Hypothyroidism refers to the exposure of body tissues to a subnormal amount of thyroid hormone. This can re-sult from a defect anywhere in the HPTA. As a conse-quence of the lack of thyroid hormone, a wide variety of physiological and clinical disturbances involving virtu-ally every organ system may result.
Primary hypothyroidism results from an inability of the thyroid gland itself to produce and secrete sufficient quantities of T4 and T3 and accounts for most cases of hypothyroidism. In iodine-sufficient areas of the world, the most common cause of primary hypothyroidism is chronic autoimmune thyroiditis (Hashimoto’s thyroidi-tis). Other causes of primary hypothyroidism include spontaneous degeneration of glandular tissue (idio-pathic hypothyroidism), thyroid ablation with radioac-tive iodine uptake (131I), and total or subtotal surgical thyroidectomy. Primary hypothyroidism is accompa-nied by an elevation in pituitary TSH secretion and cir-culating TSH levels. An enlargement of the thyroid, or goiter, usually develops with increasing duration of the primary hypothyroidism.
Biosynthetic defects in thyroid hormonogenesis may also result in an inability of the thyroid gland to produce sufficient hormone and may be due to inherited enzy-matic deficiencies or the ingestion of natural or thera-peutically administered antithyroid agents. An example in the latter category is lithium, widely used to treat psy-chiatric disorders and associated with the development of hypothyroidism and goiter. It is concentrated by the thyroid, where it inhibits thyroidal I- uptake, incorporation of I- into Tg, coupling of iodotyrosine, and, eventu-ally, thyroid hormone secretion.
Secondary hypothyroidism, or pituitary hypothy-roidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less com-mon than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tu-mor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In sec-ondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to syn-thesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration.
Tertiary hypothyroidism, or hypothalamic hypothy-roidism, results from impaired TRH stimulation of pitu-itary TSH. This may be due to a disorder that damages the hypothalamus or interferes with hypothalamic– pituitary portal blood flow, thereby preventing delivery of TRH to the pituitary. Tumors, trauma, radiation ther-apy, or infiltrative disease of the hypothalamus can cause such damage. This relatively rare form of hy-pothyroidism is also characterized by inappropriately low levels of serum TSH.
During the perinatal period, there is an absolute re-quirement for thyroid hormone for the development and maturation of the nervous and musculoskeletal sys-tems. In the perinatal nervous system, thyroid hormone plays a critical role in normal growth of the cerebral and cerebellar cortices, the proliferation of axons, the branching of dendrites, synaptogenesis, myelination, cell migration, and so on.
Thyroid hormone also plays a major role in the mat-uration of bone. A deficiency of thyroid hormone in early life leads to both delay in and abnormal develop-ment of epiphyseal centers of ossification (epiphyseal dysgenesis). Hypothyroidism-induced impairment of linear growth can lead to dwarfism in which the limbs are disproportionately short in relation to the trunk with the apparent bone age retarded in relation to chronological age.
The hallmarks of infantile hypothyroidism (e.g., re-tardation of mental development and growth) become manifest only in later infancy and are largely irre-versible. Consequently, early recognition and initiation of replacement therapy are crucial. In the absence of thyroid hormone therapy, the symptoms of infantile hy-pothyroidism include feeding problems, failure to thrive, constipation, a hoarse cry, and somnolence. In succeeding months, especially in severe cases, protuber-ance of the abdomen, dry skin, poor growth of hair and nails, delayed eruption of the deciduous teeth, and de-lay in reaching the normal milestones of development (e.g., holding up the head, sitting, walking, and talking) become evident.
In adults, the signs and symptoms of hypothyroidism include somnolence, slow mentation, dryness and loss of hair, increased fluid in body cavities (e.g., the pericardial sac), low metabolic rate, tendency to gain weight, hy-perlipidemia, subnormal temperature, cold intolerance, bradycardia, reduced systolic and increased diastolic pulse pressure, hoarseness, muscle weakness, slow re-turn of muscle to the neutral position after a tendon jerk, constipation, menstrual abnormalities, infertility, and sometimes myxedema (hard edema of subcuta-neous tissue with increased content of proteoglycans in the fluid). A goiter (i.e., enlargement of the thyroid gland) may be present.
Juvenile or adult patients with primary hypothy-roidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and re-ducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing di-etary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism.
Patients with secondary or tertiary hypothyroidism are also usually treated with thyroxine, but the serum TSH concentration is not a reliable guide to therapy. The efficacy of thyroid hormone replacement in these patients must be assessed clinically and by measure-ment of the serum T4 concentration.
The most extreme manifestation of untreated hy-pothyroidism is myxedema coma, which even if de-tected early and appropriately treated, carries a mortal-ity rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstand-ing hypothyroidism with the classic symptoms of hy-pothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the se-verely hypothyroid patient are subject to a stressful pre-cipitating event (e.g., infection, trauma, some medica-tions, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (ap-athy, confusion, psychosis, but rarely coma). Other com-mon clinical features include hypothermia, diastolic hy-pertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an inten-sive care unit for pulmonary and cardiovascular support and treated with intravenous T4 (or sometimes T3). Until coexisting adrenal insufficiency is ruled out, hy-drocortisone should also be administered.
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