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Immunohematology > Other blood group systems > Flashcards

Other blood group systems Flashcards

1
Q

Kell Blood group system antigens & frequency

A 
32 antigens:
Cellano/K2 - 99.8%
Kell/K1- 9%
Kpa & Kpb - b is more common
Jsa & Jsb - b is more common
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2
Q

Kell Blood Group system general

A

only expressed in RBCs & RBC precursors
preseent on fetal RBC
integral membrane protein w/ a high degree of di-sulfide intramolecular bonds

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3
Q

Reducing agents that will destroy Kell antigens

A 
2-mercaptoethanol (2-ME)
or dithiothreitol (DTT)
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4
Q

Antigenicity of Kell antigens

A

K antigen most immunogenic after ABO, D

associated w/ hemolytic transfusion reactions

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5
Q

Characteristics of Kell Antibodies

A

IgG class
does NOT bind complement
enzymes show no enhancement/depression of reactivity
Depressed activity w/ LISS reagents

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6
Q

K0 phenotyp

A

lack of the KEL gene
produce an antibody (anti-Ku) against Kell antigen
rare but clinically relevant

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7
Q

KX blood group system

A

KX is a carrier protein for Kell that brings it to the membrane & stabilizes it
people lacking KX have low levels of Kell antigen & form anti-KX antibody

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8
Q

KX & Kell genetic interaction

A

Genetically independent from the Kell system

if XK1 gene is not inherited, Kx antigen is not expressed & Kell antigens will not be stabilized in the RBC membrane

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9
Q

McLeod syndrome

A

reduced expression of Kell antigens
individuals have red cells w/ morphological & functional abnormalities
X linked disorder CGD (chronic granulomatous disease) -ingest but do not destroy bacteria
high bacterial infections
acanthocytes

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10
Q

Duffy Blood group summary

A

Fy (shortcut), clinical significance
IgG (37C), AHG
Enzymes destroy the antigen!

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11
Q

Duffy blood group antigens general characteristics

A

antigen’s present on birth, only on RBC, not strong immunogens
Fya & Fyb are antithetical
Fy3 antigen-epitope common to all duffy proteins

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12
Q

Duffy blood antigen statistics in White populations

A

Fy(a+b+), Fy(a+,b-), Fy(a-,b-)

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13
Q

Duffy blood antigen statistics in black populations

A

Fy(a-,b-) & FyES ( erythroid silent)

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14
Q

Duffy blood group system biochemistry

A

duffy encodes a protein called DARC, spans membrane 7x & is a G-protein coupled receptor!
binds several chemotactic cytokines

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15
Q

Duffy blood group genetics

A

Fya & Fyb are codominant alleles

FyES -recessive; Fy(a-,b-), gene promoter deletion

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16
Q

Duffy blood group system & malaria

A

duffy is a receptor for Plasmodium vivax & P. knowlesi
individuals lacking duffy Ag are 100% resistance to P. vivax & knowlesi (susceptible to falciparum though)
large portion of the black population

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17
Q

Clinical relevance of duffy antibodies

A

antibody production is stimulated by transfusion / pregnancy - HDN
can lead to delayed hemolytic transfusion reactions
anti-Fya is 20x more likely to lead to a transfusion reaction

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18
Q

Anti-Fy3 antibody

A

duffy antibody that reacts with both Fy(a+) & Fy(b+)
resistant to enzymes
similar to antiA,B antibodies

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19
Q

Characteristics of duffy antibodies

A

IgG antibody, does NOT bind complement
enzymes degrade the antigens
show dosage!

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20
Q

Kidd Blood group system summary

A 
shortcut- JK
clinically significant 
IgG antibody class (37)
AHG
enzymes enhance reactions
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21
Q

Kidd blood group system antigens

A

3: JKa, JKb, JK3
JKa & JKb are antithetical
JK3 is present when either JKa or JKb antigens are present
entirely protein, present on cells at birth, not very immunogenic

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22
Q

Kidd blood group genotype statistics

A

JK(a-,b-) found in Chinese, Filipino, & Polynesian populations

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23
Q

Kidd blood group biochemistry

A

gene encoding Kidd antigen: SLC14 (solute carrier 14) - urea transporter
can easily screen for JK(a-,b-) units by Urea experiment = these cells are resistant to hemolysis in urea

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24
Q

Kidd antibodies

A

anti-JK3 reacts w/ any JKa or JKb positive cell
IgG titer is low!! shows dosage
antibody is unstable in vivo & in vitro!!!!
WILL BIND COMPLEMENT!!!
all potentiators will enhance reactions

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25
Q

Clinical relevance of Kidd Antibodies

A

mild HDN
responsible for the majority of delayed hemolytic transfusion reactions!! (#1 cause)
titer rapidly increases in 24 hr period, BINDS COMPLEMENT

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26
Q

Lutheran blood group system summary

A

shortcut- LU
Lua - clinically significant, IgG & IgM
Lub - not clinically significant

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27
Q

Lutheran blood group system general characteristics

A

most are high-frequency antigens aka alloantibodies to this system are infrequently found (!)
antigen destroyed by DTT treatment

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28
Q

Lutheran Antigens

A

LU1 (Lua), LU2 (Lub)
not present at birth
LUb - very high frequency
LUa- low frequency

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29
Q

Blood group antigens NOT present at birth AKA impossible to cause HDFN

A 
Lutheran
Lewis
I
P1
(PILL)
30
Q

Characteristics of anti-Lua antibody

A

both IgM & IgG
does not react with DTT treated cells
demonstrates mixed field reactions
NO clinical significance in transfusion or mild HDN

31
Q

characteristics of anti-Lub antibody

A

rare antibody bc the antigen is so high frequency
IgG- most agglutinate at IAT
does not react with DTT treated cells!
associated w/ transfusion reactions, & mild HDN

32
Q

Lewis blood group system summary

A

shortcut- Le
no clinical signficance
IgM (4C) -weak reacting

33
Q

Lewis blood group system general characteristics

A

antigens are glycosphingolipids manufactured by tissue cells, secreted into body fluids & then absorbed onto RBC membrane
antiengs primarily found in watery secretions & plasma

34
Q

Development of Lewis antigens

A

development begins in first week after birth and may continue for up to 6 years
newborns type Le(a-,b-) then type Le(a+,b-) then Le(a+,b+) at 12-18 months
and finally Le(a-,b+) by 2-3 years

35
Q

Lewis antigen biochemistry

A

linked haplotype with FUT1 (H,h), FUT2 (Se,se) and FUT3 (Le,le)
FUT3 places the fucose on different location than FUT1/2
Lea- L fucose added to certain precursor
Leb- L fucose added to H antigen (will be absent in bombay)

36
Q

genotype: Le sese

predict antigens in secretions & RBC surface phenotype

A

secretions: Lea

RBC surface: Le(a+,b-)

37
Q

genotype: Le Sese

predict antigens in secretions & RBC surface phenotype

A

secretions: Lea, Leb

RBC surface: Le(a-,b+)

38
Q

Pregnancy & the lewis system changes

A

pregnancy can affect expression of Le antigens & antibodies (2 options):

  1. Le(a-,b-) woman may make anti-Le antibodies against fetal Lea/Leb
  2. Le (a-,b+) woman may type Le(a-,b-) & may make anti-Le antibodies
39
Q

Pregnancy and the lewis system mechanisms

A

changes during pregnancy may result from distribution of lewis antigens in maternal serum due to increased circulating plasma volume (drastic volume change dilute out secretory antigens)
lewis antibodies made during pregnancy will disappear upon birth

40
Q

Clinical relevance of the lewis antibodies & why

A 
NOT RELEVANT bc they can NOT cause HDFN
IgM class (weak cold reacting) & antigens aren't present at birth
only important bc they may hide clinically relevant antibodies
41
Q

Ways to eliminate Lewis antibodies to find clinically relevant antibodies

A
  1. perform antibody screens at 37C & eliminate cold agglutination from anti-Le
  2. can incorporate commercial Lewis substances that will preferentially bind any Lewis antibodies (neutralize)
42
Q

I blood group system summary

A

shortcut- big I
clinical relevance- no, except in cold autoagglutin disease
class- IgM
enhanced w/ enzymes

43
Q

I blood group system antigens

A

only one antigen - I
I & i are NOT antithetical antigens
I - expressed on adults RBC & secretions
i - expressed on cord cels & secretions

44
Q

I blood group system biochemistry

A

I antigens are found on same precursor as ABO & Lewis, just closer to RBC membrane
found on RBC, plasma & secretions
i - straight chain
I - branched chain

45
Q

Anti-I clinically insignificant form

A

anti-I is commonly encountered, low-titer, IgM, cold autoantibody (!)
can bind complement
antibodies are most often compound (anti-IH) & reacts better w/ O cells > A1 cells

46
Q

avoiding the clinically insignificant anti-I antibody

A

usually done by pre-warming techniques

pre-warm saline bottle thats used for washes (performed by hand)

47
Q

Anti-I clinically relevant antibody & mechanisms

A

strong autoanti-I found in:

  1. Mycoplasma pneumoniae -recedes w/ time
  2. cold autoagglutin disease (CAD)- reacts over a wide thermal range & is extremely high titer BINDS COMPLEMENT in lowered temp of extremity circulation & causes massive intracellular hemolysis
48
Q

Transfusing patient w/ Anti-I clinically relevant antibody

A

I- blood is extremely rare/impossible to find
prewarm blood
use blankets on patient

49
Q

anti-i antibodies

A

auto anti-i : cold, weak reacting IgM
seen in VIRAL INFECTIONS!!!
infectious mononucleosis, CMV infections

50
Q

P1 blood group system summary

A

shortcut- P1PK
clinically significant- no
class- IgM
enhanced w/ enzymes

51
Q

P antigen blood group summary

A

shortcut- GLOB group
clinically significant- YES
class - IgM & IgG
enhanced w/ enzymes

52
Q

P1PK & Globoside blood group system antigens

A

all are branching CHO antigens

antigens: P1, Pk & P produce 5 distinct phenotypes

53
Q

P1 phenotype

A

RBC express: P, P1, Pk antigens
MOST COMMON PHENOTYPE
do not produce antibodies (excluding autoimmune)

54
Q

P2 phentype

A

RBC expression: P, Pk (lacks P1)
2nd most common phenotype
produces anti-P1 antibody

55
Q

Anti-P1 antibody

A

IgM, not clinically significant

56
Q

P1k phenotype

A

RBC expression: P1 & Pk (lacks P)
very rare phenotype
produces anti-P antibody

57
Q

Anti-P antibody

A

clinically signficant IgG
associated w/ spontaneous abortions
rare

58
Q

Autoanti-P antibody

A

associated w/ autoimmune hemolytic anemia: paroxysmal cold hemoglobinuria (PCH)
known as DONATH-LANDSTEINER antibody
IgG that BINDS COMPLEMENT!!!
biphasic!! - RBCs activate complement in cold circulation, & cause hemolysis ONLY when returning to normal body temp

59
Q

Donath-Landsteiner test

A

1 set of tubes incubated at 0 - no hemolysis
1 set of tubes incubated at 37 - no hemolysis
1 set of tubes incubated at 0 & then at 37 - HEMOLYSIS

60
Q

M & N antigens group summary

A

group shortcut- MNS
clinical significance: NO
class: IgM
destroyed by enzymes!

61
Q

S & s antigen group summary

A

group shortcut- MNS
clinical significance: YES
class - IgM
variable effects w/ enzymes

62
Q

MNSs blood group system

A

5 main antigens: M,N,S,s, U

2 genes inherited as a haplotype

63
Q

MNS gene organization (2 genes)

A

GPA - encodes glycophorin A, M antigen, N antigen, demonstrates dosage
GPB- encodes glycophorin B, S antigen, s antigen, U antigen, demonstrates dosage

64
Q

Antithetical antigens that commonly show dosage

A

Cc, Ee, Kk, MN, Ss, FyaFyb & JKaJKb

65
Q

U antigen

A

on GPB gene of MNS system
antigen that is found very close to the membrane
cell that has either S or s will have U
U- cells are rare, only found in the black population

66
Q

anti-M antibody characteristics

A

class: IgM
significant: no
ficin: destroys antigen

67
Q

anti-N antibody characteristics

A

class: IgM
significant: no
ficin: destroys antigen

68
Q

anti-S or anti-s antibody characteristics

A

class: IgG
significant: yes
ficin: variable

69
Q

Anit-U antibody characteristics

A

class: IgG
significant: yes
ficin: resistant
reacts w/ all S+, s+ cells

70
Q

Antigens with enhanced agglutination after enzyme treatment

A

Rh!
Kidd!
P, I, Le

71
Q

Antigens that are destroyed after enzyme treatment

A

Duffy!

M & N!!

72
Q

High Titer Low Avidity antibodies

A

basically will always cause a 1+ no matter the dilution & are usually not clinically significant

Immunohematology (16 decks)

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