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a counter argument for PGE if you chose that answer. However, the author believes oxytocin is superior.
1) PGE rises initially that causes the uterine contractions= this would be equivalent to when someone say #of contractions per time period.
2) Oxytocin is increased when the cervix is manipulated (ie. the birth canal reflex).
Please why is estrogen not the answer, I thought estrogen would upregulate oxytocin receptors and increase oxytocin secretion?
I don't understand the last part of this question stem though... if the mother's TSH *increases* during pregnancy? Wouldn't this further increase her (and/or the fetus's) production of T4 and thus counteract the hypothyroidism?
@neonem no. Autoimmune hypothyroidism is a destruction of the thyroid gland, and a decrease in production of T3/T4.
An increase in TSH means that there is not enough T3/T4 to inhibit TRH, and so TSH is being released to stimulate the thyroid gland.
TSH, T3, T4 and thyroglobulin cannot cross the placental barrier.
@arezpr although those hormones can't cross, the autoantibodies from Hashimoto's can
TSH comes from the pituitary, and act on the thyroid. Autoantibodies attack the thyroid, so TSH doesn't work.