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Thyrotoxicosis is a metabolic imbalance that results from thyroid hormone overproduction or thyroid hormone overrelease from the gland. The most common form of thyrotoxicosis is Graves’ disease, which increases thyroxine production, enlarges the thyroid gland (goiter), and causes multiple system changes. (See Other forms of thyrotoxicosis.) Its incidence is highest between ages 30 and 40, especially in people with family histories of thyroid abnormalities.
With treatment, most patients can lead normal lives. However, thyroid storm—an acute, severe exacerbation of thyrotoxicosis—is a medical emergency that may lead to life-threatening cardiac, hepatic, or renal consequences.
Thyrotoxicosis may result from genetic and immunologic factors.
An increased incidence of this disorder in monozygotic twins points to an inherited factor, probably an autosomal recessive gene.
This disease occasionally coexists with other endocrine abnormalities, such as diabetes mellitus, thyroiditis, and hyperparathyroidism.
Thyrotoxicosis may also be caused by the production of autoantibodies (thyroid-stimulating immunoglobulin and thyroid-stimulating hormone [TSH]-binding inhibitory immuno-globulin), possibly because of a defect in suppressor-T-lymphocyte function that allows the formation of autoantibodies.
In latent thyrotoxicosis, excessive dietary intake of iodine and, possibly, stress can precipitate clinical thyrotoxicosis.
In a person with inadequately treated thyrotoxicosis, stress—including surgery, infection, toxemia of pregnancy, and diabetic ketoacidosis—can precipitate thyroid storm.
Signs and symptoms
The classic features of Graves’ disease are an enlarged thyroid (goiter), nervousness, heat intolerance, weight loss despite increased appetite, sweating, frequent bowel movements, tremor, and palpitations. Exophthalmos is considered most characteristic but is absent in many patients with thyrotoxicosis.
Many other signs and symptoms are common because thyrotoxicosis profoundly affects virtually every body system:
Central nervous system: difficulty in concentrating because increased thyroxine secretion accelerates cerebral function; excitability or nervousness due to increased basal metabolic rate; fine tremor, shaky handwriting, and clumsiness from increased activity in the spinal cord area that controls muscle tone; emotional instability and mood swings, ranging from occasional outbursts to overt psychosis
Skin, hair, and nails: smooth, warm, flushed skin (patient sleeps with minimal covers and little clothing); fine, soft hair; premature graying and increased hair loss in both sexes; friable nails and onycholysis (distal nail separated
from the bed); pretibial myxedema (dermopathy), producing thickened skin; and accentuated hair follicles, raised red patches of skin that are itchy and sometimes painful, with occasional nodule formation. Microscopic examination shows increased mucin deposits.
Cardiovascular system: tachycardia; full, bounding pulse; wide pulse pressure; cardiomegaly; increased cardiac output and blood volume; visible point of maximal impulse; paroxysmal supraventricular tachycardia and atrial fibrillation (especially in elderly people); and, occasionally, a systolic murmur at the left sternal border
Respiratory system: dyspnea on exertion and at rest, possibly from cardiac decompensation and increased cellular oxygen utilization
GI system: excessive oral intake with weight loss; nausea and vomiting due to increased GI motility and peristalsis; increased defecation; soft stools or, with severe disease, diarrhea; and liver enlargement
Musculoskeletal system: weakness (especially in proximal muscles), fatigue, and muscle atrophy; rare coexistence with myasthenia gravis; possibly generalized or localized paralysis associated with hypokalemia; and occasional acropachy (soft-tissue swelling, accompanied
by underlying bone changes where new bone formation occurs)
Reproductive system: in females, oligomenorrhea or amenorrhea, decreased fertility, higher incidence of spontaneous abortions; in males, gynecomastia due to increased estrogen levels; in both sexes, diminished libido
Eyes: exophthalmos (produced by the combined effects of accumulation of mucopolysaccharides and fluids in the retroorbital tissues that force the eyeball outward, and of lid retraction that produces the characteristic staring gaze); occasional inflammation of conjunctivae, corneas, or eye muscles; diplopia; and increased tearing.
Other forms of thyrotoxicosis
Varied forms of thyrotoxicosis may include the following.
This small, benign nodule in the thyroid gland that secretes thyroid hormone is a common cause of thyrotoxicosis. The cause of toxic adenoma is unknown. Clinical effects are essentially similar to those of Graves’ disease, except that toxic adenoma doesn’t induce ophthalmopathy, pretibial myxedema, or acropachy.
Presence of adenoma is confirmed by iodine 131 (131I) uptake and a thyroid scan, which show a single hyperfunctioning nodule suppressing the rest of the gland. Treatment includes 131I therapy or surgery to remove adenoma after antithyroid drugs achieve a euthyroid state.
Toxic multinodular goiter
Common in the elderly, this form of thyrotoxicosis involves overproduction of thyroid hormone by one or more autonomously functioning nodules within a diffusely enlarged gland.
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