1
Q
Naturally Occurring Clinically Significant
A
MarthiN Luther And Lewis Is ABOve (the) Piano
MN
Lua – Lutheran A
Lewis
I
ABO
P1
2
Q
Clinically Significant
A
(Si) Rhea nagpa-ABOrt, Killed Duffy’s Kid (para) LUBayan (na siya)
SsU
Rh
ABO
Kell
Duffy
Kidd
Lub
3
Q
Warm Antibodies (IgG)
A
RicH KID (can) DeFinitely KiLL Someone U LUB
Rh
Kidd
Duffy
Kell
Ss
U
Lub
4
Q
Cold Antibodies (IgM) Warm Antibodies (IgG)
A
MaNa (ni) LEWIS (ang) I Phone ABa
MN
Lewis
I
P1
AB
5
Q
React ONLY with AHG React at ANY Phase
A
Duffy
Kell
Kidd
6
Q
React at ANY Phase
A
lewis
7
Q
Enhanced by Enzyme - DETECTED
A
All (the) Rich Kids (around the) Globe Like I Phone
ABO
Rh
Kidd
Globoside*
Lewis
I
P1
8
Q
Unaffected by Enzymes
A
LUTHER (and) KELLY are
35 (years old)
Kell
Fy3 and Fy5
Lutheran
9
Q
Destroyed by Enzyme – NOT DETECTED
A
MeN, Xga “SIGA” (sila) DUFFY (at) ROGER, RIGHT?
MNS
Xga
Duffy: Fya and Fyb
Ch/Rg – Chido/Rogers
Yt - Cartwright
OTHER: Ge2 and Ge4, Indian antigens, JMH
10
Q
Bind Complement
A
PILAK
P
I
Lewis
ABO
Kidd
11
Q
Most common cause of DHTR
A
Kidd
12
Q
Dosage Effect
A
DR LUTHER KiM
Duffy
Rh (except D)
Lutheran
Kidd
MNSs
13
Q
Most severe cause of HDN
A
Rh (Anti-D)
14
Q
Most common D (+) genotype
A
R1R
15
Q
Most common D (-) genotype
A
rr
16
Q
Most commonly seen Rh antigen among black population
A
R0 (Dce)
17
Q
Most commonly seen Duffy phenotype among black population
A
Fy (a-b-)
18
Q
Most common blood group antigen among Chinese
A
Fy (a+b-)
19
Q
Most common Kidd phenotype among Filipinos
A
Jk (a-b-)
20
Q
Common major blood group associated with HDN
A
- ABO
- Rh
Anti-D alone
Anti-D in combination with Anti-C or Anti-E
Anti-c - Anti-Kell
- Anti-Duffy
- Anti-Kidd
kell is a kid abo rht
21
Q
Most Severe Hemolytic Transfusion Reaction (HTR)
A
ABO
22
Q
Common cause of Immediate Hemolytic Transfusion Reaction (HTR)
A
ABO
23
Q
Most common cause of Fatal Hemolytic Transfusion Reaction (HTR)
A
Clerical Errors
24
Q
Most commonly encountered Autoimmune Hemolytic Anemia (AIHA)
A
Warm AIHA with Rh specificity
25
#1 Most common bacterial contaminant of blood – Harmening 7th Ed
Staphylococcus aureus, Staphylococcus epidermidis
26
#1 Most common contaminant of donor units (platelets)
Staphylococcus epidermidis, Bacillus cereus
27
Most common parasitic complication of transfusion
Malaria
28
Most common anticoagulant-preservative solution for RBC
CPDA-1
29
Most common blood group associated with Drug-Induced Autoantibody
Kidd, Rh
30
● is the building block for ABO antigens.
H
31
discoverer OF H ANTIGEN
Karl Landsteiner
32
● Starts to develop at the 37th day of fetal life
ABO
33
ABO PEAK
○ 2-4 years (peak)
34
WHAT IMMUNOGLOBULIN IS ABO
Mixture of IgG, IgM, and IgA (predominant: IgM, primarily
reacting at room temperature)
35
Not well developed at birth (3-6 months for full
development)
ABO
36
● Genes at three separate loci:
ABO, Hh, and Se
37
Enzymes that add sugar to the basic precursor
substance
GLYCOTRANSFERASES
38
First to discover incompatibility although ABO
compatible.
Levine and Stetson
39
Second most important Blood Group System
RH
40
NAMING SYSTEM FOR RH BLOOD GROUPS
Fisher-Race – talks about genetic disposition of Rh atigen
Weiner
Rosenfield
ISBT
41
Based on the theory that antigen of the system was produced
by three closely linked set of alleles, each gene was
responsible for producing a product
FISHER-RACE (DCE)
42
Number is assigned to each antigen of the rh system in order
of its discovery.
ROSENFIELD
43
what antigen in MNS blood group is commonly encountered in
the clinical setting.
(M/N and S/s)
44
45
ARE MNSSSU ANTIGEND LOW OR HIGH PREVALENCE
LOW
46
The difference of M at N is the
amino acid at the location 1 and 5.
M: serine and glycine
N: leucine and glutamic acid
47
m and n location
glycophorin a
48
S and s antigen located ay
○ Glycophorin B
49
o Total of 72 amino acids (difference at position 29)
S: methionine
s: threonine
50
Destroyed by pretreatment of RBC with:
○ Proteolytic enzymes (trypsin, pronase, ZZAP, and other
chemicals)
○ Neuraminidase
Anti-M and Anti-N
51
enhanced by:
○ Acidification of serum to pH 6.5
○ Use of an albumin diluent
○ Preincubation of RBC in a glucose-containing solution (CPDA1)
ANTI M and ANTI N
52
can be used in paternity testing, reactive to Vicea graminea.
Anti-N
53
○ Commonly encountered in Blood Bank
● Anti-M
54
● Reported in hemodialysis patient in the past.
Autoanti-N (Anti-Nƒ)
55
55
Caused by the use of formaldehyde to sterilize membranes.
Autoanti-N (
56
Enzymatic modification of RBC with proteases but not
neuraminidase, can decrease the reactivity of some Anti-S
and Anti-s
Anti-S, Anti-s, and Anti-U
57
is unaffected by proteolytic enzymes.
● Anti-U
58
recombinant (modified)
glycophorin B.
Henshaw phenotype
59
○ Is the most common, observed exclusively in blacks.
U-
60
○ S-s-U- INDICATES
Complete loss of glycophorin B
61
○ Shows resistance to P. falciparum.
● En(a-)
62
U- Can react weakly with some examples of human
anti-U and are known as
U variants (S-s-Uvar)
63
Results from recombination of glycophorin A and B
genes
● En(a-)
64
○ Shows resistance to P. falciparum.
● En(a-)
65
Lacks all MNSs Antigens, result of recombination and
deletion of GPYA and GPYB.
Mᵏ
66
Contribute significantly to the zeta potential of red cells,
decreasing homotypic and heterotypic red cell
adhesion.
● Glycophorin A and Glycophorin B
67
Also known as Membrane Inhibitor of Reactive Lysis (MIRL): CD59
● Glycophorin A
68
■ Prevents C9 polymerization.
Membrane Inhibitor of Reactive Lysis
(MIRL): CD59
69
○ Receptor for pyelonephritogenic E. coli (UPEC).
● Glycophorin A
70
Increased Band 3 expression and osmotic resistance can be observed with Miltenberger type Ill red cells, a GYP B-A-B hybrid
● Glycophorin A
71
are receptors for P. falciparum.
● GPA and GPB
72
P. falciparum adheres to RBC via
sialic acid, which is highly expressed on glycophorins
73
relatively resistant to Plasmodium falciparum in vitro.
En(a-), kasi glycophorin deficient siya and p falciparum nakakabind lang naman siya dahil don
74
75
expression is variable between individuals and can be lost with in vitro storage.
P1
76
RBC are particularly rich in antigen, which makes up nearly 6% of the total RBC lipid.
P
77
where is P antigen locatted
○ P is more common throughout the body
■ Platelets, epithelial cells and fibroblast
○ P and Pk also found in:
■ Plasma as glycosphingolipids
■ Glycoproteins in hydatid cyst fluid
78
● May be detected in the IAT if AHG is used.
Anti-P1
79
Often detected as a weak, cold-reactive saline agglutinin
(reacts optimally at 4°C)
Anti-P1
80
Titers are often elevated in patients with.
○ Parasitic infections (e.g. Hydatid disease, and fascioliasis, C. sinensis, O. viverrini infections)
○ Bird Fancier's Lung
Anti-P1
81
elevated in Parasitic infections (e.g. Hydatid disease, and fascioliasis, C. sinensis, O. viverrini infections)
anti p1
82
elevated in bird Fancier's Lung
anti p1
83
● Separable mixture of anti P, Anti P1 and Anti Pk
anti Tja
84
Naturally occurring IgM alloantibody in the serum of Pk (and p) individuals
Alloanti-P
85
Can cause in vivo hemolysis following transfusion of P
positive (P1 and P2) RBCs
Alloanti-P
86
○ Associated with spontaneous abortions.
Alloanti-P
87
● Seen in patients with Paroxysmal Cold Hemoglobinuria (PCH)
Autoanti-P
88
biphasic hemolysin
Autoanti-P
89
s characteristic can be demonstrated in vitro in the Donath
Landsteiner test.
Autoanti-P
90
antigen may be associated with
the c-interferon and major histocompatibility class l receptors
and may modulate cell signaling via lipid rafts.
Pk
91
blood group antigens may also play a role in cellular
differentiation and neoplasia
P
92
Pk and P antigens are differentially expressed during.
○ Embryogenesis
○ Hematopoiesis
○ Intestinal mucosal differentiation
93
○ A marker of apoptosis in germinal center B cells, Burkitt
lymphoma, and lymphoblastic leukemia.
Pk antigen
94
lke is ○ Formed with the addition two additional sugars:
■ Galactose and sialic acid
95
A marker of embryonic and mesenchymal stem cells
implicated in adhesion, cell signaling, and metastasis in
renal cell and breast carcinoma.
● LKE (Luke Antigen)
96
The blood group antigen is the receptor for
Parvovirus B19
P
97
a single stranded DNA virus
associated with multiple clinical sequelae, including
aplastic crises
Parvovirus B19,
98
can bind human immunodeficiency virus (HIV) and
may confer resistance to HIV infection.
Pk
99
are receptors for Shiga toxins,
produced by Shigella dysenteriae and Enterohemorrhagic Escherichia coli (EHEC /
O157:H7) strains.
P1 and Pk antigens
100
antigen also serves as a receptor for Streptococcus
suis and Pseudomonas aeruginosa.
Pk
101
on uroepithelium are cell receptors for P-fimbriae, a bacterial adhesin and colonization factor expressed on Uropathogenic E.
coli strains
P, Pk,and LKE blood group antigens
102
Poorly developed at birth and don't reach adult levels until the
age of 15
LUTHERAN
103
appears on red cells at the orthochromatic
erythroblast stage, concurrent with binding of red cells to
laminin.
Lutheran
104
minor constituent of RBC membranes
LUTHERAN
105
the null pheotype of lutheran can make an alloantibody to lutheran glycoprotein
anti lu 3
106
Can show weakened expression of P1, i,
Indian/CD44, and Knops/CD35 antigens and
enhanced expression of CDw75
○ Autosomal dominant (In [Lu])
107
Can display subtle abnormalities, including
increased poikilocytosis and increased
hemolysis, during in vitro storage
inlu
108
■ Has weakened Lutheran, enhanced i and
CDw75, and normal P1, i, and CD44
expression.
X-linked Recessive
109
● Often an IgM, room temperature agglutinin
Anti-Lu ͣ
110
● Discovered in patient with systemic lupus diffuses.
Anti-Lu ͣ
111
Can display mixed field agglutination because not all RBCs
express detectable Lu antigens.
Anti-Lu ͣ
112
● Reacting best in the IAT
Anti Luᵇ and other Lutheran antibodies
113
● First BGS discovered through AHG testing.
kell and kx
114
there is ● Acquired K like Ag in
Streptococcus faecium infection.
115
is found on erythroid & megakaryocyte
progenitors, skeletal muscle, lymphoid organs and testis
XK (gene) protein
116
○ Completely lacks all Kell antigens.
K0K0
117
○ Completely lacks all Kell antigens.
K0K0
118
can make an
alloantibody to the Kell glycoprotein (anti Ku)
K0K0
119
Kell glycoprotein
(anti Ku)
120
○ Have significantly depressed/absent Kell antigens
● McLeod RBCs
121
○ Have no decrease in CO2 permeability.
K0K0
122
● McLeod RBCs
An X linked recessive phenotype characterized by the
absence of XK protein on RBCs (Kx antigen, XK1; ISBT
019), acanthocytes, and neuromuscular disorders.
123
individuals are incompatible with both Kell
positive and KoKo RBCs
McLeod
124
○ Depressed Kell expression
● Kmod and Gerbich-negative RBC
125
Some Kell mod individuals have increased Kx (KEL15)
expression and can develop an anti KEL5 (anti Ku)
following RBC transfusion
● Kmod and Gerbich-negative RBC
126
○ Pwedeng may Kx pero walang Kell expression.
● Kmod and Gerbich-negative RBC
127
● Septic patients and in Autoimmune hemolytic anemia
anti Kell autoantibodies
128
○ antigens are also depressed (up to 80%)
Kell
129
Often characterized by reticulocytopenia, with little or
no bilirubinemia
KELL ANTIBODIES
130
Reports have also described neonatal thrombocytopenia due
to suppression of marrow megakaryocytes
SNTI KELLQ
131
Several centers now routinely screen and refer prenatal
patients with THESE antibodies, with improved perinatal
outcomes.
Anti-K1
132
A vasoactive peptide that functions in endothelial cell
migration, neovascularization, axonal growth, and
neural crest development Kell may have only a minor
physiologic role in endothelin 3 homeostasis because
endothelin-3 is also cleaved by ECE-1, a related
endothelin converting enzyme
endothelin-3
133
McLeod RBCs have:
○ Shortened survival.
○ Decreased permeability to water.
○ Abnormal morphology (acanthocytes)
134
○ Hematologic neuromuscular abnormalities
● McLeod Syndrome
135
Typically presents with areflexia, dystonia, and
choreiform movements late in life.
● McLeod Syndrome
136
Late onset muscular dystrophy and cardiomyopathy
can also be seen.
● McLeod Syndrome
137
Can also be associated with Chronic Granulomatous
Disease
● McLeod Phenotype
138
influence of ABO IN ITS SYNTHESIS and antigenicity.
lewis
139
blood group whose precursor are h ntigens
lewis
140
synthesized in the gastrointestinal tract
and passively adsorbed onto RBCs
lewis
141
● Not intrinsic to RBCs but are on type 1 glycosphingolipids.
lewis
142
In some Tissues, Lewis Antigens are expressed.
○ Glycosphingolipids, Glycoproteins, Mucine
lweis
143
Tissues and Fluids expressing Lewis Antigens include:
○ Lymphocytes, platelets & other tissues such as the
pancreas, stomach, intestine, skeletal muscle, renal
cortex & adrenal glands, also in saliva
Lewis
144
Result from interaction of Se and Le genes.
lewis
145
Usually on RBCs of very young children and some
individuals of Polynesian, Japanese, or Taiwanese
ancestry
LEWIS
146
○ 5x more common in blacks, Africans than in Caucasians
● Le (a-b-) phenotype
147
It is speculated that they could play a role in renal graft
rejection in black, Le(a-b-) individuals.
Anti-Lea and Anti-Leb
148
○ A causative agent of gastritis and ulcers
● Helicobacter pylori
149
● Helicobacter pylori
Anti-Lea and Anti-Leb
150
Binds H, Leb, and Ley antigens via BabA recognition of a
terminal Fuca1-2 Gal. epitope
● Helicobacter pylori
151
Has been linked with a higher incidence of recurrent
Candida vaginitis and urinary tract infection.
● Lewis null and/or non-secretor phenotype
152
Protects against Norovirus infection.
Lewis null and/or non-secretor phenotype
153
phenotype associated with an increased
incidence of heart disease
Le (a-b-)
154
A ligand for the endothelial adhesion molecule E
selectin and may mediate tumor cell endothelium
interactions
● Sialyl-Lea
155
Aberrant expression of ___ occurs in many
gastrointestinal and uroepithelial cell cancers and may
contribute to tumor metastasis.
Aberrant expression of sialyl Lea occurs in many
gastrointestinal and uroepithelial cell cancers and may
contribute to tumor metastasis.
156
Also the epitope for the tumor marker CA 19 9, a useful
serologic marker for monitoring patients with
gastrointestinal and other malignancies
sialyl lea
157
Expressed on:
○ RBCs, cerebellar purkinje cells, postcapillary venule
endothelial cells, endothelial cells of glomeruli, vasa
recta, thyroid, pulmonary capillaries, alveolar type I
squamous ec & ec of collecting tubules.
DUFFY
158
- high incidence antigens (so not clinically
significant) present on all RBCs except the Duffy null
phenotype.
Fy3, Fy5, and Fy6
159
Fya and Fyb - autosomal codominant antigens.
○ Differs in
location 42
○ Fya: glycine
○ Fyb: aspartate
160
○ originally described on Fy (a-b-) RBCs
● Fy4 antigen
161
marker for African black race
Fy (a-b-) Null
162
90.8% frequency among Chinese
● Fy (a+b+)
163
Characterized by extremely weak Fyb expression
somewhat rare.
Fyx
164
Most common alloantibody encountered clinically can
be observed in Fy (a-) individuals of all races
● Anti-Fya
165
behaves like an anti-Fya+b, reacting with all Duffy
positive RBCs.
● Anti-Fy3
166
occasionally produced by sickle cell, Fy (a-b-) patients
despite the expression of Fyb on nonerythroid tissues
● Anti-Fy3
167
○ Requires the presence of Rh antigens for reactivity.
● Anti-Fy5
168
○ The epitope for an anti-Duffy monoclonal antibody that
blocks Plasmodium vivax binding.
Anti-Fy6
169
may facilitate leukocyte recruitment to the sites of
inflammation by establishing a chemokine across activated
endothelium.
DARC q
170
In patients with sickle cell disease, is associated with
increased chronic organ damage and proteinuria.
● Fy null phenotype
171
Resistant to most Plasmodium vivax strains and
Plasmodium knowlesi
● Fynu individuals
172
○ is the receptor for Plasmodium vivax
DARC
173
provides a selective advantage to populations living in
malaria endemic areas.
KIDD BLOOD GROUP SYSTE
fy null
174
antigens are expressed on:
○ RBCs
○ Descending vasa recta
Kidd
175
176
Lacks all MNSs Antigens, result of recombination and
deletion of GPYA and GPYB.
Mᵏ
177
Contribute significantly to the zeta potential of red cells,
decreasing homotypic and heterotypic red cell
adhesion.
● Glycophorin A and Glycophorin B
178
Also known as Membrane Inhibitor of Reactive Lysis
(MIRL): CD59
● Glycophorin A
179
○ Receptor for pyelonephritogenic E. coli (UPEC).
● Glycophorin A
180
Increased Band 3 expression and osmotic resistance
can be observed with Miltenberger type Ill red cells, a
GYP B-A-B hybrid.
● Glycophorin A
181
are receptors for P. falciparum.
● GPA and GPB
182
e glycosphingolipids, consisting of an
antigenically active carbohydrate moiety covalently linked to a
ceramide lipid tail.
P BLOOD GROUP SYSTEM (ISBT NO. 003 AND 028)
183
○ Pk and P1:
galactose
184
○ P:
N-acetylgalactosamine
185
is poorly expressed at birth (up to 7 years).
P1
186
expression is variable between individuals and can
be lost with in vitro storage.
P1
187
h makes up
nearly 6% of the total RBC lipid.
P antigen,
188
P and Pk also found in:
■ Plasma as glycosphingolipids
■ Glycoproteins in hydatid cyst fluid
189
Often detected as a weak, cold-reactive saline agglutinin
(reacts optimally at 4°C)
Anti-P1
190
● May be detected in the IAT if AHG is used.
Anti-P1
191
BB LEC
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