Thyroid gland Flashcards by Cindy Fieseler

thyroid anatomy

in the neck, bilobular form w/ central isthmus -‘butterfly’

follicular cells & C cells

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Follicular cells

make thyroglublin
trap iodine
produce MIT & DIT
store T3 & T4 for release when TSH stimulation occurs

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C cells

make clacitonin

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thyroid hormone precursor

tyrosine residue on the thyroglobulin

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Iodine involvement in thyroid hormones

iodide is oxidized to iodine via thyroid peroxidase (TPO) & attaches to the tyrosine residue

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T3 2 base components

MIT + DIT

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T4 2 base components

DIT + DIT

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TSH stimulation on T3 & T4

the stored T3 & T4 are cleaved from thyroglobulin droplet via lysosome ingestion when TSH stimulates thyroid

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MIT

3-monoiodiotyrosine

has one iodine in 3’ position on ring

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DIT

3,5-diiodotyrosine

has 2 iodines on 3’ & 5’ position on ring

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biologically active thyroid hormone

T3 is the most biologically active form: where iodine is missing from the OUTER ring
T4- significantly less active
T3r- removal of iodine from inner ring & has NO BIOLOGICAL ACTIVITY

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regulation of thyroid

hypothalamus secretesTRH
pituitary secretes TSH
thyroid gland releases T4 & T3 into circulation
thyroid hormones feedback & shut off TRH & TSH

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5’-deiodinase

responsible for taking of an iodine off T4 into T3 or T3r

3 types

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type 1 5’-deiodinase

MOST ABUNDANT
located in liver & kidney!
susceptible to some drugs

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type 2 5’-deiodinase

located in brain & pituitary

keeps T3 constant level in the brain

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type 3 5’-deiodinase

form deiodinates T3 to T2 & becomes completely inactive

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transport of thyroid hormones

TBG: thyroxine-binding globulin; MOST ABUNDANT
TBPA: thyroid-binding pre-albumin
albumin

higher the levels of TBG, the higher the T4 & T3 levels of bound hormone

free T3 levels in the blood

0.4%

thyroid hormone cell action

enters cell via thyroid hormone transporter
if T4 a 5’-deiodinase will convert to T3 OR if T3 it will either move on or will be converted to T2
T3 binds to thyroid nuclear receptor(TR) in nucleus
complex causes the alignment of RXR(thyroid responsive gene) & TRE (thyroid responsive element) and forms a protein of ‘action’
THYROID HORMONES ARE PROTEIN BASED BUT ACT LIKE STEROIDS!!

thyroid hormones affect

tissue growth
brain maturation
body heat production
increase 02 consumption
increase b-adrenergic receptors

thyroid effects

metabolic- increase in 02 consumption, protein catabolism, glucose levels
cardiovascular - increase heart rate, cardiac output, blood volume & decrease in peripheral vascular resistance
CNS- increase in adrenergic activity & sensitivity
GI- increase in motility

thyroid stimulating hormone TSH assay

3rd generation test method
detects 0.01 mU/L
chemiluminometric assay

serum total T4 or serum total T3 assay

RIA, chemiluminometric or immunometric

free thyroxine or free T4 or free triiodo-thyronine or free T3 assay

dialysis kit method

thyroglobulin assay

should not be in circulation bc they are in the thyroid | used to diagnose thyroid cancers

thyroid binding globulin TGB assay

may rise in pregnancy & may go down in some diseases used to determine free hormones total-TBG not used very often

thyroid stimulating antibody or TSAb or TSI

no TSH but thyroid TSH receptor is being activated by antibody

TSH receptor antibodies - TRAb or TSHR-Ab

can be stimulating or blocking antibody as it competitively binds to TSH receptor

Anti-thyroid peroxidase antibody or Anti-TPO Ab

attacks TPO which helps form thyroid hormones & process them

Graves disease general

most common hyperthyroidism- increased T3/T4 & low TSH positive for TSHR-Ab 70-100% of the cases may develop anti-TPOAb women > men

Hashimoto's thyroiditis general

hypothyroidism - low T3/T4 & high TSH looking for antibodies that inhibit hormone synthesis see anti-TPOAb in 80-99% of cases normal population has small % with anti-TPOAb

hyperthyroidism primary & secondary

primary (thyroid gland) : increase in T3/T4 & decrease in TSH secondary (pituitary): increased T3/T4 & TSH

hypothyroidism primary & secondary

primary (thyroid gland): decreased T4 & increased TSH | secondary (pituitary): decreased T4 & TSH (example: prolactin tumor)

causes of hyperthyroidism

excessive ingestion of hormone, leakage of hormone from storage, excessive hormone production: graves' disease, toxic adenoma or multinodular goiter

lab testing for grave's disease

increase in free T3/ T4 verrrry decreased TSH increased TSI/ TSH receptor Ab increased radioactive iodine uptake (RAIU) - scan shows diffuse pattern (!)

grave's treatment

surgery or use of radioactive iodine medication is liver toxic (can cause aplastic anemia) & kill very active centers in the thyroid monitor ALT, AST for liver function remission: 20-50% in USA

hypothyroidsim diseases

thyroiditis- hashimoto's or viral subacute congenital - cretinism iodine deficiency

symptoms of hypothyroidism

``` low body temp, slow movement, weight gain (!), constipation bradycardia, diastolic hypertension menstrual irregularity periorbital edema congnitive dysfunction ```

lab results for hashimoto's

``` increased TSH decreased T4 decreased Na+ due to inappropriate ADH levels increased CK due to myopathy anemia/pernicious anemia increased lipids ```

Amiodarone

used for cardiac arrhythmias is 37% iodine & can decrease thyroid hormone production inhibits conversion of T4 to T3