This question is phrased strangely, but it's essentially asking "what would happen if this woman's hypothyroidism became uncontrolled over the course of her pregnancy?"

currently her TSH is good --> well-controlled hypothryoidism HYPOTHETICAL high TSH --> her hypothyroidism must NOT be well-controlled (due to disruption of the T3/T4/TRH/TSH endocrine axis)

So, now that we understand that the question is asking "what would happen if her hypothyroidism was uncontrolled?"

Answer: cretinism

I think that this question is phrased atrociously, but far be it from me to criticize the USMLE licensing board...

This has to do with understanding two things, that maternal hypothyroidism is linked to Cretinism/neural development of the fetus, and normal pregnancy physiology. In pregnancy, increased hormones stimulate liver production of various proteins like Sex Hormone Binding Globulin (SHBG),Thyroxine Binding Globulin (TBG), etc. More TBG produced = more T3/T4 is bound. Less T3/T4 causes more TRH release, more TSH release, and more T3/T4 production until free T3/T4 levels are back to normal. In a normal pregnancy, this happens no problem. In someone with pre-existing hypothyroidism though, already has impaired T3/T4 production, and won't be able to keep up with increased demand. Their T3 will rise, but this won't result in increased T3/T4. Typically, women with Hashimoto's desiring to get pregnant will need to increase their levothyroxine dose in anticipation of this pregnancy change.

Normally maternal T3/4 are required for fetal brain development before fetal thyroid gland is formed. And after fetal thyroid gland is formed, fetal T3/4 helps in brain development. So increase TSH means decreased maternal T3/4 and thus have abn brain development. And yes T3/4 crosses placenta.

Autoimmune thyroiditis (aka Hashimoto) + pregnant--> Think about possibility of fetal hypothyroidism due to antibody mediated maternal hypothyroidism. Leads to Cretinism. Findings in infant are the 6'P (Pot belly, Pale, Puffy face, Protruding umbilicus, Protuberant tongue, and Poor Brain development.

The real thing is TSH, T3, T4 and thyroglobulin cannot cross placenta. TRH, Iodine, TSI can cross. If mother has high TSH (considering primary hypothyroidism) —> Poor brain development If mother has TSI (Hashimoto) —> cross the placental barrier —Increase in thyroid gland (May present with stridor at birth.

I think this gets at a concept related to thyroid levels and pregnancy/estrogen.

Estrogen increases the level of thyroxine-binding globulin, which temporarily decreases free T4 and T3, and increases TSH until the additional TBG becomes saturated, and normal levels are restored.

Since this patient has autoimmune thyroiditis, and requires thyroxine, when her free T4 decreases, and her TSH goes up, she wont make extra T4. So unless she increases her thyroxine dose, she will be hypothyroid --> cretinism in the fetus

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270981/

This article fails to mention poor brain development in HYPERthyroidism. The author must have meant HYPOthyroidism.

This question upsets me to no end.

My thought process was if the mother has increased TSH, she'd be using more iodine to produce T3/4. Meaning less would be able to get to the baby for brain development.

This is a very tricky question in terms of phrasing it. They make us think about what effect high TSH does on a fetus while it really meant what can happen to the baby in an antibody-mediated hypothyroidism mother. So sneaky so so sneaky...

Cretinism (congenital hypothyroidism) is the most common cause of treatable mental disability. Causes poor brain development.