Hyperthyroidism clinical symptoms

Keck FS, Loos U, Duntas L, Pfeiffer EF. Hyperthyreosis factitia acuta—Geringe klinische Symptome bei drei Fallen unter beta-Blocker-Behandlung. [Acute factitious hyperthyroidism—moderate clinical symptoms in 3 cases under beta-blocker treatment.] Klin Wochenschr 1986 64(7) 319-26. 

There are numerous thyroid gland function tests, each designed to determine the etiology of thyroid dysfunction. In general, though, when hypothyroidism is present, circulating T3 and T4 levels are down and TSH is up. The opposite is true of hyperthyroidism. In addition, free (non-protein-bound) T4 and TBG may be determined to clarify inconclusive results. In hyperthyroidism, free T4 is increased but total T4 may be normal. It is the free serum T4 that has been correlated with clinical symptoms rather than total T4. 

Because of its low oral toxicity, serious clinical consequences have only been occasionally reported following large parenteral doses (Table 7). Several cases of death by anaphylactic shock have been noted (Itokawa, 1978). The symptoms of thiamin overdosage include (at 400 mg, iv) acute mental alertness, lethargy, solemnness, mild ataxia, heaviness in the limbs, and a diminution of gut tone (Gould, 1954). Other manifestations of thiamin overdose in humans include acute hypotension and the development of hyperthyroid-like symptoms. 

Thyrotoxicosis -adrenergic blockers may mask clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm. 

Beta blockers without intrinsic sympathomimetic activity (eg, metoprolol, propranolol, atenolol) are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with sympathetic stimulation. Propranolol has been the 3 blocker most widely studied and used in the therapy of thyrotoxicosis. Beta blockers cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels. Propranolol at doses greater than 160 mg/d may also reduce T3 levels approximately 20% by inhibiting the peripheral conversion of T4 to T3. 

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. 

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. 

Clinically, the practitioner may observe conjimctival chemosis and erythema, abnormal eyelid position (lid retraction), lid lag, and proptosis. Conjunctival injection is most marked over the involved rectus muscles. Nervousness, palpitations, weight loss, hyperhidrosis, and heat intolerance are systemic symptoms occurring in more than 80% of hyperthyroid patients. Other signs, such as tremor, hyperreflexia, tachycardia, skin changes, stare, and eyelid lag, are observed in more than 60%. Additionally, goiter is present in more than 95% of Graves disease patients. In most cases, however, the laboratory confirmation of thyrotoxicosis is helpful to corroborate the diagnosis. 

Case Conclusion HP began methimazole therapy for her Graves hyperthyroidism. She also began propranolol to help control her tachycardia and tremor. During this time HP should avoid excessive exercise or other sympathomimetic drugs until her symptoms of tachycardia have subsided. HP will return to the clinic for follow-up in 4 weeks. At that time, methimazole dose, tolerability, compliance, and thyroid function tests will be reassessed. 

The clinical signs and symptoms of thyroid hormone excess or deficiency are generally vague and nonspecific (see Box 52-4). Therefore when hypothyroidism or hyperthyroidism is suspected, confirmation with laboratory tests is generally required. Guidelines for the selection of appropriate laboratory tests for thyroid function have been published... 

Despite the relatively detailed understanding of iodine metabolism and the action of THs at the molecular level, their action on the human nervous system remains poorly understood. At the clinical interface, the neuromuscular manifestations of THs are quite common. Their incidence depends primarily on how extensively and rigorously the symptoms are sought. Overall, neuromuscular dysfunction occurs in 20—80% of cases (Aminoff, 2002). In hypothyroidism, it is as high as 79%, and in hyperthyroidism it is 67%. The predominant symptoms are sensorimotor axonal neuropathy in both extremes of thyroid dysfunction. Most of these resolve with treatment for the thyroid condition. Although not documented, most patients with thyroid disease often complain of neuromuscular-type symptoms. 

Three famous physicians have contributed to our early knowledge of hyperthyroidism. Parry, an Englishman, described the disease but left it to his son to publish, in 1825, the first description of hyperthyroidism. In 1835, Graves, an Irish physician, attracted attention to the relationship between some symptoms now known to be associated with hyperthyroidism and the thyroid gland. Von Basedow in 1840 meticulously described the complete clinical symptomatology of hyperthyroidism [36]. 

All the clinical observations and the experimental data suggest that more thyroxine is made available to the target organs in thyrotoxicosis. Although the hormone s mechanism of action at a molecular level remains unknown, the hormone is known to stimulate cellular oxidation. Consequently, an excess of hormone causes the cells to perform their functions under conditions in which cellular energy is used inefficiently. This effect manifests itself in hyperthyroidism by a number of symptoms increased basal metabolism, tachycardia, muscle wasting, and excitability. 

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