L36: Transfusion Reactions, Pt. 1 Flashcards
Type 1 chains for blood groups
Antigens in secretions and plasma
Have secretor gene Se
Galactose connected to N-acetylglucosamine via 1, 3 linkage
Type 2 chains for blood groups
Antigens expressed on red cells
Galactose and N-acetylglucosamine attached via 1, 4 linkage
H antigen
Core blood group (galactose and the N-acetylglucosamine) with fucose attached to the galactose
Acts as a basis for which A and B expression is built on
A antigen
N-acetylgalactose is added galactose of H antigen
B antigen
Galactose is added to galactose of H antigen
Bombay phenotype
Absence of H antigen
hh on Type 2 chain
No fucose is available, so H antigen doesn’t form
In absence of H, there is no A or B antigens
If you type them, they look like O but react to any blood group you give them since they have anti-H
Only accept blood from other Bombay phenotypes
Para Bombay phenotype
Similar to Bombay phenotype except it has secretor gene
Has Se gene, so H, A, B or AB antigens are found in the secretions and plasma (Type 1 chain)
Expression of A or B depends on the inheritance of the pt
Antibody response that the pt makes can be mild or strong
Based on the reactivity of that antibody that they make, have to decide if you they can receive other compatible blood or only Bombay phenotype blood
Why is there no anti-A or anti-B at birth?
When baby is born, immune system hasn’t yet been exposed to bacteria which looks like A or B antigen so they can then start make naturally occuring antibodies
If reverse group is done, where there should be anti-B or anti-A, it is very weak or not present
If antibody is foundi the plasma, it is IgG passed from mother
Immune response is not developed until they start getting exposed to certain bacteria, flora from the gut
What chromosome is ABO on?
Chromosome 9
What chromosome is H antigen on?
Chromosome 19
Why is ABO expression on cord cells weak?
Due to immature type 2 chain precursors
When do embryos start to express ABO antigen?
Weak expression of ABO antigen on RBC of embryos at 5 - 6 weeks
At what age is ABO antigen developed? At what age is there an adult level?
3 - 6 months will have antigen developed
5 - 10 years will have adult level
What is the front and back type of type A?
Front: A antigen
Back: anti-B Ig
Fisher-Race system
DCE or CDE
Five major antigens: D, C, E, c, e
Whites: R1 (CDe) > r (cde) > R2 (cDE) > R0 (cDe)
Blacks: R0 (cDe) > r > R1 > R2
What antigen is most important in RH blood group?
D antigen
Rh+ means D+
Rh- means D-
Weak D
Quantitative defect in D antigen (less D than normal)
D antigen is normally formed
Weak D requires IAT (indirect antiglobilin test) to detect D presence
Won’t make anti-D since D is present, just at lower levels
Partial D
Qualitative D antigen defect (abnormal forms, missing parts of the antigen)
Will produce anti-D if they are exposed to D+ blood
Why are weak D and partial D important in labor and delivery?
Whether they are candidate for Rhogam to protect fetus from hemolytic disease of newborn
If they are partial D, should be treated as Rh- pt and be given Rhogam
Can do genotyping to see if they are partial D
Stomacytic anemia
Absence of all Rh antigens
Differentiate b/w IgG and IgM
IgG: reacts best at body temps; has to be very high titer since not very strong; most hemolysis will be extravacular (macrophage-mediated) which is not as severe as intravascular since no complement activation takes place; crosses placenta; hemolytic disease of the newborn is IgG mediated
IgM; cold-reacting antibody usually; if it reacts at body temp, it becomes very important; can cause acute hemolytic transfusion reactions and intravascular hemolysis and can be fatal
Agglutination
RBC antigen (donor red cell) + RBC antibody (pt serum/plasma) = agglutination
Indirect Coombs test
Antibody (from pt’s serum) + antigen → antigen and antibody reaction takes place (no visible agglutination since it is not strong enough) → add anti-human antibody → forms a lattice and there is visible agglutination
Direct coombs test
Detects antibodies coating patient RBC in vivo
Important test in hemolytic disease or RBC destruction
RBCs with IgG bound to membrane → add anti-human globulin → visible agglutination
What does hemolytic disease of fetus and newborn cause?
Anemia
Erythroblastosis
Hydrops: edema bc of anemia
Rising bilirubin (kernicterus) which crosses the blood-brain barrier and becomes very toxic
Rhogam
Rh immune globulin prohylaxis
Given at 28 weeks and also post-deliver or following invasive procedure or bleeding during pregnancy
Rosette test
Qualitative
Mother’s RBCs, treated with anti-D, binds to fetal Rh positive RBC wash and add RH positive RBC
Rh positive RBC forms a rosette around the fetal RBC bound with anti-D
Kleihauer betke test
Quantitative
Acid denaturation of adult hemoglobin (Hgb A)
Hgb F is not susceptible to acid denaturation
Look at percent of cells that were not subject to acid denaturation and thus calculate how much fetal D this pt had
Blood volume x %fetal cells/30 mL = RhIG dose in vials
Add extra vial to be safe
I and i group
Children with i and adults with I
Anti-I associated w/ Cold Hemagluttin Disease (CHAD) and Mycoplasma Pneumonia
Anti-i associated in infectious mononucleosis
P blood group
Anti-P1 associated w/ Paroxysmal cold hemoglobinuria (PCH), Hydatid cyst and in bird handlers (exposed to P antigens when they handle birds and make anti-P)
Lewis System, Type 1 chain
With Se gene in presence of 1H, makes Leb
Leb is receptors to Helicobacter pylori
Anti-M and anti-N
Cold reacting
Cold IgM
Becomes significant if reactive at body temp.
Anti-S, anti-s, anti-U
Will cause hemolytic disease of the newborn and hemolytic transfusion reaction
Warm IgG
Kell system
There is an association of Kell system w/ Kx antigen
If they are missing, have McLeod syndrome
Also causes X-linked chronic granulomatous disease
Kell antibodies, in addition to causing hemolytic disease of fetus/newborn, also suppress erythropoiesis; so, they both cause hemolysis and suppress erythropoiesis; pts have very severe hemolytic disease of newborn since double problem
Duffy system
Fy (a-b-) is most common Fy phenotype in African-Americans; this is protective against malaria
Higher incidence of prostate cancer in africans
Kidd
Kidd antigens cause animistic reactions
Kidd antibodies: over course of time, completely dissapears; if pt comes in and does antibody screening, it shows negative; if you give A or B type blood, will have an immediate animistic reaction; reaction will include IgG and IgM antibodies; causes severe intravascular hemolysis
Jka and Jkb are also urea transporters; they are resistant to hemolysis if you add dextrose; bc it doesn’t transport urea, it is resistant to osmotic hemolysis
