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Akshaya Rajangam

ME06, 1400829


In Course Assessment – Scenario 16
1. Mrs D’s thyroid function tests show elevated T3 and T4 levels, indicating thyrotoxicosis.
Her TSH levels are suppressed, indicating normal anterior pituitary function and normal
negative feedback system. Hence, I would infer that she has primary hyperthyroidism.
Between Graves’ disease and toxic nodular goitre, I would eliminate the possibility of the
latter due to the presence of raised TSH receptor antibodies. Therefore, the likely
diagnosis is Graves’ disease.
Graves’ disease is an autoimmune condition. The TSH-receptor antibodies bind to the
receptor, causing excess secretion of thyroxine through prolonged stimulation and
swelling of the thyroid gland. The exact mechanism behind this phenomenon is
I will not be fully certain of the diagnosis because exophthalmos, a distinct sign of
Graves’ disease, is not observed in Mrs D’s clinical examination. I will also like to analyse
the results of her radioactive iodine test to confirm the diagnosis. In Graves’ disease, the
results will show high uptake of iodine into the thyroid gland.
Mrs D may complain of other symptoms like weight loss, increased appetite,
palpitations and tremors.
2. Anxiety: Thyroxine influences cognitive function in maintaining attention and mood by
enhancing the responsiveness of the sympathetic nervous system. Thyrotoxicosis can
hyper-activate this system, causing anxiety.
Heat intolerance: Thyroid hormones increase basal metabolic rate by increasing the
transcription of genes encoding for mitochondrial uncoupling proteins. There is also
increased heat production and sweating. In thyrotoxicosis, excess heat production
coupled with increased sweating contributes to heat intolerance.
a. Iodide is transported into the follicular cells via the sodium-iodide symporter on the
basolateral surface.
b. Thyroglobulin, a large protein containing rich tyrosine residues, is synthesised in the
follicular cells. Upon completion, it is secreted into a pool of colloid in the lumen.
c. Pendrin, a sodium-independent symporter, transports iodide from the apical surface
into the colloid.

an enzyme found in the luminal end of the follicular cells. releasing T3 and T4. Lysosomes fuse with the vesicle to cleave the thyroglobulin. These lipid-soluble hormones diffuse out of the cell into the bloodstream.Akshaya Rajangam ME06. resulting in hypothyroidism. This is reflected in her thyroid function test. The structure of radioactive iodide resembles normal iodide. Once bound to this G-protein coupled receptor. The iodinated tyrosine residues can combine in pairs to form tri-iodothyronine (T3) or tetra-iodothyronine (T4). so up to 90% of the radioiodine is absorbed by thyroid follicular cells. h. subsequent second messenger activation of cAMP and Protein Kinase A lead to a variety of intracellular responses. reducing the conversion from T4 to T3. so the reserve has to be exhausted before any changes are seen. . the iodide starts to decay. TSH released from the anterior pituitary acts on a TSH receptor found on the apical surface of the follicular cells. 4. Once formed. However. Thyroxine peroxidase (TPO). storage reserve. 1400829 2 d. e. I would also assume that Mrs D was given beta blockers like propranolol to provide symptomatic relief from the enhanced sympathetic nervous response. I believe that Mrs D was most likely on Propylthiouracil. Furthermore. there is a large storage of iodinated thyroglobulin. Propylthiouracil also inhibits 5’-deiodinase in the periphery. forming a vesicle. This effectively destroys the thyroid tissue painlessly over several weeks. Propylthiouracil. This results in the loss of thyroxine synthesis. inhibits tyrosine peroxidase (TPO). preventing the addition of oxidised iodide to tyrosine residues. an anti-thyroid medication. i. Once inside the cell. g. oxidises iodide to iodine and adds the iodine to tyrosine residues in thyroglobulin. where they act on various tissues in the body. This forms mono-iodotyrosine (addition of one iodine) or diiodotyrosine (addition of two iodines). which shows a larger T4/T3 ratio of 10. emitting beta radiation from its nuclei in high concentrations. the radioiodine cannot distinguish between normal and hyperactive thyroid tissue. these hormones remain in the colloid as f. 5. The most immediate response is the endocytosis of iodinated thyroglobulin back into the follicular cell. The effects of the treatment are not seen rapidly because of the long half-life of thyroxine.

Akshaya Rajangam ME06. 1400829 3 .