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Metabolism and Diabetes in Pregnancy
1. Metabolism: The processes of biochemical reactions occurring in the body's cells that are necessary
to produce energy, repair and facilitate the growth of cells, and maintain life.
2. Diabetes: A chronic endocrine disorder of carbohydrate metabolism; can be pregestational
(type I, II) or gestational.
3. Type 1 diabetes: No insulin production.
4. Type 2 diabetes: Insulin or hypoglycemic medication is required.
5. Gestational diabetes management: Through diet and exercise, insulin, or hypo- glycemics.
6. First half of pregnancy insulin phase: It is an anabolic phase where estrogen and progesterone
stimulate more insulin production, and maternal tissue uses insulin more readily, requiring less insulin.
7. Second half of pregnancy insulin phase: It is a catabolic phase where placental hormones increase
resistance to insulin, requiring more insulin.
8. Maternal risks of pregestational diabetes: Hypoglycemia, DKA, risk of hyper- tension, preeclampsia,
spontaneous loss, risk of C-section, polyhydramnios, and exacerbation of diabetes-related diseases.
9. Newborn risks of pregestational diabetes: IUGR, hypoglycemia, asphyxia, RDS, macrosomia,
stillbirth, and congenital defects.
10. Gestational diabetes definition: Carbohydrate intolerance with first onset in pregnancy.
11. Gestational diabetes classification: Based on how it is controlled: A1 (diet and exercise) or A
(medications).
12. Post-diagnosis risk for mothers with gestational diabetes: Increased risk of developing type 2
diabetes 10 years post-diagnosis.
13. Neonatal risks of gestational diabetes: Altered fetal growth, macrosomia, hyperglycemia, and
hyperinsulinemia.
14. Insulin requirements by trimester for diabetic mothers: 1st Trimester: Less insulin; 2nd and 3rd
Trimesters: More insulin; Postpartum: Less insulin.
15. Major signs and symptoms of diabetes: Polyuria, polydipsia, polyphagia, weight loss, and
blurred vision.
16. Effects of gestational diabetes on the mother: Anemia, high C-section rate, difficult labor,
dystocia, hydramnios, risk of UTI, ketoacidosis, preeclampsia, preg- nancy loss, preterm labor, postpartum hemorrhage, poor wound healing.
17. Effects of pregestational diabetes on the baby: Birth trauma, cord prolapse, congenital anomalies
(e.g., sacral agenesis), death, respiratory distress syndrome (RDS), hypoglycemia, hypocalcemia, preterm birth, polycythemia.
18. Congenital abnormalities related to pregestational diabetes: Congenital anomalies such as
sacral agenesis.
Twice a week non-stress tests (NST) to test oxygenation, and if non-reactive, a biophysical profile (BPP).
30. Purpose of a weekly ultrasound for mothers with gestational diabetes: To check for amniotic fluid
levels.
31. Purpose of a monthly growth ultrasound for mothers with gestational diabetes: To assess
fetal growth and ensure the fetus does not grow over 4000 grams.
32. Induction criteria for mothers with gestational diabetes: If she has poor control, a large baby,
a lot of fluid, and is less than 39 weeks pregnant.
33. Test to determine if a baby will be able to breathe after delivery in cases of early induction:
Amniocentesis to check for surfactant levels.
34. Insulin management during labor for diabetes patients: An insulin drip with the primary line
interchanging between lactated ringers or D5.
35. Post-delivery outcome for gestational diabetes: It should resolve. If it re- mains, it is
considered Type 2 diabetes.
36. Next step if a mom with gestational diabetes is not responding to diet and exercise: Progress to
medication such as insulin or oral medications like glyburide or metformin.
37. Glycosylated Hgb (Hb A1c) indication: It tells the average blood sugar over the last 3 months.
38. Hb A1c level for diabetic patients: Less than 7. If greater than 8, intervention is required.
39. Definition of macrosomia or LGA in terms of birth weight: Birth weight greater than the 90th
percentile or more than 4,000 grams (8 lb, 13 oz), or 4,500 grams in diabetics.
40. Causes of macrosomia: Uncontrolled prenatal hyperglycemia, genetics, post-term
pregnancy, multiparity, and maternal obesity.
41. Effect of hyperglycemia on surfactant synthesis: Hyperglycemia interferes with surfactant
synthesis.
42. C-section rate with LGA: Because LGA can cause birth traumas.
43. Clinical manifestations of LGA: Altered behavior, congenital defects, difficulty arousing, feeding
difficulties, poor motor skills, and puffiness.
44. First hour of life for an LGA baby: Perform a heel stick to check blood glucose levels to monitor for
hypoglycemia (< 40 mg/dL).
45. Tests for signs of hypoglycemia in a baby: Check blood glucose levels immediately, perform
a CBC to check for polycythemia, and check bilirubin and calcium levels.
56. Test for monitoring antibody formation in Rh-negative mother: Indirect Coombs test.
57. Action if neonate is Rh+ and direct Coombs test is negative at birth: Give the mother RhoGAM
within 72 hours of birth.
58. Positive Coombs test in a baby: It indicates that the baby has been sensitized, meaning the
mother was sensitized.
59. Indirect Coombs test: Measures the number of RH+ antibodies in the mother.
60. Direct Coombs test: Measures if there are any RH+ cells in the baby's blood.
61. Erythroblastosis fetalis: Severe fetal anemia.
62. Hydrops fetalis: Congestive heart failure with marked fetal edema.
63. Kernicterus: Neurologic damage due to high bilirubin levels.
64. Management of sensitized pregnancy: Frequent maternal antibody titer checks, intrauterine
transfusions if high, delta optical density checks, early delivery with steroids, phototherapy, and transfusions.
65. Management protocol for RH-negative mother: Prenatal screening, RhoGAM if indirect Coombs is
negative at 28 weeks, RhoGAM following invasive procedures, and RhoGAM within 72 hours if the newborn is RH+ and direct Coombs is negative.
66. Most common cause of hemolytic disease in newborns: ABO incompatibility, particularly when the
mother is type O and the baby is type A or B.
67. Signs and symptoms of hyperbilirubinemia: Lethargy, jaundice, hypotonia, poor feeding, and
high-pitched cry.
68. Risk factors for hyperbilirubinemia: Rh factor incompatibility and ABO incom- patibility.
69. Consequences of hyperbilirubinemia: Kernicterus, which is brain damage caused by high
bilirubin levels.
70. Signs and symptoms of kernicterus: Lethargy, hypotonia, poor feeding, high-pitched cry,
back arching, and seizures.
71. Physiologic jaundice appearance in newborns: On the 2nd to 3rd day of life.
72. Bilirubin levels in physiologic jaundice: Less than 13-15 mg/dL.
73. Pathologic jaundice appearance in newborns: Within the first 24 hours of life.
74. Bilirubin levels in pathologic jaundice: Greater than 15 mg/dL.
75. Causes of pathologic jaundice: Hemolytic disease of the newborn due to blood incompatibility,
polycythemia, sepsis, asphyxia, hypoglycemia, hypothermia, late term and preterm birth.
76. Treatment for physiologic jaundice: Supportive feedings, window for UV light, and possibly
phototherapy.
77. Treatment for pathologic jaundice: Phototherapy, fiberoptic bili-blanket, and exchange
transfusions if bilirubin is greater than 25 mg/dL.
78. Nursing care for managing jaundice in newborns: Assess for risk factors, check bilirubin levels,
encourage early and adequate feeds, maintain neutral thermal environment (NTE), maintain respiratory function, monitor temperature, observe for jaundice, obtain newborn blood type and direct Coombs,
