Module 5 Flashcards by Unknown Unknown

Hypertensive disorders of pregnancy

pre-existing HTN (essential vs. secondary)
gestational HTN
pre-eclampsia
severe pre-eclampsia
eclampsia
HELLP

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gestational HTN

occurs after 20 weeks
1) with proteinuria (with or without adverse conditions)
2) without proteinuria (with or without adverse conditions)

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pre-eclampsia

HTN + proteinuria (+1 or greater) OR end-organ dysfunction OR severe consequences (eclampsia)

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RF for HTN in pregnancy

family hx
extremes of reproductive age (<20 or >35)
primigravida
multiple gestation
diabetes, renal dx, prior HTN
collagen vascular dx
no mid-trimester fall in BPO
excessive weight gain (>2 lb/week)
finger/facial edema

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Patho of pre-eclampsia

poor placentation
first stage: cytotrophoblast invades endometrium & remodels spiral arteries
second stage: cytotrophoblast invades myometrium & remodels arteries –> wider, low pressure system

pre-eclampsia occurs when this remodeling does not occur. placental ischemia –> release of inflammatory cytokines/factors that get released into maternal circulation and cause endothelial dysfunction

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Adverse outcomes of pre-eclampsia

vascular remodeling/endothelial vasospasm = HTN
kidney damage = proteinuria, liver damage = elevated enzymes
RBC traveling through damaged blood vessels sheared = hemolysis
clotting activated by endothelial injury/turbulent blood flow thrombocytopenia s/t systemic clotting –> DIC edema (increased capillary permeability)
eclampsia/headache/hemiplegia/visual disturbance (cerebral vasospasm)
cardiomyopathy
ARDS

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Nursing mgmt of pre-eclampsia

bed rest
fetal assessment (ultrasound/nonstress test)
weight gain
blood pressure measurements
proteinuria
fetal movement
general symptoms

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Severe pre-eclampsia

gestational HTN with or without proteinuria with 1+ adverse conditions

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Severe pre-eclampsia adverse conditions

severe N/V
frontal headache
visual disturbance
epigastric/RUQ pain
chest pain
SOB
leukocytosis
abnormal coagulation
thrombocytopenia
increased creatinine/uric aid
increased liver enzymes (AST, ALT, LDH, bili)
decreased albumin
fetoplacental (abnormal FHR, IUGR, oligohydramnios, absent/reversed end-diastolic flow)

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Maternal signs of severe pre-clampsia

DBP > 110
oliguria <500/day
pulmonary edema
suspected abruptio placenta

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Maternal labs for severe pre-eclampsia

platelets <100
elevated liver enzymes (AST/ALT)
plasma albumin <18
heavy proteinuria 3+ or greater

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Fetal signs of severe pre-eclampsia

IUGR
oligohydramnios
absent/reversed end diastolic flow of doppler

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S/S of eclampsia

**often not observed prior to seizures

severe headache/occipital headache
brisk reflexes
visual disturbances

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Severe pre-eclampsia treatment

1:1 nursing
calm, quiet environment
transfer to specialized unit
increased monitoring (HR/BP Q15min/4 hours until stabilized –> Q30min)
oral HTN medication
IV insertion
indwelling catheter (monitor output)
proteinuria testing
I&O documentation
O2 supplementation
VTE prophylaxis
seizure precautions (padded rails)
ensue calcium gluconate/maternal resuscitation equipment ready

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Pharmacologic management of severe pre-eclampsia

nifedipine (CCB)
labetolol (beta blocker)
hydralazine (vasodilator)
methyldopa

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Magnesium sulfate

seizure prophylaxis

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Magnesium sulfate MOA

decreases CNS irritability
blocks Ach release –> blocking neuromuscular conduction
relaxes smooth muscle of uterus (competes w/ calcium)
peripheral vasodilation
increased uterine/renal perfusion
increased prostacyclin from endothelial cells (vasodilation)
reduced platelet aggregation
inhibits RAAS

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Magnesium sulfate antidote

calcium gluconate IV

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Magnesium sulfate side effects

flushing of skin
hypotension
metallic taste
N/V
palpitations
sweating

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Magnesium sulfate toxicity

absent deep tendon reflexes
cardiac arrhythmia
CNS depression
excessive drowsiness
muscle weakness, ataxia
respiraotry depression (<12)
slurred speech
hypocalcemia + tetany (competes with calcium which is needed for muscle contraction)

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Eclampsia

new onset generalized tonic-clonic seizures assoc w/ pre-eclampsia
can occur up to 24 hours postpartum

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Gestational diabetes

insulin resistance –> diabetes after 20 weeks

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Human placental lactogen

produced ~6-30 weeks
antagonist to insulin
increases insulin resistance

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GDM & fetal development

macrosomia (>90th percentile)
hyperinsulinemia = decreased surfactant production
increased fetal BMR = fetal hypoxemia = metabolic acidosis
increased erythropoiesis = polycythemia = decreased iron for developing organs = cardiomyopathy, altered neurodevelopment, cardiac remodeling

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RF for GDM

age >25 non-white people PCOS (higher testosterone) HTN multiple gestation family hx previous macrosomia

Maternal complications of GDM

increased r/o HTN/pre-eclampsia polyhydramnios increased r/o future T2DM

Fetal complications of GDM

macrosomia hypoglycemia respiratory distress syndrome hyperbilirubinemia stillbirth future obesity

HDN

hemolytic anemia caused by isoimmunization maternal IgG antibodies attack fetal RBC d/t incompatibility of surface antigens

Types of blood incompatibility

ABO RH

ABO incompatibility

mild usually resolves on its own dose not typically result in severe hyperbilirubinemia **most common with O- mom

Rh- incompatibility

caused by Rh- mom & Rh+ baby first pregnancy: maternal IgG antibodies form when mom blood exposed to fetal blood second pregnancy: maternal IgG antibodies attack fetal RBC

HDN treatment

rhogam (prevention) phototherapy exchange transfusion IV immunoglobulin (reduces hemolysis) centesis for hydrops fetalis in utero RBC transfusion

When is rhogam given

28 days 72 hours after birth

Causes of maternal sensitization (HDN)

normal delivery spontaneous/induced abortion chorionic villlus sampling amniocentesis prenatal hemorrhage maternal trauma idiopathic **only .1 mL needed to activate maternal immune response

HDN complications

anemia hyperbilirubinemia kernicterus growth restriction hydrops fetalis

HDN complications

hyperbilirubinemia --> acute encephalopathy/kernicterus symptomatic anemia (pallor, lethargy, tachycardia, tachypnea) hydrops fetalis IUGR

HDN tests

DAT (coombs test) measures IgG antibodise cord blood IAT CBC TCB/serum bili peripheral blood smear

Maternal hormones that act as insulin antagonists

human sommatotropic hormone (human placental lactogen) estrogen progseterone prolactin cortisol insulinase (degrading enzyme)

When does fetus begin secreting insulin

10-14 weeks gestation

Hypoglycemia in pregnancy

<3.2 mmol

Pharmacotherapy GDM

insulin (first-line, doesn't cross placenta) metformin (may cross placenta) glyburide (last resort if intolerant to metformin & refusing insulin)

Hyperglycemia in pregnancy

>11

Target blood glucose levels in pregnancy

3.8-5.2 (S/S of hypoglycemia may present at <3.8)

Fetal consequences of GDM

hyperinsulinemia --> decreased surfactant/lung maturation, increased growth (macrosomia) increased O2 demand = increased erythropoiesis = decreased iron (cardiac myopathy/impaired neural development), increased r/o jaundice abnormal placenta --> preterm, IUGR perinatal asphyxia/hypoglycemia upon birth neonatal respiratory distress syndrome

Maternal consequences of GDM

higher longterm r/o of T2DM DKA macrosomia --> dystocia --> C/S or hemorrhage pre-eclampsia/HTN infection hypoglycemia (higher risk in early 1-2 trimesters as insulin need decreases)

GDDC

gestational diabetes diet controlled low glycemic diet exercise (30 min/daily) decreased fat/carbs

GDID

gestational diabetes insulin dependent insulin indicated when glucose targets cannot be maintained on diet/exercise alone

Blood glucose targets in pregnancy

FBG <5.3 1 hour postprandial <7.8 2 hours postprandial <6.7

Ferritin target in pregnancy

>15

Hemoglobin target in pregnancy

>105

Entonox

nitrous oxide

Stages of PPH

Stage 1 Stage 2 Stage 3

Stage 1 PPH

>500 SVD or >1000 CS with continued bleeding + HR higher than SBP

Stage 2 PPH

1000-1500 and HR higher than SBP

Stage 3 PPH

>1500 blood loss or hemodynamically unstable anticipated need for 3+ PRBCwithin 1 H or fibrinogen level <2.5 g/L

S/S of neonatal adaptation syndrome

**caused by exposure to SSRI/SNRi in utero respiratory distress feeding difficulty jitteriness irritabiilty temperature instability sleep problems tremors shivering restlessness convulsions jaundice rigidity hypoglycemia

Onset of NAS

0-3 days duration 2 weeks

NAS interventions

quiet, low-light enivronment STS if s/s toxicity present: respiratory support fluid replacement anticonvulsant therapy

Persistent pulmonary hypertension

failure of pulmonary vasculature to relax after extrauterine transition --> right-to-left shunting of blood thru fetal circulatory pathways can cause hypoxemia refractory to treatment

SSRI newborn complications

neonatal adaptation syndrome congenital heart defects persistent pulmonary hypertension

is breastfeeding contraindicated with SSRIs?

NESTS self-care acronym

nutritious food exercise (daily) sleep time for self-care support