unrelenting stimulation of thyroid by TSH)
What is the common treatment for hypothyroidism?
thyroid hormone replacement (usu T4)