BLD 435 FINAL EXAM ACTUAL QUESTIONS AND
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
1. state the rational for performing unexpected antibody screen on pregnant
women.
Mom makes antibody to antigen on fetus rbc's she doesn't have
mom's IgG binds to fetus rbc's, rbc's destroyed. need to be replaced and mess cleaned
up
Generalizations:
ABO common but mild weak positive DAT
Rh and other: rare but more severe and stronger DAT
2. state the two events that may lead to immunization of women.
Mom immunized during first pregnancy or by transfusion
ABO seen in first pregnancy
Second and then subsequent pregnancies get more severe. ABO can always be mild
3. suggest and discuss the information that must be investigated when a
pregnant woman has a detectable unexpected antibody and select appropriate
laboratory tests to gather some/all of the needed information.
How can we predict??
,laboratory testing
history
ABO and Rh
unexpected Ig screen
if unexpected antibody screen is negative??
if unexpected antibody screen is positive??
Is Ig clinically significant?
will Ig become clinically significant?
How much Ig is there??: titer
If you think HDN:
do ABO: Rh including weak D
do DAT:
if DAT pos: Eluate and I.D.
4. describe a "titer" and state when its performance is indicated. Interpret results
of titers and describe precautions to insure proper interpretation.
If titer is 1/16 or higher maybe HDN (if anti-K 1/8)
if less that 1/16, want to monitor over course of pregnancy
titer increase 2 tubes or 4 fold
active immunization, be afraid
titers hot bed for technical errors, run controls, be careful
,If problem: Amniocentesis normal amniotic fluid colorlesswith HDN we see color... do
spectrophotometric exam to detect bilirubin and quantitate. read at 375, 450 & 525nm
absorbance for bili max at 450
plot 375 and 525 readings draw straight line. plot 450, see how far off expected the
greater the deviation, the more the bilirubin. The more bilirubin present the greater the
red cell destruction, the more the rbc destruction the greater the danger
5. evaluate given prenatal test results and offer a decision on the level of risk of
HDFN.
Can we get the fetus/kid out?????
look at creatinine for renal maturity:
<1.5 mg/dI <35 weeks
1.8-2.9 mg/dl intermediate
>2.0 mg/di go for It
lecithin/sphingomyelin ratio
L/S ratio for pulmonary maturity
<1.5 immature
1.8 or > mature enough to
go for it
If you can't get it out transfuse it so it has some RBI’s
intrauterine transfusion may be through umbilical may just be IP
use fresh O cells neg for offending antigen mom has antibody to and probably
AB plasma or 6% Albumin
, less than 7-14* days old, CMV & Hgb S negative and irradiated
*institution policy
If no indication until birth or no emergency, evaluate when the kid hits the ground
6. describe the pathophysiology of HDFN.
Maternal immunoglobulin G (IgG) antibody crosses the placenta into the fetal
circulation, where it binds to fetal red cells or erythroid pre-cursors. The immunoglobulin
subclasses IgG1 and IgG3 are more likely than IgG2 or IgG4 to cause early and/or
severe hemolytic disease.'2
The resulting increased hematopoietic drive causes a condition termed erythroblastosis
feta-lis, with liver and spleen enlargement secondary to extramedullary hematopolesis,
and portal hy. pertension. Liver enlargement can lead to decreased production of
albumin and associated decreased plasma oncotic pressure, with generalized edema,
ascites, and effusions known as hydrops fetalis. Severe HDFN can occur as early as 18
to 20 weeks' gestation or earller with antibodies to K1 (of the KEL system), but may be
difficult to detect; severity usually increases in subsequent pregnancies. Untreated,
hydrops fe-talis, with its associated high-output cardiovascular failure secondary to
anemia, can lead to fetal death. The destruction of red cells also leads to elevated
bilirubin levels. After birth, the infant's immature liver enzymatic pathways cannot
metabolize the unconjugated bilirubin, which can increase to dangerous levels. The
hyperbilirubinemia can cause permanent brain damage, known as kernicterus.' The
maternal antibody typically decreases in the neonate over 12 weeks, with a half-life of
about 25 days.
Some antibodies may cause more prolonged anemia or delayed-onset anemia.
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
1. state the rational for performing unexpected antibody screen on pregnant
women.
Mom makes antibody to antigen on fetus rbc's she doesn't have
mom's IgG binds to fetus rbc's, rbc's destroyed. need to be replaced and mess cleaned
up
Generalizations:
ABO common but mild weak positive DAT
Rh and other: rare but more severe and stronger DAT
2. state the two events that may lead to immunization of women.
Mom immunized during first pregnancy or by transfusion
ABO seen in first pregnancy
Second and then subsequent pregnancies get more severe. ABO can always be mild
3. suggest and discuss the information that must be investigated when a
pregnant woman has a detectable unexpected antibody and select appropriate
laboratory tests to gather some/all of the needed information.
How can we predict??
,laboratory testing
history
ABO and Rh
unexpected Ig screen
if unexpected antibody screen is negative??
if unexpected antibody screen is positive??
Is Ig clinically significant?
will Ig become clinically significant?
How much Ig is there??: titer
If you think HDN:
do ABO: Rh including weak D
do DAT:
if DAT pos: Eluate and I.D.
4. describe a "titer" and state when its performance is indicated. Interpret results
of titers and describe precautions to insure proper interpretation.
If titer is 1/16 or higher maybe HDN (if anti-K 1/8)
if less that 1/16, want to monitor over course of pregnancy
titer increase 2 tubes or 4 fold
active immunization, be afraid
titers hot bed for technical errors, run controls, be careful
,If problem: Amniocentesis normal amniotic fluid colorlesswith HDN we see color... do
spectrophotometric exam to detect bilirubin and quantitate. read at 375, 450 & 525nm
absorbance for bili max at 450
plot 375 and 525 readings draw straight line. plot 450, see how far off expected the
greater the deviation, the more the bilirubin. The more bilirubin present the greater the
red cell destruction, the more the rbc destruction the greater the danger
5. evaluate given prenatal test results and offer a decision on the level of risk of
HDFN.
Can we get the fetus/kid out?????
look at creatinine for renal maturity:
<1.5 mg/dI <35 weeks
1.8-2.9 mg/dl intermediate
>2.0 mg/di go for It
lecithin/sphingomyelin ratio
L/S ratio for pulmonary maturity
<1.5 immature
1.8 or > mature enough to
go for it
If you can't get it out transfuse it so it has some RBI’s
intrauterine transfusion may be through umbilical may just be IP
use fresh O cells neg for offending antigen mom has antibody to and probably
AB plasma or 6% Albumin
, less than 7-14* days old, CMV & Hgb S negative and irradiated
*institution policy
If no indication until birth or no emergency, evaluate when the kid hits the ground
6. describe the pathophysiology of HDFN.
Maternal immunoglobulin G (IgG) antibody crosses the placenta into the fetal
circulation, where it binds to fetal red cells or erythroid pre-cursors. The immunoglobulin
subclasses IgG1 and IgG3 are more likely than IgG2 or IgG4 to cause early and/or
severe hemolytic disease.'2
The resulting increased hematopoietic drive causes a condition termed erythroblastosis
feta-lis, with liver and spleen enlargement secondary to extramedullary hematopolesis,
and portal hy. pertension. Liver enlargement can lead to decreased production of
albumin and associated decreased plasma oncotic pressure, with generalized edema,
ascites, and effusions known as hydrops fetalis. Severe HDFN can occur as early as 18
to 20 weeks' gestation or earller with antibodies to K1 (of the KEL system), but may be
difficult to detect; severity usually increases in subsequent pregnancies. Untreated,
hydrops fe-talis, with its associated high-output cardiovascular failure secondary to
anemia, can lead to fetal death. The destruction of red cells also leads to elevated
bilirubin levels. After birth, the infant's immature liver enzymatic pathways cannot
metabolize the unconjugated bilirubin, which can increase to dangerous levels. The
hyperbilirubinemia can cause permanent brain damage, known as kernicterus.' The
maternal antibody typically decreases in the neonate over 12 weeks, with a half-life of
about 25 days.
Some antibodies may cause more prolonged anemia or delayed-onset anemia.
