WHAT ARE THYROID DISORDERS?

WHAT ARE THYROID DISORDERS?

  1. 1
    WHAT IS THE MEANING OF THYROID DISORDERS?
    • Thyroid disorders involve thyroid hormone production or secretion and result in alterations in metabolic stability.
  2. 2
    WHAT ARE THE CAUSES OF THYROID DISORDERS?
    • Thyroid hormones: thyroxine (T4) and triiodothyronine (T3) are formed on thyroglobulin, a large glycoprotein synthesised within the thyroid cell. Inorganic iodide enters the thyroid follicular cell and is oxidised by thyroid peroxidase and covalently bound (organised) to tyrosine residues of thyroglobulin.
    • Iodinated tyrosine residues monoiodotyrosine (MIT) and diiodotyrosine (DIT) combine (couple) to form iodothyronines in reactions catalysed by thyroid peroxidase. Thus, two molecules of DIT combine to form T4, and MIT and DIT join to form T3.
    • Proteolysis within thyroid cells releases thyroid hormone into the bloodstream. T4 and T3 are transported by thyroid-binding globulin (TBG), transthyretin, and albumin. Only the unbound (free) thyroid hormone can diffuse into cells, elicit biologic effects, and regulate thyroid-stimulating hormone (TSH) secretion from the pituitary.
    • T4 is secreted solely from the thyroid, but less than 20% of T3 is produced there; most T3 is formed from the breakdown of T4 catalysed by the enzyme 5′-monodeiodinase in peripheral tissues. T3 is five times more active than T4. T4 may also be acted on by 5′-monodeiodinase to form reverse T3, which has no significant biologic activity.
    • Thyroid hormone production is regulated by TSH secreted by the anterior pituitary, which in turn is under negative feedback control by the circulating level of free thyroid hormone and the positive influence of hypothalamic thyrotropin-releasing hormone (TRH). Thyroid hormone production is also regulated by extrathyroidal deiodination of T4 to T3, which can be affected by nutrition, nonthyroidal hormones, drugs, and illness.
  3. 3
    WHAT ARE THE SIGNS AND SYMPTOMS OF THYROID DISORDERS?
    • Symptoms of thyrotoxicosis include nervousness, anxiety, palpitations, emotional lability, easy fatigability, heat intolerance, weight loss concurrent with increased appetite, increased frequency of bowel movements, proximal muscle weakness (noted on climbing stairs or arising from a sitting position), and scanty or irregular menses in women.
    • Physical signs include warm, smooth, moist skin, and unusually fine hair; separation of the ends of the fingernails from the nail beds (onycholysis); retraction of the eyelids and lagging of the upper lid behind the globe upon downward gaze (lid lag); tachycardia at rest, widened pulse pressure, and systolic ejection murmur; occasional gynecomastia in men; fine tremor of the protruded tongue and outstretched hands; and hyperactive deep tendon reflexes. Thyromegaly is usually present.
    • Graves’ disease is manifested by hyperthyroidism, diffuse thyroid enlargement, and extrathyroidal findings of exophthalmos, pretibial myxedema, and thyroid acropachy. In severe disease, a thrill may be felt, and a systolic bruit may be heard over the gland.
    • In subacute thyroiditis, patients have severe pain in the thyroid region, which often extends to the ear. Systemic symptoms include fever, malaise, myalgia, and signs and symptoms of thyrotoxicosis. The thyroid gland is firm and exquisitely tender on physical examination.
    • Painless thyroiditis has a triphasic course that mimics painful subacute thyroiditis. Most patients present with mild thyrotoxic symptoms; lid retraction and lid lag are present, but exophthalmos is absent. The thyroid gland may be diffusely enlarged without tenderness.
    • Thyroid storm is a life-threatening medical emergency characterised by decompensated thyrotoxicosis, high fever (often   >39.4°C   [103°F]), tachycardia, tachypnea, dehydration, delirium, coma, nausea, vomiting, and diarrhoea. Precipitating factors include infection, trauma, surgery, radioactive iodine (RAI) treatment, and withdrawal from antithyroid drugs.
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