2 forms of circulating thyroid:

1. Protein-bound fraction (>99% --> large circulating reservoir pool of thyroid hormone)
2. Free fraction (active)

~70% bind to Thyroxine-binding globulin (TBG)

the remainder bind to albumin and transthyretin

Increased estrogen (eg, preg:, OCPs, PM HRT) raises circulating TBG levels --> reduce free T4 and T3 levels

Body in response boost the production until the additional TBG becomes saturated --> increase in TOTAL T4 and T3; but the patient remains euthyroid, as level of free thyroid hormones remains normal (also TSH is in the normal range)

Scenario:

If a woman with hypothyroidism on levothyroxine wanted to take OCP, then, the levothyroxine dose might need to be increased. In those patients. TSH levels should be checked 12 weeks after starting combined OCPs

Gestational Transient thyrotoxicosis

may occur during 1st trimester

due to hCG-mediatted thyroid stimulation

geneerally associated with minimal symptoms and mild biochemmical hyperthyroidism, with resolution as hCG levels decline after 12 weeks of pregnancy.

Mild = no adverse outcomes; no treatment

More severe form occur with hyperemesis gravidarum and molar pregnancy due to very high levels of hCG in these conditions.

Menstrual irregularities occur in both hyper- and hypothyroidism but via different mechanisms:

• in hypothyroidism, low T3/T4 increased TRH, which also stimulates Prolactin which in turns inhibits GnRH;
• in hyperthyroidism, increased production of binding globulins sequester sex hormones