Hyperthyroidism
Hyperthyroidism: Excerpt from Professional Guide to Diseases (Eighth Edition)
Hyperthyroidism (also known as Graves’ disease, Basedow’s disease, or thyrotoxicosis) is a metabolic imbalance that results from thyroid hormone overproduction. The most common form of hyperthyroidism is Graves’disease, which increases thyroxine (T4) production, enlarges the thyroid gland (goiter), and causes multiple system changes.
With treatment, most patients can lead normal lives. However, thyroid storm — an acute exacerbation of hyperthyroidism — is a medical emergency that may lead to life-threatening cardiac, hepatic, or renal failure.
Causes and incidence
Hyperthyroidism may result from both genetic and immunologic factors. An increased incidence of this disorder in monozygotic twins, for example, points to an inherited factor, probably an autosomal recessive gene. This disease occasionally coexists with abnormal iodine metabolism and other endocrine abnormalities, such as diabetes mellitus, hyperparathyroidism, and thyroiditis. Hyperthyroidism is also associated with autoantibody production (thyroid-stimulating immunoglobulin and thyroid-stimulating hormone [TSH]-binding inhibitory immunoglobulin), possibly due to a defect in suppressor–T-lymphocyte function that allows the formation of autoantibodies.
In latent hyperthyroidism, excessive dietary intake of iodine and, possibly, stress can precipitate clinical hyperthyroidism. In a person with inadequately treated hyperthyroidism, stress — including surgery, infection, toxemia of pregnancy, and diabetic ketoacidosis — can precipitate thyroid storm. (See Other forms of hyperthyroidism.)
Incidence of Graves’ disease is highest between ages 30 and 40, especially in people with family histories of thyroid abnormalities; only 5% of hyperthyroid patients are younger than age 15.
Signs and symptoms
The classic features of hyperthyroidism are an enlarged thyroid (goiter), nervousness, heat intolerance, weight loss despite increased appetite, sweating, diarrhea, tremor, and palpitations. Exophthalmos is considered most characteristic but is absent in many patients with hyperthyroidism. Many other symptoms are common because hyperthyroidism profoundly affects virtually every body system:
❑ Central nervous system: difficulty in concentrating because increased T4 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, 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 the elderly); and occasionally, 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: possible anorexia; nausea and vomiting due to increased GI mobility and peristalsis; increased defecation; soft stools or, with severe disease, diarrhea; and liver enlargement
❑ Musculoskeletal system: weakness, fatigue, and muscle atrophy; rare coexistence with myasthenia gravis; generalized or localized paralysis associated with hypokalemia may occur; 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 (from the combined effects of accumulation of mucopolysaccharides and fluids in the retro-orbital 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.
Alert When hyperthyroidism escalates to thyroid storm, these symptoms can be accompanied by extreme irritability, hypertension, tachycardia, vomiting, temperature up to 106° F (41.1° C), delirium, and coma.
Diagnosis
The diagnosis of hyperthyroidism is usually straightforward and depends on a careful clinical history and physical examination, a high index of suspicion, and routine hormone determinations.
Confirming diagnosis The following tests confirm the disorder:
❑ Radioimmunoassay shows increased serum T4 and triiodothyronine (T3) concentrations.
❑ Thyroid scan reveals increased uptake of radioactive iodine (131I). This test is contraindicated if the patient is pregnant.
❑ TSH levels are decreased.
❑ Ultrasonography confirms subclinical ophthalmopathy.
❑ Antithyroglobulin antibody is positive in Grave’s disease.
Treatment
A number of approaches are used to treat hyperthyroidism, primarily antithyroid drugs, 131I, and surgery. Appropriate treatment depends on the size of the goiter, the causes, the patient’s age and parity, and how long surgery will be delayed (if the patient is an appropriate candidate for surgery).
Antithyroid drug therapy is used for children, young adults, pregnant females, and patients who refuse surgery or 131I treatment. Thyroid hormone antagonists are given to block thyroid hormone synthesis. Although hypermetabolic symptoms subside within 4 to 8 weeks after such therapy begins, the patient must continue the medication for 6 months to 2 years, depending on the clinical circumstances. Beta-adrenergic blockers may be given concomitantly to manage tachycardia and other peripheral effects of excessive hypersympathetic activity.
During pregnancy, antithyroid medication should be kept at the minimum dosage required to keep maternal thyroid function within the high-normal range until delivery and to minimize the risk of fetal hypothyroidism — even though most infants of hyperthyroid mothers are born with mild and transient hyperthyroidism. (Neonatal hyperthyroidism may even necessitate treatment with antithyroid medications and propranolol for 2 to 3 months.) Because hyperthyroidism is sometimes exacerbated in the puerperal period, continuous control of maternal thyroid function is essential. Approximately 3 to 6 months postpartum, antithyroid drug administration can be gradually tapered and thyroid function reassessed. The mother receiving low-dose antithyroid treatment may breast-feed as long as the infant’s thyroid function is checked periodically. Small amounts of the drug can be found in breast milk.
A single oral dose of 131I is the treatment of choice for patients not planning to have children. (Patients of reproductive age must not be pregnant and should give informed consent for this treatment because small amounts of 131I concentrate in the gonads. However, there have been no reports of damage to subsequently conceived children in more than 50 years of 131I use.) During treatment with 131I, the thyroid gland picks up the radioactive element as it would regular iodine. Subsequently, the radioactivity destroys some of the cells that normally concentrate iodine and produce T4, thus decreasing thyroid hormone production and normalizing thyroid size and function. In most patients, hypermetabolic symptoms diminish from 6 to 8 weeks after such treatment. However, some patients may require a second dose.
Subtotal (partial) thyroidectomy, which decreases the thyroid gland’s capacity for hormone production, is indicated for patients with a large goiter whose hyperthyroidism has repeatedly relapsed after drug therapy or patients who refuse or aren’t candidates for 131I treatment. Preoperatively, the patient may receive iodides (Lugol’s solution or saturated solution of potassium iodide), antithyroid drugs, or high doses of propranolol, to help prevent thyroid storm. If euthyroidism isn’t achieved, surgery should be delayed and propranolol administered to decrease the systemic effects (cardiac arrhythmias) caused by hyperthyroidism. After ablative treatment with 131I or surgery, patients require regular medical supervision for the rest of their lives because they usually develop hypothyroidism, sometimes as long as several years after treatment.
Therapy for hyperthyroid ophthalmopathy includes local applications of topical medications but may require high doses of corticosteroids. A patient with severe exophthalmos that causes pressure on the optic nerve may require external beam radiation therapy or surgical decompression to lessen pressure on the orbital contents.
Treatment of thyroid storm includes administration of an antithyroid drug, propranolol I.V. to block sympathetic effects, a corticosteroid to inhibit the conversion of T4 to T3 and to replace depleted cortisol levels, and an iodide to block the release of thyroid hormone. Supportive measures include administration of nutrients, vitamins, fluids, and sedatives.
Special considerations
Patients with hyperthyroidism require vigilant care to prevent acute exacerbations and complications.
❑ Record vital signs and weight.
❑ Monitor serum electrolyte levels, and check periodically for hyperglycemia and glycosuria.
❑ Carefully monitor cardiac function if the patient is elderly or has coronary artery disease. If the heart rate is more than 100 beats/minute, check blood pressure and pulse rate often.
❑ Check level of consciousness and urine output.
Alert If the patient is pregnant, tell her to watch closely during the first trimester for signs of spontaneous abortion and to report such signs immediately.
❑ Encourage bed rest, and keep the patient’s room cool, quiet, and dark. The patient with dyspnea will be most comfortable sitting upright or in high Fowler’s position.
❑ Remember, extreme nervousness may produce bizarre behavior. Reassure the patient and his family that such behavior will probably subside with treatment. Provide sedatives as necessary.
❑ To promote weight gain, provide a balanced diet, with six meals a day. If the patient has edema, suggest a low-sodium diet.
❑ If iodide is part of the treatment, mix it with milk, juice, or water to prevent GI distress, and administer it through a straw to prevent tooth discoloration.
Alert Watch for signs of thyroid storm, such as tachycardia, hyperkinesis, fever, vomiting, and hypertension.
❑ Check intake and output carefully to ensure adequate hydration and fluid balance.
❑ Closely monitor blood pressure, cardiac rate and rhythm, and temperature. If the patient has a high fever, reduce it with appropriate hypothermic measures. Maintain an I.V. line and give drugs, as ordered.
❑ If the patient has exophthalmos or other ophthalmopathy, suggest sunglasses or eye patches to protect his eyes from light. Moisten the conjunctivae often with isotonic eye drops. Warn the patient with severe lid retraction to avoid sudden physical movements that might cause the lid to slip behind the eyeball. He should avoid cigarette smoke.
❑ Avoid excessive palpation of the thyroid to avoid precipitating thyroid storm.
Thyroidectomy necessitates meticulous postoperative care to prevent complications:
❑ Watch for evidence of hemorrhage into the neck, such as a tight dressing with no blood on it. Change dressings and perform wound care, as ordered; check the back of the dressing for drainage. Keep the patient in semi-Fowler’s position, and support his head and neck with sandbags to ease tension on the incision.
❑ Check for dysphagia or hoarseness from possible laryngeal nerve injury.
❑ Watch for signs of hypoparathyroidism (tetany, numbness), a complication that results from accidental removal of the parathyroid glands during surgery.
❑ Stress the importance of regular medical follow-up after discharge because hypothyroidism may develop from 2 to 4 weeks postoperatively.
Alert Check often for respiratory distress, and keep a tracheotomy tray at bedside.
Drug therapy and 131I therapy require careful monitoring and comprehensive patient teaching:
❑ After 131I therapy, tell the patient not to expectorate or cough freely because his saliva will be radioactive for 24 hours. Stress the need for repeated measurement of serum T4 levels.
❑ If the patient is taking propylthiouracil and methimazole, monitor complete blood count periodically to detect leukopenia, thrombocytopenia, and agranulocytosis. Instruct him to take these medications with meals to minimize GI distress and to avoid over-the-counter cough preparations because many contain iodine.
❑ Tell him to report fever, enlarged cervical lymph nodes, sore throat, mouth sores, and other signs of blood dyscrasias and any rash or skin eruptions — signs of hypersensitivity.
❑ Watch the patient taking propranolol for signs of hypotension (dizziness, decreased urine output). Tell him to rise slowly after sitting or lying down to prevent orthostatic syncope.
❑ Instruct the patient receiving antithyroid drugs or 131I therapy to report any symptoms of hypothyroidism.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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