bb guy section 1 notes from Lewis through end
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| percentage of people who are Lewis (a+B+) | zero. not possible
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| isotype of most Lewis antibodies. significance? | IgM; usually not significant
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| What antigen does H. pylori use to attach to gastic mucosa? | Lewis B antigen
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| Cold agglutinin disease is associated with this RBC auto-antibody | Auto-anti-I
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| infection with this organism is associated with auto-anti-I | Mycoplasma pneumoniae
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| Auto-anti-i is associated with this infectious agent | infectious mononucleosis; EBV
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| This antigen is the parvovirus B19 receptor | P
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| paroxysmal cold hemoglobinuria is associated with auto-antibodies with this specificity | auto-anti-P
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| Is the "d" antigen a carbohydrate, lipid or a protein? | No. There is no such antigen. "d" is used as a placeholder noting the absence of D antigen
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| Name the 4 Weiner haplotypes that account for 97% of people | R1, R2, R0 and r. (~97% of blacks and whites use only these four).
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| describe racial difference in Rh haplotype differences and why that matters | “The Big Four”
Whites: R1 > r > R2 > R0
Blacks: R0 > r > R1 > R2
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| briefly outline Rh genetics/structure | 2 genes on chromosome 1; RHD,RHCE
Also RhAg packages and transports antigens to cell membrane; gene on chromosome 6
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| outline different mechanisms of D-negative phenotype | 1) caused by mutations and deletions rather than by synthetic actions of a gene product 2) Caucasians: D-negatives= deletion of RHD gene 3) African-Americans: Point mutations in RHD gene (“pseudogene”) 4) Asians: Usually have inactive RHD gene
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| A 26 yo g2p2 woman has a baby. Her Rh type was "weak D". How much Rhogam should you give her? | Most Weak D moms do not need RhIG prophylaxis
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| What are the most common partial D antigens by race? | Most common: DVI (say D “six”) in whites, DIIIa (D “three A”) in African-Americans
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| Why does partial D vs. weak D matter for moms? | Partial D moms need HDFN prophylaxis (Rhogam), while weak D‟s commonly do not (type 1,2,3)
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| Why does partial D vs. weak D matter for donor center testing? | Partial D OR weak D donor RBCs may induce anti-D in a D-negative recipient
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| Why does partial D vs. weak D matter for recipients? | Partial D recipients may make anti-D when receiving D+ RBCs, weak D recipients generally do not (type 1,2,3)
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| Describe DEL (“D-E-L”, formerly “Del”) antigen | a) Appear D-neg but have tiny amounts of D seen after elution of reagent anti-D from RBCs b) Primarily seen in Asian populations (up to 1/3 of D-negative Asians)
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| What is the G antigen? | G = Antigen present when either C or D is present
Anti-G reacts against (D+C-), (D-C+), or (D+C+) RBCs (rarely against D-C-G+)
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| What is the f antigen? | f = Present when ce is inherited (r and R0) (c in cis to e)
Anti-f is often seen with anti-e or anti-c
Can cause mild HDFN and HTR
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| Describe the dosage effect in regards to antibodies to Kidd antigens | Marked dosage effect 1) Antibodies may not react at all against cells with genetic single dose (heterozygous) Kidd antigens (Jka+,Jkb+)
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| Vicea graminea lectin reacts against | N antigen
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| Antibodies to the this blood group are famous for developing and then disappearing | Antibodies to the Kidd blood group are famous for developing and then disappearing (evanescence)
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| Glycophorin A (GPA) carries these RBC antigens | M and N
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| Glycophorin B (GPA) carries these RBC antigens | S,s, U
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| Glycophorin A (GPA) and Glycophorin B (GPB) are receptors for this organism | P. falciparum
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| M antigen frequency is? N antigen frequncy is? | a. M frequency equals N (each ~75%)
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| s antigen frequency? S antigen frequency? | s (~90%) is more frequent than S (~50%W, ~30%B)
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| What high frequency antigen can be negative in S-s- persons? | If S-s- (as seen in 2% of African-Americans), may also
be U-negative (U is extremely high frequency).
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| isotype of anti-M? significance? | IgM. usually not significant
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| isotype of anti-N? significance? | IgM. usually not significant
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| isotype of anti-S? significance? | IgG. Significant
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| isotype of anti-s? significance? | IgG. Significant
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| isotype of anti-U? significance? | IgG. Significant
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| describe the N-like antigen („N‟) | GPB terminal 5 AA sequence; matches N version of GPA; known as „N‟. Close enough to prevent most M+N- from making anti-N. Seen in all except those who lack glycophorin B.
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| Anti-N nearly exclusive to this race | Anti-N nearly exclusive to African-Americans
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| Auto-antibody to this antigen induced by hemodialysis because of formaldehyde sterilization of machine | N
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| most common Fy phenotype in African Americans | Fy(a-b-); 68%
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| Duffy antibodies: isotype and significance | IgG; significant; HTR and HDFN; anti-Fya>>anti-Fyb
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| Fy(a-b-) humans are resistant to these organisms | Plasmodium vivax and P. knowlesi infection
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| K antigen frequency: ?% whites, ?% blacks | K: 9% whites, 2% blacks
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| k antigen frequency: ?% whites, ?% blacks | k: 99.8% whites, 100% blacks
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| patients with Kell null phenotype (“K0”) develop this antibody with exposure to Kell antigens | 1) All Kell antigens decreased, Kx increased
2) Significant anti-Ku (“universal”) with exposure
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| In McLeod phenotype this is absent | 1) Kx absent, all Kell antigens markedly decreased
2) No anti-Ku, can form anti-Kx and anti-Km
(Kell “McLeod”); only McLeod RBCs compatible
3) part of McLeod “syndrome”
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| Which is the more frequent Diego antigen a. Dia b. Dib | Dia very low frequency except in some South Americans and Asians
Dib very high frequency in all populations
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| Of these Diego antigens which is more frequent A. Wra B. Wrb | Wra very low frequency
Wrb very high frequency
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| Antibody to this high frequency antigen may interfere with ABO typing due to reaction at room temperatures | Vel Antigen
Extremely high frequency antigen (>99% in all
populations)
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| The 2 most common Antibodies with “high titer, low avidity” (HTLA) features (HTLA-like antibodies) | Chido, Rodgers most frequent;
High frequency antigens that are generally clinically
benign (no HTRs or HDN)
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