pregnancy endocrine disorders Flashcards

1
Q

insulin resistance throughout pregnancy

A

Insulin sensitive 1st trimester. Insulin requirements decrease in pre-existing DM. Women at risk for severe nocturnal hypoglycemia 1st trim. Early pregnancy: Anabolic with lipogenesis. Insulin resistance late 2nd and 3rd with increased hPL, hPGH, TNFα. Women with pre-existing diabetes will double to triple their insulin requirements in 2nd and 3rd trimester

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2
Q

metabolism in late pregnancy

A

catabolic: increased lipolysis (less insulin suppression of lipolysis), Glycogen stores depleted rapidly due to fetal-placental growth requirements. Pregnant women shift from carb to fat metabolism within 12 hrs due to depleted glycogen. Pregnant women utilize fat as fuel to conserve glucose for fetal-placental unit resulting in increased ketones and risk of DKA.

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3
Q

Which women have fatter babies

A

obese women without gestational diabetes

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4
Q

plasma glucose levels in pregnancy

A

Normal pregnancy is associated with lower fasting plasma glucose, presumably due to an increase in glucose uptake by the fetoplacental unit. However, postprandial glucoses may be slightly higher and associated with hyperinsulinemia

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5
Q

gestational diabetes

A

•Glucose intolerance recognized for the first time during pregnancy. Undiagnosed Type 2 (or Type 1) with elevated A1C have risk for major malformations (3-10 weeks). Most women diagnosed before 24 weeks have IGT (pre-diabetes) and are at very high risk for developing Type 2 postpartum

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6
Q

pathophys of gestational diabetes

A

•Vast majority are overweight and insulin resistant.insulin resistance, impaired insulin secretion, and increased hepatic glucose production all contribute. The women who are not overweight have primarily an insulin secretion defect and may ave autoimmune form of diabetes.

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7
Q

GDM affects on fetus

A

The excessive transfer of glucose, amino acids, and FFAs from the mother to fetus induces fetal hyperglycemia, which results in fetal pancreatic islet hypertrophy and beta-cell hyperplasia with consequent fetal hyperinsulinemia.

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8
Q

infant morbidity associated with GDM

A

Excessive fetal growth places fetus at risk for shoulder dystocia and delivery complications. Also infant respiratory distress (hyperinsulinemia inhibits cortisol production of type II cells so lecithin is decreased), neonatal hypoglycemia (hyperinsulinemia), hyperbilirubinemia, mortality (increased insulin causes increased metabolic rate and hypoxemia) polycythemia and risk of childhood obesity/ diabetes

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9
Q

glucose tolerance test in GDM

A

blood sugar levels and insulin levels are higher in GDM

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10
Q

GDM risks to mom

A

•~50% Maternal risk of developing Type 2 DM in 5-10 years . Higher risk infection, C-section, Preeclampsia, preterm labor from polyhydramnios

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11
Q

GDM postpartum management

A

measure OGTT at 6-12 weeks post partum. If pre-diabetes us diet, exercise and possibly meds.

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12
Q

GDM diagnostic criteria

A

Following a 100g OGTT done at 24-48 weeks, or first prenatal visit if high risk: one or more of the following is diagnostic- Fasting blood glucose >95mg/dl, 1hr > 180, 2hr > 155, 3hr > 140

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13
Q

how is overt diabetes diagnosed during pregnancy

A

fasting blood glucose >126, A1C > 6.5% or random blood glucose > 200

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14
Q

Factors Associated with high BMI at 2-3 yr

A

maternal BMI, lipids, dietary fat, glucose (DM or GDM). Breast feeding is protective

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15
Q

Which form of diabetes is associated with major malformation of spine and heart

A

uncontrolled type 1 or type 2 diabetes in which hyperglycemia occurs during first trimester.

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16
Q

which criteria would support testing for diabetes at first prenatal visit

A

Obesity, Personal history of GDM or previous macrosomic infant, Family history of diabetes in a first degree relative, Polycystic ovarian ds (PCOS), High Risk Ethnic group, or Glycosuria most recs

17
Q

what is the screening method used for GDM

A

50g OGTT. If glucose >140, use diagnostic 100g OGTT.

18
Q

when does the ffetus start producing its own thyroid hormones

A

18 weeks- until then it relies on moms

19
Q

thyroid function/ hormone levels during pregnancy

A

TSH is nl or slightly decreased during 1st and 2nd trimesters due to elevated hCG. Thyroid binding globulin increases due to estrogen. Total T4 and T3 increase by 50%, but free T4 is nl. Iodine requirements increase.

20
Q

cretinism

A

mental retardation due to maternal and fetal iodine deficiency

21
Q

maternal hypothyroidism

A

most due to hashimotos. Most wmen require 25% increase in thyroid hormone supplements early in gestation. Hypothyroidism can cause neurodevelopmental delay in offspring, pregnancy loss, preterm delivery, preeclampsia, abrptio placenta

22
Q

most common cause of maternal hyperthyroidism

A

graves dz- but cant use a radioactive iodine thyroid scan during pregnancy to confirm

23
Q

maternal hyperthyroidism sx

A

Normal pregnancy mimics thyroid excess- increased HR, C.O., flow murmur, heat intolerance, vasodilation.

24
Q

subclinical hyperthyroidism

A

subclinical hyperthyroidism (suppressed TSH only) appears not to cause adverse pregnancy outcomes and treatment with antithyroid agents could be detrimental and result in fetal hypothyroidism

25
Q

gestational hyperthyroidism

A

hCG stimulation of thyrocytes may cause hyperthyroidism, resulting in transient subclincal hyperthyroidism. If HcG is abnormallly high (hyperemesis gravidarum, molar pregnancy, multiple pregnancy) symptomatic hyperthyroidism can also occur

26
Q

treatment of gestational hyperthyroidism

A

hCG levels decline in second and third trimester, resulting in spontaneous resolution of the hyperthyroid state so that it is unnecessary to treat gestational hyperthyroidism with antithyroid medication

27
Q

thyroid storm in pregnancy

A

can be precipitated in pregnancy by labor, toxemia, placenta previa, infection, or trauma. It usually occurs in individuals with untreated or poorly controlled disease with a large goiter. This is a serious medical emergency which must be considered and diagnosed quickly followed by aggressive treatment in an intensive care setting. Steroids, beta-blockers, antithyroid drugs, and cold iodine can be given as necessary.

28
Q

Effect of Hyperthyroidism on Pregnancy

A

uncontrolled may cause severe preeclampsia, increased risk of low birth weight, prematurity and placental abruption. Impairment of fetal hypothalamic-pituitary-thyroid axis, leading to congenital hypothyroidism. Placental transfer of thyroid stimulating immunoglobulin can cause neonatal Graves disease (fetal tachycardia, cardiac failure, hydrops, IUGR, fetal goiter). If mom is on antithyroid meds, fetus may not become hyperthyroid until after birth and present with irritability, poor feeding, tachycardia.

29
Q

hyperthyroidism management in mom

A

use lowest dose of antithyroid possible and titrate the total T4 in the high normal range for pregnancy (50% above non pregnant range). Don’t use TSH to titer

30
Q

post-partum thyroiditis

A

Associated with high levels of antiperoxidase (TPO) abs. Histology identical to Hashimoto’s thyroiditis. Hyperthyroid phase followed by hypothyroid phase

31
Q

Postpartum Thyroiditis–Hyperthyroid Phase

A

2-4 mos postpartum. Often clinically silent: weight loss, palpitations, nervousness, insomnia. Due to destruction of the thyroid gland and release of thyroid hormone. Treatment: Beta-blockers. Differentiate from PP exaccerbation of Grave’s

32
Q

Postpartum Thyroiditis–Hypothyroid Phase

A

Occurs 4-8 mos postpartum. Often unrecognized: fatigue, depression, weight gain. Due to continued destruction of gland. Treatment: Thyroid hormone for 6-12 months. Recheck TSH after withdrawing thyroid hormone for 6 weeks. Permanent hypothyroidism in 10-40%. Need long-term follow-up