HYPOTHYROID
STATES
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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