Graves disease: pathology
Presents with thyrotoxicosis
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Thyroid parenchyma with features of thyroid hyperactivity as seen in Graves disease with scalloping, partial follicular collapse and pseudopapillary infoldings.
The hyperthryoid clinical state of Graves disease is the result of binding of auto-antibody to the TSH receptors of thyroid follicular cells with resultant activation of follicular cells, reabsorption of stored colloid and production and release of T3 and T4.
These photomicrographs demonstrate the pathophysiology in action with activated follicular epithelium and evidence of colloid reabsorption (seen as scalloping, partial follicle collapse and epithelial infoldings).