Rh & other blood groups Flashcards

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1
Q

explain the concept of dosage (2 ways)

A
  • A person who is homozygous for an Ag expresses more of that Ag than a person who is heterozygous
  • Ab reacts strongly to homozygous Ag bc more of that specific Ag.
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2
Q

Antigens of which blood groups in this lecture are destroyed by enzyme treatment? Enhanced by enzyme
treatment?

A
  • Destroyed: M/N, S/s, Fya, Fyb

- Enhanced: C,c, D, E, e, Jka, Jkb

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3
Q

Why are Kidd antibodies so difficult to work with?

A
  • often weak: require Ag to be enzyme-treated
  • Demonstrate dosage: Homozygous Ag works better
  • Found in combo. w/ other Ab
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4
Q

Why is there a racial difference in Duffy phenotype

distribution?

A
  • among Africans bc Africa highly susceptible to P. vivax (disease carried by mosquitoes)
    => adjust to selective pressure
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5
Q

Explain the inheritance of Rh antigens.

A

Rh genes inherited as haplotype e.g. DCe (one set of gene)

e.g. If child has genotype DCe/dce, may have gotten DCe from mum & dce from dad

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6
Q

Why is the D antigen so immunogenic?

A

bc it contains ≥30 diff. epitopes: 9 epitopes exposed on extracell. surface.

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7
Q

Explain the difference between the Fisher-Race and Weiner nomenclature. What would be the W nomenclature if it’s F-R is DCe/dce

A

a) * both refers to Ag C, c, D, E, e but written diff.
- F-R: written as haplotype
- Weiner: written w/ R/r and numbers/primers (‘)
b) R1r

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8
Q

Explain the nomenclature of Wiener (for Rh nomenclature)

A
  • R = D Ag expressed
  • r = D Ag NOT expressed
  • R1 or r’ = C & e (DCe or dCe)
  • R2 or r’’ = c & E (DcE or dcE)
  • R0 or r = c & e (Dce or dce)
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9
Q
What is the class of each of the antibodies in the MNS
blood group?
A
  • Anti-M & -N: IgM or IgG

- Anti-S & -s: IgG

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10
Q

Characteristics of Ag in Rh blood group

A
  • C, e, D, E, e (d = Absence of D Ag)
  • well developed @ birth
  • enhanced by enzyme treatment
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11
Q

Characteristics of Ab in Rh blood group

A
  • IgG*
  • IR => opsinisation = phagocytose = extravascular haemolysis
  • react optimally @ 37ºC
  • detected by IAT
  • Anti-C, -c, -E, -e demonstrate dosage (strong rxn)
  • Hi clinically sig. for HTR, HDNB
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12
Q

Characteristics of Ag in Kell blood group

A
  • K, k
  • protein
  • antithetical pair expressed in co-dominant
  • well developed @ birth
  • K highly immunogenic
  • Not destroyed by enzymes but destroyed by reducing agents
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13
Q

Characteristics of Ab in Kell blood group

A
  • IgG
  • best detected @ 37ºC w/ IAT
  • Anti-K can cause HTR & HDNB
  • Finding compatible blood for a person that also expresses anti-k is hard bc rare
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14
Q

Difference b/w Weak D & partial D

A
  • Weak: Dec. expression of D Ag = considered Rh(D) pos
  • Partial: region of RHD replaced by regions of RHCE => part of D Ag is missing
    = Donors - have partial D = Rh(D) pos
    = Recipient - have partial D = Rh(D) neg so that they are given Rh(D) neg cells (as they’ll have a-D Ab = must not react)
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15
Q

Difference in testing when Rh(D) is complete vs weak/partial (type of Ig)

A

Complete: ABO FWD gp w/ IgM anti-D

Weak/partial: Weak D test using IAT w/ IgG anti-D (done donor/newborns)

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