Clinical Note

Skeletal maturation is distinct from skeletal growth. Maturation of bone results in the ossification and eventual fusion of the cartilaginous growth plates, which occurs with sufficient predictability in normal development that individuals can be assigned a specific "bone age" from radiological examination of ossification centers. Thyroid hormones profoundly affect skeletal maturation, perhaps by a direct action. Bone age is retarded relative to chronological age in children who are deficient in thyroid hormone and is advanced prematurely in hyperthyroid children. Uncorrected deficiency of thyroid hormone during childhood results in retardation of growth and malformation of facial bones characteristic of juvenile hypothyroidism or cretinism.

growth and nerve myelination are severely delayed. Overall size of the brain is reduced along with its vascu-larity, particularly at the capillary level. The decrease in size may be partially accounted for by a decrease in axonal density and dendritic branching. Thyroid hormone deficiency also leads to specific defects in cell migration and differentiation.

Autonomic Nervous System

Interactions between thyroid hormones and the autonomic nervous system, particularly the sympathetic branch, are important throughout life. Increased secretion of thyroid hormone exaggerates many of the responses that are mediated by the neurotransmitters norepinephrine and epinephrine released from sympathetic neurons and the adrenal medulla (see Chapter 40). In fact, many symptoms of hyperthyroidism, including tachycardia (rapid heart rate) and increased cardiac output, resemble increased activity of the sympathetic nervous system. Thyroid hormones increase the number of receptors for epinephrine and norepinephrine (^-adrenergic receptors) in the myocardium and some other tissues. Thyroid hormones may also increase the stimulatory G-protein (Gs) associated with adrenergic receptors and down-regulate the inhibitory G-protein (Gi), either of which results in greater production of cyclic AMP. Furthermore, sympathetic stimulation acting by way of cyclic AMP activates the type II deiodinase, which accelerates local conversion of T4 to T3. Because thyroid hormones exaggerate a variety of responses mediated by ^-adrenergic receptors, pharmacologic blockade of these receptors is useful for reducing some of the symptoms of hyperthyroidism. Conversely, the diverse functions of the sympathetic nervous system are compromised in hypothyroid states.

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