hyperthyroidism Flashcards
describe grave’s disease *
autoimmune disease Ab bind to and stimulate the TSH receptor in the thyroid and stimulate the thyroid gland - hyperthyroidism cause goitre - smooth because every cell has the receptor so whole gland grows smoothly Ab bind to muscle behind eye - exophthalmos Ab also cause pretibial myxoedema - swelling shins
problem with having too high TSH *
in long term causes arrhythmia and osteoporosis
features of hyperthyroidism *
perspiration fascial flushing muscle wasting shortness of breath - HR high, not pumping effectively breast enlargement loss of weight - increased appetite rapid pulse warm skin amenorrhea localised myxoedema brain work faster - nervous, irritability, cant sleep, aggressive, insomnia, emotional instability exophthalmos goitre increased appetite diarrhoea tremor - because B receptors are more sensitive clubbing of fingers - thyroid acropachy muscular weakness palpitations heat intolerance lid lag (eyelid delay when follow finger) lid retraction chemosis - oedema of cornea corneal scarring because cant close eyes easily so gets v dry
describe exophthalmos *
muscle behind eye become inflammed because of Ab binding to GF? receptor, produce pressure on the optic nerve - lose vision/double vision also eye lid pulled back because of increased SNS activity because of increased sensitivity of B receptors - so eye doesn’t close = red eyes eye move forward so you can see the white of the eyes at the bottom
describe pretibial myxoedema *
The swelling (non-pitting) that occurs on the shins of patients with Graves’ disease: growth of soft tissue.
overall technecium uptake in Plummer’s compared to a normal thyroid *
increased
does thyroxine increase CO and HR
yes
describe the thyroid in Grave’s *
it is smoothly enlarged Ab bind to the TSH receptor on follicular cells and all the cells grow
what can be seen when using radioactive iodine in Grave’s *
the whole thyroid gland takes it up because it is all overreactive so you see that it is enlarged `
how do you diagnose Grave’s *
blood test for TSH, fT3/4 - high TSH and low T3/4 if primary hyperthyroid look for the TSHrAb look for exophthalmos use radioactive iodine or technetium 99 (cheaper) - whole gland is enlarged - administer IV, mininmum cytotoxicity examine neck -smooth
describe Plummer’s disease *
toxic nodule goitre NOT autoimmune benign adenoma - overactive and making thyroxine 1 clone of follicular cells has grown the normal part of the thyroid shrinks - because extra thyroxine from nodule inhibits TSH by -ve feedback so there is no stimulus for the rest of the thyroid to produce thyroxine - overall still hyperthyroidism because of amount produced by nodule
difference between Grave’s and Plummers *
no Ab in plummer’s so no exophthalmos or pretibial myxoedema not smoothly enlarged Ab test is -ve
what is the appearance of a thyroid in Plummer’s with radioactive iodine *
it goes into the nodule but no where else - called a hot nodule no uptake from the rest
effect of thyroxine on the SNS *
it sensitises B receptors to normal levels of adrenaline - have a response as if there is too much adrenaline therefore there is apparent SNS activation heart rate goes up (palpatations) lose weight when you do a small amount of exercise, normally A increases slightly, with excess thyroxine the A increases dramatically causing tachycardia which patients call palpitations, tremor because of the B receptors in skeletal muscles, lid lag
describe a thyroid storm *
medical emergency - 50% mortality if untreated blood results confirm hyperthyroidism if you have 2 or more of the following and hyperthyroidism - 50% chance of death: hyperpyrexia - >41 degrees tachycardia/arrhythmia cardiac failure so breathless at rest delirium/frank psychosis hepatocellular dysfunction or jaundice
describe the mechanism of action of thionamides *
they block iodination of the tyrosine residue so inhibit thyroid peroxidase and so T3/4 synthesis also blocks the reuptake of thyroxine into the follicular cell biochem effect happens in hrs - ie stop making thyroxine clinical effect takes weeks because of the store of thyroxine in the colloid treatment regime therefore may include propranolol which is a non-selective B blocker so reduces the adrenergic effects (tremor and tachycardia) while waiting for the clinical effect of the thionamides the drugs may also supress Ab production in Grave’s and reduce conversion of T4 (PTU) inhibit coupling of iodotyrosines
describe the mechanism of action for KI to treat hyperthyroidism *
temporary inhibition of thyroid synthesis and secretion this is the Wolff-Chaikoff effect it is the autoregulatory effect of the thyroid - with too much iodine it shuts down because would never want to produce that much thyroid hormone KI inhibits iodination, H2O2 generation and thyroid peroxidase the hyperthyroid symptoms reduce in 2 days - useful for the anaesthetic vascularity and size of thyroid reduce in 10-14 days - hyperthyroid thyroid has high vascularity because it is very active - KI reduces this making surgery easier
describe the use of radio-iodine to treat hyperthyroidism *
high doses used because sometimes it is difficult to control with drugs it accumulates I the colloid, emits B particles and so destroys follicular cells
