Module 4 - OB Flashcards by Unknown Unknown

RF for heat loss in newborns

large surface area to mass ratio
thin skin
low subcutaneous fat
can’t shiver
high bmr = increased evaporation
premature or SGA
superficial blood vessels
CNS impairment (hypothalamus dysfunction

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Thermogenesis in newborns

brown fat metabolism
increased metabolic activity of organs (brain, heart, liver)

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Cold stress

cold –> thermogenesis
increased brown fat metabolism = increased free fatty acids
increased metabolism = increased oxygen demand = can lead to hypoxia/hypoxemia if demand > supply
hypoxia = pulmonary vasoconstriction = reduced pulmonary perfusion = worsening hypoxemia
loss of blood volume/oxygen = anaerobic metabolism = lactic acid

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Consequences of cold stress

hypoglycemia
metabolic acidosis
hypoxia

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How do newborns lose heat

convection
conduction
radiation
evaporation

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4 types of jaundice

unconjugated bilirubin
conjugated bilirubin
breastfeeding jaundice
breastmilk jaundice

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How is bilirubin produced

lysis of red blood cells –> heme & globulin
heme broken down into unconjugated bilirubin
unconjugated binds with albumin –> transported to liver
conjugated at liver –> bile –> GI tract –> excreted in feces/urine

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Unconjugated bilirubin characteristics

fat-soluble
can deposit into tissue
can cross BBB and accumulate in brain –> enchalopathy

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Conjugated bilirubin characteristics

water-soluble
more stable, less toxic
enters into bile then GI tract where it is converted into urobilinogen (urine) and stercobilirubin (feces)

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Physiologic jaundice

develops >24 hours
usually resolves independently in two weeks
normal as NB are born with excessive RBCs

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Pathological jaundicei

develops <24 hours
usually caused by increased hemolysis (hemolytic dx of newborn)

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Breastfeeding jaundice

caused by inadequate feeding ~day 2-5
colostrum contains natural laxative to promote voiding
less feeding = less peristalsis/pooping
dehydration = less hepatic circulation = less conjugation of bilirubin
bilirubin is reabsorbed at intestines

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Breast milk jaundice

day 5-10
r/t to factors in breast milk (beta-glucuronidase) that inhibit conjugation or decrease excretion

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RF for jaundice

increased production (polycythemia, sepsis, hemolytic anemia)
blood incompatibility ABO/RH/Hemolytic disease of newborn
poor feeding
poor voiding (bilirubin can be reabsorbed in GI tract)
bruising/trauma/assisted delivery/cephalohematoma
liver disease
acidosis/hypoxia (affect binding of bilirubin + albumin)
acidosis
lack of albumin
bowel obstruction (atresia)
family history, sibling born w/ jaundice
oxytocin used in labour (oxytocin binds with albumin)
deficiency in glucose-6-phosphate dehydrogenase/galactosemia (hemolytic anemia)
mom with GDM
ethnicity (asian, middle eastern, aboriginal)

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Bilirubin complications

Bilirubin encephalopathy = acute manifestation
kernicterus = longterm, irreversible complications

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S/S encephalopathy

lethargy
decreased tone/activity
stupor, irritability
increased tone, retrocollis/opisthotonus
minimal feeding, high pitched cry
coma
shrill cry
seizures
death

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Mechanisms of heat loss/production

cellular metabolism (heat is a byproduct)
voluntary muscle activity (crying, flexion)
peripheral vasoconstriction
nonshivering thermogenesis (brown fat metabolism)

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S/S hypothermia in newborns

acrocyanosis
cool, mottled skin
hypoglycemia
transient hyperglycemia
bradycardia
tachypnea, restlessness, shallow/irregular resps
respiratory distress, apnea, hypoxemia, metabolic acidosis
decreased activity
lethargy
hypotonia
feebel cry
poor feeding
decreased weight gain

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Mild hypothermia

35-36.3

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Moderate hypothermia

32-34.9

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Severe hypothermia

<32

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How might a fever present in a newborn?

hypothermia
*hyperthermia usually r/t external causes

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What enzyme in breast milk can cause an increase in unconjugated bilirubin?

beta-glucuronidase

RF in babies more likely to develop jaundice

preterm/early term <38 weeks
sibling hx with jaundice requiring therapy
exclusive BF
clinical jaundice within first 24 hours

APGAR

done at 1 & 5 min. repeated @ 10 mins if necessary appearance pulse grimace activity respiration

Pre-eclampsia pathophysiology

abnormal placental implantation --> trophoblsat does not adequately burrow into myometrium. spiral artery remodeling does not occur fetal perfusion demands exceed maternal supply prolonged fetal ischemia/oxidative stress --> release of inflammatory cytokines/products into maternal circulation "intervillous soup" these substances cause abnormal changes in maternal circulation --> increased permeabiilty, vasoconstriction, remodeling, endothelial dysfunction consequences: edema, hepatic dysfunction, cerebral dysfunction (seizures)

Treatment for eclampsia

magnesium sulfate

Antidote for magnesium sulfate

calcium gluconate

Fetal hemoglobin

higher affinity for oxygen difference in chains shorter lifespan than adult RBC (60 days)

What happens to fetal hemoglobin after birth

fetal RBC rapidly cleared to make room for adult RBC fetal RBC has higher affinity for O2 so needs to be destroyed to prevent hypoxia (won't release O2 @ peripheral tissue)

Physiological jaundice

normal onset >24 hours rapid fetal RBC destruction = higher bilirubin immature liver unbale to clear excess bilirubin --> jaundice

Is unconjugated bilirubin found in urine?

no when bound to albumin it is too large to pass thru glomeruli

Where is conjugated bilirubin converted into stercobilin and urobilinogen?

in the colon by intestinal flora **feeding important to establish gut microbiome in infants

Physiogical jaundice RF

premature SGA twins traumatic delivery polycythemia (GDM)

Onset of BF jaundice

first week of life

Onset of breast milk jaundice

>7 days of life & can last up to 12 weeks usually resolves on its own BF not contraindicated

Pathological increased bilirubin production

hemolysis (immune-mediated, heritable) extravasation (cephalohematoma) polycythemia sepsis DIC macrosomic infants of GDM moms

Pathological increased enterohepatic circulation

insufficient breast milk/feeding pyloric stenosis bowel obstruction ileus **longer bilirubin stays in intestine & amkes contact with brush border enzymes can unconjugate it and it returns to enterohepatic circulation

Pathological decreased clearance of unconjugated bilirubin

G6PD deficiency prematurity

Pathological metabolic conditions

hypothyroidism hypopituitarism

Pathological inborn errors of metabolism

galactosemia breast milk jaundice

Conjugated hyperbilirubinemia

conjugated bilirubin detected in serum is pathological can enter kidneys producing dark urine

Causes of conjugated hyperbilirubinemia

hep B rubella CMV herpes toxoplasmosis biliary atresia mucus plug choledochal cyst

does phototherapy work on conjugated jaundice?

cardiovascular modifications in fetus

foramen ovale - shunt between atria ductus arteriosus - joins the pulmonary artery and aorta together ductus venosus - joins the umbilical vein and inferior vena cava

heart transition during extrauterine life

blood flow from placenta stops (cord clamping) pressure in right atrium increases pushing blood into pulmonary circuit blood flow to left atrium closes the foramen ovale (functional shunt) later becomes the fossa ovalis ductus arteriosus closes after prostaglandin E1 levels fall

lung transition during extrauterine life

fetal lungs are filled with fluid (lungs not functional in utero) chloride channels pull fluid into the alveoli during labor maternal epinephrine/glucocorticoids cause active transport of sodium channels into T2 alveolar cells sodium channels cause reabsorption of fluid into lymph/circulation most lung fluid reabsorbed via sodium channels remaining squeezed out during birth + through crying

transitional tachypnea of the newborn

rapid breathing shortly after delivery of term babies onset 1-2 hours after birth caused by a delay in clearing of lung fluid usually resolves within 24-28 hours if cleared <6 hours considered a delayed transition

onset of respiratory distress syndrome

immediate

first period of reactivity

0-60 minutes postpartum HR 160-180 RR 40-60 very alert, exploratory, active

second period of reactivity

occurs 6-8 hours after birth lasts 10min-several hours tachycardia + tachypnea increased muscle tone, changes in skin color, mucus production

period of relative inactivity

period of decreased responsiveness lasting min-hours

minimum number of feeds in the first 24 hours

when is cluster feeding most common

first 24-36 hours infants may feed multiple times in an hour

what amount of weight loss in the first 4-5 days would indicate more assessment?

7-10%