Chapter 26: Concurrent Disorders during Pregnancy Flashcards Preview

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Flashcards in Chapter 26: Concurrent Disorders during Pregnancy Deck (54)
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1

CHO metabolism in normal pregnancy

  • First Trimester:
    • inc insulin release-->hypoglycemia especially w/ a problem w/ n/v
  • Second & Third Trimester:
    • placental hormones (hPL) inc resistance to insulin and dec glucose tolerance --> dec effectiveness of insuiln
      • allows glucose to be available to the fetus

2

etiology of DM

  • caused by partial or complete lack of insulin secretion by the beta cells of the pancreas
    • w/o insulin glucose accumulates --> energy depletion and hyperglycemia
  • body tries to dilute glucose load by any means:
    • polydopsia: inc thirst
    • fluid from intracellular space drawn into vascular bed-->dehydration at cellular level but fluid vol excess in vessels
      • kidneys attempt to excrete large vols of fluid and heavy solute load of glucose --> polyuria and glucosuria
  • b/c glucose stays in blood and can't be metabolized, the body breaks down fat and protein to get energy --> ketosis
  • complications of hyper/hypoglycemia fluctuations which can cause vascular damage (esp in the kidneys, eyes, heart)

3

effects of DM on early pregnancy

  • during early pregnancy, maternal metabolic rates and energy needs change little 
    • but insulin release in response to glucose levels accelerates --> significant hypoglycemia may occur (esp in women experiencing nausea, vomiting)
  • in an uncomplicated pregnancy, availability of glucose and insulin favors the development and storage of fat during the 1st half pregnancy which prepares the mother for rise in energy use by the fetus during the 2nd half of pregnancy

4

effects of DM on late pregnancy

  • when fetal growth accelerates during 2nd half of pregnancy, levels of placental hormones (hPl, estrogen, and progesterone) create resistance to insulin in maternal cells
    • allows for more glucose available for fetus --> so hormones are diabetogenic effect and leave the woman with insufficient insulin and episodes of hyperglycemia
  • the fetus continues to draw nutrients (glucose and AAs) from maternal blood --> earlier than normal switch from CHO metabolism by gluconeogensis (so form glucose form fat/protein)
    • causes high levels of fatty acids which inhibits uptake of glucose-->more glucose available for fetus

5

effects of DM on birth

  • maintenance of normal maternal glucose levels is essential during birth to reduce neonatal hypoglycemia
    • women with DM usually maintain glucose testing and administration of insulin to day before scheduled induction or C/S
  • after admission with NPO, glucose level is checked and continuous infusion of insulin and glucose is started based on hourly glucose levels

6

effects of DM on postpartum period

  • need for additional insulin falls during postpartum period
    • BF is encouraged for newborn and also b/c added calorie intake by mom helps lower the amount of insulin needed in women with type 1 or 2 DM
      • in women with GDM, usually need no insulin after birth but inc risk for later development of type 2 DM

7

classification of DM

  • Type 1: insulin dependent, b/c pancreas makes no insulin
    • obtain HgA1C
    • prone to ketosis
  • Type 2: non insulin dependent
    • insulin is required to contorl maternal blood glucose levels
      • insulin does not cross placenta
    • oral hypoglycemics are NOT taken during pregnancy b/c potential teratogen
  • GDM: inset of glucose interolerance during pregnancy
    • may be asymptomatic
    • disappears but inc risk of DM later in life

8

influence of pregnancy on diabetes

  • symptoms: polyphagia, polyuria, polydipsia
  • hypoglycemia is common during 1st trimester
    • insulin needs may dec
  • hyperglycemia is common during 2nd and 3rd trimester
    • insulin needs may inc
  • illness, diarrhea, n/v complicate control
  • exercise: assists in regulation of hyperglycemia and may keep off GDM
  • if hypoglycemic rxn occurs, drink OJ then low fat milk
  • possible induction b/w 38-40 wks as long as metabolic control is maintained and fetal growth w/in stds
  • labor inc energy needs and inc needs for insulin
  • once placenta is delivered insulin needs drop-->risk for hypoglycemia

9

factors associated with DM

  • family hx
  • hx of more than 2 spontaneous abortions
  • hydramnios
  • previous baby w/ a weight over 4000 g
  • previous baby w/ unexplained congenital anomalies
  • high parity
  • obesity
  • recurrent monilial vaginitis

10

maternal effects r/t preexisting DM

  • hypoglycemia, hyperglycemia, and ketosis inc incidence of spontaneous abortion or major fetal malformations
  • pre-eclampsia
  • ketoacidosis is a threat to woman with Type 1 DM and is often precipitated by missed doses of insulin or infection
    • can lead to fetal/maternal death if untreated
  • UTIs and monilial vaginitis
  • hydramnios
  • premature ROM
  • during labor, if child has macrosomia-->difficult labor, dystocia, consequent injury to the infant

11

fetal effect r/t pre-existing maternal DM

  • effects on fetus depend on timing and severity of maternal hyperglycemia and degree of vascular impairment
  • risks:
    • malformations of the fetus (dec risk if woman maintains normal blood glucose): NTDs, caudal regression syndrome, cardiac defects
    • variations in fetal size: related to maternal vascular integrity
      • fetal macrosomia results when elevated levels of blood glucose stimulate excess fetal  insulin production --> C/S and shoulder dystocia
    • vascular impairment leads to dec placental perfusion
      • can be caused by vasoconstriction which occurs in preeclampsia
      • dec supply of glucose and O2 --> IUGR and oligohydramnios

12

fetal surveillance done on IDM

  • U/S: starting at 20-22 weeks
    • can also help document fetal growth rates
  • AFP
  • NST
  • CST
  • kick counts
  • BPP

13

4 major neonatal effects r/t pre-existing maternal DM

  • hypoglycemia: high risk b/c of accelerated fetal insulin production during pregnancy
    • constant stimulation of hyperglycemia leads to hyperplasia and hypertrophy of pancreas
  • hypocalcemia
    • during last half of pregnancy, large amounts of calcium are transported across the placenta from the mother to the fetus
      • at birth, the transfer is stopped, leading to dramatic dec in amount of calcium
    • assoc with preterm birth, perinatal asphyxia
  • hyperbilirubinemia
    • fetus experiencing recurrent hypoxia compensates by production of add'l RBCs (polycythemia)-->excess RBCs broken done-->more bilirubin
  • RDS
    • fetal hyperinsulinemia retards cortisol production which is necessary for synthesis of surfactant
  • maintain normal blood glucose in mom to reduce incidence and severity of neonatal complications

14

lab test for maternal assessment of DM

  • baseline renal function should be assessed w/ a 24 hour urine collection for total protein excretion and creatinine clearance and protein excretion
    • random urine sample checked at each prenatal visit for UTIs which are common in diabetes
  • thyroid function tests: inc risk of co-existing thyroid fcn dz
  • HbA1C: accurate msmt of avg glucose concentrations during the preceding 2-3 mos
    • not affected by intake or restriction of food

15

therapeutic mgmt of DM

  • goals: maintain normal blood glc, facilitate the birth of a healthy baby, avoid accelerated impairment of blood vessels
  • preconception: establish optimal time to undertake pregnancy, identifying if diabetes complications, determining degree of glycemic control, instruct a woman how to use glucometer, having the woman take a daily prenatal vitamin 400 mcg folic acid
  • diet: 30 kcal/kg/day
    • 40-45% carbs, 12-20% protein (60 g), up to 40% dat
    • 3 meals w/ 2 snacks: bedtime snack should include a complex carb and a protein
  • SMBG
  • insulin therapy

 

 

16

GDM: risk factors

  • overweight or obese
  • maternal age >25 yo
  • previous birth outcome often assoc with GDM: neonatal macrosomia, maternal HTN, infant with unexplained congenital anomalies, previous fetal death
  • GDM in prior pregnancy
  • hx of abnormal glucose tolerance
  • hx of diabetes in first degree relative
  • member of African American, Hispanic/Latino, American Indian, Asian American, or Pacific Islanders

17

Diagnostic Testing for DM

  • 1 hr glucose screen - routine test on all pregnant women between 24 & 26 weeks
    • Non-fasting
    • Glucola
      • 50 g of glucose is given, blood draw 1 hr later
    • If greater than 140mg/dl then GTT
  • Elevated hA1C will show blood glucose level for 6-8 weeks

18

Glucose Tolerance Test

  • 3 hour glucose tolerance test: gold standard for dx of diabetes
    • fasting 
    • ingest 100 grams or oral glucose solution
    • dx if FBS > or equal to 95 or
      • 2 or more of these values occur:
        • 1 hour >180
        • 2 hour >155
        • 3 hour >140

19

maternal, fetal, and neonatal effects of GDM

  • similar to preexisting DM
  • but GDM is not assoc with an inc risk of ketoacidosis or spontaneous abortion
  • b/c GDM develops after 1st trimester (critical period of fetal organ development) is usually not assoc with an inc in congenital malformations
  • poorly controlled GDM assoc with inc neonatal morbidity and mortality
  • fetal complications: macrosomia (leads to birth injuries or C/S), neonatla hypoglycemia, hypocalcemia, hyperbilirubinemia, and RDS
  • BF may reduce later development of Type 2 DM in the baby

 

20

mgmt of diet with GDM

  • should provide calories and nutrients for maternal and fetal health, result in euglycemia, avoid ketosis, and promote appropriate weight gain
  • eliminate simple sugars from sweets
  • 30 kcal/kg/day is recommended
    • if a woman is obese, restricted to 25 kcal/kg/day
  • smaller percent of carbs to limit hyperglycemia
    • carbs at breakfast limited to 30 g b/c of inc levels of cortisol and growth hormone at that time of day
    • protein foods to help satisfy hunger
    • evening snack to prevent ketosis at night
  • divide calories among 3 meals and at least 3 snacks

21

exercise and SMBG with GDM

  • exercise can improve cardiorespiratory fitness
    • graduated exercise program should be recommended
  • evaluate blood glucose: fasting blood glucose (no food for previous 4 hours) and postprandial blood glucose (2 hrs after each meal)
    • if fasting is above 95 or postprandial above 120 repeatedly, then insulin is started

22

fetal surveillance with GDM

  • begin to identify fetal compromise as early as 28 weeks if woman has poor glycemic control or by 34 weeks in low risk women
  • includes: 
    • kick counts
    • U/S for fetal growth and amniotic fluid vol
    • BPP
    • NST
    • CST
    • amniocentesis for lung maturity

23

nursing care during labor with DM

  • short acting (regular) insulin
  • maintain blood glucose b/w 70-90
  • hourly fingersticks
  • position left side: b/c of large fetus or hydramnios
  • check urine for ketones hourly (report 2+)
  • continuous EFM

24

nursing care post delivery with DM

  • sliding scale insulin
  • continuous IV with 5% glucose
  • check for ketones
  • encourage BF

25

chorioamnionitis

  • bacterial infection of the amniotic cavity
  • chorioamnionitis --> postpartum endometritis
  • inc risk of sepsis in the newborn

26

assessment findings with chorioamnionitis

  • uterine tenderness and contractions
  • inc temperature
  • maternal and fetal tachycardia
  • foul odor to amniotic fluid
  • inc WBC count

27

nursing considerations w/ chorioamnionitis

  • monitor:
    • maternal V/S and FHR
    • uterine contractions and activity
    • results of blood culture
  • medications: abx after cultures
  • prepare for: 
    • amniocentesis for gram stain and WBC
    • delivery of the fetus
    • neonatal cultures after delivery

28

cytomegalovirus (CMV)

  • type of herpesvirus
  • isolated from urine, saliva, blood, cervical mucus, semen, breast milk, and stool
  • transmission may occur thru contamination of any of these fluids, but close personal contact is required
  • children often can acquire CMV in a day care center
    • inc risk again at adolescence w/ activities such as kissing, sexual intercourse
  • after a primary infection, the virus becomes latent, but can become periodically reactivated and shedding of the virus can occur
    • primary infection more likely to cross placenta
  • seroconversion (change in blood test from negative to positive indicates development of Abs in response to infection) and a rise in IgM Abs can detect a primary infection that has occurred in the last 4-8 mos

29

fetal and neonatal effects of CMV

  • 10% of newborns are symptomatic at birth
    • these infants show full cytomegalic inclusion dz
  • another 10% of the group showing CMV infection at birth will develop late onset signs like developmental delay, seizure activity, enlargement of the spleen and liver, chorioretinitis, dental defects, and hearing loss

30

therapeutic mgmt of CMV

  • no effective therapy is available for congenital CMV
  • U/S may identify manifestations like cranial abnormalities or growth restriction
  • antiviral agents (ganciclovir or foscarnet) can be used for severe infections, but these drugs are toxic and only temporarily stop the shedding
  • primary prevention (hand washing, warning about risk of multiple sexual partners) is most effective