Thyroid gland Flashcards
thyroid anatomy
in the neck, bilobular form w/ central isthmus -‘butterfly’
follicular cells & C cells
Follicular cells
make thyroglublin
trap iodine
produce MIT & DIT
store T3 & T4 for release when TSH stimulation occurs
C cells
make clacitonin
thyroid hormone precursor
tyrosine residue on the thyroglobulin
Iodine involvement in thyroid hormones
iodide is oxidized to iodine via thyroid peroxidase (TPO) & attaches to the tyrosine residue
T3 2 base components
MIT + DIT
T4 2 base components
DIT + DIT
TSH stimulation on T3 & T4
the stored T3 & T4 are cleaved from thyroglobulin droplet via lysosome ingestion when TSH stimulates thyroid
MIT
3-monoiodiotyrosine
has one iodine in 3’ position on ring
DIT
3,5-diiodotyrosine
has 2 iodines on 3’ & 5’ position on ring
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
regulation of thyroid
hypothalamus secretesTRH
pituitary secretes TSH
thyroid gland releases T4 & T3 into circulation
thyroid hormones feedback & shut off TRH & TSH
5’-deiodinase
responsible for taking of an iodine off T4 into T3 or T3r
3 types
type 1 5’-deiodinase
MOST ABUNDANT
located in liver & kidney!
susceptible to some drugs
type 2 5’-deiodinase
located in brain & pituitary
keeps T3 constant level in the brain
type 3 5’-deiodinase
form deiodinates T3 to T2 & becomes completely inactive
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
