Thyroid disorder in pregnancy

What primary hormonal change causes the rise in Thyroid Binding Globulin (TBG) during pregnancy, and when does it plateau? +1

It is driven by estrogen-driven glycosylation from the corpus luteum. It triples by 20 weeks of gestation.+2

Why are measurements of Total T4 and Total T3 considered unreliable for diagnosis during pregnancy?

Because total thyroid hormone levels increase significantly due to the rise in TBG, making them an inaccurate reflection of thyroid status.

What is "Hormone Spillover Syndrome" in the first trimester, and what causes its biochemical picture?

It occurs when high levels of hCG (which shares an alpha unit with TSH) stimulate TSH receptors. This results in raised free T4 and lowered TSH.+1

How does maternal thyroxine transfer to the fetus change before and after 12 weeks' gestation? +1

Before 12 weeks: Maternal T4 (but not fT3) crosses the placenta for fetal brain development. After 12 weeks: The placenta prevents significant passage, and the fetal thyroid functions independently.+1

What is the compensatory role of Deiodinase II (D2) as gestation advances, especially if fT4 is low? +3

It increases in concentration to convert T4 into the active T3 locally (predominantly in the brain) to ensure adequate fetal development despite low systemic fT4.+2

What are the defining clinical features of Cretinism (untreated congenital hypothyroidism)? +1

Mental retardation, growth failure, macroglossia, coarse facial features, umbilical hernia, hypotonia, and prolonged neonatal jaundice.

Which laboratory test is considered the "best screen" for hypothyroidism in pregnancy?

Thyroid Stimulating Hormone (TSH).

How is "Subclinical Hypothyroidism" biochemically defined in a pregnant patient?

Normal fT4 levels with a raised TSH in an asymptomatic patient.

Should thyroxine dose adjustments be guided by clinical symptoms or laboratory findings? +2

They must be guided by laboratory findings using trimester-specific reference ranges, as symptoms often mimic normal pregnancy.+2

What are the major maternal and fetal complications associated with hyperthyroidism/Graves' disease?

Maternal: Preeclampsia (PET), heart failure, and thyroid storm. Fetal: IUGR, prematurity, stillbirth, and tachycardia.+2

What are the clinical "good indicators" of thyrotoxicosis that distinguish it from normal pregnancy?

Failure to gain weight despite good appetite, resting tachycardia >100 bpm that fails to slow with Valsalva, and onycholysis.

Why is Propylthiouracil (PTU) preferred over Carbimazole/Methimazole in the first trimester?

Because Carbimazole/Methimazole are associated with Aplasia Cutis (scalp defects) in the fetus. PTU has fewer associated adverse effects early on.

What is the target range for fT4 and fT3 when treating hyperthyroidism with antithyroid drugs? +1

Levels should be maintained in the high normal range to minimize the risk of inducing fetal hypothyroidism.+1

Why is Radioactive Iodine (I131) strictly contraindicated during pregnancy?

It crosses the placenta and binds to/destroys the fetal thyroid gland.

In the management of Thyroid Storm, why is Iodide administered several hours after the antithyroid drug (PTU)?

To prevent the thyroid gland from using the iodide to build up and store more thyroid hormones before the synthesis is blocked by PTU.

What is the relationship between hypothyroidism and amniotic fluid volume? +1

Hypothyroidism is linked to oligohydramnios (due to reduced fetal renal perfusion), whereas hyperthyroidism may cause polyhydramnios.+1