lifespan Flashcards
blood types
determined by genetics
- ABO antigens
- develop antibodies against antigens they dont have
ABO antibodies
not present at birth and develop between 2-8 months of age
blood group AB
has A and B antigens
blood group A
has A antigen
blood group B
has B antigen
blood group O
does not have either A or B antigen which is why its universal donor
Rh factor
determines whether blood has type D Rh antigen and determines this through being “positive or negative”
Rh positive
has type D antigen
- most common blood type
Rh negative
does not have type D antien
most common blood type
O Rh+
Hemolytic disease of the newborn (HDN) general
mother is Rh negative and fetus is Rh positive; interface of vessels are closed off until delivery and maternal cells can develop antibodies if blood type is different than baby’s
HDN specifics
- baby blood dosent cross with mothers blood until delivery
- blood wont cross but antibodies will for second baby
- develops in first pregnancy and harms baby in second pregnancy
- preventable
HDN treatment
Rh immunoglobulin
- at 28 weeks and within 72 hours of delivery
postpartum hemorrhage
losing more than 500ml of blood and will cause hypovolemic shock
4T’s of postpartum hemorrhage
Tissue (retained placenta)
Tone (uterine atony)
Trauma
Thrombin (coagulation disorders)
antepartum hemorrhage
prior to delivery; a risk factor for postpartum hemorrhage
chorioamnionitis
risk factor for post partum hemorrhage; infection of placenta and amniotic fluid
fetal macrosomia
large infant; risk factor for postpartum hemorrhage
maternal anemia
risk factor for postpartum hemorrhage
maternal obesity
risk factor for post partum hemorrhage due to it yielding fetal macrosomia
multifetal gestation
many fetuses causing risk for postpartum hemorrhage
preeclampsia
high BP putting at risk for postpartum hemorrhage
uterine contraction
oxytocin secretion from hypothalamus stimulates uterine contraction during delivery
uterine atony treatment
oxytocin, crytalloid fluids (if hypovolemic shock) and fundal massage
fundal massage
helps uterus respond to pressure and increase contraction
neonatal jaundice/hyperbilirubinemia
occurs due to high production with immature circulation which causes recirculation
- emergency if within 24 hours but onset usually 48-72 hours
bilirubin
product of hemoglobin breakdown
- excreted via stool
- if unconjugated and lipid soluble it is toxic to cells and accumulates in CNS
bilirubin encephalopathy (Kernicterus)
neurological condition that occurs due to jaundice where bilirubin deposits on on basal ganglia
grade 1 jaundice
face and neck
grade 2 jaundice
face, neck, chest, back
grade 3 jaundice
from knees up minus arms
grade 4 jaundice
whole body except feet
grade 5 jaundice
entire body
unconjugated bilirubin
the gap between total bilirubin and conjugated bilirubin
breastfeeding as treatment for jaundice
eliminates extra bilirubin because it has colostrum which acts as a laxative to excrete the bilirubin
phototherapy as a treatment for bilirubin
bilirubin is transformed to photobilirubins when exposed to blue-green light which is hydrophilic and easily excreted
exchange transfusion
taking away blood that is present and replacing it with new blood not high in bilirubin
syndromes
group of symptoms or condition which consistently occur together or are associated with a set of symptoms
- can be genetic or “de Novo” (new)
down syndrome
Trisomy 21; error in meiosis
2 risk groups for down syndrome
- if older than 25 due to aged oocytes
- familial link for chromosomal ‘robertsonian translocation’
fetal echocardiogram as screening for down syndrome
cardiac defects can be an identifier and results will show ‘higher translucency’ between 10-13 weeks
serum markers as screening for down syndrome
hCG levels are high
GI issues associated with down syndrome
large tongue, TE fistula, intestinal obstruction, hirschsprung disease, imperforated anus, GERD
large tongue in down syndrome
makes it difficult for child to latch
TE fistula in down syndrome
can cause chocking because esophagus is ‘blind’ and it does not connect to the GI
hirschsprung disease
malfunctioning portion of large intestine
- diagnosed quickly d/t lack of BM
treatment for GI issues with feeding
intermittent feeds, upright positioning
thickened formula as a treatment for GI issues
decreases vomiting as a result of reflux but not reflux itself
atopic dermatitis ‘eczema’
chronic inflammation of the skin; allergen triggered
- damaged epidermal barrier puts at risk for infection
- children with this may have more allergies
atopic dermatitis treatment
corticosteroid cream, antihistamine cream, moisturizer cream
pulmonary and aortic valves
semilunar valves
semilunar valves
pulmonary and aortic valves
tricuspid and mitral valves
atrioventricular valves
atrioventricular valves
tricuspid and mitral valves
murmur
implies turbulent blood flow due to valves not being able to close properly or at all
- if it goes away after changing position it is benign (innocent)
diastole murmur
worse because theres more flow due to valves being open
VSD (ventricular septal defect)
leading CHD; systolic murmur
- blood shunted to right side; high pressure to low pressure
- cardiac silhouette enlarges over time
ASD
blood shunts left to right
right side of heart in VSD
ventricle overload, increased pulmonary flow causing overall fatigue and tachypnea, coagulation due to increased pressure
left side of heart in VSD
decreased cardiac output, decreased perfusion, decreased BP
VSD treatment
optimize CO with fluid restriction, diuretics, ace inhibitors high calorie low volume formulas
TOF (tetralogy of Fallot)
VSD, pulmonary outflow tract stenosis, RV hypertrophy (very thick), overriding aorta
pulmonary outflow tract stenosis
thickening in pulmonary vein
if little RVOT stenosis
VSD shunting L–>R
if high RVOT stenosis
VSD shunting R –> L
- will see cyanosis b/c unoxygenated blood enters left side
hypercyanotic spells (TET spells)
extreme cyanosis during times of stress
- 2 main triggers are crying and hypovolemia
crying as a trigger for TET spells
hyperventilation–> tachycardia–> hyperpnea–> vasoconstriction–> reduced perfusion–> right to left shunting–> hypoxemia
hypovolemia (dehydration) as a trigger for TET spells
drop in BP –> lower L ventricle pressure –> right to left shunting
- risk of hypoxic brain injury
- risk of seizure
- giving O2 will not help, it will be a trigger
TET spell treatment goal
goal is to decrease right to left shunting
treatment of TET spell
knee to chest position
fluid bolus
morphine (vasodilatory)
B blocker
COA (coarctation of the aorta)
narrowed aorta
- low BP, low perfusion, difference in pressure between upper and lower limbs
- dilate to help treat
