Term
| regardless of DM, what is the major fuel source for the developing fetus? what is the effect of this on the mother? |
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Definition
| carbohydrates (coming from the mother) - which means the mother will normally have a mild fasting hypoglycemia (60-70 mg/dL ) and a postprandial hyperglycemia. |
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Term
| what are other normal effects of pregnancy on the mother in terms of glucose metabolism besides mild fasting hypoglycemia/postprandial hyperglycemia? what is largely responsible for these changes? |
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Definition
| increased plasma volume, a progressive increase in tissue insulin resistance, increase in insulin secretion (to maintain euglycemia), suppressed glucagon response, and increased prolactin and cortisol. many of these changes are due to human placental lactogen (HPL - insulin antagonist from the placenta), which has GH-like effects on the mother - creating an insulin-resistant environment in her. |
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Term
| what is the normal/healthy response to the HPL-mediated insulin-resistant environment in pregnant women? |
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Definition
| creating of more insulin and normalization of glucose levels |
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Term
| what is the diabetogenic state which occurs to some pregnant pts? |
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Definition
| in this state, the mother can no longer make enough insulin to overcome the insulin-resistant environment mediated by HPG and *glucose levels trend higher than usual. therefore, pregnancy induced hyperinsulinemia + pregnancy induced hyperglycemic environment = *gestational diabetes (GDM). |
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Term
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Definition
| gestational diabetes is any degree of hyperglycemia diagnosed during pregnancy (7% of pregnancies). pregnancy induced DM may unmask the onset of beta-cell defects (hallmark of GDM), where the pregnant pt's glucose goes up postprandially, but then does not fall. these pts generally do not have nocturia or hematuria (may be asymptomatic) and their glucose values usually revert to normal immediately following delivery. |
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Term
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Definition
| usually after 24-28 wks, once the placenta has started to produce HPL (if you see hyperglycemia before the first trimester, the pt had undiagnosed DM before getting pregnant). |
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Term
| what are the possible immediate complications of GDM? |
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Definition
| preeclampsia, polyhydramnios, fetal macrosomia, birth trauma, neonatal metabolic complications (hypoglycemia, hyperbilirubinemia, hypocalcemia, erythremia), fetal growth disorders, neural tube defects, and alteration of obstetrical management issues (increased frequency of C-sections) |
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Term
| what do the mother/offspring risk developing later w/GDM? |
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Definition
| perinatal mortality/birth trauma (shoulder dystocia), later development of DM in the mother, later development of DM in the fetus (type II), increased risk of *obesity/glucose intolerance/DM developing when newborn is teen/young adult, and development of *metabolic syndrome* in the mother (hyperglycemia, increased lipids, HTN). |
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Term
| what can a mother w/GDM do to reduce risk of developing type II DM? what ethnicity is at particular risk for this? |
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Definition
| *lifestyle modifications to achieve normal body weight* hispanic women are at particular risk for this. |
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Term
| what is the pathogenesis of insulin resistance? |
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Definition
| insulin sensitive cells such as skeletal/adipose/hepatic cells develop impaired glucose transport due to a disruption in insulin signaling. one mechanism for this is *increased phosphatidyl 3-kinase - which *inhibits tyrosine kinase activity. |
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Term
| what characterizes the placenta's role in GDM? |
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Definition
| the placenta is the primary interface between the mother and fetus, responsible for transferring glucose from the mother to child. however, if the placenta increases expression of TNF-alpha, IL-6, and leptin and these substances accumulate - they can antagonize insulin, leading to resistance and hyperglycemia. |
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Term
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Definition
| an infant at birth w/increased amounts of body fat - due to overexposure to insulin, which is a growth hormone. this leads to increase adipose in fat cells - not just subcutaneous, but in the liver (visceral fat: responsible for insulin resistance and metabolic syndrome). |
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Term
| what is the pathogenesis of macrosomia? |
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Definition
| maternal insulin does not cross the placenta, but glucose does. if the mother has hyperglycemia - so does the baby, and it has to increase it's own insulin production - to the point of fetal hyperinsulinemia (whose body responds by reducing blood glucose and laying down more fat). |
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Term
| what are GDM risks related to ethnicity? |
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Definition
| there is a higher prevalence of GDM in african amerians, hispanics, native americans, and east asian islanders. |
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Term
| what are GDM risk factors not related to ethnicity? who does not need to be screened? |
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Definition
| a body mass index > 25, hx of abnormal glucose tolerance, hx of adverse pregnancy outcome (previous overweight baby etc), a 1st degree relative w/DM, and women > 25. *pts w/o any of these characteristics or ethnic background do not need to be screened for GDM - but everyone generally gets screened at least once prenatally* |
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Term
| what GDM screening procedure has good sensitivity and specificity? |
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Definition
| the 50 g glucose challenge test (GCT) |
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Term
| how is the GDM screening procedure carried out? |
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Definition
| at *24-28 wks, the pt is given a 1 hr 50 gm glucose challenge. if their serum glucose is still >140 mg/dl, this is considered a positive screening test and the 100 gm 3 hour oral glucose tolerance test is performed. then if 2+ of the following values: pt's fasting serum glucose is >95, 1 hour is >180, 2 hour is >155, or 3 hour is >140 mg/dl - this test is positive and the pt is diagnosed w/GDM. (also if the screening test is just below 140, then it repeating the test is probably a good idea). |
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Term
| what is the most common and significant neonatal complication of GDM? |
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Definition
| macrosomia, which is a birth wt > 90th percentile for gestational age/sex. usually, normalization of maternal glucose will prevent this - but it can still occur outside of normalized maternal glycemia (may be due to other factors). |
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Term
| why does GDM require intensive therapy? |
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Definition
| intensive management of GDM is associated w/a decrease in mortality and morbidity in infants and w/appropriate therapy, fetal death is not detectably higher than in the general population. |
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Term
| what are the goals of GDM therapy? |
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Definition
| fasting serum glucose < 90 mg/dl, 1 hour postprandial less than 120 mg/dl, and a normal Hgb A1C (< 6.5) |
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Term
| how is GDM therapy carried out? |
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Definition
| lifestyle modifications are enacted for 1 week, after which blood sugars are retested (specifically look for blood sugar trends in the 3rd trimester). if lifestyle modifications do not have enough of an effect, insulin therapy (more common) or sulfonylureas (less common) are administered. |
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Term
| what is the rate of congenital anomalies affecting children w/DM? |
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Definition
| children w/DM have a 4-10x increase in congenital anomalies - so need to test for these (AFP for neural tube defect etc). |
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Term
| what is the challenge w/using the Hgb A1C to check pts glucose levels? |
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Definition
| pregnant pts's bodies change drastically, and since this is a 3 month test - it may not be sensitive to more subtle changes w/in that window. therefore there is a fructosamine 10 day fingerstick test which is not as standardized, but may give more specific information about that pt's stage in pregnancy. |
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Term
| what is a consideration for PCOS (polycystic ovarian syndrome) and GDM? |
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Definition
| PCOS pts use metformin, which can create an insulin resistant environment - so they probably need to stay off this drug for the first trimester. |
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Term
| what is the vicious GDM cycle? |
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Definition
| children born to mothers w/GDM are more likely to develop DM, and if they become parents, they are more likely to develop GDM and so on. |
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Term
| are low birth wt babies also at risk for DM? |
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Definition
| yes, along w/high birth wt babies |
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