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HIGH RISK OB STUDY GUIDE 2024|2025 QUESTIONS AND CORRECT ANSWERS

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HIGH RISK OB STUDY GUIDE 2024|2025 QUESTIONS AND CORRECT ANSWERS

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HIGH RISK OB STUDY GU
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HIGH RISK OB STUDY GU

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Subido en
5 de noviembre de 2024
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Escrito en
2024/2025
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HIGH RISK OB STUDY GUIDE 2024|2025
QUESTIONS AND CORRECT ANSWERS


Study Guide: High Risk OB

1) Review the pathophysiology of diabetes. The pancreas does not produce enough insulin to
allow necessary carb metabolism and/or there is diminished tissue response to insulin.
With inadequate amounts of insulin or defects in insulin action, glucose cannot enter the
cells but remains circulating in the blood. The body cells become energy depleted while
the blood glucose level remains elevated. Fats and proteins in the body tissues are then
oxidized by the cells as a source of energy. This results in wasting of fat and muscle tissue
of the body, negative nitrogen balance due to protein breakdown, and ketosis due to fat
metabolism. The blood with elevated levels of glucose is very osmotic, so it pulls water
from the cells into the vasculature, which results in cellular dehydration. The high level of
glucose eventually spills over into the urine. Osmotic pressure of glucose in the urine
prevents reabsorption of water into the kidney tubules, causing extracellular dehydration.
♥ How does gestational diabetes differ from other types? GD has an onset of the 2nd or 3rd
trimester. It’s defined as glucose intolerance and the severity is variable.
♥ What hormones influence diabetes in pregnancy? Human placental lactogen (hPL);
prolactin; elevated levels of cortisol and glycogen. When are these present and
increase? hPL is low in the first trimester but begins rising by the end of the first
trimester. As a result of increased levels of hPL and placental maturation, insulin
requirements may double or quadruple by the end of pregnancy.
2) What affects does diabetes have on the development of a fetus?
♥ Presence of severe maternal ketoacidosis greatly ↑ risk of fetal death;
♥ presence of congenital anomalies is 6-10%. These anomalies often involve the:
o heart (septal defects; coarctation of the aorta; transposition of the great
vessels),
o the CNS (hydrocephalus; meningomyelocele; anencephaly, spina bifida),
o the skeletal system (sacral agenesis, which only appears in IDMs.
♥ Excessive growth (macrosomia) due to high levels of fetal insulin production
because of high levels of maternal glucose crossing the placenta causes LGA
babies.
♥ If mom has vascular involvement, the fetus may have IUGR due to decreased
perfusion of the placenta.
3) What affects does diabetes have on the fetus in utero and understand the patho behind it? Ex.
Excessive fetal urination, increased blood glucose, increased insulin circulation, etc. Excessive
fetal urination due to fetal hyperglycemia is thought to result in polyhydramnios. The fetal
hyperglycemia is the result of high levels of maternal glucose readily crossing the
placenta.
4) What potential problems could occur due to diabetes in pregnancy (understand the patho)?
♥ Pre-eclampsia—eclampsia occurs more often especially when there are already
diabetic vascular changes.
♥ Ketoacidosis may occur more rapidly in pregnant woman due to the
hyperketonemia state associated with accelerated starvation in the fasting state.
This is because maternal glucose is being diverted to the fetus, so fat is being
broken down instead during the fasting state and fat breakdown produces
ketones.
♥ There are higher postprandial glucose levels b/c of ↓ gastric motility and the
insulin-antagonizing effects of hPL
♥ If fetal-macrosomia exist, then labor dystocia can occur.
♥ ↑ risk for UTIs and monilial vaginitis b/c of glycosuria, which creates a favorable
environment for bacterial growth.
♥ Worsened retinopathy
5) What problems occur in newborns due to diabetes (understand the patho)?
♥ Hypoglycemia—once delivered, maternal glucose supply is severed, but the IDM

, lOMoAR cPSD| 37668344




continues producing high levels of insulin, which depletes the NBs blood glucose within
hours after birth. IDMs also less ability to release glucagon and catecholamines, which
normally stimulate glucagon breakdown and glucose release.
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