Thyroid disorders are common among women of childbearing years. However, the diagnosis of thyroid disorders during pregnancy is confounded by the normal alteration in thyroid physiology. Serum TSH levels decrease at the end of the first trimester, mirroring the increase in serum hCG levels; hCG is thyrotropic and causes a slight increase in serum free T4 concentrations. With the drop in serum hCG as pregnancy progresses, serum free T4 levels decline and may decrease below the nonpregnant reference range by the third trimester. Furthermore, women with hyperemesis gravidarum may have more pronounced changes in serum TSH and free T4 levels, rendering the differentiation between true hyperthyroidism and gravid physiology even more challenging. Once recognized, proper management of thyroid dysfunction is essential for a healthy pregnancy. Abnormalities in maternal thyroid function can adversely affect the fetus both directly, via transplacental passage of abnormal maternal hormone concentrations, TSH receptor antibodies, or prescribed antithyroid medications, and indirectly, via altered maternal gravid physiology. Graves disease affects ∼0.2% of all pregnancies. To optimize fetal thyroid function, antithyroid drug dosage must be titrated to maintain the maternal free T4 level at or just above the NONpregnant reference range. At the end of the 2nd trimester, ultrasound monitoring is required to assess the presence of fetal Graves disease, which can occur even in levothyroxine (L-T4) replaced hypothyroid women with I-131 ablated Graves disease. For hypothyroid women, L-T4 dosage must be adjusted (average increase ∼45%) to maintain the serum TSH <2.5 mIU/L, which replicates the normal TSH decline throughout gestation. Elevations in maternal serum TSH levels during pregnancy have been adversely associated with alterations in the offsprings cognitive performance.