Endocrine & Metabolic Disorders in Pregnancy PDF

Endocrine & Metabolic Disorders Dr. Christi Camarena, DNP, RNC-OB, C-EFM CSUS School of Nursing N137 Nursing the Childbearing Family The following content is protected and may not be shared, uploaded, or distributed. This PowerPoint Presentation is protected by U.S. copyright law. I am the excl...

Endocrine & Metabolic Disorders Dr. Christi Camarena, DNP, RNC-OB, C-EFM CSUS School of Nursing N137 Nursing the Childbearing Family The following content is protected and may not be shared, uploaded, or distributed. This PowerPoint Presentation is protected by U.S. copyright law. I am the exclusive owner of the copyright in the course materials that I create. You may not reproduce, distribute, display, post, or upload my course materials or recordings or course materials in any other way — whether or not a fee is charged — without my express written consent. The following Textbook is used throughout this presentation: Maternity and Women’s Health Care, 13th edition. Lowdermilk, Cashion, Alden, Olshansky & Perr., Elsevier Inc., 2024  1. Differentiate the types of diabetes mellitus and their respective risk factors in pregnancy. 2. Compare insulin requirements during pregnancy, postpartum, and lactation. 3. Identify maternal and fetal risks or complications associated with diabetes in pregnancy. 4. Develop a plan of care for pregnant women with pre-gestational or gestational diabetes. 5. Explain the effects of hyperemesis gravidarum on maternal and fetal well-being. 6. Discuss the management of the client with hyperemesis gravidarum. 7. Explain the effects of thyroid disorders on pregnancy. Objectives 8. Loading… Compare the management of pregnant women with hyperthyroidism with one who has hypothyroidism. 9. Discuss the care management for the client with phenylketonuria during the perinatal period. 10. Examine the effects of maternal phenylketonuria on the pregnancy outcome. 11. Describe the effects of maternal diabetes on the newborn, including congenital anomalies, macrosomia, birth trauma, perinatal hypoxia, respiratory distress syndrome & hypoglycemia. Endocrine Disorders Diabetes Mellitus Infants of Mothers with Diabetes Hyperemesis Gravidarum Thyroid Disorders Maternal Phenylketonuria  Metabolic changes associated with pregnancy Normal pregnancy is characterized by alterations in metabolic status related to rising levels of estrogen and progesterone Glucose crosses the placenta, but insulin does NOT Fetus will begin to secrete its own insulin at adequate levels @10-14 weeks “Diabetogenic” effect in 2nd and 3rd trimesters (decreased glucose tolerance and Loading… increased insulin resistance) Delivery of placenta results in abrupt drop in circulating placental hormones and reversal of diabetogenic effect Breastfeeding uses maternal glucose Pregestational Diabetes Mellitus (DM) Pathogenesis Hyperglycemia resulting from defects in insulin secretion, insulin action, or both Type 1 diabetes → huge risk pregnancy = goal is to prenatal care to prevent hypoglycemia in fetus right at birth Islet B-cell destruction → no insulin production Absolute insulin deficiency Type 2 diabetes → usually undiagnose until pregnancy → don’t need to memorize this Insulin resistance Relative insulin deficiency Other (disease, injury, etc.) Note: if A1C is above 10 then its infertility A1C = 3 months reading  Gestational DM Classification You’ll be set for the type once dx during pregnancy n no transition Gestational diabetes mellitus (GDM) Carbohydrate intolerance with the onset or first recognition occurring during pregnancy. A1 –diet controlled A2-medication controlled → start diet first then add med  Gestational Diabetes (GDM A1 or A2): Intrauterine fetal death Maternal Risk Factors: Family history, hx of IUFD and/or unexplained congenital anomalies, hx of macrosomic fetus, maternal obesity, HTN, glycosuria, advanced maternal age, hx of GDM during previous → newborn weight more than 4000g → glucose in the urine pregnancy GDM screening usually occurs at 24 to 28wks, unless risk factors are present Know 2 steps ACOG recommends two-step method Very sweet syrup n take at once then sit there until blood draw HbA1c 5.7-6.4 → technically not a dx tool Treatment begins immediately → prefer IV and no poke Priority is dietary modification Insulin → not the safest choices but if its the only option Always good to be more aggressive in tx than not tx enough Metformin → would be on somebody on prior pregnancy and unable to take insulin Hemoglobin A1c levels are normally lower in pregnant patients because RBCs turn over more rapidly during pregnancy. Therefore, the estimation of glycemic control provided by the test applies to only the previous 2 to 6 weeks Complications of DM ***Pre-conceptional counseling decreases perinatal mortality, preterm birth, and congenital anomalies*** Maternal risks & Fetal & neonatal risks & complications: complications: SAB (as high as 30%) Congenital malformations (cardiac & CNS) Spontaneous abortion r/t hyperglycemia Macrosomia=increased risk of C/S → all the c/s risks Respiratory Distress Syndrome → hypoxia HTN, pre-eclampsia, preterm birth, and maternal mortality Prematurity Too much amniotic fluids Polyhydramnios=increased risk of IUFD (r/t poor glycemic control) placental abruption, uterine → can cause the placenta to separate from Macrosomia*=increased risk of birth injury the uterus = bleeding or increase pressure dysfunction, and PPH Postpartum hemorrhage (40-50% of diabetic pregnancies) Increased risk for infections (UTI’s) (*disproportionate increase in shoulder, trunk and Ketoacidosis (may occur at blood chest size) → instead of head since its normally the largest = birth complications of trying to get the baby out glucose levels >200mg/dL, especially Hypoglycemia at birth r/t high levels of in response to stress), DKA insulin  Intrapartum: Period of labor and delivery DM Management Determine delivery date/mode Antepartum: Period of pregnancy and before child birth Optimally 39 to 40 weeks, vaginal More frequent prenatal visits C/S for EFW>4500 grams Estimate fetal weight Diet education and modification is IV therapy/Insulin infusion → can be IV drip n injection but pt scared individualized (based on BMI) FREQUENT blood glucose monitoring Lots of NPO Exercise-ideally after meals Just walking 30 min after Postpartum: Period after child birth Insulin (Table 29.4) or oral hypoglycemics Insulin requirements decrease (50-60%) with the → Dont need to know the dose but know what med Glucose monitoring (6-8 times/day) delivery of the placenta, which was the main source of insulin resistance Regular schedule (eat, meds, sleep) Encourage breastfeeding Fetal Surveillance Anti-diabetogenic effect Labs, ultrasounds, NST, AFI, BPP → don't need to know ab this since the physician will be responsible Carbohydrates used in milk production (decreases insulin needs) Consider "fasting" Follow up re-screening (6-12 week PP) Lifetime risk factor Anything below 60 is bad Birth control options → not estrogen base for type 2 or non hormonal choices in general Infants of Mothers with Diabetes Second recording Az baby have more risk of complication than A1 baby Pathophysiology Macrosomia, Birth Trauma, and Perinatal Hypoxia Respiratory Distress Syndrome Hypoglycemia Loading… Polycythemia and Hyperbilirubinemia https://www.health4mom.org/how-diabetes-affects-you-your-baby/  Just there = no need to memorize Pathophysiology Early pregnancy: Ketoacidosis is thought to be the cause of congenital anomalies Later in pregnancy: Insufficient maternal insulin results in maternal hyperglycemia and increased glucose crossing the placenta Fetal glucose level 70-80% of maternal value Frequent maternal hyperglycemia=fetal pancreas hyperplasia=hyperinsulinemia → the pancreas have to work overtime Insulin is a growth hormone: Macrosomia: Birthweight greater than 4000 grams or 8 lbs. 13 oz. Large for Gestational Age (LGA): Birth weight greater than the 90th percentile for gestational age Nursing interventions are specific to the neonate’s particular problem. https://womendeliver.org/publications/diabetes-and-pregnancy/  Macrosomia, Birth Trauma and Perinatal Hypoxia Macrosomia (occurs in about 35% of DM pregnancies) Increased body fat, plethoric, enlarged internal organs, excessive glycogen, and fat stores Infants of mothers with diabetes can be LGA but physiologically immature Excessive shoulder size can lead to dystocia and associated trauma: Fractured clavicle or humerus Brachial plexus injury Facial nerve injury Perinatal hypoxia occurs more often in infants of mothers with diabetes Multifactorial Elevated Hgb n Hct High amount of insulin in blood Polycythemia & Hyperbilirubinemia-Hyperinsulinism increases newborn metabolic rate=increased O2 demand mild hypoxia Increased RBC production → high risk for jaundice Respiratory Distress Syndrome (RDS) RDS less common with improved maternal glucose management and antepartum surveillance Risk of RDS decreases after 38 weeks Hyperglycemia and hyperinsulinemia delays synthesis of surfactant in the fetus → create surface force n promote fluid clearance Late preterm birth may be indicated in cases where maternal glycemic control cannot be achieved as an inpatient or for those mothers who have abnormal antepartum fetal testing https://healthjade.net/wp-content/uploads/2019/12/infant-respiratory- distress-syndrome.jpg  Hypoglycemia Blood glucose concentration inadequate to support neurologic, organ, and tissue function Don't memorize this but know first 24hr should be For term baby with DM mom only ⑭ Signs and Symptoms: jitteriness, apnea, tachypnea, greater than 40 but any time after that then above 45 hypotonia, decreased activity, and cyanosis, however, many infants remain asymptomatic Macrosomic, LGA, and preterm infants have highest risk of hypoglycemia Constant exposure to high levels of glucose, hyperplasia of the fetal pancreas occurs Disruption of the maternal glucose supply occurs with the clamping of the umbilical cord. Frequently occurs in first 1-6 hrs of life, but it takes several days for the newborn to regulate insulin https://pediatrics.aappublications.org/content/127/3/575 Significant hypoglycemia can result in seizures There is a direct correlation between temperature regulation, glucose homeostasis, and respiratory distress A disruption in one system challenges the others. Other Endocrine Disorders Hyperemesis Gravidarum Thyroid Disorders Maternal Phenylketonuria  Normal nausea and vomiting occurs in 50%-80% of all pregnancies, starts at about 4 to 10 weeks of gestation and Hyperemesis ends by 20 weeks of gestation Gravidarum Hyperemesis gravidarum is excessive, prolonged vomiting accompanied by any of the following: Weight loss Dehydration Electrolyte imbalance & Ketonuria Nutritional deficiencies Cause is not well understood Assessment: signs of dehydration, r/o infections, labs (electrolytes & thyroid panel), psychosocial assessment, height, weight, and vital signs First line tx Interventions: IV therapy, Vitamin B6 & Unisom (ACOG #1 choice), Anti-emetics (not proven safe in pregnancy), corticosteroids and enteral or parental nutrition as a last resort → usually have PICC line cos infusion a lot Once vomiting has stopped, begin with fluids and a bland diet, small amounts, frequent intervals, advance as tolerated Of everything → NPO Thyroid Disorders ***Fetus depends on maternal thyroid hormones until 18wks, normal T4 levels in early pregnancy are critical for normal brain development*** → identify which type of disorders when given s/s in exam Hyperthyroidism Hypothyroidism Rare in pregnancy, cases in pregnancy are In the U.S. it is usually caused by autoantibodies, usually caused by Graves’ disease however; iodine deficiency is a major cause worldwide Clinical manifestations Clinical manifestations: Heat intolerance, diaphoresis, fatigue, Weight gain, lethargy, decrease in exercise anxiety, emotional lability, capacity, cold intolerance, hair loss, brittle tachycardia, weight loss, goiter, very nails, dry skin, constipation, and elevated low levels of TSH levels of TSH Untreated=increased risk of SAB, preterm Untreated=infertility, increased risk of SAB, pre- birth, IUFD, pre-eclampsia & heart failure eclampsia, placental abruption, preterm birth, IUFD, low birth weight Primary treatment during pregnancy is Primary treatment is levothyroxine and low normal Propylthiouracil (PTU) and Methimazole TSH levels (MMI), and rarely surgery → no reactive iodine (RAI) PTU recommended 1st trimester, MMI for the remainder of the pregnancy  Maternal Phenylketonuria Only 1 question → the mother having PKU n its ab breast-feeding AKA Phenylalanine Hydroxylase Deficiency PKU was the first inborn error of metabolism to be universally screened in the U.S. (1961) Inborn error of metabolism resulting in deficiency of the enzyme phenylalanine hydrolase, which impairs the body’s ability to metabolize foods with protein (amino acids). Treatment: phenylalanine restricted diet, indefinitely. Should be started pre-conception and continue throughout pregnancy. High levels of phenylalanine can result in fetal microcephaly, cognitive impairments, seizures, growth impairment, and congenital heart defects. Breastfeeding is safe for women with PKU as long as the baby does not also have PKU. Infants with PKU have phenylalanine levels tested frequently and modify the feeding plan accordingly.  20 questions but 15 will be about diabetes and 2 in thyroid with 1 in PKU Summary: Pregestational vs. Gestational DM Gestational DM Classifications Maternal, Fetal and Newborn Complications of DM Management of DM in Pregnancy, Labor, PP Newbon Hypoglycemia Hyperemesis Management Hyperthyroid vs. Hypothyroid Maternal PKU & Breastfeeding