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Hyperthyroidism - Causes, Symptoms And Treatment

Alternative names :- Thyrotoxicosis; Overactive thyroid

Hyperthyroidism (also known as Graves' disease, von 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, if left untreated. hyperthyroidism may lead to a thyroid storm - an acute exacerbation of hyperthyroidism that constitutes a medical emergency that can lead to life threatening cardiac, hepatic, or renal failure.

Incidence of Graves' disease is highest between ages 30 and 40, especially in a patient with a family history of thyroid abnormalities. However, it may occur in young children and adolescents as well. It's more prevalent in women than in men by an 8 to 1 ratio.

What causes Hyperthyroidism ?

Although the exact mechanism of hyperthyroidism isn't understood, it has a hereditary component and is usually associated with other autoimmune endocrinopathies.

Graves' disease is an autoimmune disorder characterized by the production of auto antibodies that attach to and then stimulate thyroidstimulating hormone (TSH) receptors on the thyroid gland. A goiter is an enlarged thyroid gland, either the result of increased stimulation or a response to increased metabolic demand. Goiter occurs in iodine-deficient areas of the world, where the incidence increases during puberty (a time of increased metabolic demand). These goiters commonly regress to normal size after puberty in males, but not in females. The cause of sporadic goiter in non-iodine-deficient areas is unknown. Endemic and sporadic goiters are nontoxic and may be diffuse or nodular. Toxic goiters may be uninodular or multinodular and may secrete excess thyroid hormone.

Pituitary tumors with TSH producing cells are rare, as is hypothalamic disease causing thyroid releasing hormone (TRH) excess, thyrotoxicosis may result from both genetic and immunologic factors including:

  • increased incidence in monozygotic twins, pointing to an inherited factor, probably an autosomal recessive gene
  • occasional coexistence with other endocrine abnormalities, such as type 1 diabetes mellitus, thyroiditis, and hyperparathyroidism
  • defect in suppressor T-lymphocyte function permitting production of autoantibodies (thyroid-stimulating immunoglobulin and TSH-binding inhibitory immunoglobulin)
  • clinical thyrotoxicosis precipitated by excessive dietary intake of iodine or, possibly, stress (patients with latent disease)
  • stress, such as surgery, infection. toxemia of pregnancy, or diabetic ketoacidosis, can precipitate thyroid storm (inadequately treated thyrotoxicosis)
  • medications, such as lithium and amiodarone
  • toxic nodules or tumors

Signs and symptoms of Hyperthyroidism

Signs and symptoms of hyperthyroidism include:

  • enlarged thyroid (goiter)
  • nervousness
  • heat intolerance and sweating
  • weight loss despite increased appetite
  • frequent bowel movements
  • tremor and palpitations
  • exophthalmos (characteristic, but absent in many patients with thyrotoxicosis).

Because thyrotoxicosis profoundly affects virtually every body system, other common signs and symptoms include:

  • central nervous system difficulty concentrating due to accelerated cerebral function; excitability or nervousness caused by increased basal metabolic rate from T 4; 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 (central nervous system)
  • integumentary system - moist. smooth, warm, flushed skin (patient sleeps with minimal covers and little clothing); fine, soft hair; premature patchy graying and increased hair loss in both sexes; friable nails and onycholysis (distal nail separated from the bed); pretibial inyxedema (non pitting edema of the anterior surface of the legs, dermopathy), producing thickened skin; accentuated hair follicles; sometimes itchy or painful raised red patches of skin with occasional nodule formation; microscopic examination showing increased mucin deposits (skin, hair, and nails)
  • cardiovascular system - systolic hypertension; tachycardia; full, bounding pulse; wide pulse pressure; cardiomegaly; increased cardiac output and blood volume; visible point of maximal impulse; paroxysmal supra ventricular tachycardia and atrial fibrillation (especially in elderly people); and occasional systolic murmur at the left sternal border
  • respiratory system - increased respiratory rate and dyspnea on exertion and at rest, possibly due to cardiac decompensation and increased cellular oxygen use
  • gastrointestinal system excessive oral intake with weight loss; nausea and vomiting due to increased GI motility and peristalsis; increased defecation; soft stools or, in severe disease, diarrhea; liver enlargement
  • musculoskeletal system - weakness, fatigue, and muscle atrophy; coexistence with myasthenia gravis (rare); possibly generalized or localized paralysis associated with hypokalemia; and, rarely, acropachy (soft-tissue swelling accompanied by underlying bone changes where new bone formation occurs)
  • reproductive system - oligomenorrhea or amenorrhea, decreased fertility, increased incidence of spontaneous abortion (females), gynecomastia due to increased estrogen levels (males), diminished libido (both sexes)
  • special sensory organs - exophthalmos due to combined effects of accumulated mucopolysaccharides and fluids in the retro-orbital tissues of the eyes, forcing the eyeball outward and causing lid retraction, thereby producing a characteristic staring gaze; occasional inflammation of conjunctivae, corneas, or eye muscles; diplopia; and increased tearing.

When thyrotoxicosis escalates to thyroid storm, a life-threatening medical emergency, possible symptoms include:

  • high fever, possibly up to 106° F (41.1° C)
  • tachycardia, pulmonary edema, hypertension, shock
  • tremors, emotional liability, extreme irritability, confusion, delirium, psychosis, apathy, stupor, coma
  • diarrhea, abdominal pain, nausea and vomiting, jaundice, hyperglycemia.

Possible complications of hyperthyroidism include:

  • muscle wasting, atrophy, and paralysis
  • visual loss or diplopia
  • heart failure, arrhytlmias
  • hypoparathyroidism after surgical removal of thyroid
  • hypothyroidism after radioiodine treatment.
Diagnosis information

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. These tests confirm the disorder:

  • Radioimmunoassay shows increased serum T 4 and triiodothyronine (T 3) concentrations.
  • Thyroid scan reveals increased uptake of radioactive iodine (1311). This test is contraindicated if the patient is pregnant.
  • TSH levels are decreased.
  • TRH stimulation test indicates hyperthyroidism if the TSH level fails to rise within 30 minutes after the administration of TRH.
  • Ultrasonography confirms subclinicalophthalmopathy.

Treatment of Hyperthyroidism

The primary forms of therapy include:

  • antithyroid drugs
  • single oral dose of 131
  • surgery.

Appropriate treatment depends on:

  • severity of thyrotoxicosis
  • causes
  • patient age and parity
  • how long surgery will be delayed (if the patient is an appropriate candidate for surgery).

Antithyroid therapy includes antithyroid drugs for children, young adults, pregnant women, and patients who refuse surgery or 131 I treatment. Antithyroid drugs are preferred in patients with new-onset Graves' disease because of spontaneous remission in many of these patients; they're also used to correct the thyrotoxic state in preparation for 131I treatment or surgery. Treatment options include:

  • thyroid hormone antagonists, including propylthiouracil (PTU) and methimazole (Tapazole), to block thyroid hormone synthesis (Hypermetabolic symptoms subside within 4 to 8 weeks after therapy begins, but remission of Graves' disease requires continued therapy for 6 months to 2 years.)
  • propranolol (lnderal) until antithyroid drugs reach their full effect, to manage tachycardia and other peripheral effects of excessive hypersympathetic activity resulting from blocking the conversion of t4 to the active T3 hormone
  • minimum dosage needed to keep maternal thyroid function within the high-normal range until delivery, and to minimize the risk of fetal hypothyroidism, with PTU as the preferred agent (during pregnancy)
  • possibly antithyroid medications and propranolol for neonates for 2 to 3 months because most infants of hyperthyroid mothers are born with mild and transient thyrotoxicosis (neonatal thyrotoxicosis) caused by placental transfer of thyroid stimulating immunoglobulins
  • continuous control of maternal thyroid function because thyrotoxicosis is sometimes exacerbated in the puerperal period; antithyroid drugs gradually tapered and thyroid function reassessed after 3 to 6 months postpartum
  • periodic checks of infant's thyroid function with a breast-feeding mother on low-dose antithyroid treatment due to the possible presence of small amounts of the drug in breast milk, which can rapidly lead to thyrotoxicity in the neonate
  • single oral dose of 1311 (radioiodine ablation), the treatment of choice for patients not planning to have children (pregnancy is the sole contraindication for this treatment). (Patients of reproductive age must give informed consent for this treatment because 131 concentrates in the gonads.)

During treatment with 131 I. the thyroid gland picks up the radioactive element as it would regular iodine. The radioactivity destroys some of the cells that normally concentrate iodine and produce T 4' thus decreasing thyroid hormone production and normalizing thyroid size and function.

In most patients, hypermetabolic symptoms diminish 6 to 8 weeks after such treatment (although some patients may require a second dose). However, a major and very common adverse effect of 131 is hypothyroidism. In fact, most patients become hypothyroid, either immediately after treatment or shortly thereafter. These patients should expect lifelong thyroid replacement treatment with T4 (thyroxine [Synthroid]).

Surgical treatment of hyperthyroidism involves subtotal thyroidectomy to decrease the thyroid gland's capacity for hormone production (in patients who refuse or aren't candidates for 131 treatment). Treatment before and after surgery includes:

  • iodides (Lugol's solution or saturated solution of potassium iodide), antithyroid drugs, and propranolol to relieve hyperthyroidism preoperatively (if patient doesn't become euthyroid, surgery should be delayed, and antithyroid drugs and propranolol given to decrease the systemic effects [cardiac arrhythmias] of thyrotoxicosis)
  • lifelong regular medical supervision because most patients become hypothyroid, sometimes as long as several years after surgery.

Treatment of ophthalmopathy includes:

  • local application of topical medications such as prednisone acetate suspension or, possibly, high doses of corticosteroids
  • calcium channel blockers, such as diltiazem and verapamil, to block the peripheral effects of thyroid hormones
  • external-beam radiation therapy or surgical decompression (for severe ex0phthalmos causing pressure on the optic nerve and orbital contents).

Emergency treatment of thyroid storm includes:

  • antithyroid drug to stop conversion of T4 to T3 and to block sympathetic effect; corticosteroids to inhibit the conversion of T4 to T3: and iodide to block the release of thyroid hormone
  • supportive measures, including the administration of nutrients, vitamins, fluids, oxygen, hypothermia blankets, 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 her heart rate is more than 100 beats/minute. check blood pressure and pulse rate often.
  • Check level of consciousness and urine output.
  • If the patient is pregnant. tell her to watch closely for signs of spontaneous abortion during the first trimester and 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 family that such behavior will probably subside with treatment. Provide sedatives. as necessary.
  • To promote weight gain. provide a balanced diet with six meals per 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.
  • Watch for signs of thyroid storm (tachycardia, hyperkinesis, fever, vomiting, 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 l.V.line and give drugs. as ordered.
  • If the patient has exophthalmos or another ophthalmopathy. suggest sunglasses or eye patches to protect her 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.
  • Avoid excessive palpation of the thyroid to avoid precipitating thyroid storm.

Postoperative care

Thyroidectomy necessitates meticulous postoperative care to prevent complications:

  • Check often for respiratory distress. and keep a tracheotomy tray at the bedside.
  • 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 her 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 hypo para thyroidism (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 2 to 4 weeks postoperatively.

Drug therapy monitoring

Drug therapy and 131 therapy require careful monitoring and comprehensive patient teaching:

  • After 131 therapy. tell the patient not to expectorate or cough freely because her 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 her to lake these medications with meals to minimize GI distress and avoid over the-counter cough preparations because many contain iodine.
  • Tell her to report fever. enlarged cervicallymph 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 her 10 rise slowly after sitting or lying down to prevent orthostatic syncope.
  • Instruct the patient receiving antithyroid drugs or 131 therapy to report any symptoms of hypothyroidism.

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