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Hypothyroidism - Causes, Symptoms And Treatment

Alternative names :- Myxedema; Adult hypothyroidism

Hypothyroidism results from hypothalamic, pituitary or thyroid insufficiency or resistance to thyroid hormone. The disorder can progress to life-threatening myxedema coma. Hypothyroidism is more prevalent in women than men; in the United States. the incidence is increasing significantly in people ages 40 to 50. Hypothyroidism occurs primarily after age 40. After age 65, the prevalence increases to as much as 10% in females (3% in males).

The severity of hypothyroidism varies widely. Patients are classified as "subclinical hypothyroid" if diagnostic findings show thyroid hormone abnormalities, but they do not exhibit any symptoms. Others have moderate symptoms that can be mistaken for other diseases and states. Advanced hypothyroidism may cause severe complications, the most serious one of which is myxedema.

What causes Hypothyroidism?

Hypothyroidism may reflect a malfunction of the hypothalamus. pituitary. or thyroid gland. all of which are part of the same negative-feedback mechanism. However, disorders of the hypothalamus and pituitary rarely cause hypothyroidism. Primary hypothyroidism. a disorder of the gland itself, is most common.

Chronic autoimmune thyroiditis. also called chronic lymphocytic thyroiditis, occurs when auto antibodies destroy thyroid gland tissue. Chronic autoimmune thyroiditis associated with goiter is called Hashimoto's thyroiditis. The cause of this autoimmillie process is unknown. Even so, heredity has a role. and specific human leukocyte antigen subtypes are associated with greater risk.

Causes of hypolliyroidism in adults include:

  • inadequate production of thyroid hormone. usually after thyroidectomy or radiation therapy (particularly with radioactive iodine); inflammation; chronic autoimmune thyroiditis (Hashimoto's disease); or such conditions as amyloidosis and arcoidosis (rare)
  • pituitary failure to produce thyroidstimulating hormone (TSH), hypothalamic failure to produce thyroid-releasing hormone (TRH), inborn errors of thyroid hormone synthesis, iodine deficiency (usually dietary), or use of such antithyroid medications as propylthiouracil.

Signs and symptoms of Hypothyroidism

Typical, vague, early clinical features of hypothyroidism include weakness, fatigue, forgetfulness, sensitivity to cold, unexplained weight gain, and constipation. Other signs and symptoms include:

  • characteristic myxedematous signs and symptoms of decreasing mental stability; coarse, dry, flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; uppereyelid droop; dry, sparse hair; and thick, brittle nails (as disorder progresses) .
  • cardiovascular involvement, including decreased cardiac output, slow pulse rate, signs of poor peripheral circulation and, occasionally, an enlarged heart.
  • anorexia, abdominal distention, menorrhagia, decreased libido, infertility, ataxia, and nystagmus; reflexes with delayed relaxation time (especially in the Achilles tendon)
  • progression to myxedema coma, usually gradual but possibly developing abruptly, with stress aggravating severe or prolonged hypothyroidism, including progressive stupor, hypoventilation, hypoglycemia, hyponatremia, hypotension, and hypothermia.

Possible complications of hypothyroidism include:

  • heart failure
  • myxedema coma
  • infection
  • megacolon
  • organic psychosis
  • infertility.
Diagnosis information

Diagnosis of hypothyroidism is based on:

  • radioimmunoassay showing low triiodothyronine (T3) and thyroxine (T4) levels
  • increased TSH level greater than 2.0 for primary hypothyroidism; decreased with hypothalamic or pituitary disorder
  • thyroid panel differentiating primary hypothyroidism (thyroid gland hypofunction), secondary hypothyroidism (pituitary hyposecretion of TSH), tertiary hypothyroidism (hypothalamic hyposecretion of TRH), and euthyroid sick syndrome (impaired peripheral conversion of thyroid hormone due to a suprathyroidal illness such as severe infection) (see Thyroid test results in hypothyroidism)
  • basal body temperature less than 97.8°F (36.6°C) (in women, axillary temperatures taken for 3 days starting in the morning on the second day of menstruation)
  • elevated serum cholesterol, alkaline phosphatase, and triglyceride levels
  • normocytic, normochromic anemia . low serum sodium levels, decreased pH, and increased partial pressure of carbon dioxide, indicating respiratory acidosis (myxedema coma).

Treatment of Hypothyroidism

The purpose of treatment is to replace the deficient thyroid hormone. Levothyroxine is the most commonly used medication. The lowest dose effective in relieving symptoms and normalizing the TSH is used. Life-long therapy is needed. Medication must be continued even when symptoms subside. Thyroid hormone levels should be monitored yearly after a stable dose of medication is determined.

After replacement therapy has begun, report any symptoms of increased thyroid activity ( hyperthyroidism ) such as restlessness, rapid weight loss, and sweating.

Myxedema coma is a medical emergency that occurs when the body's level of thyroid hormones becomes extremely low. It is treated with intravenous thyroid replacement and steroid therapy. Supportive therapy of oxygen, assisted ventilation, fluid replacement, and intensive-care nursing may be indicated.

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HYPOTHYROIDISM IN CHILDREN

A deficiency of thyroid hormone secretion during fetal development and early I infancy results in infantile cretinism (congenital hypothyroidism). Hypothyroidism in infants is seen as respiratory difficulties, cyanosis, persistent jaundice, lethargy, excessive somnolence, large tongue, abdominal distention, poor feeding, abnormal deep tendon reflexes, and hoarse crying. Prompt treatment of hypothyroidism in infants prevents physical and mental retardation.

Older children who suffer from hypothyroidism have similar symptoms to those of adults, plus poor skeletal growth and late epiphyseal maturation and dental development. Sexual maturation may be accelerated in younger children and delayed in older children.

Cretinism is three times more common in girls than boys. Early diagnosis and treatment allow the best prognosis; infants treated before age 3 months usually grow and develop normally. Athyroid children who remain untreated after age 3 months and children with acquired hypothyroidism who remain untreated beyond age 2 years have irreversible mental retardation, although their skeletal abnormalities are reversible with treatment.

Special considerations

  • Prevention, early detection, comprehensive parent teaching, and psychological support are essential. Know the early signs. Be especially wary if parents emphasize how good and how quiet their new baby is
  • Inform parents that the child will require lifelong treatment with thyroid supplements. Stress the need to comply with the treatment regimen to prevent further mental impairment.
  • Provide support to help parents deal with a child who may be mentally retarded. Help them adopt a positive but realistic attitude and focus on their child's strengths rather than her weaknesses. Encourage them to provide stimulating activities to help the child reach her maximal potential. Refer them to appropriate community resources for support.
  • To prevent infantile cretinism, emphasize the importance of adequate nutrition during pregnancy, including iodine­rich foods and the use of iodized salt or, in case of sodium restriction, an iodine supplement.

SPECIAL NEEDS

Watch for hypertension and heart failure in the elderly.

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Special considerations

To manage treatment of the patient with hypothyroidism:

  • Provide a high-bulk, low-calorie diet and encourage activity to combat constipation and promote weight loss. Administer cathartics and stool softeners as needed.
  • Mter thyroid replacement begins, watch for symptoms of hyperthy roidism, such as restlessness, sweating, and excessive weight loss.
  • Tell the patient to report any signs of aggravated cardiovascular disease, such as chest pain and tachycardia.
  • To prevent myxedema coma, tell the patient to continue the course of thyroid medication even if symptoms subside.
  • Warn the patient to report infection immediately and to make sure any physician who prescribes drugs for her knows about the underlying hypothyroidism.

Myxedema coma care Treatment of myxedema coma requires supportive care:

  • Check frequently for signs of decreasing cardiac output (such as decreased urine output).
  • Monitor temperature until stable. Provide extra blankets and clothing and a warm room to compensate for hypothennia. Rapid rewarming may cause vasodilation and vascular collapse.
  • Record intake and output and daily weight. As treatment begins, urine output should increase and body weight decrease; if not, report this immediately.
  • Avoid sedation when possible or reduce dosage because hypothyroidism delays metabolism of many drugs.
  • Maintain a patent I.V. line. Monitor serum electrolyte levels carefully when administering I.V. fluids.
  • Monitor vital signs carefully when administering levothyroxine because rapid correction of hypothyroidism can cause adverse cardiac effects. Report chest pain or tachycardia immediately.
  • Check arterial blood gas values for hypercapnia, metabolic acidosis, and hypoxia to determine whether the patient who's severely myxedematous requires ventilatory assistance.
  • Administer corticosteroids as Ordered.
  • Because myxedema coma may have been precipitated by an infection, check possible sources of the infection, such as blood and urine, and obtain sputum cultures.


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