The thyroid gland lies in the neck in front of the trachea and just below the larynx. During pregnancy there is an increase in thyroid stimulation from increased estrogen, hCG, and other factors.
For many years it was thought that the thyroid gland itself enlarges during pregnancy. Current studies show that there is really very little actual enlargement of the gland. This is especially true in pregnant North American women who have diets relatively rich in iodine. A noticeable enlargement in the gland for these women would not be normal, and would require further evaluation.
The fetus needs a steadily increasing supply of maternal glucose (among other nutrients). One of the basic actions of thyroid hormones is to stimulate enzymes concerned with metabolism of nutrients, particularly the oxidation of glucose. The result of an increase in thyroid activity is an increase in the processing of glucose.
To properly process glucose, the mother will increase her own oxygen consumption. In fact, the pregnant woman does experience an increase in the basal metabolic rate (BMR) by about 20-30%.
Side effects of this kind of metabolic rate increase are very similar to signs of hyperthyroidism. They can include, fatigue, a feeling of anxiety, emotional lability, excessive sweating, heat intolerance, warm skin, breathlessness, ankle edema, full pulse, higher pulse rate and increased pulse pressure. It's often difficult to differentiate between symptoms of normal pregnancy, and a state of hyperthyroidism.
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Symptoms of normal pregnancy differ from those of hyperthyroidism.
To properly evaluate thyroid function and hormonal changes, it's important to remember the key features of hormone action. If a hormone molecule is bound, it's unable to interact with cell receptors. Only the "free" hormone is available to stimulate cell activity.
There are 2 thyroid hormones: the major hormone, thyroxine, T4, and triiodothyronine, T3. As we said earlier, during pregnancy there is an increase in thyroid stimulation. One reason this occurs is:
When assessing lab results of thyroid function, it's important to note the results of more than one test. For example note the "free" or "unbound" T4, the total T4, TBG, and TSH. Also, though the total T4 in a nonpregnant person ranges from 5 to 12 micrograms/dl, it ranges from 10 to 17 micrograms/dl during pregnancy. The increase in total T4 would give the appearance of hyperthyroidism, unless we knew that only the "free" or "unbound" T4 stimulates gland activity. True hyperthyroidism occurs in only 0.08% of pregnancies.
There are other sources of tissue and/or thyroid stimulation during pregnancy.
Please review this information about Hypothyroidism and Pregnancy, and the recommendations from the American Thyroid Association. Experts agree that pregnant women who underproduce thyroxine may have children with lower IQs and other learning problems.
According to this article, what is the most frequent cause of the inability of the maternal thyroid to produce enough thyroxine?
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Since glucose is needed for fetal growth, a benefit of increased thyroid activity during pregnancy is an increase in the processing of glucose.
Calcitonin is another hormone produced by the thyroid cells. The calcitonin-producing cells monitor the calcium level in the blood. If the blood calcium level rises, calcitonin is produced. Calcitonin then acts on bone cells to remove calcium from the blood and store it in bone, and on kidney cells to increase the excretion of calcium.
Calcitonin levels rise during pregnancy. The increase is stimulated by increased serum calcium and influenced by estrogen and hPL. The increased calcitonin inhibits calcium and phosphorus release from the bones, helping to conserve the mother's skeleton.