**Abstract**

DG presents with three main presentations: hyperthyroidism with diffuse goiter, infiltrative ophthalmopathy and pre-tibial myxedema. Patients with Graves' Disease can rarely develop severe hyperthyroidism. The hyperthyroidism of Graves' Disease is characterized immunologically by the lymphocytic infiltration of the thyroid gland and by the activation of the immune system with elevation of the circulating T lymphocytes. In GD, goiter is characteristically diffuse. May have asymmetric or lobular character, with variable volume. The clinical manifestations of hyperthyroidism are due to the stimulatory effect of thyroid hormones on metabolism and tissues. Nervousness, eye complaints, insomnia, weight loss, tachycardia, palpitations, heat intolerance, damp and hot skin with excessive sweating, tremors, hyperdefecation and muscle weakness are the main characteristics. In the laboratory diagnosis, biochemical and hormonal exams will be done to assess thyroid hormones and the antithyroid antibodies. Additionally, imaging tests may be performed, such as radioactive iodine capture in 24 hours, ultrasonography, thyroid scintigraphy and fine needle aspiration. It is necessary to make the differential diagnosis of Graves' Disease for thyrotoxicosis, subacute lymphocytic thyroiditis and toxic nodular goiter. The treatment of DG aims to stop the production of thyroid hormones and inhibit the effect of thyroid hormones on the body. Hyperthyroidism caused by DG can be treated in the following ways: it may be the use of synthetic antithyroid medicines, thionamides, MMI being a long-term medicine, it allows a single daily dose, and adherence to treatment occurs, a disadvantage is that it cannot be used in pregnant women; beta-blockers, preferably used in the initial phase of DG with thionamides; radioactive iodine therapy (RAI), being the best cost–benefit and preventing DG recurrence; finally the total thyroidectomy, causing the withdrawal of the thyroid gland. Therefore, it should be discussed with the patient what is the best treatment for your case, with a view to the post and against each approach. If the patient develops Graves ophthalmopathy, in lighter cases the artificial tears should be used, and in more severe cases can be used as treatment, corticosteroids, orbital decompression surgery, prisms and orbital radiotherapy. In addition, the patient should keep their body healthy, doing exercise and healthy eating, following the guidance of their doctor.

**Keywords:** Graves' Disease, Hyperthyroidism, Goiter, Thyroid hormones

## **1. Introduction**

GD presents with three main presentations: hyperthyroidism with diffuse goiter, infiltrative ophthalmopathy and dermopathy (pretibial myxedema). Patients with Graves' Disease rarely may develop severe hyperthyroidism (thyroid storm or thyrotoxic crisis) [1]. Consider tests for thyroid dysfunction for people if there is a clinical suspicion of thyroid disease, but bear in mind that only an isolated symptom may not be associated with this disease [2].

## **2. Hyperthyroidism**

Graves' Disease hyperthyroidism is characterized immunologically by lymphocytic infiltration of the thyroid gland and by activation of the immune system with elevation of circulating T lymphocytes, appearance of autoantibodies that bind to the TSH receptor (TRAb) and that stimulate glandular growth and function [3–5]. The reasons for triggering this autoimmune process have not yet been fully understood, but factors such as susceptibility genetics, constitutional factors such as sex hormones and changes in immune function, and factors environmental factors (stress, iodine intake and the action of infectious agents) [6, 7].

From a clinical point of view, the hyperthyroidism of Graves' Disease is characterized by diffuse enlargement and hyperactivity of the gland thyroid, associated or not with infiltrative ophthalmopathy and, more rarely, localized myxedema. Excess thyroid hormones can lead to the development of serious complications such as congestive heart failure, cardiomyopathy and arrhythmias, mainly atrial fibrillation (10–30%). It is also associated with increased bone resorption, increased calcium and phosphorus excretion in urine and faeces, with a consequent decrease in bone mineral density and risk of fractures in women elderly [1, 3].


### **3. Dermopathy (pretibial myxedema)**

It affects only 5 to 10% of patients with GD and is almost associated with ophthalmopathy (usually severe) and high levels of TRAb [8]. Exceptionally, it has seen in euthyroid patients with GD [1] or with Hashimoto's thyroiditis [9]. It consists of within the thickening of the skin, particularly within the pretibial area, because of the buildup of the glycosaminoglycans. The evidence is shown in plaques and on them; the skin is type of thickened, with the looks of orange rind and violet color. Sometimes a Dermopathy involves the entire lower leg and should reach the feet. Rarely (less than 1% of cases), it can be seen in other places (hands or shoulders), especially after prolonged trauma [8, 10]. Very rarely, pretibial myxedema is the initial manifestation of GD [1, 11].

*Graves' Disease: Hyperthyroidism, Symptoms, Causes and Treatment DOI: http://dx.doi.org/10.5772/intechopen.97578*
