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immunohema

immunohematology

QuestionAnswer
Most fatal transfusion reactions are caused by Clerical errors
Samples must be collected when 3 days of schedule transfusion
Blood bank must have 2 unique patient identifiers date of collection and initials
When can a electronic crossmatch replace an Immediate spin crossmatch When 2 blood types are on the file and antibody screen is negative
In a emergency,you can uncrossmatched group O with Rh-negative packed RBCs
Transfusion therapy used for blood loss,insufficient proteins for hemostasis
A unit of whole blood or packed RBCs should increase hemocrit 3% or hemoglobin level 1.0-1.5
Leukocyte reduced filters can prevent non hemoltic transfusion, reduce the risk of HLA and CMV infection
When can you used factor IX Patient with Hemoglobin B
Replacement of massive transfusion within 24 hours 10 units of blood in a adult
Irradiation Gamma or electron treatment of cellular blood
All cellular blood components to be irradiated necessary for bone marrow transplatation
How much plateletpheresis be prepared from one donor 3 X 10/11 platelets
Needle stick accident with infectious blood Hep B immuneglobulin
Life threating neutropenia Granulocytes pheresis
Anaphylaxis Washed or deglycerolized RBCs
Repeated febrile transfusion reactions leukocyte reduced RBCs
Directed donation from a blood relative Irradiated RBCs
Cryoprecipitate Factor VIII deficiency
FFP Vitamin K deficiency and hemorrhage
Factor VIII Hemo A
Factor IX Hemo B
Fibrinogen deficiency Cryoprecipitate
Increase oxygen-carrying capacity RBCs
Bone marrow transplant patient with anemia unresponsive to iron and vit B12 therapy Irradiated RBCs
Lewis antibodies are capable of binding complement and enhanced by enzymes
Lele genotype Common in blacks
Le(a-b+)Lewis phenotype most common in whites or blacks
What is formed when a second L-fucose is added to the #4 carbon of N-acetyl-D Le/b antigen
What expression is needed for a Le/a substance Le gene
What is needed to form Le/b substance Le and Se genes
Glycoprotein Lewis antigens in secretions
Absorbed from plasma onto RBC membranes Glycolipids
Anti M and anti N do not bind complement or react with enzymes
IgG antibodies Anti S and anti s
Anti U IgG antibody associated with transfusion reactions and HDN
P1 antigen Poorly develope at birth
Anti P1 IgM antibody and cold reactive
Anti-PP1 Pk Produced by all P individuals early in life, without RBCs sensitization
Found as a naturally occurring alloantibody in sera of all Pk individuals Anti P
PCH Caused by autoantibodies that demonstrate anti P
Anti I Weak, naturally occurring IgM, detect at 4C
Pathogenic anti I Strong cold autoagglutinin with high titer at 4C
Anti i is a rare IgM agglutinin
Develope at birth and not destroyed by enzymes Kell blood group antigens
Kell blood group antigens Destroyed by DTT, ZZAP,and glycine-acid-EDTA
This antigen is rated second only to D antigen in immunogencity K
What antigens are destroyed by enzymes and ZZAP Fy-a and Fy-b
Common cause for delayed hemolytic transfusion reactions Kidd system antibodies
Anti jka/jkb demonstrate dosage and are IgG antiglobin reactive
Lu(a-b-) rare from 3 different genectic backgrounds
Antibody detection cells will not routinely detect antibody specificity Anti-Kpa
Which blood system is associated with resistance to P.vivax malaria Duffy
Which antibodies does not fit with the others with respect to the optimum phase Anti-P1
Lewis system Not manufactured by RBC as other antigens
Soluble substance secreted into plasma and secretions In plasma glycolipids
Soluble substance secreted into plasma and secretions in secretions glycoproteins
Adsorbed onto RBC’s and Tissues as Glycolipids
Le a and b are not alleles
Genotype is lele, Have gene, but mutated May form Lewis Antibodies, Common in blacks Le (a=b=)
Le (a=b+) secretors
Le (a+b=) non-secretors
What happens when Le a and b both in secretions b only adsorbed onto RBC
Le (a=b=) first 10 days
Le and sese have Leª in saliva
Naturally occurring; don’t require exposure Lewis antibodies
Lewis Antibodies Usually IgM; rarely IgG
M,N,S,s are known as Alleles
MNS System Wide range of reaction temperatures M,N sometimes 18⁰C S,s usually AHG
Phenotypes P1 (most common) P2 p P1k P2k
IgM, cold reacting, Enhanced by enzyme treatment, May be associated with parasitic infections P System
present on all adult cells Anti I antigen
Anti I antigen absent on cord blood cells
Anti I antibody Reactive with all adult cells; anti-i rare, reacts with cord cells
Anti I antibody Cold reactive, best at 4 degrees
K (kell), k (Celano), Kpa (20% freq. in blacks), Kpb, Jsa, Jsb Major antigens
Kidd System Genetics: chromosome 18
Chromosome #1,Present on fetal cells in uteroFya-b- phenotype associated with Malaria Duffy System
appears as an inseparable combination of anti-Fya+b Fy3
what happens to anti-Fy 3,4,5 during treatment Not destroyed by enzymes
Genetics: Lu gene, chromosome 19,Antigens: Lua low frequency, Lub high frequency Lutheran System
refers to the presence of the antigen on a panel +
O refers to the absence of the antigen
An antibody will only react with cells that have the corresponding antigen antibodies will not react with cells that do not have the antigen
Landsteiner’s Rule Individuals DO NOT make allo-antibodies against antigens they have.
P1 substance is found sometimes derived from hydatid cyst fluid
Lea and Leb substance is found soluble antigen found in plasma and saliva
I substance is found can be found in breast milk
Sda substance is found human or guinea pig urine
Dithiothreitol (DTT) is a thiol and will denature Kell antigens
Autoadsorption technique in which the autoantibody is removed from the patients serum using their own red cells
Created by: hintonworld
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