Thyroid disease in pregnancy Flashcards

1
Q

What are the clinical features of thyroid disease in pregnancy?

A

Classical features such as heat intoleance, constipation, fatigue, palpitations and weight gain may resemble those of normal pregnancy and so new presentations can be difficult to detect

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2
Q

What investigations are used to diagnose thyroid disease in pregnancy?

A
  • Free T4
  • Free T3
  • TSH

NB: thyroid hormone reference ranges are unlikely to be useful in pregnancy due to physiological changes such as plasma volume expansion, increased TBG, and relative iodine deficiency.

Total T3 and T4 should not be used.

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3
Q

What is the target TSH level in pregnancy?

A

TSH < 4mmol/l

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4
Q

What physiological changes to thyroid hormone regulation occur during pregnancy?

A

Increased thyroxine-binding globulin (TBG) - this increases the levels of total thyroxine but does not affect the free thyroixine level

First trimester - decrease in TSH and a rise in fT4 concentrations in normal pregnancy

Later gestations - fall in fT4 concentration

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5
Q

What are the most common causes of thyrotoxicosis in pregnancy?

A

Graves’ disease/autoimmune thyrotoxicosis - affects 2 per 1,000 pregnancies (most common cause of maternal hyperthyroidism causing 95% of cases)

Transient gestational hyperthyroidism - activation of TSH-R by HCG

Other causes (5%):

  • toxic adenoma,
  • subacute thyroiditis
  • toxic multinodular goitre
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6
Q

What are the clinical features of Graves’ disease?

A
  • tremor,
  • sweating,
  • insomnia,
  • hyperactivity
  • anxiety
  • goitre,
  • Graves’ ophthalmopathy,
  • tachycardia,
  • hypertension with a wide pulse pressure,
  • weight loss
  • pretibial myxoedema
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7
Q

What are the risks of untreated thyrotoxicosis in pregnancy?

A
  • Miscarriage
  • Maternal heart failure
  • Premature labour
  • FGR
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8
Q

What trimester does transient gestational hyperthyroidism usually occur and why?

A

First - levels of HCG are highest and may activate the TSHr. . HCG levels will fall in the second and third trimester

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9
Q

What is the management (monitoring and medical)of hyperthyroidism during pregnancy?

A

Antenatally

Monitoring TFTs - should be checked every 2-4 weeks to ensure biochemical euthyroidism (TSH <4mmol/L). Maternal free thyroxine should be kept in the upper third of the normal reference range to avoid hypothyroidism. NB: 1/3 are able to stop treatment during pregnancy

Medical

  • Beta blockers - can be used before antithyroid drugs take effect
  • 1st trimester: Propylthiouracil (PTU).
  • For the rest of pregnancy: Carbimazole.

Surgery - rarely done but can be considered if retrosternal goitre is causing upper airways obstruction due to tracheal compression, or if there is a suspicion of malignancy or failed medical therapy

Postnatally - TFTs monitoring at 6-8 weeks postnatal check with GP

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10
Q

How should babies born to mothers with TSHr antibodies in Graves’ be managed postnatally?

A

Review after birth by neonatology team to exclude thyroid dysfunction associated with maternal antibody passage

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11
Q

What are the side effects associated with PTU and carbimazole?

A
  • PTU - severe hepatic injury
  • Carbimazole - risk of congenital abnormalities is higher than with PTU if used in the first trimester
  • Both - agranulocytosis [safety-net + check WCC]

PTU/carbimazole should be continued at lowest acceptable doses according to TFTs as higher doses may cross the placenta and cause fetal hypothyroidism.

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12
Q

Which hyperthyroidism treatments are contraindicated in pregnancy?

A
  • block-and-replace regimes should not be used in pregnancy
  • radioiodine therapy is contraindicated - completely obliterates the fetal thyroid gland
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13
Q

What investigation done in the third trimester can help determine risk of neonatal thyroid problems in maternal thyrotoxicosis?

A

TSH receptor stimulating antibodies- checked at 30-36 weeks gestation to help determine the risk of neonatal thyroid problems

These Abs cross the placenta and the risk of fetal Graves’ disease after 20 weeks is proportional to their level, although still very low overall, as <10% of Graves’ disease is associated with high levels of antibodies

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14
Q

What are the clinical features of thyroid storm in pregnancy? What can it mimic?

A
  • excessive sweating,
  • pyrexia,
  • tachycardia,
  • atrial fibrillation,
  • hypertension,
  • hyperglycaemia,
  • vomiting,
  • agitation
  • cardiac failure

May be associated with labour and it can mimic imminent eclampsia.

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15
Q

What is the management of thyroid storm in pregnancy?

A
  • PTU
  • High dose corticosteroids
  • Beta-blockers - block peripheral effects of thyroixine
  • Supportive rehydration
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16
Q

What are the three stages of post-partum thyroiditis?

A

Three stages

  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Normal thyroid function (but high recurrence rate in future pregnancies)
17
Q

What antibodies may be found in post-partum thyroiditis?

A

Thyroid peroxidase antibodies are found in 90% of patients

18
Q

What is the management of postpartum thyroiditis?

A

Thyrotoxic phase: propranolol (anti-thyroid drugs are avoided as the thyroid is not overactive

Hypothyroid phase: thyroxine.

19
Q

How common is hypothyroidism in pregnancy? What are the most common causes?

A

Affects 1%

  • Iodine deficiency (most common cause globally)
  • AI Hashimoto’s thyroiditis (most common cause in developed world)
20
Q

What is the management of hypothyroidism in pregnancy?

A

Antenatally

Monitoring TFTs - should be checked in each trimester to ensure biochemical euthyroidism (TSH <4mmol/L) and more often if necessary

Medical

  • Thyroxine - continue as normal but adjust dose throughout pregnancy according to TFTs. Higher doses required, up tp 50% higher, as early as 4-6 weeks of pregnancy.

Postnatally

  • Advise that breastfeeding is safe on thyroxine
  • Monitor TSH 6-8 weeks postpartum at GP
21
Q

What are the risks of hypothyroidism in pregnancy?

A

Maternal T4 levels are most important in the first trimester of pregnancy, where suboptimal replacement therapy is associated with developmental delay and pregnancy loss in some studies.

Corrected hypothyroidism does not affect pregnancy outcomes