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BLOOD BANKING > Blood Banking > Flashcards

Blood Banking Flashcards

1
Q

First recorded blood transfusion performed.

A

Pope Innocent VIII

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2
Q

Performed blood transfusion to Pope Innocent

A

Jiacomo de San Genesio

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3
Q

Discovered circulatory system

A

William Harvey

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4
Q

Animal to animal transfusion

A

Richard Lower

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5
Q

Animal to human transfusion

A

Jean Baptiste Denis

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6
Q

First to work on blood transfusion and blood preservation technique

A

Charles Drew

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7
Q

Sodium phosphate (Na3PO4)

A

Braxton Hicks

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8
Q

Sodium Citrate

A

Albert hustin

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9
Q

Determined minimum non-toxic amount of citrate needed to prevent coagulation

A

Richard Lewisohn

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10
Q

Citrate dextrose

A

Rous and Turner

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11
Q

Acid Citrate Dextrose

A

Loutit and mollison *

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12
Q

Utilized glycerol to extend lifespan by 10 years

A

Audrey Smith

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13
Q

Citrate phosphate dextrose as standard

A

Gibson

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14
Q

First vein-vein transfusion using special cannulas

A

Edward Lindemann

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15
Q

Syringe valve apparatus

A

Unger

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16
Q

ABO group

A

Karl Landsteiner

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17
Q

Fourth ABO blood group: AB

A

Alfred von Decastello and Adriano Sturli

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18
Q

MN and P system

A

Karl Landsteiner and Philip levine

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19
Q

RH blood group

A

Karl landsteiner and alexander weiner

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20
Q

World first blood bank in Chicago under the leadership of Dr. Bernard Fantus

A

Cook County hospital

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21
Q

First community-based blood center

A

Erwin Memorial Blood Bank

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22
Q

Book authored by Karl Landsteiner

A

Book authored by Karl Landsteiner

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23
Q

Discovered the ABO blood group system

A

Karl Landsteiner

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24
Q

Remains the leading cause of death in hemolytic transfusion reaction fatalities (FDA)

A

Transfusion of wrong ABO group

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25
Q

According to FDA, the most common cause of death is TRALI or NCPE

A

Fiscal year 2009

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26
Q

Basic sugar precursors in ABO blood group

A

Paragloboside/Glycan

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27
Q

Amorphic. It does NOT code for any enzymes and is merely representative of A and B gene absence

A

O gene

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28
Q

Higher concentrations of transferases (810,000 to 1,170,000 Ag sites on an A1 adult RBC)

A

A gene

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29
Q

610,000 to 830,000 Ag sites

A

B gene

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30
Q

B enzyme compete more efficiently for H substance than the A enzyme A-600,000 sites B-720,000 sites

A

A and B gene

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31
Q

Described the theory for the inheritance of the ABO blood group

A

Bernstein

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32
Q

An individual inherits one ABO gene from each parent and these two genes determine which ABO antigen is present in RBC

A

Co-dominance

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33
Q

Inheritance pattern of ABO

A

Autosomal

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34
Q

A and B blood group are

A

Codominant

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35
Q

Amorph, as no detectable antigen is produced in response to the inheritance of this gene

A

O gene

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36
Q

Group O phenotype
In heritance of two genes that are non-functional

A

Autosomal recessive

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37
Q

Possible genotype for O phenotype

A

OO

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38
Q

Possible genotype for A phenotype

A

A1A1, A1A2,A1,O

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39
Q

Possible genotype for A2 phenotype

A

A2A2, A2O

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40
Q

Posible genotype for B phenotype

A

BB,BO

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41
Q

Possible genotype for A1B phenotype

A

A1B

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42
Q

Posible genotype for A2B phenotype

A

A2B

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43
Q

enzyme coded by H gene with L-fucose immunodominant sugar

A

Alpha-2-L-Fucosyltransferase

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44
Q

Enzyme coded by A gene with GalNAc immunodominant sugar

A

Alpha-3-N-acetylgalactosaminyltransferase

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45
Q

Enzyme coded by B gene with D-galactose as immunodominant sugar

A

Alpha-3-D-Galactosaminyltransferase

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46
Q

Composition of paragloboside

A

Glucose, Galactose, GalNAc, Galactose

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47
Q

Jansky Nomenclature (O, A ,B,AB)

A

I,II,III,IV

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48
Q

Moss nomenclature (O,A,B,AB)

A

IV,III,II,I

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49
Q

Antigen frequency of ABO

A

O>A>B>AB

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50
Q

ABO antigen formation

A

37th Day of fetal Life

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51
Q

Full expression of ABO antigen which remain constant for life

A

2-4 years

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52
Q

Location of ABO antigens in the body

A

RBC, endothelial cells, platelets, lymphocytes, epithelial cells and secretion

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53
Q

ABO antigen forms on RBC

A

Glycoproteins, glycolipids, or glycosphingolipids

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54
Q

ABO antigens are synthesized on type 2 Precursor chains refer to a ____ linkage

A

Beta 1-4 linkage

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55
Q

ABO antigen type present in the secretion

A

Glycoproteins

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56
Q

ABO antigens are synthesiszed on type 1 precursor chains refer to a ____ linkage

A

Beta 1-3 linkage

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57
Q

ABH Substances can be found in:

A

Digestive juices, Urine, Bile, Saliva, Tears,Amniotic fluid, Milk, Pathologic fluids

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58
Q

Excessive ABH substance in secretion can be oberved in: (PIC)

A

Pseudomembranous ovarian cyst, Intestinal obstruction, Carcioma of stomach and pancreas

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59
Q

Determination of secretor status (Ag+ Saliva+Agcells=No agglutination)

A

Hemagluttination Inhibition Assay with Saliva

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60
Q

H1 and H2 forms of H antigen

A

Unbranched Straight Chain

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61
Q

H3 and H4 forms of H antigen

A

Complex Branched Chains

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62
Q

Reactivity of Anti H or Anti-H lectin with ABO blood groups

A

O>A2>B>A2B>A1>A1B

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63
Q

Reacts with Anti-A1 and Anti-A

A

A1

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64
Q

Reacts with Anti-A only

A

A2

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65
Q

MF with Anti-A1 and anti-AB

A

A3

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66
Q

Reacts only with Anti-AB, but no reaction to Anti-A

A

Ax

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67
Q

MF reaction with Anti-A and Anti-AB, but on few agglutination (<10%)

A

Aend

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68
Q

Weak/No reaction with anti-A and Anti-AB

A

Am

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69
Q

No reaction with Anti-A and anti-AB

A

Ael

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70
Q

No reaction with Anti-A and anti-AB, but only present in siblings

A

Ay

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71
Q

Small agglutinates within predominantly unagglutinated cells

A

Mixed field

72
Q

Method used to confirm the presence of Am, Ay, and Ael antigens

A

Adsoprtion and Elution of anti-A

73
Q

More antigenic sites for A and less for H

A

A1

74
Q

Less antigenic sites for A and More for H

A

A2

75
Q

Predominantly Aa and Ab and uncoverted H3 and H4 antigenic sites

A

A2 RBCs

76
Q

Aa, Ab,Ac,Ad determinants with no unconverted H3 and H4 antigen sites

A

A1 RBCS

77
Q

Reacts with Anti-B and Anti- AB

A

B subgroup

78
Q

MF reaction with anti-B and anti-AB (Most frequent B subtype)

A

B3

79
Q

Weak reaction with anti-B and Anti-AB

A

Bx

80
Q

No/Weak reaction with Anti-B and Anti-AB

A

Bm

81
Q

Bm subtype can be converted to B if incubated with:

A

Uracil diphosphate

82
Q

No reaction with Anti-B and anti-AB (Extremely rare phenotype)

A

Bel

83
Q

Homozygous inheritance of the h gene results in the inability to form H antigen

A

Bombay Phenotype

84
Q

First reported the Bombay Phenotype

A

Dr Y.M Bhende in 1952 in Mumbai, India

85
Q

Genotype of Bombay phenotype

A

hh genotype non-secretor

86
Q

The inheritance pattern of Bombay phenotype

A

Autosomal recessive

87
Q

Mutation in FUT-1

A

Silenced H gene

88
Q

Mutation in FUT-2

A

Silenced Se gene

89
Q

Serum of Bombay phenotype

A

Anti-A, Anti-B, Anti-AB, Anti-H

90
Q

Bombay individuals are phenotyped as:

A

Oh

91
Q

Bombay phenotype forward and reverse typing

A

No Agglutination at Anti-H and with agglutination in O cells

92
Q

Absent or only trace amount of A, B, H antigens on RBCs with normal expression in the secretion

A

Para-Bombay phenotype

93
Q

genotype of para-bombay phenotype

A

hh, secretor

94
Q

Para-Bombay phenotype is caused by:

A

Mutated FUT1 gene w/ or w/o active FUT2 or silenced FUT1 gene with an active FUT2 gene

95
Q

Individuals normally produce antibodies directed against the A and/or B babsent from their RBC

A

Naturally Occuring antibodies

96
Q

ABO antibodies are produced at:

A

Birth

97
Q

When are ABO antibodies starts to be detected

A

3-6 months of age (4-6 mos.)

98
Q

Predominant form of ABO antibody

A

Predominantly IgM (IgM, IgG, or IgA)

99
Q

ABO antibodies react at:

A

Room temperature (20-24) or below

100
Q

ABO antibodies activate compliment at:

A

37 degree celcius

101
Q

IgG ABO antibody which is present only on O individuals

A

Anti-A,B (not a combination of A and B but is only a cross reacting antibody)

102
Q

Primarily IgM and IgG may be found on O individuals

A

Anti-A and Anti-B

103
Q

Plants or seed extracts that agglutinate human cells with some degree of specificity

A

Lectins

104
Q

Anti-A1 lectin

A

Dolichos biflorus

105
Q

Anti-B lectin

A

Banderia simplicifolia (Griffona Simpliforia)

106
Q

Anti-H lectin

A

Ulex Europeus

107
Q

Anti-N lectin

A

Vacia Graminea

108
Q

Anti-M lectin

A

Iberis amara

109
Q

Anti-T,Th

A

Arachis hypogenea

110
Q

Anti-Tn

A

Salvia Sclarea

111
Q

Using Antisera (Anti-A, Anti-B) to detect antigens on patient’s RBCs

A

Forward grouping/Direct/Front/Cell Typing

112
Q

Used as preservative in Blood typing

A

Sodium azide and Formalin

113
Q

Ensure the reactivity of the antisera
Control cell should be weakly reactive for the antigen being tested.

A

Positive control

114
Q

Ensure the specificity of the antisera

A

Negative control

115
Q

Using reagent RBCs to detect ABO antibodies in the patient’s serum

A

Reverse typing/Indirect/Back/ Serum typing

116
Q

Universal RBC donor

A

Type O

117
Q

Universal Plasma donor

A

Type AB

118
Q

Universal plasma recipient

A

Type O

119
Q

Universal RBC recipient

A

Type AB

120
Q

One SOLID agglutinate

A

4+

121
Q

several LARGE agglutinates with CLEAR background

A

3+

122
Q

MEDIUM agglutinates, CLEAR background

A

2+

123
Q

SMALL agglutinates,TURBID background

A

1+

124
Q

TINY agglutinates, Turbid background

A

W+

125
Q

No agglutination or hemolysis

A

0

126
Q

Partial/complete hemolysis

A

Positive reaction

127
Q

Hemolysis-Presence of free HB in serum (see notes for more info)

A

H grading 10=score

128
Q

Nonspecific aggregation like a stack of coins

A

Rouleaux

129
Q

Conditions that cause weaker reactions

A

Leukemia
Chromosome Translocation
Hemolytic diseases
Hodgkin’s disease
Hypogammaglobulinemia (CLL)/ Immunodeficiency

130
Q

Acquired A phenomenon is caused by: (PT)

A

Proteus mirabilis
Tn activation

131
Q

Acquired B phenomenon is caused by : (EPICC)

A

E.coli(086)
Proteus Vulgaris
Intestinal obstruction
Carcinoma of Colon and rectum
C. Tetani infx

132
Q

Blood type of patients with Acquired B phenomenon

A

A1

133
Q

Mechanism of Acquired B phenomenon

A

Deactylation of GalNAc

134
Q

Resolution of Acquired B phenomenon can be done using: (5)

A

Acetic Anhydride
Acidified Anti-B
Monoclonal Anti-B
Secretor status
Autocontrol

135
Q

Most common source of ABO discrepancies

A

Technical errors

136
Q

In cases of emergency situation:

A

O Rh Neg pRBCS

137
Q

Group I discrepancies are present in:

A

Reverse grouping

138
Q

Causes of Group I discrepancies (Newborn, elderly, hypogammaglobinemia,Agammaglobulinemia,ABO subgroups)

A

Weakly reacting/Missing antibodies

139
Q

Resolution for Group I discrepancy

A

Incubate px serum with rgt at ROOM TEMP for 15-30minutes or add more plasma or serum to the test

140
Q

If after incubation at room temp, G-I discrepancy is not resolve:

A

Incubate at ref temp (4 degrees Celcius) for 15 minutes

141
Q

Done after incubation at ref temp. in G-1 and 2 discrepancy

A

Include O cell control and autocontrol

142
Q

Additional method in resolving G-1 discrepancy

A

Determine Px age and history

143
Q

Group II discrepancy problem:

A

Forward grouping

144
Q

Probable cause in Group II discrepancy (ABO subgroups, weakened/depression of A or B antigen, Pseudoantigen)

A

Weakly reacting or missing Antigen

145
Q

Additional method in resolving G-2 discrepancy

A

Enzyme Treatment

146
Q

Rare Group II discrepancies

A

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
Q

Group III discrepancy problem:

A

Forward and reverse grouping

148
Q

Probable cause of Group III discrepancy (inc. globulin, inc. fibrinogen, plasma expanders, Wharton’s jelly)

A

Plasma or protein abnormalities

149
Q

Resolution for group III discrepancy

A

Microscopic exam,
Saline replacement
Wash saline 3x (6-8 if cord cells)

150
Q

Group IV discrepancy problem

A

Forward and reverse grouping (Miscellaneous)

151
Q

Causes of Group IV discrepancies (5)

A

Cold reactive autoAb
Unexpected ABO isoagglutinins and non-ABO antibodies
More than one ABO group RBCs
Polyagglutination

152
Q

Used to disperse IgM-related Agglutinations

A

0.01M DTT (Dithietreitol)

153
Q

Rare Group IV discrepancies

A

Antibody to acriflavine
Cis-Ab phenotype

154
Q

ISBT #004

A

Rh Blood Group System

155
Q

RHD and RHCE genes are proposed by:

A

Tippett

156
Q

Chromosome location of Rh blood group system

A

1

157
Q

RHAG gene is located at:

A

16

158
Q

Involved the presence of 3 separate genes D, C, and E and their alleles c and e

A

Fisher-Race Nomenclature

159
Q

Based on the notion that a single locus on a gene carries entire Rh system

A

Wiener Nomenclature

160
Q

A system that assigns a number to each antigen in order of its discovery or recognized relationship to the Rh system

A

Rosenfield (Alpha-numeric terminology)

161
Q

A system that adopted a 6-digit number for each authenticated antigen

A

International Society of Blood transfusion

162
Q

First 3 numbers in ISBT represent:

A

System

163
Q

Last 3 numbers in ISBT represent:

A

Antigenic specificity

164
Q

Rh Subtype common in blacks

A

Weak D

165
Q

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

A

Rh antigen

166
Q

Immunogenicity (most to least)

A

D>c>E>C>e

167
Q

Causes of Weak D reaction

A

Positional D
Genetic Weak D
Partial D/D mosaic

168
Q

Major problem in C in trans to Rh D that causes a weak reaction with anti-D antisera

A

Steric hindrance

169
Q

As DONOR: partial D individual is considered as

A

Rh positive

170
Q

As RECIPIENT: partial D individual is considered as:

A

Rh negative

171
Q

C and E are not expressed on RBCs causing increased D antigens

A

Rh deletion (D–/D–)

172
Q

No antigen expression on RBCs which is caused by abnormalities in transmembrane proteins

A

Rh Null (—/—)

173
Q

Rh null causes ____ on RBCs

A

Stomatocytosis

174
Q

Rh null characterize by mutation in RHAG gene with normal RhD and RhCE genes

A

Regulator Type

175
Q

Rh null characterize by mutation in RhCE gene,deleted RhD gene,with normal RHAG gene

A

Amorphic type

BLOOD BANKING (5 decks)

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