Hx of large for gestational age infant hydramnios o Stillbirth miscarriage or

Hx of large for gestational age infant hydramnios o

This preview shows page 36 - 38 out of 53 pages.

Hx of large for gestational age infant, hydramnios o Stillbirth, miscarriage, or an infant w congenital anomalies during previous preg o Fam hx of type 2 diabetes (1 st degree relative) o Ethnicity - Pathophysiology o Body requires constant source of energy, provided by glucose
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Once glucose enters a cell, may undergo oxidative (glycolysis) or nonoxidative (glycogen synthesis) metabolism In response to glucose ingestion pancreatic beta cells of islets of Langerhans secrete insulin (hormone that promotes uptake of glucose into cells) o Changes in carb, protein, & fat metabolism in normal preg are profound o 1 st half of pregnancy anabolic phase associated w inc storage of fat & protein, along w inc in secretion of estrogen & progesterone these events lead to maternal hyperplasia & hyperinsulemia inc insulin production prompts an inc tissue response to insulin & inc uptake & storage of glycogen & fat in the liver & tissues o 2 nd hald of preg catabolic phase associated w breakdown of protein & fat also an inc insulin resistance caused by the heightened production of placental hormones (insulinase & human placental lactogen), cortisol, GH these hormones are diabetogenic & act as insulin antagonists in women who cannot meet the inc needs for insulin production, this change leads to an altered carb metabolism & progressively hyperglycemia o During this time, developing fetus continuously removes glucose & aa , substances that easily cross the placenta, from maternal circulation Bc insulin does not cross placenta, the fetus must inc its own insulin production Fetal hyperinsulemia develops & acts as a GH that contributes to an inc in fetal size (marosomia), & a dec in pulmonary surfactant production When preg woman’s BG levels remain abnormally elevated, there is a constant transport of maternal glucose across the placenta This glucose load prompts fetus to produce insulin at greater rate to use the glucose - Maternal and Perinatal Morbidity & Mortality o Changes in maternal milieu that characterize the diabetic state can have profound effects on the growth & development of fetus, inc risk of perinatal morbidity&mortality, & exert adverse effects throughout life o Physiological adaptations induced by preg can unmask latent maternal diabetes or result in transient worsening of preexisting vascular compromise o Diabetic W are 4x more likely to develop preeclampsia or eclampsia than are nondiabetic W & 2x as likely to experience SAB o Rates of infection, hydramnios, PPH, c/s birth are inc o In long term, GDM is associated w impaired insulin tolerance & the manifestation of diabetes in later life o Major fetal effects w diabetes include a 5fold inc in perinatal death & 2-3fold inc in rate of congenital malformations o Early in preg fetus is @ risk for congenital malformations & poor fetal growth o Risk of congenital defects is 4-8% greater w type 1 or type 2 diabetes o Congenital defects result from teratogenic effects of hyperglycemia during the time of organogenesis during early gestational wks o
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