Grave's disease: Symptoms, Diagnosis, Treatments

Symptoms
In Graves' disease, all of the clinical features of thyrotoxicosis mentioned above may occur. In addition, diffuse thickening of the thyroid gland, protrusion of the eye, lid retraction, lid lag, ocular motility disorder, optic nerve disorder may occur. The patient seemed to have a slight protrusion of the eyeball, and the professor asked him to try the thyroid gland, but he could definitely touch the enlarged thyroid gland. Among the clinical features mentioned above, thyroid ophthalmopathy is a characteristic feature of Graves' disease, which is not seen in other thyrotoxicosis. It is caused by thickening of the autoantibody in the extraocular muscle and elevation of the intraocular pressure. It is rarely seen in other thyroid diseases with autoantibody besides Graves' disease.

Diagnosis
The first thing to do in a patient suspected of elevated thyroid function is to measure TSH and free T4. If TSH decreases and free T4 increases, it can be classified as primary thyroid hyperfunction. If it shows diffuse thyroid hyperplasia, anti - TPO Ab (+), ophthalmopathy or dermatosis, it can be diagnosed as Grave 's disease. We can diagnose multinodular goiter or toxic adenoma without primary thyroid hyperplasia diffuse thyroid hypertrophy, anti - TPO Ab (-), ophthalmopathy and dermatosis. When TSH normal or increased, free T4 increases, a tumor that secretes TSH may be suspected. TSH is decreased and free T4 is normal, T3 toxicosis is increased by measuring free T3, and subclinical hyperthyroidism is normal.
In Graves' disease, T3, T4, and free T4 levels are elevated by the presence of autoantibody stimulating thyroid hormone secretion, and TSH levels are decreased by negative feedback. RAI uptake increases. Anti - TPO Ab in Thyroid autoantibody test is positive in more than 80% of patients but not specific. Anti - TSH receptor Ab is useful for confirmation, but not routine.

Treatments
The primary treatment for Grave's disease is anti-thyroid drug. There are PTU and methimazole types, and methimazole is generally preferred due to side effects of PTU. The mechanism of action is to inhibit thyroid hormone production and lower the thyroid autoantibody level. From 3 to 4 weeks after the start of treatment, the TFT and clinical features are assessed to evaluate the response to treatment. It is said to be between 18 and 24 months, but recurrence is common. Hepatitis and agranulocytosis are the main adverse reactions. In this case, the drug should be discontinued and the treatment modi- fied immediately. In addition, β-blockers are used to control the adrenergic symptom. Β-blocker has no effect on thyroid function and is used to control symptoms. It is effective to control throbbing, sweating, anxiety, and tachycardia.
Radioiodine therapy can be used for recurrence after drug treatment and for recurrence after surgery, but it is an absolute contraindication during pregnancy or lactation. Side effects may include hypothyroidism.
Surgery is a method that can be performed when there is no response to medication or if it frequently recurs. Pre-operative anti-thyroid drug and KI are used. To avoid a thyrotoxic crisis and to reduce blood flow to the preoperative thyroid gland. Anti-thyroid drugs should be administered first and KI should be used.

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