CEP WK6 - THYROID GLAND Flashcards
CELLS IN THYROID
thyroid follicular cells (produce thyroid hormones) & C-cells (make calcitonin)
THYROID HORMONES
- made by thyroid follicular cells
- control metabolism, regulate growth
CONTROL OF THYROID HORMONE SECRETION
- hypothalamus releases TRH (+ve feedback to pituitary to release TSH (-ve feedback) to thyroid to release T3 & T4 to the target tissue
- T3 has negative feedback loop (high T3 = less TSH made)
HOW THYROID HORMONES MADE
- iodine absorbed from bloodstream & concentrated in follicles then thyroperoxidase (TPO) binds iodine to tyrosine residue in thyroglobulin molecules to form MIT & DIT
- MIT + DIT = T3
- DIT + DIT = T4
1. TSH binds to TSH receptor on membrane
2. iodine taken up by Na/I symporter
3. iodination of tyrosyl residues in thyroglobulin by TPO
4. coupling of iodotyrosyl residue by TPO (to make MIT/DIT)
T3/4 RATIO
- these are usually bound to TBG (increase in pregnancy as oestrogen increases TBG so the TSH level will drop)
- T3 is active & we store T4 which we convert to T3 by mono-deiodination
TESTS OF THYROID FUNCTION
- hyperthyroidism = high T3/4 & low TSH
- hypothyroidism = low T3/4 & high TSH
HYPERTHYROIDISM
- caused by external iodine, excess T3/4, TSH secreting pituitary adenoma , neonatal
- symptoms are rapid HR, atrial fibrillation, ankle swelling, short breath
- weight loss, diarrhoea, increased appetite
- main consequences are graves, toxic nodular goitre, thyroiditis
- diagnosed by high T4/3 levels & low TSH & clinical features, measuring TPO antibodies, doing isotope uptake scan (toxic nodular disease is when uptake is only in toxic nodule & not rest of thyroid)
Graves disease
- autoimmune disorder caused by pathogenic antibodies to TSH receptor on thyroid follicular cells
- due to genetic + environmental factors
- no negative feedback as TSH receptor in pituitary is always active so thyroid hormones are always made
- symptoms are eyelid lag, swelling, puffy eye
TREATING HYPERTHYROIDISM
- anti-thyroid drugs (thonamides) inhibit TPO enzyme to block iodine uptake e.g. carbimazole (used to prep patient for treatment, rapid control, well tolerated)
- surgery e.g. thyroidectomy (could lead to hypothyroidism)
- radioactive (131-I) therapy - capsule, one dose cures
HYPOTHYROIDISM
- caused by treatments of hyperthyroidism leading to hypothyroidism, iodine deficiency, Hashimoto thyroiditis
- mainly caused by iodine deficiency (goitre is compensatory mechanism to try to capture as much f little iodine available into thyroid) but we prevent it with supplements
- treated with levothyroxine (if TSH level too low after levothyroxine, the dose is too high)
- leads to slow HR, heart failure, weight gain, vitiligo, depression
HASHIMOTO THYROIDITIS
inflammation of thyroid leads to goitre & swelling & then as this inflammation dies down, there is shrinkage & fibrosis of thyroid so can’t release hormones like normal (less T3/4) (autoimmune thyroiditis)
GOITRE
- enlargement of thyroid gland (more common in F)
- a thyroid nodule is enlarged thyroid gland you can feel as a lump, but when they become visible, it is called a goitre
ASSESSMENT OF THYROID NODULES
- assess thyroid function (check serum TSH levels)
- assess thyroid size (symptoms, CT or MRI)
- assess thyroid pathology by doing fine needle aspiration or radionuclide (nodule that doesn’t take up radioactive substance = cancerous)
ULTRASOUND
guides fine needle aspiration (stick needle in nodule & aspirate cells (withdraw fluid & look for cancer) under ultrasound guidance
THYROID ANATOMY
- in neck, brownish-red, between C5-T1
- R&L lobes united by narrow isthmus & is inferior to thyroid cartilage of larynx
