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77 Cards in this Set
- Front
- Back
where is thyrotropin releasing hormone made and what does it increase
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TRH is made in the hypothalamus and increases prolactin levels
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what will decrease TRH
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dopamine
somatostatin glucocorticoids |
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what will increase TRH
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cold
emotional stress illness seratonin catacholamines |
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what are the steps for TH secretion
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TRH released from hypothalamus
TRH binds to thyrotropes on anterior pituitary anterior pituitary secretes TSH/thyrotropin TSH binds to GPCR on thyroid gland causing thyroid gland to produce thyroid hormone |
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how does thyrotropin stimulating hormone stimulate thyroid hormone release
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by binding to GPCR on thyroid gland causing it to secrete thyroid hormone
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what happens to TSH/TRH if there are low levels of TH
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increase production of TSH (anterior pituitary gland) and TRH (hypothalamus)
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what happens to TSH/TRH if there is too much TH
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decrease in production of TSH and TRH
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what are the thyroid hormones
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T4 - levothyroxine
- delivery molecule - 4 iodine T3 - liothyronine/tri-iodothyronine - active molecule |
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what form is thyroid hormone given as a drug
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T4
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what are some of the roles of thyroid hormone
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basometabolism
temp regulation energy use strorage of nutrients |
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what happens to a fetus/new born that does not get enough TH
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cretinism (severe type of mental disorder due to lack of TH)
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what is the source of tyrosine
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thyroglobulin (Tg)
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what all must be added together to make thyroid hormone
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2 tyrosines and then addition of iodine
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where is thyroid hormone made
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colloids/follicular lumen of thyroid epithelium
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how is thyroglobulin synthesized
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Tg is made in the ER
travels to golgi travels to lumen *in the lumen Tg sits and waits for addition of iodine |
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where does Tg get glycosylated
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in the golgi
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if one iodine is added to tyrosine what is that
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monoiodotyrosine (MIT)
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if two iodine are added to tyrosine what is that
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di-iodotyrosine (DIT)
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what is thyroid hormone built on
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thyroglobulin (Tg)
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what is the sequence of events in order for the making of T3/T4 from Tg
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iodine is added to Tg via thyroid peroxidase and hydrogen peroxide
depending on how many iodine is added you can have DIT or MIT the thyroglobulin is reacted with thyroid peroxidase + hydrogen peroxide again to couple two tyrosine together making T3 or T4 THE THYROID HORMONE (T3/T4) IS NOT MADE UNTIL IT GETS REMOVED FROM Tg |
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when does Th get cleaved from Tg
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when you go back into epithelial cells
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what puts iodine on tyrosine
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thyroid peroxidase + hydrogen peroxide
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what directly stimulates synthesis of TH
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TSH/thyrotropin
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what indirectly stimulates the synthesis of TH
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TRH
low T3/T4 |
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what stimulates all aspects of TH synthesis
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TSH
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how is T3/T4 secreted
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Tg w/ precursor for T4/T3 is endocytosed into a endosome
the endosome combines with a lysosome after fusion of the endosome and lysosome, ENZYMES IN LYSOSOME CLEAVE OFF T3/T4 T3/T4 is exported into the blood Tg is broken down and recycled |
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how does T3/T4 circulate
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bound to protein
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what is the activity and affinity of bound/unbound T3/T4
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T3 is only active when unbound
T4 is not active whether bound or unbound T3 has less of affinity for the protein compared to T4 b/c you want to release T3 faster from the proteins |
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which type of TH is found more in our blood
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T4
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what occurs in the conversion of T4 to T3 (metabolism of TH)
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5' deiodinase converts T4 to T3 by removing and Iodine.
- depenending on which the iodine is removed from T4 you can form T3 or REVERSE T3 (inactive form of T3) |
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what are the inactive forms of T3
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bound T3
reverse T3 |
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what kind of receptor are thyroid hormone receptors
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nuclear
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where are TH receptors located
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inside the nucleus of the cell of almost every tissue
THEY DON'T HAVE EXTERNAL DOMAIN |
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what are the forms of TH receptor
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alpha
beta |
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what are the isotypes of 5' deiodinase
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D1
D2 |
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what is differentiates TH receptors from steroid receptors
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TH receptors can bind to DNA w/o the ligand (hormone)
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what are the properties of TH receptors
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once they bind hormone they act as transcription factors and regulate (up or down) gene expression/transcription depending on whether they recruit activators or repressors
TH receptors have non genomic activities (functions/activities outside the nucleus but inside the cell) |
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where do TH receptors bind
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they bind to DNA at thyroid response elements (TRE)
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what can bind to TH receptors and what do they activate
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T3 and T4 can both bind to TH receptors but only T3 gets activated
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what receptors are TRE associated with
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alpha/beta TH receptors
retinoid receptors they have also been associated w/ a combo btwn TH receptor and other intracellular receptors such as retinoid receptors |
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what is TRE part of
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the DNA that TH receptor binds to
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what activates gene expression
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ONLY T3 ACTIVATES GENE EXPRESSION
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what are examples of nuclear receptors
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Vit A, Vit D, retinoic acid, steroid receptors
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what does serca 2a do
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ATP dependent Ca pump
pumps Ca back into the sarcoplasmic reticulum when we want our muscles to relax |
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what regulates serca 2a
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phospholamban (PLB)
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what does phospholamban
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regulates serca 2a
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when is PLB used
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when we want to contract
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how is PLB inactivated and when does this occur
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PLB is inactivated when it gets phosphorylated by a kinase
this occurs when we want our muscle to relax |
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what effects does T3 have on the heart
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increases gene expression/translation of Serca 2A (this puts more Serva 2a on SR and allows us to pump Ca back in quicker)
increases gene expression/translation of alpha myosin heavy chain (this gives us a greater contractility) down regulates the gene expression/translation of PLB (this takes away the inhibition of Serca 2a allowing us to pump more Ca in) |
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how does T3 increase HR
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because greater contractility (due to increase of alpha myosin heavy chain) and greater relaxation (due to increase of Serca 2A)
you have a quicker HR because you are contracting harder and relaxing quicker |
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what happens to your HR when there is excess TH
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tachycardia due to increase in force of contraction and rate of relaxation
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what happens to your HR when there is little TH
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bradycardia
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how does T3 mediate changes in gene expression that directly affect the function of the heart
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by changing the gene expression/transcription of
ALPHA MYOSIN HEAVY CHAIN PLB SERCA 2A |
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how does T3 indirectly effect the heart
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by altering the sensitivity to catecholamines (upregulates Beta 1 adrenoceptors which increase HR by binding epinephrin)
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how does T3 effect the HR
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upregulation of B1 adrenoceptors
upregulation of Serca 2A upregulation of alpha myosin heavy chains downregulation of PLB |
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what kind of thyroid dysfunction will you see insulin resistance
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hyperthyroidism (thyrotoxicosis)
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what effects does TH have on cholesterol
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TH upregulates LDL receptors on the liver which take up cholesterol from the blood into the liver
TH converts cholesterol into bile acids TH enhances the lipolytic effects of catecholamines (epinephrin) |
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what happens in iodine deficiency
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hypothyroidism b/c not enough iodine to make thyroid hormone
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what happens in thyroiditis
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may have hypothyroidism
inflammation of the thyroid low or normal T3/T4 high TSH/TRH |
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is there a goiter in ion deficiency
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yes
GOITER DUE TO EXCESS Tg -in response to low TH the hypothalamus is upregulated making TRH which goes to the anterior pituitary and makes more TSH telling the thyroid gland to make more TH. THYROID GLAND CAN'T MAKE MORE TH B/C NO IODINE BUT IT DOESN'T KNOW THAT AND MAKES A LOT OF Tg WHICH ENLARGES THE GLAND |
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what occurs in primary hypothyroidism
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thyroid gland isn't functioning properly and you can't produce sufficient TH
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what is hyperthyroidism
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FREE thyroid hormone in circulation is elevated
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what is graves disease
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AUTOIMMUNE DISEASE
hyperthyroidism due to auto-antibodies bind to TSH receptors on the thyroid gland and cause TH production |
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what are TRH/TSH levels in graves disease
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low TRH/TSH
low TSH b/c the hypothalamus is telling the pituitary gland to stop making TSH, TRH is also low b/c the body is trying to drop TH levels TH REMAINS HIGH B/C THE TSH RECEPTORS ON THE THYROID GLAND ARE NO LONGER RESPONDING TO TSH BUT THE AUTOANTIBODIES OF GRAVES DISEASE |
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what occurs in thyroid nodules
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not immune cause
hyperthyroidism part of thyroid gland ignores signals from pituitary gland or hypothalamuc and just produces TH |
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is there a goiter in thyroid nodules
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goiter but no exopthalmos
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what happens if someone is hyperthyroid for an extended period
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osteoporosis (bone loss) may occur due to the TH causing bone turnover, and excess TH causes a lot of bone turnover
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what occurs in central hypothyroidism
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don't make enough TSH/TRH therefore can't make enough TH
secondary(pituitary) - TSH tertiary(hypothalamus) - TRH |
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what is hashimotos thyroiditis
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autoimmune disease
autoantibodies against thyroid peroxidase or Tg (thyroid proteins) thyroid epithelium undergoes apoptosis and you lose thyroid function high TSH/TRH |
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what is the most common cause of hypothyroidism
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hashimotos thyroiditis
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is there a goiter in hashimotos thyroiditis
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goiter b/c inflammation not b/c gland working too hard
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when is non goiterous hypothyroidism seen
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in patients who's thyroids have been killed by radioactive iodine
burned out graves - after period of hyperthyroidism TH production diminishes |
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what are the causes of hypothyroidism
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pituitary defect - tumors therefore don't make enough TSH
thyroid gland dysfunction -iodine deficiency -cancers hashimoto's thyroiditis |
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what is the range of hypothyroidism
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subclinical
myxedema hyponatriemia |
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what is hyponatriemia
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impared Na absorption due to lack of TH
TH upregulates Na/K ATPase therefore if TH is low we lose Na in urine |
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what is myxedema
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need to get IV TH immediately, hydrophilic mucopolysaccharides in tissue
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when does exopthalmos occur
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only in graves disease
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