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BSNC 5000 > Module 4 - OB > Flashcards

Module 4 - OB Flashcards

1
Q

RF for heat loss in newborns

A

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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2
Q

Thermogenesis in newborns

A

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

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3
Q

Cold stress

A

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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4
Q

Consequences of cold stress

A

hypoglycemia
metabolic acidosis
hypoxia

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5
Q

How do newborns lose heat

A

convection
conduction
radiation
evaporation

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6
Q

4 types of jaundice

A

unconjugated bilirubin
conjugated bilirubin
breastfeeding jaundice
breastmilk jaundice

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7
Q

How is bilirubin produced

A

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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8
Q

Unconjugated bilirubin characteristics

A

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

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9
Q

Conjugated bilirubin characteristics

A

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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10
Q

Physiologic jaundice

A

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

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11
Q

Pathological jaundicei

A

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

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12
Q

Breastfeeding jaundice

A

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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13
Q

Breast milk jaundice

A

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

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14
Q

RF for jaundice

A

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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15
Q

Bilirubin complications

A

Bilirubin encephalopathy = acute manifestation
kernicterus = longterm, irreversible complications

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16
Q

S/S encephalopathy

A

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

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17
Q

Mechanisms of heat loss/production

A

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

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18
Q

S/S hypothermia in newborns

A

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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19
Q

Mild hypothermia

A

35-36.3

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20
Q

Moderate hypothermia

A

32-34.9

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21
Q

Severe hypothermia

A

<32

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22
Q

How might a fever present in a newborn?

A

hypothermia
*hyperthermia usually r/t external causes

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23
Q

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

A

beta-glucuronidase

24
Q

RF in babies more likely to develop jaundice

A

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

25
Q

APGAR

A

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

26
Q

Pre-eclampsia pathophysiology

A

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)

27
Q

Treatment for eclampsia

A

magnesium sulfate

28
Q

Antidote for magnesium sulfate

A

calcium gluconate

29
Q

Fetal hemoglobin

A

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

30
Q

What happens to fetal hemoglobin after birth

A

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)

31
Q

Physiological jaundice

A

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

32
Q

Is unconjugated bilirubin found in urine?

A

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

33
Q

Where is conjugated bilirubin converted into stercobilin and urobilinogen?

A

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

34
Q

Physiogical jaundice RF

A

premature
SGA
twins
traumatic delivery
polycythemia (GDM)

35
Q

Onset of BF jaundice

A

first week of life

36
Q

Onset of breast milk jaundice

A

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

37
Q

Pathological increased bilirubin production

A

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

38
Q

Pathological increased enterohepatic circulation

A

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

39
Q

Pathological decreased clearance of unconjugated bilirubin

A

G6PD deficiency
prematurity

40
Q

Pathological metabolic conditions

A

hypothyroidism
hypopituitarism

41
Q

Pathological inborn errors of metabolism

A

galactosemia
breast milk jaundice

42
Q

Conjugated hyperbilirubinemia

A

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

43
Q

Causes of conjugated hyperbilirubinemia

A

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

44
Q

does phototherapy work on conjugated jaundice?

A

no

45
Q

cardiovascular modifications in fetus

A

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

46
Q

heart transition during extrauterine life

A

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

47
Q

lung transition during extrauterine life

A

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

48
Q

transitional tachypnea of the newborn

A

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

49
Q

onset of respiratory distress syndrome

A

immediate

50
Q

first period of reactivity

A

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

51
Q

second period of reactivity

A

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

52
Q

period of relative inactivity

A

period of decreased responsiveness lasting min-hours

53
Q

minimum number of feeds in the first 24 hours

A

5

54
Q

when is cluster feeding most common

A

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

55
Q

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

A

7-10%

BSNC 5000 (11 decks)

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