Endo Disorders of Pregnancy Flashcards

1
Q

How does insulin response change during pregnancy? (2)

A
  • Insulin sensitivity increases in 1st trimester
    • Store fat while fetus is very small
  • Insulin resistance occurs in 2nd and 3rd trimester
    • Less glucose taken up by mother’s tissues, so can send glucose to growing baby
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2
Q

Healthy women maintain their sugar levels normal throughout pregnancy

A
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3
Q

Name 2 reasons that obese women have bigger babies.

A

Higher glucose levels

Higher TG levels

*This occurs even if the women don’t have gestational diabetes

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4
Q

What maternal glucose disorder produces major organ malformations?

A

Undiagnosed T2D during pregnancy

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5
Q

Compare the effect on the baby of undiagnosed T2D and gestational diabetes

A

Undiagnosed Type II diabetes -> organ malformations

Gestational diabetes -> big babies

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6
Q

How do we define GDM? (2)

A

Glucose intolerance recognized for the first time during pregnancy

*Excluding women with A1C above 6.5, FBG over 125, or random over 200 (overt diabetes)

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7
Q

What is the pathophysiology of gestational diabetes?

A
  1. Pregnancy causes insulin resistance
  2. Beta cells cannot produce sufficient insulin to compensate for insulin resistance
  3. Hyperglycemia
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8
Q

What should you consider in thin women with gestational diabetes?

A

They may have late onset Type 1 Diabetes instead

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9
Q

What is the major risk to the mother of gestational diabetes?

A

50% of mothers with GDM go on to develop T2D in the next 10 years

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10
Q

How should you manage GDM during pregnancy? (2)

How should you manage GDM post-partum? (3)

A

During pregnancy, lifestyle changes & insulin if necessary

After pregnancy,

  1. Postpartum oral glucose tolerance test
  2. Lifestyle changes & primary prevention
  3. Contraception
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11
Q

How do glucose and TG’s get across the placenta?

How does maternal insulin cross the placenta?

A

Glucose and TG’s freely diffuses across placenta

Maternal insulin cannot cross placenta

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12
Q

Name 4 potential effects on the baby of GDM

(size, glucose, heart, lungs)

A
  • Macrosomia (big baby)
  • Hyperglycemia in utero, followed by immediate hypoglycemia
  • Cardiac hypertrophy
  • Respiratory distress syndrome due to lung immaturity
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13
Q

How are TSH, TBG, total T4, and free T4 affected by pregnancy?

What causes this?

A
  • TSH is low early in pregnancy and later normalizes
    • due to hCG
  • TBG and total T4 increase
    • due to estrogen
  • Normal T4
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14
Q

A woman with hx of total thyroidectomy becomes pregnant. How should you adjust her levothyroxine dose?

A

Increase

More will be bound (increased TBG) and more will get degraded (placenta)

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15
Q

How are hyperemesis and thyroid function connected?

A
  • Hyperemesis is due to high bHCG
  • High bHCG can cause hyperthyroidism due to binding at TSH receptor
  • Both occur early in pregnancy (when hCG is highest)
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16
Q

Describe the pathogenesis of postpartum thyroiditis

A
  1. Anti-TPO Ab’s (Hashimoto’s) are suppressed during pregnancy
  2. After childbirth, rebound high levels of Ab’s
  3. Rapid destruction of thyroid causes hormone release and ensuing thyrotoxicosis
  4. Hyperthyroidism occurs initially, followed by hypothyroidism
17
Q

Where is fetal insulin from?

How is this affected by GDM?

A
  • Fetus synthesizes its own insulin
    • Mom’s can’t cross the placenta
  • However, glucose can freely cross placenta
  • GDM -> hyperglycemia in baby -> high fetal insulin production -> later insulin resistance
18
Q

Does mom’s amount of thyroid hormone synthesis change during pregnancy?

A

YES

Free thyroid hormone stays the same, but there is more TBG and so more thyroid hormone must be made total

19
Q

Is postpartum thyroiditis a hyperthyroid or hypothyroid state?

A

First hyperthyroid, then hypothyroid later

*BUT, it’s never increased production of thyroid hormones (only increased release)