Any enlargement of the thyroid gland is called as a goiter. Terminology related to thyroid disorders is shown in Box 863.1.
Hyperthyroidism is a condition caused by excessive secretion of thyroid hormone. Causes of hyperthyroidism are listed in Table 863.1.
Clinical characteristics of hyperthyroidism are nervousness, anxiety, irritability, insomnia, fine tremors; weight loss despite normal or increased appetite; heat intolerance; increased sweating; dyspnea on exertion; amenorrhea and infertility; palpitations, tachycardia, cardiac arrhythmias, heart failure (especially in elderly); and muscle weakness, proximal myopathy, and osteoporosis (especially in elderly).
The triad of Graves’ disease consists of hyperthyroidism, ophthalmopathy (exophthalmos, lid retraction, lid lag, corneal ulceration, impaired eye muscle function), and dermopathy (pretibial myxoedema).
In most patients, free serum T3 and T4 are elevated. In T3 thyrotoxicosis (5% cases of thyrotoxicosis), serum T4 levels are normal while T3 is elevated. Serum TSH is low or undetectable (< 0.1 mU/L) (Box 863.2).
Undetectable or low serum TSH along with normal levels of T3 and T4 is called as subclinical hyperthyroidism; subtle signs and symptoms of thyrotoxicosis may or may not be present. Subclinical hyperthyroidism is associated with risk of atrial fibrillation, osteoporosis, and progression to overt thyroid disease.
Features of primary and secondary hyperthyroidism are compared in Table 863.2.
|Parameter||Primary hyperthyroidism||Secondary hyperthyroidism|
|1. Serum TSH||Low||Normal or high|
|2. Serum free thyroxine||High||High|
|3. TSH receptor antibodies||May be positive||Negative|
|4. Causes||Graves’ disease, toxic multinodular goiter, toxic adenoma||Pituitary adenoma|
Evaluation of hyperthyroidism is presented in Figure 863.1.
Hypothyroidism is a condition caused by deficiency of thyroid hormones. Causes of hypothyroidism are listed in Table 863.3. Primary hypothyroidism results from deficient thyroid hormone biosynthesis that is not due to disorders of hypothalamus or pituitary. Secondary hypothyroidism results from deficient secretion of TSH from pituitary. Deficient or loss of secretion of thyro-tropin releasing hormone from hypothalamus results in tertiary hypothyroidism. Secondary and tertiary hypothyroidism are much less common than primary. Plasma TSH is high in primary and low in secondary and tertiary hypothyroidism. Differences between primary and secondary hypothyroidism are shown in Table 863.4.
|Parameter||Primary hypothyroidism||Secondary hypothyroidism|
|1. Cause||Hashimoto’s thyroiditis||Pituitary disease|
|2. Serum TSH||High||Low|
|3. Thyrotropin releasing hormone stimulation test||Exaggerated response||No response|
|4. Antimicrosomal antibodies||Present||Absent|
Clinical features of primary hypothyroidism are: lethargy, mild depression, disturbances in menstruation, weight gain, cold intolerance, dry skin, myopathy, constipation, and firm and lobulated thyroid gland (in Hashimoto’s thyroiditis).
In severe cases, myxoedema coma (an advanced stage with stupor, hypoventilation, and hypothermia) can occur.
Laboratory features in hypothyroidism are shown in Box 863.3.
Normal serum thyroxine (T4 and FT4) coupled with a moderately raised TSH (>10 mU/L) is referred to as subclinical hypothyroidism. It is associated with bad obstetrical outcome, poor cognitive development in children, and high risk of hypercholesterolemia and progression to overt hypothyroidism.
Evaluation of hypothyroidism is presented in Figure 863.2