Blood Banking Flashcards
1
Q
First recorded blood transfusion performed.
A
Pope Innocent VIII
2
Q
Performed blood transfusion to Pope Innocent
A
Jiacomo de San Genesio
3
Q
Discovered circulatory system
A
William Harvey
4
Q
Animal to animal transfusion
A
Richard Lower
5
Q
Animal to human transfusion
A
Jean Baptiste Denis
6
Q
First to work on blood transfusion and blood preservation technique
A
Charles Drew
7
Q
Sodium phosphate (Na3PO4)
A
Braxton Hicks
8
Q
Sodium Citrate
A
Albert hustin
9
Q
Determined minimum non-toxic amount of citrate needed to prevent coagulation
A
Richard Lewisohn
10
Q
Citrate dextrose
A
Rous and Turner
11
Q
Acid Citrate Dextrose
A
Loutit and mollison *
12
Q
Utilized glycerol to extend lifespan by 10 years
A
Audrey Smith
13
Q
Citrate phosphate dextrose as standard
A
Gibson
14
Q
First vein-vein transfusion using special cannulas
A
Edward Lindemann
15
Q
Syringe valve apparatus
A
Unger
16
Q
ABO group
A
Karl Landsteiner
17
Q
Fourth ABO blood group: AB
A
Alfred von Decastello and Adriano Sturli
18
Q
MN and P system
A
Karl Landsteiner and Philip levine
19
Q
RH blood group
A
Karl landsteiner and alexander weiner
20
Q
World first blood bank in Chicago under the leadership of Dr. Bernard Fantus
A
Cook County hospital
21
Q
First community-based blood center
A
Erwin Memorial Blood Bank
22
Q
Book authored by Karl Landsteiner
A
Book authored by Karl Landsteiner
23
Q
Discovered the ABO blood group system
A
Karl Landsteiner
24
Q
Remains the leading cause of death in hemolytic transfusion reaction fatalities (FDA)
A
Transfusion of wrong ABO group
25
According to FDA, the most common cause of death is TRALI or NCPE
Fiscal year 2009
26
Basic sugar precursors in ABO blood group
Paragloboside/Glycan
27
Amorphic. It does NOT code for any enzymes and is merely representative of A and B gene absence
O gene
28
Higher concentrations of transferases (810,000 to 1,170,000 Ag sites on an A1 adult RBC)
A gene
29
610,000 to 830,000 Ag sites
B gene
30
B enzyme compete more efficiently for H substance than the A enzyme A-600,000 sites B-720,000 sites
A and B gene
31
Described the theory for the inheritance of the ABO blood group
Bernstein
32
An individual inherits one ABO gene from each parent and these two genes determine which ABO antigen is present in RBC
Co-dominance
33
Inheritance pattern of ABO
Autosomal
34
A and B blood group are
Codominant
35
Amorph, as no detectable antigen is produced in response to the inheritance of this gene
O gene
36
Group O phenotype
In heritance of two genes that are non-functional
Autosomal recessive
37
Possible genotype for O phenotype
OO
38
Possible genotype for A phenotype
A1A1, A1A2,A1,O
39
Possible genotype for A2 phenotype
A2A2, A2O
40
Posible genotype for B phenotype
BB,BO
41
Possible genotype for A1B phenotype
A1B
42
Posible genotype for A2B phenotype
A2B
43
enzyme coded by H gene with L-fucose immunodominant sugar
Alpha-2-L-Fucosyltransferase
44
Enzyme coded by A gene with GalNAc immunodominant sugar
Alpha-3-N-acetylgalactosaminyltransferase
45
Enzyme coded by B gene with D-galactose as immunodominant sugar
Alpha-3-D-Galactosaminyltransferase
46
Composition of paragloboside
Glucose, Galactose, GalNAc, Galactose
47
Jansky Nomenclature (O, A ,B,AB)
I,II,III,IV
48
Moss nomenclature (O,A,B,AB)
IV,III,II,I
49
Antigen frequency of ABO
O>A>B>AB
50
ABO antigen formation
37th Day of fetal Life
51
Full expression of ABO antigen which remain constant for life
2-4 years
52
Location of ABO antigens in the body
RBC, endothelial cells, platelets, lymphocytes, epithelial cells and secretion
53
ABO antigen forms on RBC
Glycoproteins, glycolipids, or glycosphingolipids
54
ABO antigens are synthesized on type 2 Precursor chains refer to a ____ linkage
Beta 1-4 linkage
55
ABO antigen type present in the secretion
Glycoproteins
56
ABO antigens are synthesiszed on type 1 precursor chains refer to a ____ linkage
Beta 1-3 linkage
57
ABH Substances can be found in:
Digestive juices, Urine, Bile, Saliva, Tears,Amniotic fluid, Milk, Pathologic fluids
58
Excessive ABH substance in secretion can be oberved in: (PIC)
Pseudomembranous ovarian cyst, Intestinal obstruction, Carcioma of stomach and pancreas
59
Determination of secretor status (Ag+ Saliva+Agcells=No agglutination)
Hemagluttination Inhibition Assay with Saliva
60
H1 and H2 forms of H antigen
Unbranched Straight Chain
61
H3 and H4 forms of H antigen
Complex Branched Chains
62
Reactivity of Anti H or Anti-H lectin with ABO blood groups
O>A2>B>A2B>A1>A1B
63
Reacts with Anti-A1 and Anti-A
A1
64
Reacts with Anti-A only
A2
65
MF with Anti-A1 and anti-AB
A3
66
Reacts only with Anti-AB, but no reaction to Anti-A
Ax
67
MF reaction with Anti-A and Anti-AB, but on few agglutination (<10%)
Aend
68
Weak/No reaction with anti-A and Anti-AB
Am
69
No reaction with Anti-A and anti-AB
Ael
70
No reaction with Anti-A and anti-AB, but only present in siblings
Ay
71
Small agglutinates within predominantly unagglutinated cells
Mixed field
72
Method used to confirm the presence of Am, Ay, and Ael antigens
Adsoprtion and Elution of anti-A
73
More antigenic sites for A and less for H
A1
74
Less antigenic sites for A and More for H
A2
75
Predominantly Aa and Ab and uncoverted H3 and H4 antigenic sites
A2 RBCs
76
Aa, Ab,Ac,Ad determinants with no unconverted H3 and H4 antigen sites
A1 RBCS
77
Reacts with Anti-B and Anti- AB
B subgroup
78
MF reaction with anti-B and anti-AB (Most frequent B subtype)
B3
79
Weak reaction with anti-B and Anti-AB
Bx
80
No/Weak reaction with Anti-B and Anti-AB
Bm
81
Bm subtype can be converted to B if incubated with:
Uracil diphosphate
82
No reaction with Anti-B and anti-AB (Extremely rare phenotype)
Bel
83
Homozygous inheritance of the h gene results in the inability to form H antigen
Bombay Phenotype
84
First reported the Bombay Phenotype
Dr Y.M Bhende in 1952 in Mumbai, India
85
Genotype of Bombay phenotype
hh genotype non-secretor
86
The inheritance pattern of Bombay phenotype
Autosomal recessive
87
Mutation in FUT-1
Silenced H gene
88
Mutation in FUT-2
Silenced Se gene
89
Serum of Bombay phenotype
Anti-A, Anti-B, Anti-AB, Anti-H
90
Bombay individuals are phenotyped as:
Oh
91
Bombay phenotype forward and reverse typing
No Agglutination at Anti-H and with agglutination in O cells
92
Absent or only trace amount of A, B, H antigens on RBCs with normal expression in the secretion
Para-Bombay phenotype
93
genotype of para-bombay phenotype
hh, secretor
94
Para-Bombay phenotype is caused by:
Mutated FUT1 gene w/ or w/o active FUT2 or silenced FUT1 gene with an active FUT2 gene
95
Individuals normally produce antibodies directed against the A and/or B babsent from their RBC
Naturally Occuring antibodies
96
ABO antibodies are produced at:
Birth
97
When are ABO antibodies starts to be detected
3-6 months of age (4-6 mos.)
98
Predominant form of ABO antibody
Predominantly IgM (IgM, IgG, or IgA)
99
ABO antibodies react at:
Room temperature (20-24) or below
100
ABO antibodies activate compliment at:
37 degree celcius
101
IgG ABO antibody which is present only on O individuals
Anti-A,B (not a combination of A and B but is only a cross reacting antibody)
102
Primarily IgM and IgG may be found on O individuals
Anti-A and Anti-B
103
Plants or seed extracts that agglutinate human cells with some degree of specificity
Lectins
104
Anti-A1 lectin
Dolichos biflorus
105
Anti-B lectin
Banderia simplicifolia (Griffona Simpliforia)
106
Anti-H lectin
Ulex Europeus
107
Anti-N lectin
Vacia Graminea
108
Anti-M lectin
Iberis amara
109
Anti-T,Th
Arachis hypogenea
110
Anti-Tn
Salvia Sclarea
111
Using Antisera (Anti-A, Anti-B) to detect antigens on patient's RBCs
Forward grouping/Direct/Front/Cell Typing
112
Used as preservative in Blood typing
Sodium azide and Formalin
113
Ensure the reactivity of the antisera
Control cell should be weakly reactive for the antigen being tested.
Positive control
114
Ensure the specificity of the antisera
Negative control
115
Using reagent RBCs to detect ABO antibodies in the patient's serum
Reverse typing/Indirect/Back/ Serum typing
116
Universal RBC donor
Type O
117
Universal Plasma donor
Type AB
118
Universal plasma recipient
Type O
119
Universal RBC recipient
Type AB
120
One SOLID agglutinate
4+
121
several LARGE agglutinates with CLEAR background
3+
122
MEDIUM agglutinates, CLEAR background
2+
123
SMALL agglutinates,TURBID background
1+
124
TINY agglutinates, Turbid background
W+
125
No agglutination or hemolysis
0
126
Partial/complete hemolysis
Positive reaction
127
Hemolysis-Presence of free HB in serum (see notes for more info)
H grading 10=score
128
Nonspecific aggregation like a stack of coins
Rouleaux
129
Conditions that cause weaker reactions
Leukemia
Chromosome Translocation
Hemolytic diseases
Hodgkin's disease
Hypogammaglobulinemia (CLL)/ Immunodeficiency
130
Acquired A phenomenon is caused by: (PT)
Proteus mirabilis
Tn activation
131
Acquired B phenomenon is caused by : (EPICC)
E.coli(086)
Proteus Vulgaris
Intestinal obstruction
Carcinoma of Colon and rectum
C. Tetani infx
132
Blood type of patients with Acquired B phenomenon
A1
133
Mechanism of Acquired B phenomenon
Deactylation of GalNAc
134
Resolution of Acquired B phenomenon can be done using: (5)
Acetic Anhydride
Acidified Anti-B
Monoclonal Anti-B
Secretor status
Autocontrol
135
Most common source of ABO discrepancies
Technical errors
136
In cases of emergency situation:
O Rh Neg pRBCS
137
Group I discrepancies are present in:
Reverse grouping
138
Causes of Group I discrepancies (Newborn, elderly, hypogammaglobinemia,Agammaglobulinemia,ABO subgroups)
Weakly reacting/Missing antibodies
139
Resolution for Group I discrepancy
Incubate px serum with rgt at ROOM TEMP for 15-30minutes or add more plasma or serum to the test
140
If after incubation at room temp, G-I discrepancy is not resolve:
Incubate at ref temp (4 degrees Celcius) for 15 minutes
141
Done after incubation at ref temp. in G-1 and 2 discrepancy
Include O cell control and autocontrol
142
Additional method in resolving G-1 discrepancy
Determine Px age and history
143
Group II discrepancy problem:
Forward grouping
144
Probable cause in Group II discrepancy (ABO subgroups, weakened/depression of A or B antigen, Pseudoantigen)
Weakly reacting or missing Antigen
145
Additional method in resolving G-2 discrepancy
Enzyme Treatment
146
Rare Group II discrepancies
BGSS (Blood group specific soluble substances) - neutralize the reagent with Anti-A and Anti-B
Antibodies to low incidence antigens - has contaminating antibody
Chimerism - True and artificial chimerism
147
Group III discrepancy problem:
Forward and reverse grouping
148
Probable cause of Group III discrepancy (inc. globulin, inc. fibrinogen, plasma expanders, Wharton's jelly)
Plasma or protein abnormalities
149
Resolution for group III discrepancy
Microscopic exam,
Saline replacement
Wash saline 3x (6-8 if cord cells)
150
Group IV discrepancy problem
Forward and reverse grouping (Miscellaneous)
151
Causes of Group IV discrepancies (5)
Cold reactive autoAb
Unexpected ABO isoagglutinins and non-ABO antibodies
More than one ABO group RBCs
Polyagglutination
152
Used to disperse IgM-related Agglutinations
0.01M DTT (Dithietreitol)
153
Rare Group IV discrepancies
Antibody to acriflavine
Cis-Ab phenotype
154
ISBT #004
Rh Blood Group System
155
RHD and RHCE genes are proposed by:
Tippett
156
Chromosome location of Rh blood group system
1
157
RHAG gene is located at:
16
158
Involved the presence of 3 separate genes D, C, and E and their alleles c and e
Fisher-Race Nomenclature
159
Based on the notion that a single locus on a gene carries entire Rh system
Wiener Nomenclature
160
A system that assigns a number to each antigen in order of its discovery or recognized relationship to the Rh system
Rosenfield (Alpha-numeric terminology)
161
A system that adopted a 6-digit number for each authenticated antigen
International Society of Blood transfusion
162
First 3 numbers in ISBT represent:
System
163
Last 3 numbers in ISBT represent:
Antigenic specificity
164
Rh Subtype common in blacks
Weak D
165
Polypeptides in nature and reside in transmembrane proteins
Not soluble and not expressed on the tissues
Well-developed at birth and can easily cause HDFN
Rh antigen
166
Immunogenicity (most to least)
D>c>E>C>e
167
Causes of Weak D reaction
Positional D
Genetic Weak D
Partial D/D mosaic
168
Major problem in C in trans to Rh D that causes a weak reaction with anti-D antisera
Steric hindrance
169
As DONOR: partial D individual is considered as
Rh positive
170
As RECIPIENT: partial D individual is considered as:
Rh negative
171
C and E are not expressed on RBCs causing increased D antigens
Rh deletion (D--/D--)
172
No antigen expression on RBCs which is caused by abnormalities in transmembrane proteins
Rh Null (---/---)
173
Rh null causes ____ on RBCs
Stomatocytosis
174
Rh null characterize by mutation in RHAG gene with normal RhD and RhCE genes
Regulator Type
175
Rh null characterize by mutation in RhCE gene,deleted RhD gene,with normal RHAG gene
Amorphic type
