Give 2 exact answer
Answer: Synthesis of antibodies to TSH receptors
In Graves' disease (diffuse toxic goiter), the pathogenesis is based on the production of TSH receptor antibodies (TRAb), specifically thyroid-stimulating immunoglobulins (TSI). These IgG autoantibodies bind to and continuously stimulate the TSH receptor on thyroid follicular cells, mimicking TSH action - leading to unregulated thyroid hormone synthesis and diffuse thyroid enlargement.
The highlighted answer in the image (synthesis of antibodies to TSH receptors) is correct.
Why the others are wrong:
- Antibodies to hepatocytes - unrelated to thyroid pathology
- Antibodies to thyroglobulin - seen in Hashimoto's thyroiditis (hypothyroidism), not Graves'
- Increased sensitivity to catecholamines - a consequence of hyperthyroidism (upregulation of beta-adrenergic receptors), not the basis of pathogenesis
2 answers sugest
If forced to pick 2 answers, they would be:
1. Synthesis of antibodies to TSH receptors ✅ (PRIMARY - definitive answer)
The core autoimmune mechanism of Graves' disease. TSI/TRAb continuously stimulate the thyroid independent of TSH.
2. Increased sensitivity to catecholamines ✅ (SECONDARY - contributory mechanism)
Excess thyroid hormone upregulates beta-adrenergic receptors, increasing catecholamine sensitivity. This contributes to many clinical features (tachycardia, tremor, sweating) and is considered part of the pathogenetic picture in some exam contexts.
Why not thyroglobulin antibodies? - Those are a marker of autoimmune thyroid disease in general but are NOT the pathogenic basis of toxic (hyperfunctioning) goiter specifically.
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