In our last blog we discussed the role of the thyroid and how it produced thyroid hormones
This time we are looking at how this can go wrong; with either overproduction of the thyroid hormones or under production.
This is as the name suggests when there is too much thyroid hormones in the circulation. Typically, this results from thyroid gland hyperactivity, most commonly Graves’ disease, toxic multinodular goitre and toxic adenoma. We looked at the hypothalamic-pituitary-thyroid axis in the last blog; rarely causes of hyperthyroidism can affect this axis; for example, a TSH-producing pituitary tumour.
No matter the cause the symptoms of hyperthyroidism reflect the function of the thyroid hormone, increase metabolism. So, patients with hyperthyroidism present with fatigue, anxiety, heat intolerance, weight loss despite increased appetite, increase perspiration and palpitations.
This is the opposite, there is not enough thyroid hormones being produced. This condition can either be acquired or congenital. If the condition is congenital it is usually the result of dysplasia or aplasia. The cause of acquired hypothyroidism is most commonly autoimmune such as hashimoto’s thyroiditis. The reduction of the hormones causes a reduction of the basal metabolic rate as well as generalized myxedema. This reflects the typical clinical findings or fatigue, cold intolerance, periorbital oedema, constipation and weight gain. Acquired hypothyroidism can either be primary or secondary. Autoimmune comes under the primary bracket as this is an insufficient hormone production due to the thyroid gland itself. Whereas secondary is a pituitary disorder affecting the production of TSH and therefore under stimulating the thyroid to produce thyroid hormones.
Both hypo- and hyperthyroidism can be picked up on blood tests for serum levels of thyroid hormone. In hyperthyroidism the levels of free T4 and T3 are increased and unless due to a TSH secreting tumour the levels of TSH are low, due to the negative feedback system that T3 and T4 have on the pituitary and the hypothalamus. Where as in hypothyroidism the free T3 and T4 would be low. The amount of TSH depends on whether it is a primary or a secondary hypothyroidism; primary there is increased TSH, again due to the negative feedback loop not functioning, whereas secondary hypothyroidism there is a decreased TSH as that is the cause of the reduced T3 and T4. Once the type of hyper/hypothyroidism has been determined, more investigations need to be carried out in order to discover the cause. This includes serum thyroglobulin levels, serum thyroid antibodies such as thyroid peroxidase antibodies (Grave’s/Hashimoto’s disease), ultrasound of the thyroid and iodine uptake studies.
The treatment of hypothyroidism is relatively simple, the thyroid hormones need to be replaced so therefore they are given in tablet form as L-thyroxine which is synthetic T4. This is due to the prolonged half-life of T4 compared to T3. This requires regular follow up checks for TSH and thyroid hormone levels. For hyperthyroidism, symptomatic relief can be achieved through use of beta-blockers such as propranolol, to improve the patient’s tachycardia, high blood pressure and tremors. Anti-thyroid drugs can also be used, such as carbimazole, this is a pro drug that is converted to methimazole after absorption. This inhibits the thyroid peroxidase enzyme that we discussed in the last blog from coupling and iodinating the tyrosine residues on thyroglobulin, therefore inhibiting the production of T3 and T4. Surgery and radioactive iodine ablation are also treatment options, these would then cause the patient to become hypothyroid, so lifelong thyroxine would need to be taken in these cases.