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426 Blood Bank > W3 > Flashcards

W3 Flashcards

1
Q

Genetics of Rh antigen

A
  • RHD and RHCE
  • Chromosome 1
  • A single haplotype
  • Ro: highly prevalent in African ancestry
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2
Q

Biochemistry of Rh

A

Protein RhD: present or not (deletion)
Protein RhCE: C/c and E/e
Serves as a structural support for RBC’s wall
RhAG: required for expression of Rh antigens

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3
Q

Name scheme

A
  1. Fisher-Race: 1 gene - 1 product, DCE
  2. Wiener: 1 gene - 3 products, R1-R2-Ro-Rz and r, r’, r’’, ry
    * Ro: prevalent in Black, r is very rare in Asian
  3. Rosenfield: Rh antigen is given a number, Ag’s present –> # positive, Ag’s absent –> # negative
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4
Q

Antibody of Rh

A

Ig, unexpected
D: no dosage, CE: dosage
Enhanced by enzyme / Resistant to chemical
Ab persist for years after transfusion or pregnancy
Lead to extravascular hemolysis
Immunogenicity: D>c>E>C>e

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5
Q

Ab of D, C/c, E/e

A
  1. D: most immunogenic, present or absent, weak or partial, no dosage
  2. C/c: Differ 1 aa, dosage
  3. E/e: Differ 1 aa, dosage, anti-E is often and go with anti-c
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6
Q

Antigen f

A
  • Compound antigen
  • Present only on cells having c and e in the same haplotype
  • Occurs less often than big 5
  • Can cause rxn
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7
Q

Antigen G

A
  • Present on cells having D positive OR C positive

- Important for mom/baby studies

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8
Q

Rh Null

A
  • Missing RhAG –> Rh gene is not expressed
  • Amorph: Gene RhD, RhCE are inactive
  • -> True Rh Null show Stomatocytes and mild anemia. They can make anti-Rh29: react with all Rh antigens
  • D– : Missing RhCE –> Highest single expression of D. They can make anti-Rh17: react with all from of RhCE proteins
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9
Q

RhIg (Rhogam)

A
  • Anti-D from human
  • Given to Dneg pregnant women at 26-28 weeks & at delivery (trauma, abortion, miscarriage)
  • 1 dose negate 30mL whole blood
  • Prevent anti-D formation
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10
Q

Kell antigen

A
  • KEL gene: chromosome 7
  • XK gene: X chromosome
  • The default: k/Kpb/Jsb
  • No KEL gene has multiple mutation (K; Kpa/Kpc; Jsa)
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11
Q

Biochemistry of Kell

A
  • Only on RBC
  • Fetal as early as 10 wks
  • Enzymatic activity but unclear
  • On RBC wall, Kx antigen is a part of Xk protein which is linked with Kell by a disulfide bond (Km)
  • k = Cellano
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12
Q

Antibody of Kell

A
  • Ag is unimpacted by enzymes
  • Ag is destroyed by DTT
  • Show dosage technically
  • IgG, unexpected
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13
Q

Kk antibody

A
  • Anti-K: can cause HDFN (lower than anti-D) by suppressing erythropoiesis in baby
  • k antigen : 99% pop. has this antigen –> Cellano
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14
Q

Kpb/Kpa/Kpc

A
  • Kpb: high frequency
  • Kpa/Kpc: low frequency
    + Kpa 2% in pp at European ancestry
    + Kpc more rare
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15
Q

Jsb/Jsa

A

Jsb: high
Jsa: low - 20% in African ancestry

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16
Q

Km and Kx antigen

A
  • High frequency
  • Kx antigen: on XK protein (encoded by XK gene)
  • Km antigen: the di-sulfide bond between XK and Kell protein
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17
Q

McLeod Syndrome

A
  • Lacking XK protein –> lack Kx antigen and Km antigen
  • X-linked condition and exclusive to males
  • Result in McLeod Phenotype
  • Kell antigen: trace (due to missing Km bond)
  • Assoc. with chronic granulomatous dz due to the deletion on part of X chromosome with includes XK and CYBB
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18
Q

Null of Kell

A
  • Ko: produce anti-Ku
  • No assoc. pathology
  • Kx antigen increase (as no Kell tail cover), and no Km
  • Kell antigen: none
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19
Q

MNSs family

A
  • Haplotype on chromosome 4
  • Ns>Ms>MS>NS
  • Total 46 antigens have been described
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20
Q

Biochemistry of MNSs

A
  • Glycophorin A: M/N - differ 2aa at 1 and 5
  • Glycophorin B: S/s - differ 1aa at 29
  • Glycophorin B has ‘N’ - assemble structure of N
  • Can be used by Plasmodium falciparum
  • Expressed on cord cells
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21
Q

Antibody of MNSs

A
  • Destroyed by enzyme
  • Dosage: important (M/N)
  • Anti-M and anti-N: IgM (even many cases show IgG), react at cooler temp., insignificant if not react at 37C
  • Anti-S and anti-s: IgG, significant and rarer than M/N
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22
Q

Anti-M/N antibody

A
  • Anti-M: with bacterial infx (can naturally occur), like pH 6.5
  • Anti-N: Anti-Nf (after exposure to formaldehyde), common in dialysis patients
  • True anti-N rare (due to N on GPB)
23
Q

En(a) - Envelope

A
  • Envelop
  • On all RBC with M OR N
  • En(a)= is M=N= due to GPA deletion
  • Unexpected Ab
24
Q

S/s

A
  • Significant Ab: IgG, unexpected
  • S: 50% pop
  • s: 90% pop
  • Destroyed by enzyme
25
Q

U (Universal)

A
  • U= means S=s=: exclusive in African ancestor
  • Anti-U: significant, can cause HTR and HDFN
  • Unexpected Ab
  • Can make true anti-N
26
Q

MkMk

A
  • Complete deletion of GPA and GPB
  • Cell: M=N=S=s= –> Null phenotype
  • Can make all Ab
  • No hematological difference on RBC
27
Q

Mur

A
  • GPB mutation common 9% in SE Asia
  • 2nd most immunogenic after ABO in some Asian countries –> need routine AbSC test
  • Capable of HTR and HDFN
28
Q

Kidd genetics

A
  • On chromosome 18

- Jka/Jkb: codominant

29
Q

Biochemistry of Kidds

A
  • Express on cord cells
  • Urea transporter: Jka=Jkb= increase the lysing time of RBC by 2M urea from 1min to 30min
  • Jka/Jkb is located on the 4th extracellular loop of Kidd protein
30
Q

Jka/Jkb

A
  • Enhanced results with serum: Ab are better at fixing complement
  • Need polyclonal antisera (have both anti-IgG and anti-C3)
  • Need to check pt’s history
31
Q

Jk3

A
  • Null phenotype: pp missing both Jka and Jkb will make anti-Jk3
  • Common in Polynesian population (Hawaii)
32
Q

Duffy genetics

A
  • Chromosome 1

- Fya/Fyb: codominant –> destroyed by the enzyme

33
Q

Biochemistry of Duffy

A
  • Chemokine receptor: DARC
  • Used by Plasmodium vivax to enter RBC
  • Found on tissue throughout body
34
Q

Ab of Duffy

A
  • IgG, unexpected Ab
  • Dosage
  • Found on cord cells
  • Can cause HTR and HDFN
  • Show up with other Ab
35
Q

Ab of Kidd

A
  • IgG
  • Dosage
  • Enhanced by enzyme
  • Assoc. with intravascular hemolysis
  • Fade in vivo: cause linked delay HTR
  • Show up with other Ab –> Honor history
36
Q

GATA box mutation

A
  • Found in African ancestry (67%)
  • Suppress all Fy antigen on RBC
  • Fyb still found on tissue –> Even miss on RBC, no anti-Fyb Ab made.
  • Resistant to P. vivax
37
Q

Null of Duffy

A
  • Rarer, in European ancestry
  • Fya=Fyb= people w/o GATA mutation: make Fy3, Fy5, Fy6 antigen
  • Antibody of Fy3,5,6 all react with Fya, Fyb (can’t differentiate)
  • Fy3, Fy5: resistant to enzyme (different from Fya/Fyb - destroyed by the enzyme)
  • Fy5: absent on Rh Null cells
38
Q

Glob genetics

A
  • Two genes: P1PK, P –> interplay makes phenotype
  • Make sugar antigen (not proteins as others)
  • From Gb2, can make Pk, P (same way) and P1 (another way) antigen - depends on a different mechanism
39
Q

Biochemistry of Glob

A
  • Like ABH: composed of sugar
  • 5 main phenotypes:
    + P1: P1, P, Pk
    + P2: P, Pk
    + p: None
    + P1k (very rare): P1, Pk
    + P2k (very rare): Pk
40
Q

Ab of Glob

A
  • Naturally occuring
  • Anti-P1: variable reactivity, IgM, neutralized with P1 substance
  • Anti-P: insignificant
  • Anti-PP1Pk: Anti-Tja, can seperate out 3 Abs
41
Q

Disease assoc. with Glob

A
  1. PCH: auto-antiP, Syphilis, after viral infection, biphasic hemolysis,
  2. Spontaneous abortion: Anti-PP1Pk (placenta’s rich of P antigen –> miscarry early)
  3. Anti-P1: assoc. with pigeon eggs, liver flukes, hydatid cyst
  4. P1 receptor: used for Shiga toxin and E. coli
42
Q

Lewis genetics

A
  • 2 genes: Lewis, Secretor

- Interplay –> phenotype

43
Q

Biochemistry of Lewis

A
  • Sugar –> insignificant
  • Type 1 chain
  • Not found in fetal cells
  • Pregnant women can become Lewis neg temporary
  • Secretor gene convert type 1 chain into H chain
  • Lewis gene add Fucose to
    + type 1 chain –> Lea
    + H chain –> Leb
44
Q

Ab of Lewis

A
  • Can be naturally occurring
  • Show up during pregnancy
  • IgM
  • Neutralized by saliva
45
Q

Lea/Leb antigen

A
  • Not antithetical
  • No dosage
  • Genotype: combination of LE and Secretor gene
    + LE gene: Le (add fucose)/le (not add fucose)
    + Secretor gene: Se (H chain made)/se (only type 1)
46
Q

I biochemistry

A
  • Sugar
  • i: linear chain vs I: branched chain
  • I: not found on cord cells, slowly appear over first 18 months
47
Q

Ab of I

A
  • IgM (naturally occurring)
  • Enhanced by enzyme
  • Auto anti-I: common - found in most adults, can be neutralized by milk (not affect as due to temp.)
  • Like cold temp
  • Anti-IH: React with compound antigen b/w I and H antigen. Tend to show up in A1 pt
48
Q

Disease assoc. with I

A
  • Cold agglutination disease (CAD): due to high titer of auto anti-I
  • M. pneumoniae
  • Epstein Barr virus
49
Q

Null phenotype of I

A
  • ii

- Rare: never develop branched chains

50
Q

Lutheran

A
  • Lu(a): low freq, cause mixed field, may be considered as significant
  • Lu(b): high freq, significant
  • Dominant inhibitor: In(lu) –> suppress Lu gene
  • True Null: LuLu –> can make anti-Lu(ab)
51
Q

HTLA (High Titer Low Avidity)

A
  • Rxn stay 1+ even dilute or no
  • Chido/Rogers: C4d absorbed on RBC, neutralized by plasma
  • Bg: Remnant of HLA on RBC, neutralized by chloroquine, Bg(a)/Bg(b)
52
Q

Diego

A
  • Anion exchanger
  • Di(a)/Di(b)
  • Di(a): low freq, found in Native American (esp. South) and Mongolian population.
  • Di(b): high freq
  • Mom/baby study
  • Clinically significant
53
Q

High-frequency Antibody

A
  • Mimic warm autos, except not binding to themselves –> A/C: negative
  • Special panel
  • Check pt’s history
  • Perform full antigen typing, look for something odd
54
Q

Low-frequency Antibody

A
  • Found by accident: incompatible XM, explained rxn
  • Special panel
  • Check pt’s history
  • Antigen typing is less helpful (as they are low-frequency)

426 Blood Bank (9 decks)

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