## Mechanism of Action of Antithyroid Drugs ### PTU vs Methimazole: Key Differences | Feature | PTU | Methimazole | |---------|-----|-------------| | Blocks TPO | Yes | Yes | | Inhibits peripheral T4→T3 conversion | Yes | No | | Onset of action | Faster | Slower | | Preferred in pregnancy | 1st trimester | No (teratogenic) | | Agranulocytosis risk | ~0.2% | ~0.3% | **Key Point:** PTU has a dual mechanism — it blocks thyroid peroxidase (TPO) AND inhibits peripheral deiodination of T4 to T3 via 5'-deiodinase inhibition. This makes it uniquely effective in acute thyroid storm. **Key Point:** Methimazole ONLY blocks TPO; it does NOT affect peripheral conversion of T4 to T3. ### Iodine's Mechanism **High-Yield:** Iodine (Lugol's solution, Saturated Solution of Potassium Iodide [SSKI]) works through the **Wolff-Chaikoff effect** — it inhibits thyroid peroxidase and also decreases thyroid hormone release from the gland. It is used acutely in thyroid storm (after PTU/methimazole has been given). ### Beta-Blockers: Symptomatic Relief Only **Key Point:** Beta-blockers (propranolol, atenolol) do NOT reduce thyroid hormone synthesis or secretion. They provide **symptomatic relief** of adrenergic manifestations (tachycardia, tremor, anxiety) in hyperthyroidism. Propranolol has the added benefit of mild inhibition of peripheral T4→T3 conversion, but this is not its primary mechanism. **Warning:** Beta-blockers are NOT antithyroid drugs — they do not treat the underlying thyroid disorder. ### Why Option 3 is Incorrect Beta-blockers directly reduce thyroid hormone **secretion** — this is FALSE. They reduce the **peripheral effects** of thyroid hormones (sympathomimetic symptoms) but do not alter thyroid function or hormone levels. The thyroid continues to produce and release T3 and T4 normally; the patient simply feels better because adrenergic symptoms are suppressed. [cite:KD Tripathi 8e Ch 42]
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