Monday, May 29, 2017

Hypothyroidism in Adults



Hypothyroidism
, a state of low serum thyroid hormone, results from hypothalamic, pituitary, or thyroid insufficiency. The disorder can progress to life-threatening myxedema coma. Hypothyroidism is more prevalent in women than in men.

Etiology
Hypothyroidism results from inadequate production of thyroid hormone, usually because of dysfunction of the thyroid gland due to surgery (thyroidectomy), radiation therapy (particularly with 131I), inflammation, chronic autoimmune thyroiditis (Hashimoto’s disease) or, rarely, conditions such as amyloidosis and sarcoidosis. It may also result from pituitary failure to produce thyroid-stimulating hormone (TSH), hypothalamic failure to produce thyrotropin-releasing hormone, inborn errors of thyroid hormone synthesis, inability to synthesize thyroid hormone because of iodine deficiency (usually dietary), or the use of antithyroid medications such as propylthiouracil.
In patients with hypothyroidism, infection, exposure to cold, and sedatives may precipitate myxedema coma.

Signs and symptoms:
Typically, the early clinical features of hypothyroidism are vague and may include fatigue, forgetfulness, sensitivity to cold, unexplained weight gain, and constipation. As the disorder progresses, characteristic myxedematous signs and symptoms appear, such as decreasing mental stability; dry, flaky, inelastic skin; puffy face, hands, and feet; hoarseness; periorbital edema; upper eyelid droop; dry, sparse hair; and thick, brittle nails.
Cardiovascular involvement leads to decreased cardiac output, slow pulse rate, signs of poor peripheral circulation and, occasionally, an enlarged heart. 

Other common effects include anorexia, abdominal distention, menorrhagia, decreased libido, infertility, ataxia, and nystagmus. Reflexes show delayed relaxation time (especially in the Achilles tendon).
Progression to myxedema coma is usually gradual, but when stress aggravates severe or prolonged hypothyroidism, coma may develop abruptly. Clinical effects include progressive stupor, hypoventilation, hypoglycemia, hyponatremia, hypotension, and hypothermia.

Diagnosis
:
Radioimmunoassay confirms hypothyroidism with low triiodothyronine (T3) and thyroxine (T4) levels.
Supportive laboratory findings include:
  • increased TSH level when hypothyroidism is due to thyroid insufficiency; 
  • decreased TSH level when hypothyroidism is due to hypothalamic or pituitary insufficiency
  • elevated levels of serum cholesterol, alkaline phosphatase, and triglycerides
  • normocytic, normochromic anemia.
In myxedema coma, laboratory tests may also show low serum sodium levels as well as decreased pH and increased partial pressure of carbon dioxide, indicating respiratory acidosis.

Treatment:
  • Therapy for hypothyroidism consists of gradual thyroid hormone replacement with levothyroxine and, occasionally, liothyronine.
  • During myxedema coma, effective treatment supports vital functions while restoring euthyroidism. To support blood pressure and pulse rate, treatment includes I.V. administration of levothyroxine and hydrocortisone to correct possible pituitary or adrenal insufficiency. 
  • Hypoventilation requires oxygenation and respiratory support.
  • Other supportive measures include fluid replacement and antibiotics for infection.

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