Ziekte van Graves II: Pathofysiologie

Graves' disease begins when the immune system fails to maintain tolerance, allowing plasma cells to produce and release thyroid-stimulating immunoglobulins or TSI.

These antibodies bind to thyroid-stimulating hormone receptors or TSH-R on thyroid follicular cells and mimic the action of thyroid-stimulating hormone or TSH.

With the receptors continuously overstimulated by the antibodies, the thyroid gland produces and releases large amounts of thyroxine or T4 and triiodothyronine or T3 without normal regulatory control.

Microscopically, follicular cells become tall and crowded, vascularity increases, and colloid stores are rapidly depleted, leaving wavy edges.

The same immune response targets fibroblasts expressing TSH receptors in the orbit and skin.

It causes swelling around the eyes, known as periorbital edema, protrusion of the eyes called exophthalmos, and thickened patches on the shins, referred to as pretibial myxedema.

Excess T4 and T3 in the blood raise the metabolic rate, increasing heat production and heart rate.