Match each clinical presentation and thyroid laboratory profile with its most accurate und… — USMLE Step 2 CK

Match each clinical presentation and thyroid laboratory profile with its most accurate underlying pathophysiologic mechanism.

A 28-year-old woman with weight loss and tachycardia. Labs: TSH $<0.01$ $\mu$ U/mL, elevated free T4, and a diffuse radioactive iodine uptake of $65\%$ (normal $8-25\%$ ).Stimulation of the thyroid gland by IgG autoantibodies
A 35-year-old woman with fever and severe anterior neck pain. Labs: TSH $<0.01$ $\mu$ U/mL, elevated free T4, radioactive iodine uptake of $<1\%$ , and markedly elevated serum thyroglobulin.Release of preformed thyroid hormone from inflamed and disrupted follicles
A 42-year-old medical worker with anxiety and a nonpalpable thyroid. Labs: TSH $<0.01$ $\mu$ U/mL, elevated free T4, radioactive iodine uptake of $<1\%$ , and undetectable serum thyroglobulin.Suppression of the hypothalamic-pituitary-thyroid axis by exogenous hormone ingestion
A 45-year-old man with palpitations and bitemporal hemianopsia. Labs: TSH $6.5$ $\mu$ U/mL (normal $0.4-4.0$ $\mu$ U/mL), elevated free T4, and elevated serum alpha-subunit levels.Autonomous, neoplastic secretion of thyrotropin

Answer

The correct matches map the varying combinations of TSH, free T4, radioactive iodine uptake, and thyroglobulin to their distinct thyrotoxic etiologies (Graves disease, subacute thyroiditis, exogenous thyroid hormone, and a TSH-secreting pituitary adenoma).

Evaluating thyrotoxicosis requires a stepwise approach. An inappropriately elevated TSH with high free T4 indicates a central cause, most commonly a TSH-secreting pituitary adenoma (further supported by high alpha-subunits and compressive mass effects like bitemporal hemianopsia). In primary hyperthyroidism (suppressed TSH), a high radioactive iodine uptake (RAIU) signifies overproduction of hormone, such as in Graves disease caused by TSH-receptor autoantibodies. If RAIU is low, the hyperthyroidism is either from follicular destruction (subacute thyroiditis) or exogenous hormone use. Serum thyroglobulin successfully differentiates these two: it is elevated during follicular destruction but suppressed by exogenous hormone administration.

Step-by-Step Solution

Evaluate TSH and free T4 levels to establish the level of the defect.

Three patients have primary hyperthyroidism (low TSH, high free T4), while one has central hyperthyroidism (high TSH, high free T4).

This immediately isolates the central hyperthyroidism case (TSH-secreting adenoma).

Analyze the radioactive iodine uptake (RAIU) for the primary hyperthyroidism cases.

One patient has high/diffuse uptake (Graves disease), while two have severely decreased uptake.

High RAIU indicates de novo hormone production. Low RAIU indicates either release of preformed hormone or an exogenous hormone source.

Use serum thyroglobulin to distinguish the remaining two cases of primary hyperthyroidism with low RAIU.

The patient with elevated thyroglobulin and a tender neck has subacute thyroiditis. The patient with undetectable thyroglobulin has exogenous hormone ingestion.

Thyroglobulin is co-secreted during endogenous thyroid hormone release but is completely suppressed when exogenous hormone causes thyrotoxicosis.

Key Concept

The diagnostic workup of thyrotoxicosis relies on TSH and free T4 to identify the primary vs. central source, followed by radioactive iodine uptake and thyroglobulin to differentiate mechanisms of primary hyperthyroidism.

Question

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Topics

More questions from this topic