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60 Cards in this Set
- Front
- Back
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What is sensitization |
Antibodies are bound to the RBCs, but they are not crosslinking |
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DAT Vs IAT |
DAT: Directly detects the presence of IgG bound to RBCs
IAT: Detects the presence of IgG in the serum using test cells. |
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Human Leukocyte Antigen (HLA) |
HLA-aby results from transfusions or pregnancy. It causes a poor clotting response to transfusions and needs matched platelet types to repair. |
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Panel-Reactive Antibody (PRA) |
A test to see to how many HLA types the patient will react to. |
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HLA Typing |
The letter indicates the gene locus, and the number is the antigen.
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HLA Typing Microtoxicity test |
Donor or recipient WBC (HLA source) Incubated with comercial MHC allels Ab
Compliment added which kills cells with bound Ab
Pink dye added that only enters dead cells, these cells are positive for the tested allele |
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HLA Typing Mixed Lymphocyte reaction |
Mixes donor a recipient WBCs. If they attack eachother, they will multiply which is detected by the uptake of radioactive thymodine.
Detects compatibility, but not specific HLA type |
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Blood Type sugars |
A = GalNAc
B = Galactose
AB = Both
O = Neither |
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Forward Typing Vs Reverse Typing |
Forward: Detects antigen on the cell surface.
Reverse: Detects the presence of antibodies in the serum. |
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INST Number |
ABO = 1
Rh = 4 |
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ABO history |
First described by Landsteiner in the early 1900s
von Decastello and Sturli discovered the ABO type. |
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Where are ABO antigen's not found? |
The CSF |
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When Dose a human begin expressing ABO antigens? |
Weekly expressed at 5-6 weeks, fully expressed at 2-4 years of age. |
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H antigen |
Adds a L-fucose to terminal galactose to common oligosaccharide chains.
A and B antigens cannot stick to the RBC without the H antigen.
O types, have a lot of unused H-antigen, AB types have very little. |
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Chromosome 9 |
Has 3 Loci; A, B, O
A: N=acetylgalactoseaminyltransferase – N-acetylgalactosamine
B: D-galactosyltransferase – D-galactose
O: enzymatically inactive
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A1 type |
80% of types A
Have both branched and linear antigen
Positive/agglutinate with anti-A antisera –
Positive with Dolichos biflorus (lectin) |
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A2 Type |
20% of type A individuals – Linear ag – Fewer A antigen copies than A1 phenotype – Positive/agglutinate with anti-A antisera – Can produces Anti- A1 – Negative with Dolichos biflorus (lectin) |
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Rare A types |
Weak or no agglutination with anti-A & anti-A,B • No agglutination with anti-A1 • Presence or absence of anti-A1 in plasma • Strong agglutination with anti-H (lectin) • Presence of A and H in saliva • Adsorption and elution studies |
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ABO Phenotypes |
A1 Type = A1A1 / A1A2 / A1O
A2 Type = A2A2 / A2O
B Type = BB / BO
A1B Type = A1B
A2B Type = A2B
O Type = OO |
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What is special about Anti A1? |
Dose not agglutinate A2, otherwise insignificant.
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Group A with aquired B antigen |
Disease of lower GI tract • Cancer of the colon • Intestinal obstruction • Gram negative septicemia -Bacterial deacetylating enzyme: *Removes acetyl group leaving galactosamine - D-galactose -Pt anti-B doesn’t agglutinate autologous RBC -Patients should receive Group A RBC for transfusion |
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B(A) Phenotype |
Patient has a small amount of A antigen despite being type B.
Often exposed by bacterial infections where it causes agglutination |
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Secreter Status |
Se and se alleles • Se – FUT2 – L-fucosyltransferase – L-fucose to type 1 oligosaccharide
These individuals secrete soluble A, B and H antigens in their body fluids
Dominant mutation
Tested with a basic agglutination test |
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Rh Type Discovery |
Landsteiner and Weiner in the 1930s
A child was still born after having a sever reaction to ABO compatible blood.
Mother's RBC reacted 80% of the time with the fathers at temps between 20-37c
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Rh Protein |
Produce a 416 AA polypeptide with no carbohydrate residues.
Only appear on the RBC membrane, and will not be recognized by the body if seperated.
The Rh protein serves as a cation transporter and plays a role in membrane integerety.
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Rh Genetics |
Two genes located on the first chromosome
RHD: Allele, D. Code for D antigen (d = negative)
RHCE: Allele's, RHCE / RHCe / RHcE /RHce / Codes for CE, Ce, cE, ce
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Wiener Rh Terminology |
8 possible alleles
R0, R1, R2, Rz r, r', r", ry
R = D(Rh+) r = Rh-null
1/' = C
2/" = E
RZ /ry = CE
0 = ce |
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Wiener to fisher |
R1 = DCe R0 = Dce r = dce r' = dCe ry = dCE |
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Rosenfiled Notation |
D = 1 / C = 2 / E = 3 / c = 4 / e = 5
Example: D+, C+, E-, c+, e+ = 1,2-3,4,5 |
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Inffering Genotype |
Infering genotype |
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D antigen |
Very Immunogenic: 85% of D-negative patients produce anti-D when exposed, so they should only reciev D- transfusions
C on the opposite chromosome weakens D |
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Weak D expression |
Genetic: Mostly seen in Blacks -Requires IAT to detect
Position effect: Ce (r') Inherited to the RHD gene - Detect with monoclonal Anti-D at RT
Partial (Mosaic) D: parts of the D-antigen complex missing -Ab to missing D components -Reacts with monoclonal anti-D at RT -Anti-D on antibody when screening a D positive patient.
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G antigen |
If negative for D&C then negative for G
Comes with: RHD, RHCe, RHCE
Anti-G reacts with C or D positive cells
This patient should not D or C blood |
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Weird Phenotypes |
D-deletion
Rh-mod: Minimal Rh expression, a modified RHAG |
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Rh-null |
No antigens expressed which compromises membrane integrity
Normal type: Caused by mutant RHAG gene
Amorphic Type: RHD deletion, no RHCE expression, RHAG expression normal |
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Rh Anttbodies |
Produced after trasfusion or pregnancy
Reactivity: D > c > E > C > e
IgG(1) Ab which bind at 37C
Agglutiante with IAT
If Anti-E is present look for anti-c as well. These patients need -c and -E blood for transfusions |
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LW blood group |
Anti-LW reacts like Anti-D -Reacts 4+ with D+ cells -locus on chromosome 19
Alleles: LW^a , LW^b , LW
LW is spontanious mutation, the Ab produced to it are rare but clinically significant. |
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Extravascualr Vs Intravascular Hemolysis |
Extra: IgG or complement binds the RBC and opsonizes it, then it is cleared by phagocytes in the spleen.
Intra: Complement is fixed and mediates the cells destruction. |
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Kell Blood Group Misc'. |
Discovered by Coombs in 1946 as an antibody on a patient named Kelleher using an AHG test.
It is associated with HDFN
Anti-Kell is produced to the 32 types of kell antigen
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What is a negative function of Kell? |
It's antigens are microbial receptors
Fya and Fyb are attachment sites for malaria strains. |
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Kell on the RBC |
K+ appears in fetuses at 10 week, k+ appears at 7 weeks.
4,000-18,000 kell antigens per RBC
An integral membrane glycoprotein; Covalently link to Kx group, play role in zinc binding, high number of disulfide bonds, damaged by sulfhydral agents (DTT)
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How Immunogenic is Kell? |
KEL 1 is slightly less immmunogenic then D, so 1/10 patients exposed to it will produce antibodies. |
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Kell alleles |
K/k*
Kpa/Kpb*
Jsa/Jsb*
KEL11*/KEL17 (Wka)
KEL14/KEL24
VLAN/VONG (rare)
* = Common |
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K0 and K-null |
Lack all KEL antigens, but do express Kx
Alloantibody is either anti-Ku or anti-KEL5
Ku antigen is found on all RBC except K0, 'u' for universal. They can only receive blood from other Ku, which are rare. |
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Most common KEL groups |
White: KEL2/k, KEL4/Kpb, KEL7/Jsb
Black: Same, but KEL6/Jsa is much more common
These are all coded on the 7th chromosome |
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Anti-KEL Chracteristics |
Can be triggered by pregnancy or transfusion leading to IgG reactions, or by Bacterial infection which triggers and IgM response.
This dose not cause the fixation of complement, but can cause sever transfusion reactions and HDFN
Not effected by enzyme treatment, decreased LISS binding, PEG enhanced binding, Destroyed by DTT |
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Anti-K |
Very Sever Transfusion Reactions with extravascular hemolysis, sever HDFN
Causes fetal anemia by destroying circulating RBC and surpresing erythropoiesis by destroying RBC precursers. |
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Kx Blood Group |
#019
X chromosome - XK1 - Kx ag
Independent from Kell
K0 = Elevated Kx
If kell Ag Denatured Kx is increased |
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McLeod Phenotype |
Appears with Kell-null and leads to a weak exprsion of k, Kpb and Jsb
Very rare condition in males, X-linked given by the mother
No Kx, leading to abnormalities of the RBC
Women are carriers
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McLeod Syndrome |
RBC defects: Rigid, Short life span, compensated anemia, reticulocytosis, bilirubinemia, splenomegaly, reduced serum haptoglobin
Muscle and nerve disorders, progresive multiple sclerosis like condition
Leads to cardion megaly in mid life |
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Chronic Granulomatous Disease |
Inability of phagocytes to form NADH Oxidase, leading to the generation of H2O2
XK1 gene has deletions associated with the disease
Mcleod Ab: Anti-KL (Anti-Km and Kx if transfused) |
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Duffy Geneotypes |
Fy(a+b+), (a+b-) or (a-b+) are the most common in whites.
Fy(a-b-) is most common in blacks
#008 |
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Duffy Antigens |
Fya, Fyb, Fy3, Fy5, Fy6: These are glycoproteins.
Only expressed on RBC and can be found in cord blood.
Ficin/papain Suceptible: Fya, Fyb, Fy6
Ficin/papain Resistant: Fy3, Fy5
These are receptors for inflammatory drugs |
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Duffy Genetics |
DARC gene on chromosome 1
Syntenic with Rh Locus (same arm, but to far to link)
Fya and Fyb are codomanent
Fyx is weekend by Fyb: Can absorb and elute anti-Fyb, and there is no Fyx antibody
Fy (FyFy) or (Fy a-b-) = no Duffy antigen. Caused by a change in promorter region of mRNA transcription |
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Duffy Ab |
Formed after transfusions or pregnancy
Creates IgG AHG phase
Dose not bind complement
Rare HDFN transfusion reaction
Anti-Fya more common than Anti-Fyb
Enhanced in LISS |
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Duffy Dosage Reaction Strength |
Strong Reaction: Fya/Fya or Fyb/Fyb Fy(a-b+) or Fy(a+b-)
Normal or Weak reaction: Fya/Fyb o Fy(a+b+)
Fy(a-/b-) imparts a resistence to Plasmodium |
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Kidd Ag |
#009
These are glycoproteins that are not denatured by enzyme reganets
Genetic Locus for JK is on Chromosome 18
Jk3 is co-dominante with Jka and Jkb
Jk is silent, and prodcues no antigens: Common in Polynesia, Philipinos and Chinese |
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Kidd testing |
Jk(a-b-) Resistant to lysis with 2M urea, this is the only test for the rare genotype |
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Anti-Kidd Ab |
Very weak in vitro, but lead to sever hemolisis in vivo as they can fix complement
Test with broad spectrun HGA (Anti-IgG and Anti-C3
Delayed transfusion reactions. |
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Anti-Kidd Ab Reaction Strength |
Strong reaction if: Jka/Jka or Jkb/Jkb or Jka-b+ or Jka+b-
Weak reaction if: Jka/Jkb or Jka+b+
Hard to store and enhanced by enzymes |
