7.4 Hyperthyroidism
Key Features
Hyperthyroidism is a hypermetabolic condition associated with elevated levels of free T4, free T3, or both.
The incidence of hyperthyroidism is between 0.05 and 1.3%, with most cases consisting of subclinical disease.
It is caused by excess synthesis and secretion of thyroid hormone by the thyroid.
Hyperthyroidism′s causes include diffuse toxic goiter (Graves’ disease), toxic multinodular goiter, and toxic adenoma.
Thyrotoxicosis is the presence of an excess of thyroid hormone (T4 and/or T3) in the body, which may be due to overproduction of thyroid hormone by the thyroid gland, increased release of thyroid hormone in such conditions as thyroiditis, and exogenous ingestion of thyroid hormone preparations. Hyperthyroidism refers to causes of thyrotoxicosis in which the thyroid produces excess thyroid hormone.
Clinical
Signs
Signs include sinus tachycardia, atrial fibrillation, hyperreflexia with rapid relaxation of tendon reflexes, tachycardia, lid lag and stare, hair loss, goiter, warm and moist skin, muscle weakness and wasting, and onycholysis.
Symptoms
Symptoms include fatigue, weakness, heat intolerance, weight loss with increased appetite, palpitations, diarrhea, oligomenorrhea or amenorrhea, insomnia, brittle hair, shakiness, difficulty concentrating, irritability, or emotional lability.
Etiology
The etiology of thyrotoxicosis is broadly divided into two categories:
Hyperthyroidism secondary to increased synthesis of hormone. This condition is associated with high radioactive iodine uptake (RAIU). Causes include:
A. Graves’ disease: the most common cause of hyperthyroidism, discussed more fully later in this chapter
B. Toxic multinodular goiter: arises in the setting of a long-standing multinodular goiter; usually affects patients > 50 years of age; occurs when certain nodules develop autonomous function
C. Toxic adenomas: a single benign thyroid nodule (adenoma) that becomes autonomous
D. Iodine-induced hyperthyroidism: can develop, though uncommonly, after an iodine load, such as following administration of contrast agents used for angiography or CT or iodine-rich drugs such as amiodarone
E. Thyroid-stimulating hormone (TSH)-producing pituitary adenomas
Hyperthyroidism secondary to thyroiditis (with release of preformed hormone into the circulation) or an extrathyroidal source of thyroid hormone. This condition is associated with low RAIU. Causes include:
Thyroiditis: painless and postpartum thyroiditis, subacute painful or de Quervain thyroiditis (see Chapter 7.7)
Exogenous and ectopic: factitious ingestion; excessive thyroid hormone
Graves’ Disease: Key Points
30 cases per 100,000 persons per year
Female/male ratio of 10:1
Peak age of onset 40 to 60 years
Autoimmune condition with TSH-receptor antibodies (TSHR Abs, also called thyroid-stimulating immunoglobulins, or TSIs)
Clinical evidence of Graves’ ophthalmopathy in 25 to 30% of patients with Graves’ disease
The ocular manifestations of thyroid-associated ophthalmopathy include eyelid retraction, proptosis, chemosis, periorbital edema, and altered ocular motility.
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