WorksheetsRECALL CORNER OTHER BLOOD GROUPS
Total questions: 131
Worksheet time: 1hrs 6mins
Name
Class
Date
1.
The P blood group was first described in 1927 by which researchers?
a)
Karl Landsteiner and Philip Levine
b)
Levine and Stetson
c)
Wiener and Landsteiner
d)
Coombs and Mourant
2.
Can react in any phase of testing
a)
Rh
b)
Lewis
c)
kidd
d)
P1
e)
I
3.
ABO
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
4.
Rh
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
5.
Kell
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
6.
Kidd
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
7.
Duffy
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
8.
S
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
9.
s
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
10.
U
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
11.
Lutheran (Lub)
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
12.
Lutheran (Lua)
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
13.
I
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
14.
Lewis
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
15.
M
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
16.
N
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
17.
P1
a)
Clinically significant alloantibodies
b)
Clinically insignificant alloantibodies
18.
Rh
a)
Warm antibodies
b)
Cold antibodies
19.
Kell
a)
Warm antibodies
b)
Cold antibodies
20.
Duffy
a)
Warm antibodies
b)
Cold antibodies
21.
Kidd
a)
Warm antibodies
b)
Cold antibodies
22.
M
a)
Warm antibodies
b)
Cold antibodies
23.
N
a)
Warm antibodies
b)
Cold antibodies
24.
P1
a)
Warm antibodies
b)
Cold antibodies
25.
Rh
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
26.
ABO
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
27.
Kidd
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
28.
Lewis
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
29.
P1
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
30.
I
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
31.
Duffy
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
32.
MNS
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
33.
Xga
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
34.
Kell
a)
Enhanced by enzymes
b)
Destroyed by enzymes
c)
Unaffected by enzymes
35.
Rh (except D)
a)
Antibodies that exhibit dosage effect
b)
Binds complement
36.
ABO
a)
Antibodies that exhibit dosage effect
b)
Binds complement
37.
I
a)
Antibodies that exhibit dosage effect
b)
Binds complement
38.
Lewis
a)
Antibodies that exhibit dosage effect
b)
Binds complement
39.
P
a)
Antibodies that exhibit dosage effect
b)
Binds complement
40.
Kidd
a)
Antibodies that exhibit dosage effect
b)
Binds complement
41.
Duffy
a)
Antibodies that exhibit dosage effect
b)
Binds complement
42.
MNSs
a)
Antibodies that exhibit dosage effect
b)
Binds complement
43.
Lutheran
a)
Antibodies that exhibit dosage effect
b)
Binds complement
44.
Anti-P1 is neutralized by
a)
Hydatid cyst fluid, pigeon droppings, turtle doves' egg whites
b)
Plasma or serum, saliva
c)
Serum only (contains complement)
d)
Urine
e)
Breast milk
45.
Anti-Lewis is neutralized by
a)
Hydatid cyst fluid, pigeon droppings, turtle doves' egg whites
b)
Plasma or serum, saliva
c)
Serum only (contains complement)
d)
Urine
e)
Breast milk
46.
Anti-Sda can be neutralized by
a)
Hydatid cyst fluid, pigeon droppings, turtle doves' egg whites
b)
Plasma or serum, saliva
c)
Serum only (contains complement)
d)
Urine
e)
Breast milk
47.
Anti-I can be neutralized by
a)
Hydatid cyst fluid, pigeon droppings, turtle doves' egg whites
b)
Plasma or serum, saliva
c)
Serum only (contains complement)
d)
Urine
e)
Breast milk
48.
Hydatid cyst fluid
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
49.
Pigeon droppings
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
50.
Turtle doves' egg whites
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
51.
Plasma or serum
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
52.
Saliva
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
53.
Serum (contains complement)
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
54.
Urine
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
55.
Breast milk
a)
Anti-P1 is neutralized by this
b)
Anti-Lewis is neutralized by this
c)
Anti-Chido/Rogers is neutralized by this
d)
Anti-Sda can be neutralized by
e)
Anti-I can be neutralized by
56.
Abnormal RBC seen in Rh null phenotype
a)
Stomatocytes
b)
Acanthocytes
c)
Elliptocytes
d)
Hereditary spherocytosis, Congenital acanthocytosis, Southeast Asian Ovalocytosis
57.
Abnormal RBC seen in McLeod Phenotype
a)
Stomatocytes
b)
Acanthocytes
c)
Elliptocytes
d)
Hereditary spherocytosis, Congenital acanthocytosis, Southeast Asian Ovalocytosis
58.
Abnormal RBC seen in Leach Phenotype
a)
Stomatocytes
b)
Acanthocytes
c)
Elliptocytes
d)
Hereditary spherocytosis, Congenital acanthocytosis, Southeast Asian Ovalocytosis
59.
Abnormal RBC seen in Diego Phenotype
a)
Stomatocytes
b)
Acanthocytes
c)
Elliptocytes
d)
Hereditary spherocytosis, Congenital acanthocytosis, Southeast Asian Ovalocytosis
60.
Stomatocytes
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
61.
Acanthocytes
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
62.
Elliptocytes
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
63.
Hereditary spherocytosis
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
64.
Congenital acanthocytosis
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
65.
Southeast asian ovalocytosis
a)
Abnormal RBC seen in Rh Null Phenotype
b)
Abnormal RBC seen in McLeod Phenotype
c)
Abnormal RBC seen in Leach Phenotype
d)
Abnormal RBC seen in Diego Phenotype
66.
Phenotype resistant to Plasmodium vivax merozoites
a)
Fy (a-b-)
b)
M-N-
c)
Pk antigen
67.
Phenotype resistant to Plasmodium falciparum merozoites
a)
Fy (a-b-)
b)
M-N-
c)
Pk antigen
68.
Fy(a-b-)
a)
Phenotype resistant to Plasmodium vivax merozoites
b)
Phenotype resistant to Plasmodium falciparum merozoite
69.
M-N-
a)
Phenotype resistant to Plasmodium vivax merozoites
b)
Phenotype resistant to Plasmodium falciparum merozoite
70.
Receptor for Shiga toxin
a)
Fy (a-b-)
b)
M-N-
c)
Pk antigen
71.
Antibody enhanced by acidification
a)
Anti-M
b)
Ani-N
c)
Anti-P
d)
Anti-I
e)
Anti-i
72.
Antibody seen in patients dialyzed with formaldehyde sterilized equipment
a)
Anti-M
b)
Ani-N
c)
Anti-P
d)
Anti-I
e)
Anti-i
73.
Paroxysmal cold hemoglobinuria
a)
Anti-M
b)
Ani-N
c)
Anti-P
d)
Anti-I
e)
Anti-i
74.
Cold agglutinin associated with Mycoplasma pneumoniae
a)
Anti-M
b)
Ani-N
c)
Anti-P
d)
Anti-I
e)
Anti-i
75.
Antibody associated with infectious mononucleosis and alcoholic cirrhosis
a)
Anti-M
b)
Ani-N
c)
Anti-P
d)
Anti-I
e)
Anti-i
76.
Most common cause of HDN
a)
ABO
b)
Rh (anti-D)
c)
ABO incompatibility
77.
Immediate transfusion reaction
a)
ABO
b)
Rh (anti-D)
c)
ABO incompatibility
78.
Most severe cause of HDN
a)
ABO
b)
Rh (anti-D)
c)
ABO incompatibility
79.
most serious transfusion reaction
a)
ABO
b)
Rh (anti-D)
c)
ABO incompatibility
80.
Notorious for delayed transfusion reaction
a)
Kidd
b)
Clerical error
c)
Diego
d)
Xg
e)
Scianna Sc2
81.
Most common cause of severe and fatal hemolytic transfusion reaction
a)
Kidd
b)
Clerical error
c)
Diego
d)
Xg
e)
Scianna Sc2
82.
Antigen used to study Mongolian ancestry
a)
Kidd
b)
Clerical error
c)
Diego
d)
Xg
e)
Scianna Sc2
83.
Sex-linked, frequent in females
a)
Kidd
b)
Clerical error
c)
Diego
d)
Xg
e)
Scianna Sc2
84.
Mennonite population
a)
Kidd
b)
Clerical error
c)
Diego
d)
Xg
e)
Scianna Sc2
85.
C4 complement
a)
Chido or Rogers
b)
Gerbich
c)
Cromer
d)
Knops
86.
Glycophorin C and D
a)
Chido or Rogers
b)
Gerbich
c)
Cromer
d)
Knops
87.
Decay Accelerating Factor
a)
Chido or Rogers
b)
Gerbich
c)
Cromer
d)
Knops
88.
Complement receptor 1
a)
Chido or Rogers
b)
Gerbich
c)
Cromer
d)
Knops
89.
CD44 or Immune adhesion molecule
a)
Indian
b)
HLA on RBCs
c)
Sda
d)
Ch, Rg, Yka Csa JMH,* Kna McCa
90.
Bennett-Goodspeed, Bga, Bgb, Bgc
a)
Indian
b)
HLA on RBCs
c)
Sda
d)
Ch, Rg, Yka Csa JMH,* Kna McCa
91.
Mixed-field and refractile microscopically
a)
Indian
b)
HLA on RBCs
c)
Sda
d)
Ch, Rg, Yka Csa JMH,* Kna McCa
92.
High-titer, low avidity ab
a)
Indian
b)
HLA on RBCs
c)
Sda
d)
Ch, Rg, Yka Csa JMH,* Kna McCa
93.
Bga
a)
HLA B7
b)
HLA B17
c)
HLA A-28
94.
Bgb
a)
HLA B7
b)
HLA B17
c)
HLA A-28
95.
Bgc
a)
HLA B7
b)
HLA B17
c)
HLA A-28
96.
I and I antigens genes are found on
a)
Chromosome 19
b)
Chromosome 4
c)
Chromosome 22
d)
Chromosome 6
e)
Chromosome 1
97.
Fya and Fyb antigens are located at the long arm of
a)
Chromosome 19
b)
Chromosome 4
c)
Chromosome 22
d)
Chromosome 6
e)
Chromosome 1
98.
high-prevalence antigens but expressed in a reciprocal relationship that is developmentally regulated
a)
I and i antigen
b)
Duffy antigen
c)
Kell antigen
d)
Kidd antigen
e)
Lutheran antigen
99.
was named for Mr. Duffy, a multiply transfused hemophiliac who in 1950 was found to have the first described example of anti-Fya
a)
I and i antigen
b)
Duffy antigen
c)
Kell antigen
d)
Kidd antigen
e)
Lutheran antigen
100.
Clinically significant and destroyed by enzymes
a)
I and i antigen
b)
Duffy antigen
c)
Kell antigen
d)
Kidd antigen
e)
Lutheran antigen
101.
Identified on fetal RBCs as early as 6 weeks gestational age and are well developed at birth
a)
Fya and Fyb antigens
b)
K0 or K null
c)
Kx
102.
Receptors for Plasmodium vivac and Plasmodium knowlesi
a)
Fya and Fyb antigens
b)
K0 or K null
c)
Kx
103.
During the first 18 months of life one slowly decreases as the other increases until adult proportions are reached, adult RBCs are rich in and have only trace amounts of .. antigen
a)
I and i antigen
b)
Duffy antigen
c)
Kell antigen
d)
Kidd antigen
e)
Lutheran antigen
104.
At birth, infant RBCs are rich in
a)
i
b)
I
105.
Found in trace amount when adult phase is reached
a)
i
b)
I
106.
Individuals who do not change their I status after birth
a)
I and I antigens
b)
Weak D
c)
Rare I Adult / I negative
107.
Conditions associated with increased i antigen on RBCs include thos with shortened marrow maturation time or dyserythropoiesis
a)
I and I antigens
b)
Weak D
c)
Rare I Adult / I negative
108.
Chronic dysrtyrhopoetic anemia type II or hereditary erythroblastic multinucleanty with positive acidified serum (HEMPAS); with much greater i activity on RBCs that control cord RBCs
a)
I and I antigens
b)
Weak D
c)
Rare I Adult / I negative
109.
Almost undetectable at birth
a)
i
b)
I
110.
Rich when adult proportions are reached
a)
i
b)
I
111.
common autoantibody that can be found in virtually all sera although testing at 4C and/or against enzyme0treated RBCs may be required to detect reactivity
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
112.
Found in the serum of many normal healthy individuals
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
113.
Weak, naturally occurring, saline-reactive IgM agglutinin
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
114.
Not associated with in vivo red cell agglutination
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
115.
Potent cold autoagglutinin that demonstrated high titer and reacts over a wide thermal range (0 to 30C)
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
116.
Patients with Mycoplasma pneumoniae often develop strong cold agglutinins with I specificity and can experience a transient episode of acute abrupt hemolysis just as the infection begins to resolve
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
117.
Listeria monocytogenes organism from patients with cold autoimmune hemolytic anemia has been reported to absorb anti-i and stimulate the production in rabbits
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
118.
IgM cold agglutinin and reacts optimally at 4C
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
119.
Associated with infectious mononucleosis (Epstein-Barr virus infection) and some lymphoproliferative disease
a)
Anti-I
b)
Benign Anti-I
c)
Pathologic Anti-I
d)
Autoanti-I
e)
Anti-i
120.
Which Duffy phenotype is Very rare among whites?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
121.
Which Duffy phenotype is Very rare among whites, never been recorded sa mga chines, BUT prevalent sa mga BBC aka black americans?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
122.
Which Duffy phenotype have NEVER ever ever ever been recorded to chinese?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
123.
Which Duffy phenotype is Prevalent among chinese (90.8%?)
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
124.
Which Duffy phenotype is Prevalent among blacks (68%)?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
125.
Which Duffy phenotype is super RARE among blacks (1%) BUT prevalent in whites (49%) and rare den medyo in chinese (8.9%)?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
126.
Which Duffy phenotype is not that rare but not that common (parang G6PD in the Philippines eme) in whites (34%), 22% in black americans but super duper unique and rare sa mga chinese (0.3%)?
a)
Fy (a+ b-)
b)
Fy (a+ b+)
c)
Fy (a-b+)
d)
Fy (a- b-)
127.
short dosage reacting more strongly with RBCs that have a double dose than RBCs from heterozygotes
a)
Anti-Jka and Anti-Jkb
b)
Anti-I
c)
Anti-i
128.
Ab usually do not bind complement
a)
Anti-Jka and Anti-Jkb
b)
Anti-I
c)
Anti-i
129.
has clinical significance in transfusion and are an uncommon cause of HDFN
a)
Anti-Jka and Anti-Jkb
b)
Anti-I
c)
Anti-i
130.
More commonly observed
a)
Anti-Fya
b)
Anti-Fyb
131.
Both Anti-Jka and Anti-Jkb are which type of immune antibody?
a)
IgG
b)
IgM
100 %
