Immuno Exam 3: Pregnancy

what test is done on the first prenatal visit

maternal blood tests

3 Types of maternal Blood tests

-HCG (pregnancy confirmation)

-Anitgen typing of RBC (AOB and RH)

-Indirect Coombs test

Indirect Coombs test

screen for antibodies that can cause hemolysis of fetus/newborn

what does it mean if Indirect Coombs is postive

mother is already sensitized bad

what does it mean if Indirect Coombs is negative

mother is not sensitized
can be given rhogam if needed

3 types of RBC antigens

- ABO

-Rh-D

-Atypical antigens

6 possible ABO genotypes

AA, AO, BB, BO, AB, OO

4 types of ABO phenotypes (Blood types)

Type A, B, O, or AB

type A

AA or AO

type B

BB or BO

type O

OO

Type AB

AB

what blood type is a universal donor and which is a universal recipeint

universal recipient: AB

universal donor: O

type A blood

A antigens present on red blood cells (self)

body makes anti-B antibodies (recognizes non-self if exposed)

type B blood

B antigens present on red blood cells (self)

body makes anti-A antibodies (recognizes self if exposed)

why is type O a universal donor

blood could be accepted by people wth other blood types without rejection

type O blood

do NOT have A or B antigens

body makes anti-A and anti-B antibodies (recognizes non-self if exposed)

why is type AB blood a universal recipient

people with type AB blood can be given type A, B, and O blood without rejection

Type AB blood

A and B antigens present on red blood cells (self)

body does NOT make anti-A or anti-B antibodies

what is the root cause of blood transfusion errors

a problem with documentation

ABO blood transfusion incompatability

A and B antigens are very immunogenic

corresponding antibodies (anti A and B) are strongly hemolytic

wif the mother's blood type is incompatible with the blood type of the fetus

• mother's immune system can recognize the fetal tissue as "non self

"• mother creates antibodies against the fetus' RBC

• RBC antibodies can cross the placental barrier and damage/kill fetal RBC

why are A and B antigens less immunogenic during gestation than in children/adults

because they're not well developed during gestation

transfusion vs fetal hemolytic disease

fetal/newborn hemolytic disease is MILD compred to adult transfusion reactions because antigens are less well developed during fetal/newborn

Rh antigens

RBC surface antigens (Rh factor= Rhesus factor)

is there a prophylatic therapy for blood type incompatibility?

no

Rh-D antigen

most immunogenic of Rh antigens

only Rh antigen with a medical prophylatic therapy

possible Rh-D phenotypes

Rh-D "positive": Dd, DD

Rh-D "negative": dd

Rh-D incompatibility

occurs when an Rh-d (negative) mother ispregnant with an Rh-D (positive) fetus.

The mother's immunesystem recognizes the Rh-D antigen as non-self.

chances of contributing D if father is Dd vs DD

DD then 100% chance of contributing D•

Dd then 50% chance of contributing D, 50% chance ofcontributing d (lack)

alloimmunization

immune response to foreign antigens after exposure to genetically different cells or tissues

process of alloimmunization

1. maternal sensitization

2. maternal production of IgG antibodies

3. Maternal antibodies cross placenta to fetus

4. antibody mediated hemolysis in fetal RBC

how does maternal Rh-D sensitization occur

mom exposed to "non-self" antiges BEFORE or DURING pregnancy/delivery

Rh- mom exposed to Rh+ blood AT ANY POINT in her life

Rh- mom initial exposure to Rh-D antigen and after exposure

primary immune response is slower and weaker compared to future exposures IgM anti-D does not cross placenta

secondary conversion to anti-D IgG production (immunoglobulin class switching), crosses placenta

when are anti-D IGM found in ciruclation after Rh- mom is exposed to Rh-D antigen

anti-D IGM found in ciruclation 8 weeks-6 months after exposure

if exposure and Rh-D sensitization is durig pregnancy/delivery...

the baby is UNAFFECTED

• IGM response occurs first and IGG response is weeks/months later (IGG crosses the placenta and can affect fetus)

• The lag in maternal immune response to fetal antigen often means the pregnancy is over before the fetus is affected (it has already been born!).•

if exposure and sensitization of Rh-D occurs before pregnancy/delivery...

the baby is AFFECTED earlier in gestation and more severely

• Subsequent pregnancies after 1st Rh-D baby

• FIRST pregnancy if mother was previously exposed/sensitized in another way

4 risk factors affecting maternal sensitization

-volume of blood exposure

-extent of maternal immune response

-fetus homozygous vs heterozygous for D antigen (Dd or DD)

-concurrent presence of ABO incompatability

how does volume of blood exposure affect risk of maternal Rh-D sensitization?

smaller embryo/fetus--> less blood volume

complication types of the fetus of blood type incompatability in pregnancy

-anemia--> erythroblastosis fetalis

-juandice--> kernicterus

-hydrops fetalis

anemia (low RBC count) results in

-decreased oxygen carrying capacity

-increased cardiac workload; tachycardia

-erythroblastosis fetalis

erythroblastosis fetalis

an anemic blood disease of a fetus or newborn, characterized by erythroblasts in the circulating blood

jaundice

yellowing of the skin and whites of the eyes caused by excess bilirubin (product of heme breakdown ) in the blood

kernicterus

a life-threatening form of brain damage caused by excessive jaundice

hydrops fetalis

a severe, life-threatening edema in the fetus/newborn

bilirubin during pregnancy

bilirubin from breakdown of fetal hemoglobin can be cleared via placenta to maternal circulation → bilirubin is conjugated and excreted by mom

bilirubin after delivery

infant has low levels of glucuronyl transferase enzyme→ cannot conjugate and clear the bilirubin as efficiently

baby with high serum bilirubin--> jaundice

what is required for determining the risk of Rh incompatability for each pregnancy

good prenatal care

when can alloimmunization be prevented

If Rh- mom has not been exposed to Rh antigen because this means she hasn't been sensitized

when is it too late to prevent alloimmunization?

Rh- mom is already exposed and sensitized to Rh antigen

who should be treated with Rh IgG injections

all unsensitized Rh- moms possibly carrying an incompatible fetus

what does Rh IgG do

-provides passive immunity

-supresses the immune response to Rh+ blood in non-sensitized Rh- females

-prevents maternal sensitization and formation of active Rh-D antibodies

-prevents Rh hemolytic disease in Rh+ neonates

ONLY effective for current pregnancy, not future ones

routine administration of Rh IgG in Rh- moms at risk

• mid-pregnancy (around 28 weeks gestation)

• within 72 hours after delivery (can admin up to 2 weeks after delivery if initial window missed)

as needed administration of Rh IgG in Rh- moms at risk

•Post-miscarriage/termination

• Post-ectopic pregnancy

• After prenatal tests such as amniocentesis and chorionic villus biopsy -(puncture/rupture)

• After injury to the abdomen during a pregnancy

contraindications to Rh IgG

Rh+ individuals

brands of anti-D immune globulin

rhogam, rhoplac, rho-sdf, hyperrho S/D, micrhogam

route of admins for anti-D immune globulin

brand specific IM or IV

which conditions would you give 300mcg of anti-D immune globulin

antenatal and postpartum, 2nd and 3rdtrimester pregnancy miscarriage/terminations,transplacental hemorrhage

which conditions would you give 50mcg of anti-D immune globulin

1st trimester pregnancy miscarriage/terminations

how do you know when alloimunization occurs after maternal sensitization?

maternal and fetal montioring

maternal monitoring of alloimmunization

antibody titers

invasive fetal monitoring of alloimmunization

-amniocentesis

-percutaneous cord blood

non-invasive fetal monitoring of alloimmunization

-ultrasound

-cerebral artery doppler ultrasound

-non-stress test (NST)

maternal antibody titers, what do higher levels mean? what do lower levels mean?

higher levels--> greater immune response against a specific antigen

lower levels--> rarely result in severe hemolytic disease

what info is obtained in invasive fetal monitoring

fetal antigen status, presence of anemia or increased levels of bilirubin

what info is obtained in non-invasive fetal monitoring methods (like ultrasound)?

assess fetal grwoth, development, and presence of hydrops

middle cerebral artery dopplr ultrasound

-assesses fetal anemia

-faster flow with fewer RBC (less viscous)--> increased HR

non-stress test (NST)

-not harmful to fetus

-used after 28 weeks gestation

-uses monitors on maternal abdomen to measure fetal heart rate and maternal contractions

goal of non-stress test

-measure fetal HR in response to own movement

-increase movement ocrrelates with increased HR

reactive vs non-reactive non-stress test results

reactive- blood flow, O2 is adequate

non-reactive: rule out other causes (asleep, meds, etc) but O2 may not be adequate

when is early delivery

~32-35 weeks gestation

betamethasone

administered in anticipattion of an early delivery to induce production of surfactant in the fetal lungs

lubricates air sacs of the lung--> hasten lung development, imrpoves survival outsdie of the womb

betamethasone also decreases the risk for...

-brain bleed (intraventricular hemorrhage)

-necrotizing enterocolitis (severe intestine infection)

-mortality

corticosteroid

will suppress meternal immune system to lead o reduced alloimmunization effects

dose of betamethasone

12mg x2 doses

intrauterine transfusion use

used when possibility for severe anemia at <35 weeks gestation