Thyroid disorders

Thyroid disorders encompass a variety of disease states affecting thyroid hormone production or secretion that result in alterations in metabolic stability. Hyperthyroidism and hypothyroidism are the clinical and biochemical syndromes resulting from increased and decreased thyroid hormone production, respectively. 

The thyroid hormones thyroxine (T4) and triiodothyronine (T3) are formed on thyroglobulin, a large glycoprotein synthesized within the thyroid cell. Inorganic iodide enters the thyroid follicular cell and is oxidized by thyroid peroxidase and covalently bound (organified) to tyrosine residues of thyroglobulin. 

The iodinated tyrosine residues monoiodotyrosine (MIT) and diiodoty-rosine (DIT) combine (couple) to form iodothyronines in reactions catalyzed by thyroid peroxidase. Thus, two molecules of DIT combine to form T4, and MIT and DIT join to form T3. 

Thyroid hormone is liberated into the bloodstream by the process of proteolysis within thyroid cells. T4 and T3 are transported in the bloodstream by three proteins thyroid-binding gjobulin, thyroid-binding preal-bumin, and albumin. Only the unbound (free) thyroid hormone is able to diffuse into the cell, elicit a biologic effect, and regulate thyroid-stimulating hormone (TSH) secretion from the pituitary. 

T4 is secreted solely from the thyroid gland, but less than 20% of T3 is produced there the majority of T3 is formed from the breakdown of T4 catalyzed by the enzyme 5 -monodeiodinase found in peripheral tissues. T3 is about five times more active than T4. 

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Other Inflammatory Muscle Disorders Endocrine Myopathies Thyroid Disorders Adrenal Disorders Pituitary Disorders Parathyroid Disorders Pancreatic Disorders Drug-Induced and Toxic Myopathies Management of Muscle Disease... 

Approximately one-third of patients with MDD do not respond satisfactorily to their first antidepressant medication.37 In such cases, the clinician must evaluate the adequacy of antidepressant therapy, including dosage, duration, and patient compliance.17 Treatment reappraisal also should include verification of the patient s diagnosis and reconsideration of clinical factors that could be impeding successful therapy, such as concurrent medical conditions (e.g., thyroid disorder), comorbid psychiatric conditions (e.g., alcohol abuse), and psychosocial issues (e.g., marital stress).16... 

Discuss the prevalence of thyroid disorders, including subclinical (mild) and overt (typical signs and/or symptoms present) hypothyroidism and hyperthyroidism. 

O In most patients with thyroid hormone disorders, the measurement of a serum thyroid-stimulating hormone (TSH) level is adequate for the diagnosis of hypothyroidism and hyperthyroidism. The target TSH for most patients being treated for thyroid disorders should be the mean normal value of 1.4 milliunits/L or 1.4 microunits/mL (target range 0.5-2.5 milliunits/L or 0.5-2.5 microunits/mL). 

The assessment of patients for thyroid disorders entails a history and physical examination. In many patients with subclinical or mild thyroid disease, there may be an absence of specific signs and symptoms, and the physical examination may be normal. Various diagnostic tests can be used, including serum thyroid hormone(s), TSH, and thyroid antibody levels and imaging techniques to evaluate patients for thyroid disorders. Normal values for selected laboratory tests are given in Table 41-1. 

The laboratory assessment of patients with suspected thyroid disorders must be based on the continuum of disease from subclinical or mild to overt (Fig. 41-2). 

Success of therapy for thyroid disorders must be based not only on short-term improvement of the patient s clinical status and abnormal laboratory values but also on achievement of a long-term euthyroid state. Maintaining the TSH level in the normal range improves symptoms and reduces the risk of long-term complications. 

Endocrine disorders (hypogonadism and pituitary, adrenal, and thyroid disorders)... 

Chap. 41 - Thyroid Disorders Universal Program Number 014-999-07-057-H04... 

G Levy, MH MacGillivray, JA Procknal. Riboflavin absorption in children with thyroid disorders. Pediatrics 50 896-900, 1972. 

Iodine, most ancient of the therapeutic agents for thyroid disorders, inhibits the secretion of thyroid hormone by retarding both the pinocyto-sis of colloid and proteolysis. This effect is observed in euthyroid as well as hyper thyroid persons. 

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