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Locus
Specofoc position of a gene on a chromosome.
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Humans have how many chromosomes?
23 pairs
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Alleles
Alternate forms of a gene at a specific locus.
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Gene
Encode amino acids that make up protein chains.
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Traits
Observable expressions of a gene.
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Amorphic genes
No observable product.
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Genotype.
Is the exact allelic genes occupying a given locus on a pair of chromosomes.
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Phenotype
Is the observable expression of a gene (trait).
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ABO Blood group incidence.
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RBC Antigen Precursor substance
Oligosaccaride chain + red cell protein.
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Type 1 precursor substance found where?
Body secretions
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Type 2 precursor substance found where?
RBC
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What is the difference in type 1 and type 2 precursor substance
Bonds.
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Formation of ABO antigens controlled by genes at
ABO, Hh, Se loci
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Glycosyltransferase
Specific enzyme that produce ABO and H substances by transfer of an immonodominant sugar.
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Immunodominant Sugar.
The sugar that occupies the terminal position on the precursor substance and determines the blood group speceficity.
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H antigen gene, transferase, and sugar.
- H gene
- fucosyltransferase
- Fucose
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A gene, transferase, sugar
- A gene
- Glalctosaminyltransferase.
- N-acetylgalactosamine (galnac)
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B gene, transferase, sugar
- B gene
- Galactosyltransferase
- D-galactose
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O gene, transferase, sugar.
- O gene
- No functional enzyme.
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Amount of h substance by blood type least to greatest
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2 blood types that will react to Anti-H
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Bombay Phenotype.
- Gene does not express ABO or H substance.
- Produces Anti-H
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A3 subgroup
Causes mixed field reactions on ABO typing.
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Sub groups of A
- A1 (principle subgroup)
- A2 (priniciple subgroup)
- A3
- Ax
- Am
- Ael
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Domicile Biflorus
Anti-A1 lectin.
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Ulex Europaeus
Anti-H lectin
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Vicia Graminea
Anti-N Lectin
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Anti-A and Anti-B able to he detected at what age?
First few months.
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Antibody production reaches adult level at what age?
5-10 years of age.
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A and B group individuals produce what type of corisponding antibodies?
Primarily IgM and a little IgG
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Dominant class of antibody produced by a type O individual.
IgG
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Anti A1
- Produced in 1-8% of A2 individuals.
- 22-35% of individuals with A2B
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Allo antibodies reactive at ISS
- Anti M
- Anti N
- Anti Le(a)
- Anti Le(b)
- Anti P1
- Anti K
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Cold reactive Auto-Antibodies
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Individuals missing antibodies
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ABO discrepancy (cells)
- Mixed cell populations:
- 1. Transfusions with out of group ABO cells.
- 2. Transplant (bone marrow, stemcells).
- 3. Chimerism wich are changes in erythropoetic tissue.
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ABO discrepancy (cell coating)
- Antibody coated cells
- Cold reactive auto-abs
- Whartons jelly.
- SST or Gel tube
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Aquired B phenotype ( ABO discrepancy)
- Microbial enzymes modify A antigen to resemble B antigen.
- Ussually ascociated with Proteus Septicemia.
- Will forward as AB
- Reverse as A
- Use anti-B lectin to test , will not affect true B antigen
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How to resolve ABO discrepancy.
- Check sample ID.
- Prepare new washed cell suspension and retest.
- Extend room temp incubation and include auto control.
- Test with lectins.
- Get patient diagnosis history.
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Secretor substances found in saliva
All corresponding ABO antigens and H substance. (H only for O)
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Rh factor prevalence.
- 15% negative.
- 85% positive.
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% of people that will produce Anti-D
80% of D neg people
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Rh protein
- Polypetide
- 417 aminoacids.
- Passes through RBC 12 times.
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Rh null and other Rh depletion Phenotypes will effect what other Antigen systems?
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D Antigen structure.
- Mosaic of proteins, RhD gene codes for 416 amino acid Rh proteins.
- Embedded in bilipid layer of RBC membrane.
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Rh blood group has how many known Ag.
At least 45
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Cw
- Low frequency Allele. (1-2%)
- Altered C gene or gene varient due to single amino acid change.
- Found in C+ individuals but individual can make Anti-C.
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G Antigen
- High frequency compound antigen.
- Due to presence of serine on 103rd position of the Rh polypetide.
- Only rr individuals do not have G antigen.
- Individuals with G transfused with D neg, C neg blood
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f antigen
- Results from c and e on CIS position ( same chromosome).
- cDe or cde.
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V antigen
- Compound antigen.
- cDe or cde (e varient or VS)
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rhi antigen
- Results from Ce in CIS position ( same chromosome).
- Ussually seen in Rh positive individuals with Anti-C
- F not expressed because c&e in trans position.
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Anti D reagents
- Poly/monocolonal blend that readily detect D antigen on most D+ cells.
- Weak D cells may require prolonged incubation.
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Weak D or Du phenotype
- Weak form of D antigen.
- Mutation or RhD gene codes for less D antigen on RBC.
- Cis trans position codes for suppression of expression of d antigen om RBC.
- Partial D mosaic.
- Loss of some D antigen or epitope.
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Rh Null Phenotype.
- Phenotype in which individual has no rh protein on cells.
- May have hemolytic anemia associated with cell membrane abnormalities.
- Abetalipoproteinemia
- Acanthocytes
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ABO HDN
- Immune Anti-A or Anti-B
- Most common.
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Rh Incompatability HDN
- Anti- D,C, c, E, e.
- Moste severe.
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Other blood group HDNs
Anti- Kell Duffy Kidd
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DAT interpretation
- If positive RBCs are sensitized >> probable HDN.
- IF negative>>RBCs not sensitized>>probably not HDN (ABO HDN can give negative DAT).
- Control must be negative.
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Rh Immune Globulin Dosage
- 1 dose protects against 15ml PC or 30ml WB.
- Can also be given if Rh- cells are given to + recipiant.
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When to give Rhogam
- Mother Rh and Du negative.
- Must not already produce Anti-D.
- Infant Is Rh pos Du pos.
- Transplecental Hemmorrhage occurs.
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Rosette test
- Incubate maternal blood with anti-d.
- Add D indicator cells.
- Indicator cells with attached antibody should rosette around any Rh positive infant blood.
- If negative give One RhoGam.
- If positive perform quantitative test.
- false Positive -mother is weak D.
- False negative if infant is weak D.
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Kleihauer-Betke principle.
- Fetal hemaglobin is insoluble in acidic solution.
- Fetal cells stain orange while adult cells dissolve into ghost cells.
- Count number of fetal cells out of 500 ghost cells.
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Fetal Cell RhoGam calculation.
- Devide fetal cells counted by 500 ghost cells.
- Multiply result by 100 to get %.
- Multiply % by 50
- Then divide by 30.
- Number = number of RhoGam doses to give.
- If > 0.5 round up and add one.
- If < 0.5 round down.
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Mn system.
- 40 antigens in system many low incidence.
- Inherit GYPA or GYPB on chromosome 4.
- Both are single pass protein of 131 amino acids seperated into three regions.
- Both M and N are cold reacting and not clinically significant.
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Ss system.
- 40 antigens in MNSsU.
- Inheritance-GYPB gene on chromosome 4.
- GYPB gene produces glycophorin B
- Single pass protein composed of 72 amino acids.
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Big S antigen.
Substitutes methionine on the 29th position of the glycophorin B molecule.
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Little s gene.
Substitutes threonine amino acid in the 29th position of the glycophorin B molecule.
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U antigen.
- Found on RBCs of all SsU positive.
- Absent from S-s- cells.
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Anti-M
- Reacts best at ISS phase.
- Enzymes destoy the Ab.
- Rarely binds complement.
- No invitro hemolysis.
- Causes very few HTRs.
- Mild to severe HDNs.
- Prevelent in 22% of population.
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Anti-N
- Reacts best at ISS phase.
- Enzymes destroy it.
- Rarely binds complement.
- No invitro hemolysis.
- Rarely causes HTRs.
- Causes moderate HDNs.
- Prevelant in 28% of population.
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Anti Big S
- Reacts beat In AHG phase.
- Enzymes have variable effect.
- Binds some complement.
- No Invitro Hemolysis.
- Causes HTRs and Mild HDNs.
- 45% whites.
- 69% whites.
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Anti little s
- Reacts best at AHG phase.
- Binds a little complement.
- No invitro hemolysis.
- Causes HTRs and mild to severe HDNs.
- 11% whites
- 3% blacks.
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Anti U
- Reacts best at AHG phase.
- Enzymes do not change.
- Rarely binds complement.
- No invitro hemolysis.
- Causes HTRs and mild to severe HDNs.
- <1% of population.
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Lewis system.
- Le (a) and Le(b) antigens coded by Le gene.
- Le dominant and le recessive genes are alleles
- Lewis Antigens are not intrinsic to red blood cells, they are glycoproteins adsorbed from plasma.
- Le gene without Se gene = Le(a) antigen.
- Le gene with se gene = Le(b) antigen.
- Null phenotype is absence of Le gene. (a-b-)
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Le sese gene.
- Phenotype: Le(a+b-)
- Plasma secretions: Le(a)
- Rbc antigen: Le(a)
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Le Se gene.
- Phenotype: Le(a-b+)
- Plasma secretion: Le (b)
- Rbc antigens: Le(a) and Le(b)
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le le se se genes
- Phenotype: Le (a-b-)
- Plasma secretions: none.
- RBC antigens: none
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le le se genes
- Phenotype: Le(a-b-)
- Plasma secretions: none
- RBC antigens: none.
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Lewis Antibodies
- Always IgM antibodies.
- Rarely clinically significant.
- Neutrilized by plasma containing blood group substances.
- Seen frequently in serum of pregnant woman.
- Do not cross the placenta or cause hdn.
- Poorly developed at birth.
- Developes after about 2 years.
- Can bind comlement and cause some invitro hemolysis.
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Lutheran System
- First reported in a patient with lupus who developed anitbody.
- Set of 19 antigens numbered Lu1 - Lu 21
- 10 and 15 are obsolete.
- Inheritance is 4 pairs of allelic genes on chromosome 19.
- Lu (a) and Lu (b) are codominant genes.
- Lu(a) found in 8% of polulation.
- Lu(b) found in 99.8-100% of population.
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Anti-Lu(a)
- Cold reacting IgM.
- Causes mixed field agglutination.
- May also be IgG and IgA.
- Some dosage effect.
- IgG may cause a Mild HDN.
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Anti-Lu (b)
- Antibody is rare because Lu(b) is high incidence Ag.
- Usually IgG
- Reacts best at AHG
- May cause mild and delayed transfusion reactions.
- Not significant cause of HDNs.
- May also be cold reacting IgM.
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Ii System.
- Inheritance is 2 anitegens: li
- 2 phenotypes
- 1 gene: IGnT on chromosome 6
- Codes for enzymes.
- B-1>>>6 N-acetylglucosaminyltransferase.
- Converts straight chain i antigen into branched chain I antigen.
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Anti Big I
- Common as IgM cold reactive antibody.
- Often ascociated with Mycoplasma Pneumoniae (primary atipical pneumonia).
- Patients with infectious mononeucleosis often have transient anti-I
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Anti-i
- Rare autoantibody associated with IM, AML, and Cirrhosis.
- IgG type always clinicaly significant.
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