Hyperthyreoosia

Hyperthyreoosia is not a standard medical term. It is commonly viewed as a misspelling or variant of hyperthyroidism, the condition characterized by excess thyroid hormone production, or of thyrotoxicosis, the clinical syndrome caused by elevated thyroid hormones from any source. The term may therefore refer to either the source of excess or its hormonal effects.

Most cases arise from Graves’ disease, toxic multinodular goiter, or a toxic adenoma. Less common causes include thyroiditis (inflammation of the thyroid), postpartum thyroiditis, or exogenous thyroxine intake. Autoimmune stimulation or nodular disease leads to increased synthesis or release of T4 and T3, resulting in a hypermetabolic state.

Symptoms reflect this acceleration of physiology and can include weight loss with maintained or increased appetite, heat intolerance, sweating, tremor, palpitations, anxiety, irritability, insomnia, and menstrual changes. A goiter may be present, and eye involvement can occur with Graves’ disease, sometimes with visual symptoms.

Diagnosis relies on laboratory testing and sometimes imaging. The typical pattern is suppressed or undetectable TSH with elevated free T4 and often free T3. TSH receptor antibodies support Graves’ disease. A thyroid uptake scan helps distinguish causes: high uptake in Graves’ disease or toxic nodular disease, low uptake in thyroiditis or in exogenous hormone exposure.

Treatment depends on the underlying cause and may include antithyroid drugs (such as methimazole), beta-blockers for symptom relief, and definitive therapies like radioactive iodine ablation or thyroidectomy. Pregnancy requires special management considerations. With appropriate treatment, thyroid function can be restored to normal in most patients, though relapse or overtreatment is possible.