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Give an example of an Ab to a high
frequency Ag? What % of the popn would
you expect to have this Ab?
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Anti-k (2%) b/c k Ag is seen in 98% of the
population.
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What do sulfhydryl reagents destroy?
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Kell Ags and most IgM Abs
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What is a high titre, low avidity Ab? Give an example.
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An Ab that shows rxn in IAT. Rxns are weak but don’t get diluted out; Chido, Rogers
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What may be the cause if you experience an unexpected rxn during an IAT XM?
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Donor unit is DAT pos; Pt has an Ab to a low frequency Ag
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What are some ways to enhance weak Ab rxns? (6)
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Use potentiators: LISS, PEG, BSA, enzymes; increase serum:cell ratio, increase incubation time (max 60 mins), fresher panel cells, fresher pt cells
Wash panel cells 1x to remove preservative
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What are cold alloAbs? What type of Ig are they? What rxn phase are they detected at? Give some examples.
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IgM Abs that react best at IS or RT (colder temps) Examples include –P1, -M, -N, -Lea, -Leb
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What are ways to avoid having rxns w/ cold Abs (in general – non-specific)?
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Skip the IS phase, use only anti-IgG for IAT (don’t use C3), do auto-adsorption or use REST, use sulfhydryl reagents (destroy most IgM Abs
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How can you remove rxns involving the cold Abs –M, or –N?
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Treat the panel w/ enzymes (will destroy the M, N Ags)
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How can you remove rxns involving Lewis Abs?
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Use Lewis substance (saliva of Lewis pos secretions) – it neutralizes the Abs
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How can you remove rxns involving –P1 Abs?
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Use P1 substance (pigeon egg whites) or hydatid cyst fluid
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What type of autoAb is the most common?
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Warm autoAb
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What is WAIHA? What are the causes of WAIHA?
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Warm autoimmune hemolytic anemia; Idiopathic, disease related (cancer, lupus), medications
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How can rxns w/ warm autoAbs be enhanced?
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Use potentiators: LISS, enzymes, PEG
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What blood product should be issued to a pt w/ a warm autoAb?
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The least incompatible blood product!
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How can rxns w/ warm autoAbs be avoided?
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Do adsorption @ warm temp -WARM: warm Ab removal method (ZZAP soln = enzymes + DDT); Elution: elute the Abs off the RCs???
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