hypothyroidism Flashcards
axis DIAGRAM
TRH= TSH= T3/4
what goes on in a follicle DIAGRAM
I- goes into follicular cell where its convered into I2 by oxidation then moves into colloid containing thyroglobulin+ stored thyroxine I2= monoiodotyrosine= thyroxine, which moves out and becomes T4
feature of primary hypothyroidism (myxoedema)
autoimmune damage (antibodies against thyroid gland)= lower T3/4+ high TSH
symptoms of primary hypothyroidism
deep voice, depression/tiredness, cold intolerance, weight gain with lower appetite, constipation, bradycardia
2 types of thyroid hormones
T4 is a prohormone converted into T3 by deiodinase in deiodination 80% T3 from deiodination of T4, 20% from thyroidal secretion
effect of T3
T3 binds to thyroid hormone receptor and retinoid x receptor, which all bind to thyroid response element to cause an altered gene expression
treatment of primary hypothyroidism and dosage
thyroxine/levothyroxine sodium/tetraiodothyronine given usually, T3 less common T4 given orally as a tablet, with TSH reference ranger used as guidance for dose
treatment of secondary
a SMALL group of patients have pituitary tumour/ post-pituitary surgery, so TSH is low, so can’t be used as a guide levothyroxine still given orally, but free (active) T4 middle of reference range is used
treatment of myxoedema coma
very rare complication of hypothyroidism T3 given instead intravenously, as more potent and quicker acting. T4 then given after
T4 vs T3
T3 not given for primary and secondary, as no trial has shown its effectiveness combined treatment also not usual, as T3 can be toxic if too much given (tremor, anxiety)
pharmacokinetics (half life, activity, circulation)
T4 half life 6 days, T3 2.5 DAYS also T4 active orally more than 99% T3/4 bound to mostly thyroxine binding globulin
why free T4 measured rather than plasma bound
plasma protein bound can vary- increases in pregnancy/treatment with oestrogens falls with malnutrition/liver disease/ drugs that compete for protein binding sites
