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Final

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  1. Locus
    Specofoc position of a gene on a chromosome.
  2. Humans have how many chromosomes?
    23 pairs
  3. Alleles
    Alternate forms of a gene at a specific locus.
  4. Gene
    Encode amino acids that make up protein chains.
  5. Traits
    Observable expressions of a gene.
  6. Amorphic genes
    No observable product.
  7. Genotype.
    Is the exact allelic genes occupying a given locus on a pair of chromosomes.
  8. Phenotype
    Is the observable expression of a gene (trait).
  9. ABO Blood group incidence.
    • O 45%
    • A 40%
    • B. 11%
    • AB. 4%
  10. RBC Antigen Precursor substance
    Oligosaccaride chain + red cell protein.
  11. Type 1 precursor substance found where?
    Body secretions
  12. Type 2 precursor substance found where?
    RBC
  13. What is the difference in type 1 and type 2 precursor substance
    Bonds.
  14. Formation of ABO antigens controlled by genes at
    ABO, Hh, Se loci
  15. Glycosyltransferase
    Specific enzyme that produce ABO and H substances by transfer of an immonodominant sugar.
  16. Immunodominant Sugar.
    The sugar that occupies the terminal position on the precursor substance and determines the blood group speceficity.
  17. H antigen gene, transferase, and sugar.
    • H gene
    • fucosyltransferase
    • Fucose
  18. A gene, transferase, sugar
    • A gene
    • Glalctosaminyltransferase.
    • N-acetylgalactosamine (galnac)
  19. B gene, transferase, sugar
    • B gene
    • Galactosyltransferase
    • D-galactose
  20. O gene, transferase, sugar.
    • O gene
    • No functional enzyme.
  21. Amount of h substance by blood type least to greatest
    • O
    • A2
    • B
    • A2B
    • A1
    • A1B
  22. 2 blood types that will react to Anti-H
    • O
    • A2
  23. Bombay Phenotype.
    • Gene does not express ABO or H substance.
    • Produces Anti-H
  24. A3 subgroup
    Causes mixed field reactions on ABO typing.
  25. Sub groups of A
    • A1 (principle subgroup)
    • A2 (priniciple subgroup)
    • A3
    • Ax
    • Am
    • Ael
  26. Domicile Biflorus
    Anti-A1 lectin.
  27. Ulex Europaeus
    Anti-H lectin
  28. Vicia Graminea
    Anti-N Lectin
  29. Anti-A and Anti-B able to he detected at what age?
    First few months.
  30. Antibody production reaches adult level at what age?
    5-10 years of age.
  31. A and B group individuals produce what type of corisponding antibodies?
    Primarily IgM and a little IgG
  32. Dominant class of antibody produced by a type O individual.
    IgG
  33. Anti A1
    • Produced in 1-8% of A2 individuals.
    • 22-35% of individuals with A2B
  34. Allo antibodies reactive at ISS
    • Anti M
    • Anti N
    • Anti Le(a)
    • Anti Le(b)
    • Anti P1
    • Anti K
  35. Cold reactive Auto-Antibodies
    • I
    • H
    • IH
  36. Individuals missing antibodies
    • Elderly
    • Infants
  37. 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.
  38. ABO discrepancy (cell coating)
    • Antibody coated cells
    • Cold reactive auto-abs
    • Whartons jelly.
    • SST or Gel tube
  39. 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
  40. 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.
  41. Secretor substances found in saliva
    All corresponding ABO antigens and H substance. (H only for O)
  42. Rh factor prevalence.
    • 15% negative.
    • 85% positive.
  43. % of people that will produce Anti-D
    80% of D neg people
  44. Rh protein
    • Polypetide
    • 417 aminoacids.
    • Passes through RBC 12 times.
  45. Rh null and other Rh depletion Phenotypes will effect what other Antigen systems?
    • Fy
    • LW
    • Ss (GPB)
  46. D Antigen structure.
    • Mosaic of proteins, RhD gene codes for 416 amino acid Rh proteins.
    • Embedded in bilipid layer of RBC membrane.
  47. Rh blood group has how many known Ag.
    At least 45
  48. 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.
  49. 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
  50. f antigen
    • Results from c and e on CIS position ( same chromosome).
    • cDe or cde.
  51. V antigen
    • Compound antigen.
    • cDe or cde (e varient or VS)
  52. 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.
  53. Anti D reagents
    • Poly/monocolonal blend that readily detect D antigen on most D+ cells.
    • Weak D cells may require prolonged incubation.
  54. 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.
  55. Rh Null Phenotype.
    • Phenotype in which individual has no rh protein on cells.
    • May have hemolytic anemia associated with cell membrane abnormalities.
    • Abetalipoproteinemia
    • Acanthocytes
  56. ABO HDN
    • Immune Anti-A or Anti-B
    • Most common.
  57. Rh Incompatability HDN
    • Anti- D,C, c, E, e.
    • Moste severe.
  58. Other blood group HDNs
    Anti- Kell Duffy Kidd
  59. 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.
  60. Rh Immune Globulin Dosage
    • 1 dose protects against 15ml PC or 30ml WB.
    • Can also be given if Rh- cells are given to + recipiant.
  61. When to give Rhogam
    • Mother Rh and Du negative.
    • Must not already produce Anti-D.
    • Infant Is Rh pos Du pos.
    • Transplecental Hemmorrhage occurs.
  62. 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.
  63. 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.
  64. 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.
  65. 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.
  66. 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.
  67. Big S antigen.
    Substitutes methionine on the 29th position of the glycophorin B molecule.
  68. Little s gene.
    Substitutes threonine amino acid in the 29th position of the glycophorin B molecule.
  69. U antigen.
    • Found on RBCs of all SsU positive.
    • Absent from S-s- cells.
  70. 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.
  71. 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.
  72. 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.
  73. 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.
  74. 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.
  75. 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-)
  76. Le sese gene.
    • Phenotype: Le(a+b-)
    • Plasma secretions: Le(a)
    • Rbc antigen: Le(a)
  77. Le Se gene.
    • Phenotype: Le(a-b+)
    • Plasma secretion: Le (b)
    • Rbc antigens: Le(a) and Le(b)
  78. le le se se genes
    • Phenotype: Le (a-b-)
    • Plasma secretions: none.
    • RBC antigens: none
  79. le le se genes
    • Phenotype: Le(a-b-)
    • Plasma secretions: none
    • RBC antigens: none.
  80. 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.
  81. 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.
  82. 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.
  83. 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.
  84. 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.
  85. 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
  86. Anti-i
    • Rare autoantibody associated with IM, AML, and Cirrhosis.
    • IgG type always clinicaly significant.
Author:
 moses1424
ID:
 90181
Card Set:
 Final
Updated:
2011-06-11 18:16:01
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finals
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