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Understand Thyroid – A Functional Myriad, and Clear Skepticism on Hypothyroidism

Dr. K. V. Narasimha Raju & Dr. B. Swapna

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Whether hypothyroidism is due to Endemic Colloid Goiter, Idiopathic Colloid Goiter, Thyroiditis, destruction of the thyroid gland by Irradiation, or Surgical removal of the thyroid gland, the physiologic effects and the clinical presentation are the same.

Clinical Presentation of Hypothyroidism
The clinical manifestations of hypothyroidism include Cretinism and Myxedema. Cretinism refers to hypothyroidism developing in infancy or early childhood. This disorder was formerly fairly common in areas of the world where dietary iodine deficiency is endemic. It has now become much less frequent because of the widespread supplementation of foods with iodine. On rare occasions cretinism may also result from inborn errors in metabolism (e.g., enzyme deficiencies) that interfere with the biosynthesis of normal levels of thyroid hormone (sporadic cretinism).

Clinical features of cretinism include impaired development of the skeletal system and central nervous system, with severe mental retardation, short stature, coarse facial features, a protruding tongue, and umbilical hernia. The severity of the mental impairment in cretinism seems to be directly influenced by the time at which thyroid deficiency occurs in utero. Normally, maternal hormones that are critical to fetal brain development, including T3 and T4, cross the placenta. If there is maternal thyroid deficiency before the development of the fetal thyroid gland, mental retardation is severe. In contrast, reduction in maternal thyroid hormones later in pregnancy, after the fetal thyroid has developed, allows normal brain development.

Hypothyroidism developing in older children and adults results in a condition known as Myxedema, or Gull’s disease. Manifestations of myxedema include generalized apathy and mental sluggishness that in the early stages of disease may mimic depression. Individuals with myxedema are cold intolerant, and often obese. Mucopolysaccharide-rich edema accumulates in skin, subcutaneous tissue, and a number of visceral sites, with resultant broadening and coarsening of facial features, enlargement of the tongue, and deepening of the voice. Bowel motility is decreased, resulting in constipation. Pericardial effusions are common; in later stages the heart is enlarged, and heart failure may supervene.

Laboratory evaluation has a vital role in the diagnosis of suspected hypothyroidism because of the nonspecific nature of symptoms. Measurement of the serum TSH is the most sensitive screening test for this disorder. The serum TSH is increased in primary hypothyroidism because of a loss of feedback inhibition of thyrotropin-releasing hormone (TRH) and TSH production by the hypothalamus and pituitary, respectively. The TSH concentration is not increased in persons with hypothyroidism caused by primary hypothalamic or pituitary disease. Serum T4 is decreased in individuals with hypothyroidism of any origin.

The symptoms of hypothyroidism are often subtle. They are not specific (which means they can mimic the symptoms of many other conditions) and are often attributed to aging. Patients with mild hypothyroidism may have no signs or symptoms. The symptoms generally become more obvious as the condition worsens and the majority of these complaints are related to a metabolic slowing of the body.

Symptoms (Descending Order of Frequency):

  • Tiredness, weakness
  • Dry skin
  • Feeling cold
  • Hair loss
  • Difficulty concentrating and poor memory
  • Constipation
  • Weight gain with poor appetite
  • Dyspnea
  • Hoarse voice
  • Menorrhagia (later oligomenorrhea or amenorrhea)
  • Paresthesia
  • Impaired hearing

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