Overview
The Mechanism That Connects the Syndromes
Thyroiditis is inflammation of the thyroid gland, but the clinical priority changes sharply with the cause.
NCLEX-RN
NCLEX-RN
Thyroiditis is inflammation of the thyroid gland, but the clinical priority changes sharply with the cause. The central distinction is whether thyroid hormone is leaking from injured follicles or being newly synthesized by an overactive gland. In destructive thyroiditis, damaged follicles release stored thyroxine (T4) and triiodothyronine (T3) into the circulation. The patient can look hyperthyroid—palpitations, tremor, heat intolerance, anxiety, and weight loss—but the gland is not manufacturing excess hormone. This is why antithyroid drugs such as methimazole and propylthiouracil do not help. They block synthesis, not release of hormone that is already stored. Subacute thyroiditis, also called de Quervain or granulomatous thyroiditis, is usually a post-viral inflammatory process. A recent viral illness may precede painful thyroid enlargement. Inflammation ruptures follicles, producing a temporary thyrotoxic phase. Once stored hormone is depleted, a hypothyroid phase may follow before recovery. The typical subacute course has four stages: 1. Thyrotoxic phase: usually during the first 1 to 4 weeks, with suppressed TSH and elevated free T4 and T3. 2. Hypothyroid phase: often around weeks 4 to 8, when hormone stores are exhausted and...
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