Thyroid Pregnancy Flashcards

0
Q

First, maternal total or bound thyroid hormone levels increase with serum concentration of thyroid-binding globulin. Second, the level of thyrotropin (also known as thyroid-stimulating hormone [TSH]), which plays a central role in screening for and diagnosis of many thyroid disorders, decreases in early pregnancy because of weak stimulation of TSH receptors caused by substantial quantities of human chorionic gonadotropin (hCG) during the first 12 weeks of gestation.

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1
Q

Maternal thyroid volume is 30% larger in the third trimester than in the first trimester (1). In addition, there are changes to thyroid hormone levels and thyroid function throughout pregnancy.

A

True

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2
Q

Physiologic thyroid changes during pregnancy are considerable and may be confused with maternal thyroid abnormalities. Maternal thyroid volume is 30% larger in the third trimester than in the first trimester (1). In addition, there are changes to thyroid hormone levels and thyroid function throughout pregnancy. Table 1 depicts how thyroid function test results change in normal pregnancy and in overt and subclinical thyroid disease. First, maternal total or bound thyroid hormone levels increase with serum concentration of thyroid-binding globulin. Second, the level of thyrotropin (also known as thyroid-stimulating hormone [TSH]), which plays a central role in screening for and diagnosis of many thyroid disorders, decreases in early pregnancy because of weak stimulation of TSH receptors caused by substantial quantities of human chorionic gonadotropin (hCG) during the first 12 weeks of gestation. Thyroid hormone secretion is thus stimulated, and the resulting increased serum free thyroxine (T4) levels suppress hypothalamic thyrotropin-releasing hormone, which in turn limits pituitary TSH secretion. After the first trimester, TSH levels return to baseline values and progressively increase in the third trimester related to placental growth and production of placental deiodinase (2). These physiologic changes should be considered when interpreting thyroid function test results during pregnancy (Table 1).

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3
Q

Maternal T4 is transferred to the fetus throughout the entire pregnancy and is important for normal fetal brain development.

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4
Q

Hyperthyroidism is characterized by a decreased TSH level and an increased free T4 level (Table 1).

A

Decrease tsh

Increased free t4

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5
Q

Hyper-thyroidism occurs in 0.2% of pregnancies; Graves disease accounts for 95% of these cases

A

Graves’ disease accounts 95%

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6
Q

The signs and symptoms of hyperthyroidism include

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nervousness, tremors, tachycardia, frequent stools, excessive sweating, heat intolerance, weight loss, goiter, insomnia, palpitations, and hypertension

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7
Q

Distinctive symptoms of Graves disease are

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ophthalmopathy (signs include lid lag and lid retraction) and dermopathy (signs include localized or pretibial myxedema).

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8
Q

Inadequately treated maternal thyrotoxicosis is associated with a greater risk of severe preeclampsia and maternal heart failure than treated, controlled maternal thyrotoxicosis

A

True

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9
Q

*The level of TSH decreases in early pregnancy because of weak TSH receptor stimulation due to substantial quantities of human chorionic gonadotropin during the first 12 weeks of gestation. After the first trimester, TSH levels return to baseline values.

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T

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10
Q

Overt hyperthyroidism

A

Tsh decrease

Free t4 increase

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11
Q

Subclinical hyperthyroidism Decrease No change

A

Tsh decrease

Free t4 no change

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12
Q

Overt hypothyroidism Increase Decrease

A

Tsh increase

Free t4 decrease

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13
Q

Subclinical hypothyroidism Increase No change

A

Tsh increase

Free t4 no change

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14
Q

Inadequately treated hyperthyroidism is associated with an increase in

A

medically indicated preterm deliveries, low birth weight, and possibly fetal loss

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15
Q

In most cases of maternal hyperthyroidism, the neonate is euthyroid. Fetal and neonatal risks associated with Graves disease are related either to the disease itself or to thioamide treatment of the disease.

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16
Q

large proportion of thyroid disease in women is mediated by antibodies that cross the placenta, there is a legitimate concern about the risk of development of immune-mediated hypothyroidism and hyperthyroidism in the neonate.

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T

17
Q

Pregnant women with Graves disease can have thyroid-stimulating immunoglobulin and TSH-binding inhibitory immunoglobulins, also known as thyrotropin-binding inhibitory immunoglobulins, that can stimulate or inhibit the fetal thyroid, respectively.

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T

18
Q

. In some cases, maternal TSH-binding inhibitory immunoglobulins may cause transient hypothyroidism in neonates of women with Graves disease

A

T

19
Q

1–5% of these neonates have hyperthyroidism or neonatal Graves disease caused by the transplacental passage of maternal thyroid-stimulating immunoglobulin

A

T but incidence is low because of the balance of stimulatory and inhibitory antibodies as well as thioamide treatment

20
Q

The possibility of fetal thyrotoxicosis should be considered in all women with a history of Graves disease (5). If fetal thyrotoxicosis is diagnosed, consultation with a clinician with expertise in such conditions is warranted.

A

The incidence of neonatal Graves disease is unrelated to maternal thyroid function. The neonates of women with Graves disease who have been treated surgically or with radioactive iodine-131 before pregnancy and whose mothers required no thioamide treatment are at higher risk of neonatal Graves disease because they lack suppressive thioamide

21
Q

Routine evaluation of fetal thyroid function, including fetal thyroid ultrasonographic assessment, umbilical cord blood sampling, or both, is not recommended (13, 14). However, because maternal hyperthyroidism can be associated with fetal hydrops, growth restriction, goiter, or tachycardia, fetal thyroid disease should be considered in the differential diagnosis in these cases, and consultation with an expert may be appropriate (15

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