Medication and Teaching
The Therapeutic Problem: Excess Hormone Production
Graves disease is an autoimmune cause of hyperthyroidism.
REx-PN
REx-PN
Graves disease is an autoimmune cause of hyperthyroidism. Thyroid-stimulating immunoglobulins bind to thyroid-stimulating hormone receptors and keep signalling the gland to produce thyroid hormone. The thyroid behaves as though it is receiving a constant demand signal: it synthesizes and releases excess thyroxine (T4) and triiodothyronine (T3). Too much thyroid hormone accelerates metabolic and adrenergic activity. The patient may have heat intolerance, sweating, tremor, anxiety, weight loss despite increased appetite, diarrhoea, palpitations, and exercise intolerance. An experienced nurse pays close attention to the heart rate and rhythm because persistent hormone excess can produce atrial fibrillation, worsen angina, or precipitate heart failure. Antithyroid therapy has two different goals: - Thionamides, primarily methimazole, reduce new thyroid hormone synthesis. - Radioactive iodine destroys overactive thyroid tissue and provides definitive treatment. Neither treatment corrects severe adrenergic symptoms immediately. A beta-blocker may be prescribed while hormone production is being controlled because it reduces tachycardia, tremor, and palpitations during the transition to euthyroidism.
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