Hyperthyroidism primary

If sgns of hyperthyroidism (eg, nervousness snxiety, increased appetite, elevated body temperature, tachycardia, moderate hypertension or flushed, warm, moist skin) are apparent, the nurse reportsthese to the primary health care provider before the next dose is due because it may be necessary to decrease the daily dosage. 

The patient with hyperthyroidism is likely to have cardiac symptoms such as tachycardia or palpitations. Propranolol, a adrenergic blocking drug (see Chap. 21), may be prescribed by tlie primary health care provider as adjunctive treatment for several weeks until tlie therapeutic effects of tlie antithyroid drug are obtained. 

Primary hyperthyroidism Graves disease Toxic multinodular goiter... 

Blockers are usually used as adjunctive therapy with antithyroid drugs, RAI, or iodides when treating Graves disease or toxic nodules in preparation for surgery or in thyroid storm. /3-Blockers are primary therapy only for thyroiditis and iodine-induced hyperthyroidism. 

Increased = Decreased N = Normal X = Contraindicated Pregnancy Primary hypothyroidism Secondary hypothyroidism Hyperthyroidism... 

Juvenile or adult patients with primary hypothyroidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and reducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing dietary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism. 

The three primary methods for controlling hyperthyroidism are antithyroid drug therapy, surgical thyroidectomy, and destruction of the gland with radioactive iodine. 

In 50 women taking levothyroxine either for primary thyroid failure or for hypothyroidism secondary to radioiodine treatment for hyperthyroidism, there was no difference between the two groups in terms of bone density at the hip or spine and no difference from the reference population (31). In addition, there was no correlation between bone density and circulating thyroid hormone concentrations or duration of levothyroxine replacement. These findings are reassuring, although large studies of fracture risk are required, in view of previous evidence of an adverse effect of levothyroxine on bone mineral density, especially in post-menopausal women (32). 

Patients with beta-thalassemia major have an increased risk of primary hypothyroidism. In 23 patients with beta-thalassemia amiodarone was associated with a high risk of overt hypothyroidism (33 versus 3% in controls) (43). This occurred at up to 3 months after starting amiodarone. The risk of subclinical hypothyroidism was similar in the two groups. In one case overt hypothyroidism resolved spontaneously after withdrawal, but the other patients were given thyroxine. After 21-47 months of treatment three patients developed thyrotoxicosis, with remission after withdrawal. There were no cases of hyperthyroidism in the controls. The authors proposed that patients with beta-thalassemia may be more susceptible to iodine-induced hypothyroidism, related to an underlying defect in iodine in the thyroid, perhaps associated with an effect of iron overload. 

Primary hyperthyroidism Graves disease Thyroid adenoma/carcinoma Secondary hyperthyroidism... 

Thyroid disorders can be divided into two primary categories conditions that increase thyroid function (hyperthyroidism) and conditions that decrease thyroid function (hypothyroidism).8 There are several different types of hyperthyroidism and hypothyroidism, depending on the apparent etiology, symptoms, and age of onset of each type. The types of hyperthyroidism and hypothyroidism are listed in Table 31-1. Although we cannot review the causes and effects of all the various forms of thyroid dysfunction at this time, this topic is dealt with elsewhere exten-sively.6,8,56 74... 

The clinical manifestations of hyperthyroidism and hypothyroidism are listed in Table 31-2. From a pharmacotherapeutic standpoint, hyperthyroidism is treated with drugs that attenuate the synthesis and effects of thyroid hormones. Hypothyroidism is usually treated by thyroid hormone administration (replacement therapy). The general aspects and more common forms of hyperthyroidism and hypothyroidism are discussed here, along with the drugs used to resolve these primary forms of thyroid dysfunction. 

Thyroid hormone preparations used clinically are listed in Table 31-3. The primary problems associated with these agents occur with overdosage. Symptoms of excess drug levels are similar to the symptoms of hyperthyroidism (see Table 31-2). Presence of these symptoms is resolved by decreasing the dosage or changing the medication. 

Peak serum thyrotropin levels occur 20-30 seconds after intravenous TRH injection in healthy individuals. In hyperthyroidism, the serum thyrotropin level is suppressed. In primary hypothyroidism, thyrotropin levels are high and the thyrotropin response to TRH may be accentuated. In secondary (pituitary) hypothyroidism, serum thyrotropin levels are "inappropriately" normal or low (using a sensitive TSH assay) TSH often fails to rise after TRH administration. In tertiary (hypothalamic) hypothyroidism, the baseline serum thyrotropin level may be normal or low and the thyrotropin response to TRH may be normal or blunted. 

Failure of the thyroid to produce sufficient thyroid hormone is the most common cause of hypothyroidism and is known as primary hypothyroidism. Secondary hypothyroidism occurs much less often and results from diminished release of TSH from the pituitary. Treatment of hypothyroidism is achieved by the replacement of thyroid hormone, primarily T4. A synthetic preparation of T4 is available, levothyroxine (Synthroid ), which has been a popular choice for hypothyroidism because of its consistent potency and prolonged duration of action. No toxicity occurs when given in physiological replacement doses. Desiccated animal thyroid is also available at a lesser cost. Overdoses cause symptoms of hyperthyroidism and can be used as a guide in clinical management. Hypothyroidism is not cured by the daily intake of thyroid hormone it is a life-long regimen. 

The most significant of the abnormalities observed in a hypothyroid brain is a hypoplastic neuropile, i.e., a marked reduction in the number of connections between neurons [102], This has been observed both in the cerebrum and the cerebellum. For instance a permanent and dramatic reduction in the arborization of the dendritic tree of the Purkinje cell is observed in the hypothyroid cerebellum [103]. The length of the primary dendritic trunk is increased and a deficit in the number, density and branching of the dendritic spines is noticed. In contrast neonatal hyperthyroidism accelerates development of spines. Similar findings have been reported for the cerebrum, i.e., reduction in length and branching of pyramidal neurons, of the density of axonal terminals and of the number of spines [102],... 

Thyroid Disease. Elevated blood pressure or other adverse cardiovascular effects can result when patients with Graves disease receive adrenergic agonists with vasopressor activity. This is due to the increased catecholamine activity associated with hyperthyroidism. The primary agent to be avoided or used cautiously is topically applied phenylephrine for pupillary dilation. 

Humans cannot synthesise vitamins in the body except some vitamin D in the skin and nicotinamide from tryptophan. Lack of a particular vitamin may lead to a specific deficiency syndrome. This may be primary (inadequate diet), or secondary, due to failure of absorption (intestinal abnormality or chronic diarrhoea), or to increased metabolic need (growth, pregnancy, lactation, hyperthyroidism). 

Basedow hyperthyroidism BCG vaccine Erythematodes visceralis Granulomatosis infantisepticum Hypogammaglobulinaemia Polymyalgia rheumatica Primary biliary cholangitis Sarcoidosis Vasculitis... 

The thioamides are often used as primary therapy for hyperthyroidism. They are also used as adjunctive therapy to achieve euthyroidism in patients prior to surgery or radioactive iodine therapy. The thioamides primarily inhibit... 

Acute symptomatic hypocalcemia may be seen in hospitalized patients for various reasons. Rapid remineralization of bone after surgery for primary hyperparathyroidism (hungry bone syndrome), treatment for hyperthyroidism, or treatment for hematological malignancy may result in hypocalcemia. Acute hemorrhagic or edematous pancreatitis is frequently complicated by hypocalcemia. Vitamin D deficiency may also be associated with hypocalcemia because of impaired intestinal absorption of calcium and skeletal resistance to PTH. Osteomalacia and rickets are discussed in a later section of this chapter. 

Coexistent primary hyperparathyroidism Other endocrine disorders Hyperthyroidism Hypothyroidism Acromegaly... 

Elevated concentrations of telopeptides and DPD have been reported in osteoporosis, Paget s disease, metastatic bone disease, primary and secondary hyperparathyroidism, hyperthyroidism, and other diseases with increased bone... 

Hypothyroidism and hyperthyroidism are the two primary pathological conditions that involve the thyroid glands. Laboratory testing of thyroid hormones is used to diagnose and document the presence of thyroid disease, a condition that often presents with vague and subtle symptoms. Accurate measurement of thyroid hormone concentrations is key to the proper diagnosis of thyroid gland dysfunction. 

The determination of serum TSH by RIA proved very valuable in assessing the elevated TSH values in primary hypothyroidism. However, because these assays could only detect 1 mU of TSH per fiter, most conventional RIAs could not distinguish normal values from the subnormal values associated with hyperthyroidism. 

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