HYPERTHYROIDISM: CAUSES AND SYMPTOMS

Hyperthyroidism is a hypermetabolic condition caused by excessive production of thyroid hormones. This is also called thyrotoxicosis. The prevalence is low 0.3 to 0.6% in population.

Symptoms: Increase irritability, sweating, palpitation, SOB, loss of weight despite increase appetite (classical feature), increase bowel movement, malabsorption, loss of appetite, etc.

Signs: Tachycardia, tremor, warm and moist peripheries due to increased cutaneous blood flow and sweating, arrhythmias, etc.

CAUSES:
Causes of thyrotoxicosis are divided into two types: (I) those associated with frank hyperthyroidism and increased production and secretion of thyroid hormones from the gland,
and (2) those that are not.

TSH measurement shows suppressed level with highly increased thyroid hormones in all cases (except in pituitary adenomas where TSH is inappropriately secreted). For follow up of treatment measurement of free T4 and T3 should be done with TSH until TSH returns to normal.

Graves ‘disease
There is presence of TSH mimicking autoantibodies to TSH receptor. There is diffused goiter due to thyroid hyperplasia, Opthalmopathy, myxedema and hyperthyroidism. It predominately affects female. There is staring eyes with forward protrusion of eyeball and lid lagging behind globe. During this condition there is long period of hyperthyroidism and again hypothyroidism ensues due to excess damage of thyroid cells. Iodine-131 can be used therapeutically to treat hyperthyroidism due to Graves’ and other thyroid disorders, this radioiodine interferes with Organification of iodine, inhibits thyrocytes replication by inducing radiation damage thus controlling thyroid Overactivity. Male to female ratio is 5:1 in having this disease. Laboratory test shows very high level of T3, T4 with low or undetectable TSH except in those rare conditions where there is TSH secreting pituitary adenoma or pituitary resistance to thyroid hormones. TSH within the euthyroid reference range eliminates the diagnosis of hyperthyroidism. When TSH is low and T4 within normal range T3 should be measured as it is highly increased during Graves’s disease and in multinodular toxic goiter (T3-toxicosis).

Toxic Nodular Goiter (Plummer’s disease)
This occurs by autonomously functioning thyroid tissue without requiring TSH. Here multiple sites within thyroid gland autonomously produce thyroid hormones. The biochemical diagnosis of hyperthyroidism is suppression of TSH but thyroid hormones lies at URL. Radioiodine is the treatment of choice. MNG usually results from a low-grade, probably intermittent stimulus to the thyroid gland from iodine deficiency, goitrogens (foods that induce hypothyroidism and goiter in the diet such as cabbage, broccoli, cauliflower, and brussels sprouts), decreased thyroid hormone production, or an autoimmune disease, which causes multiplication and growth of small groups of thyroid cells.

TSH-secreting pituitary tumour
Rarely adenomas of pituitary gland secreting TSH (TSHomas) may produce hyperthyroidism. There is persistence of TSH secretion despite overproduction of thyroid hormones. There is thyroid gland Overactivity and hyperplasia leading to goiter.

Iodine Induced
In individual with goiter due to previous iodine deficiency, chronic administration of excess iodine in the diet can induce a hyperthyroid state. This phenomenon (sometimes called the Jod-Basedow phenomenon) and occurs in patients who already have pre-existing thyroid autonomy, expression of which may have been masked by lack of iodine.

hCG secreting Trophoblastic tumor
Here hCG functions as TSH since it has common alpha subunit and its receptor and TSH receptor have similar ligand binding domain.

[Amiodarone is anti-arrhythmic drug that contain 1-12 mg iodine, this prevent peripheral conversion of T4 to T3 with increased production of rT3 and it also inhibits both iodine uptake by thyroid and entry of T4 into cells and can cause both iodine induced hypothyroidism and hyperthyroidism]. This is also a wolf chaikof effect. Some develop hyperthyroidism if the medication leads to inflammation of the thyroid gland (subacute thyroiditis) and subsequent leakage of stored thyroid hormone into the circulation.

Subclinical hyperthyroidism
Here TSH is suppressed but normal concentration of T3 and T4, usually in URL.

Hyperthyroidism or NTI
Suppressed TSH but elevated fT4 is common picture but it’s difficult to differentiate whether this is due to NTI or hyperthyroidism. A raised T4 is uncommon in NTI. The typical signs and symptoms of hyperthyroidism are absent in NTI. Laboratory pattern shows low T4 and TSH. Here illness decreases 5’ monodeiodinase activity, less T4 is converted to T3. This leads to decreased T3 but high rT3.