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Flashcards in thyroid Deck (23):

function of thyroid hormones

- normal growth and development
- maintain metabolic activity and oxygen requirements especially brain
- regulate lipid and carbohydrate metabolism and thus body weight

control of thyroid hormone is by HPA


thyroid anatomy and supply

- consists of 2 lobes connected by the isthmus
- deep to sternohyoid muscle
- anterior to recurrent laryngeal nerve and tracheal cartilage ring 2 & 3
- has ANS innervation
- supplied by superior and inferior thyroid artery



- colloid is made up of thyroglobulin
- Tg is a glycoprotein that stores thyroid hormone
- Tg is a cancer marker (normally circulates in blood in low levels)


follicular epithelium

inactive thyroid = cuboidal
active thyroid = FSH makes cells columnar

produce Tg
closely associated with capillaries


parafollicular cells

- between follicles
- produce calcitonin hormone



- inflammation of thyroid
- increased thyroid hormone in thyroid releases into the blood circulation
- leads to high thyroid function = high Tg in blood


factitious thyrotoxicosis

when patients take thyroid hormones deliberately and subsequently make themselves thyrotoxic
- patients present with weight loss and all typical features of an overactive thyroid
- however, Tg is very low b/c thyroid has gone to sleep


iron deficiency leads to

- compensatory enlargement of thyroid (endemic goitre)

- in pregnancy may lead to fetal thyroid not developing properly and irreversible damage to developing CNS


thyroid hormone synthesis

- 90% thyroid hormone produced in thyroid gland is T4
- most T3 bound to proteins such as thyroid binding globulin and albumin acts as a buffer against acute changes in T4 production and for iodine recycling



drug given to patients with an overactive thyroid hormone

- inhibits peroxidase enzyme, thus reducing iodine uptake into thyroid and decrease thyroid hormone production


thyroid hormone control mechanisms

1. hypothalamus release TRH
2. pituitary release TSH
3. stimulates thyroid gland
4. thyroid produces thyroid hormones (T4 & T3)
-T3 also produced locally at target organs

-T3 & T4 has a negative feedback at hypothalamus and pituitary
-TSH has negative feedback on pituitary


thyrotoxicosis hormones and signs/symptoms

overactive thyroid with high T4/T3 and low TSH

-nervousness, increased sweating
-weight loss
-weakness and tiredness

-skin changes
-eye signs


causes of thyrotoxicosis

1. graves disease
= autoimmune production of an antibody that stimulates TSH receptors

2. multi-nodular goitre
= hyperfunctioning regions of thyroid gland, not suppressed by circulating thyroid hormone

3. thyroiditis
4. drugs
5. toxic nodule


metabolism of thyroid hormone

when T4 is released and reaches target organs (esp liver & kidney) it locally turns into T3. T3 is the form that has metabolic activity in the periphery

thyroid hormone is metabolised, broken down and excreted by liver and kidneys


high T4, low TSH

if high T4 appropriate feedback = less TSH which normally inhibit thyroid with decreased T4

therefore, overactive thyroid causing increased T4 release, with normal pituitary

- in some conditions of pregnancy HCG can be high cause overactivity of thyroid


low T4, high TSH

if low T4 appropriate feedback = more TSH which normally stimulates thyroid with more T4

therefore underactive thyroid causing decreased T4 release, with normal pituitary


thyroid hormone synthesis: iodide 'trapping'

- iodide conc in plasma is extremely low
- iodide is trapped by a sodium-iodide symporter (NIS)
- active transport of 2 Na+ ions results in the entry of 1 iodide molecule against its conc gradient


where is the sodium-iodide symporter found?

-gastric mucosa
-ciliary body eye
-salivary glands
-differentiated thyroid cancer cells


iodide oxidation

oxidation of iodide is catalysed by thyroid peroxidase (TPO)

in the presence of H2O2, TPO iodinates tyrosine residues in Tg

TPO is inhibited by carbimazole


storage and release of thyroid hormone

- large store of thyroid hormone (T4/T3) incorporated into Tg (~50 day supply)

- thyroid hormone release involves endocytosis of Tg (colloid) from follicular space

- endosomes fuse with lysosomes

- degradation of Tg --> T4 or T3 and released

- thyroid gland only place where T4 synthesied but T3 also from peripheral deiodination of T4

- T4 & T3 metabolised by many organs esp liver/kidneys


TSH stimulates what aspects of thyroid hormone synthesis

- increase iodide into follicular lumen

- increased BF

- increased Tg, TPO and H202

- increased endocytosis and degradation of Tg

- increased release of T4


peripheral metabolism of thyroid hormones

T4 is the main thyroid hormone in plasma

T3 is also released from thyroid
-80% is generated by peripheral metabolism from T4 by removal of a single iodine atom


primary hypothyroidism

=hashimotos disease

high TSH, low T4, +ve TPO antibodies

- adult onset slow
- can affect all organ systems
- decrease in energy metabolism e.g. low basal metabolic rate +/- slightly low body temperature
- decreased protein synthesis