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Blood Bank > Mixed Flash Cards > Flashcards

Mixed Flash Cards

1
Q

5 types of Acute Immunologic Transfusion Reactions

A 
Hemolytic, Intravascular
Febrile
Allergic
Anaphylactic 
TRALI (Transfusion Related Acute Lung Injury)
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2
Q

Cause of Hemolytic, Intravascular transfusion reaction

A

Immediate destruction of donor RBCs by recipient Ab

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3
Q

Clinical Signs of Hemolytic, Intravascular transfusion rxn

A

Fever; chills; shock; renal failure; DIC; pain in the chest, back and flank

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4
Q

Most serious Acute Immunologic Transfusion Reaction

A

Hemolytic, intravascular

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5
Q

Usually due to transfusion of ABO-incompatible blood

A

Hemolytic, intravascular

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6
Q

Laboratory findings in Hemolytic Intravascular Transfusion Reaction

A

HGB in urine & serum
Mixed-field DAT
decrease haptoglobin, hgb, hct

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7
Q

Cause of febrile transfusion reaction

A

Anti-leukocytes Abs or cytokines

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8
Q

Medicine that can be use to premedicate febrile transfusion reaction

A

Antipyretics (aspirin, acetaminophen)

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9
Q

Clinical Signs of Febrile Transfusion Reaction

A

Increase greater than or equal to 1 degree Celsius during or after transfusion

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10
Q

Cause of Allergic Acute Immunologic Transfusion Reaction

A

foreign plasma protein

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11
Q

Treatment for Allergic Transfusion Reaction

A

Antihistamines

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12
Q

Clinical Signs of Allergic Transfusion Reaction

A

Hives(urticaria), wheezing

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13
Q

Cause of Anaphylactic Transfusion Reaction

A

Anti-IgA in IgA deficient recipient

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14
Q

Rare but dangerous kind of transfusion reaction

A

Anaphylactic

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15
Q

Clinical Signs of Anaphylactic transfusion reaction

A

Pulmonary edema, bronchospams

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16
Q

Treatment for Anaphylactic transfusion reaction

A

Epinephrine

Transfuse with washed products

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17
Q

Most common cause of tf-related deaths in U.S

A

TRALI (transfusion related acute lung injury)

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18
Q

Cause of TRALI

A

Unknown. Possible donor Abs to WBC Ags

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19
Q

Transfusion reaction that recommended the use of plasma from female donors to reduce this transfusion reaction fatalities

A

TRALI

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20
Q

Clinical signs of TRALI

A

Fever; chills; coughing; respiratory distress; fluid in the lungs; decrease BP within 6 hrs of tf.

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21
Q

4 types of Acute Nonimmunologic Transfusion reactions

A

Sepsis
TACO (Transfusion-associated circulatory overload)
Nonimmune hemolysis
Hypothermia

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22
Q

Cause of TACO

A

too large a volume or too rapid rate of infusion

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23
Q

Cause of Hypothermia (Acute nonimmunologic tf rxn)

A

Rapid infusion of large amounts of cold blood

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24
Q

Cause of Nonimmune hemolysis (Acute nonimmunologic tf rxn)

A

Destruction of RBCs due to extremes of temp, addition of meds to unit

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25
Q

3 types of Delayed Immunologic Transfusion Reactions

A

Hemolytic, extravascular
Alloimmunization
TA-GVHD (Transfusion associated - Graft vs Host disease)

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26
Q

Type of Delayed nonimmunologic Transfusion reaction

A

Iron overload

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27
Q

Cause of Hemolytic, Extravascular ( Delayed transfusion reaction)

A

Donor RBCs sensitized by recipient IgG ab & removed from circulation

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28
Q

Laboratory findings in Hemolytic, Extravascular ( delayed tf rxn)

A

Increased Bili; Mixed-field DAT; decreased Haptoglobin; decrease Hgb & Hct; (+) antibody screening

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29
Q

Kidd Ab usually cause this type of delayed transfusion reaction

A

Hemolytic, extravascular

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30
Q

Cause of alloimmunization (delayed transfusion reaction)

A

Development of abs to foreign RBCs, WBCs, plt, plasma protein ff transfusion

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31
Q

Cause of TA-GVHD

A

Viable T lymphs in donor blood attack the recipient

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32
Q

Cause of Iron Overload (delayed nonimmunologic tf rxn)

A

Build up of iron in body

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33
Q

Composition of RhIG (Rh immune globulin)

A

Anti-D derived from pools of human plasma

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34
Q

RhIG means

A

Rh immune globulin

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35
Q

Purpose of RhIG

A

prevent immunization to D

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36
Q

Ag are on the

A

cells

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37
Q

Ab are on the

A

serum

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38
Q

Substance recognized as foreign and react with a complementary antibody or cell receptor

A

Antigens

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39
Q

Immunoglobulin developed in response to the presence of antigens

A

Antibodies

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40
Q

Type of antibody that is from another species

A

Hetero/Xenoantibodies

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41
Q

Type of antibody that is from individuals of the same species

A

Alloantibodies

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42
Q

Body’s own antigens

A

Autoantibodies

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43
Q

Discoved by Karl Landsteiner in 1900s

A

ABO Blood Group

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44
Q

Most significant for transfusion practice

A

ABO Blood Group

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45
Q

1st blood group discovered

A

ABO Blood Group

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46
Q

Landsteiner’s Rules for the ABO Blood Group

A
  1. A person doesn’t have Ab to his own Ag

2. Each person has Ab to the Ag he lacks

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47
Q

Develops as early as the 37th day of fetal life

A

ABO Ag

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48
Q

expression is fully develope by 2 to 4 years of age and remains constant for life

A

ABO Ag

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49
Q

ABO Ag are controlled by

A

Secretor (Se) gene

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50
Q

Inherited Homozygous (SeSe) or Heterozygous (Sese) genotype

A

Secretors

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51
Q

Inherited the sese genotype

A

Non-secretors (no ABH substance in secretions)

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52
Q

What are the ABO Abs

A

Anti-A
Anti-B
Anti-A,B

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53
Q

Absent at birth and start to appear around 3-6 months

A

ABO Abs

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54
Q

Developed shortly after birth ff exposure to ABO-like Ags in the environment

A

Naturally occuring Abs

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55
Q

Optimal temp for reactivity of IgM

A

24 deg celsius or lower

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56
Q

Develop in response to exposure to ABO-incompatible RBCs

A

Immune type Ab

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57
Q

Antibody that can cross the placenta

A

IgG

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58
Q

Structure of IgG

A

monomer

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59
Q

Number of Ag-binding sites of IgG

A

2

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60
Q

Optimal temp for reactivity of IgG

A

37 deg celsius

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61
Q

Ab that reacts best in IAT

A

IgG

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62
Q

Ab that can cause HDFN

A

IgG

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63
Q

Structure of IgM

A

Pentamer

64
Q

Number of Ag-binding sites of IgM

A

10

65
Q

Detection of Ags on patient’s RBCs with known antisera

A

Forward Blood Group Typing

66
Q

Detection of ABO Abs in serum of patients with Known RBCs

A

Reverse Blood Group Typing

67
Q

Type of Ag found in Blood type A person

A

A

68
Q

Type of Ag found in Blood type B person

A

B

69
Q

Type of Ag found in Blood type O person

A

H

70
Q

Type of Ag found in Blood type AB person

A

A, B

71
Q

Type of Ab found in Blood type A person

A

Anti-B

72
Q

Type of Ab found in Blood type B person

A

Anti-A

73
Q

Type of Ab found in Blood type O person

A

Anti-A, Anti-B

74
Q

Type of Ab found in Blood type AB person

A

None

75
Q

Cause by decreased amounts of Ag on RBCs

A

ABO subgroups

76
Q

2 main A subgroups

A

A1, A2

77
Q

Anti-A1 lectin

A

Dolichos Biflorus

78
Q

6 types of Weak A Subgroups

A

A3, A(x), A (end), A(m), A(y), A(el)

79
Q

Shows mixed field agglutination with Anti-A or anti-A, B reagents

A

A3 (Weak A Subgroup)

80
Q

RBCs are not agglutinated by Anti-A rgt but agglutinate with most examples of Anti-A,B

A

Ax (Weak A Subgroup)

81
Q

Also shows mixed field agglutination with Anti-A and anti-A,B but only a = 10% of RBCs agglutinate

A

A(end) (Weak A Subgroup)

82
Q

RBCs are not agglutinated or only weakly agglutinated by anti-A or anti-A,B

A

A(m) (Weak A Subgroup)

83
Q

RBCs are not agglutinated by anti-A or anti-A,B; with detectable amount of A glycosyltransferase

A

A(y) (Weak A Subgroup)

84
Q

Very rare and less frequent ABO subgroup

A

B Subgroups

85
Q

Anti-B lectin

A

Griffonia simpliciforia (prev. Banderiae simpliciforia)

86
Q

4 types of B Subgroups

A

B3, Bx, Bm, B(el)

87
Q

mixed field agglutination with anti-B and anti-A,B

A

B3 (Weak B Subgroup)

88
Q

weak agglutination with anti-B and anti-A,B

A

Bx (Weak B Subgroup)

89
Q

unagglutinated by anti-B or anti-A,B; B glycosyltransferase is present

A

Bm (Weak B subgroup)

90
Q

RBCs are not agglutinated by anti-A or anti-A,B; no detectable amount of A glycosyltransferase

A

A(el) (Weak A Subgroup)

91
Q

unagglutinated by anti-B or anti-A,B; no B glycosyltransferase is present

A

B(el) (Weak B subgroup)

92
Q

Lacks the H gene (hh genotype)

A

Bombay phenotype

93
Q

Absence of A,B and H Ag

A

Bombay phenotype

94
Q

Can only be transfused with blood from another Bombay

A

Bombay phenotype

95
Q

No reaction to Anti-H lectin

A

Bombay phenotype

96
Q

Anti-H lectin

A

Ulex europaeus

97
Q

Type of ABO discrepancies that is due to weakly or missing Abs

A

Group I

98
Q

Anti-A = 0
Anti-B = 0
A1 cells = 0
B cells = 0

What type of ABO discrepancies is this?

A

Group I

99
Q

Type of ABO discrepancies that is due to weakly reacting or missing Ag

A

Group II

100
Q

Associated with diseases of the digestive tract (e.g., cancer of colon)

A

Acquired B phenomenon

101
Q

Anti-A = 4+
Anti-B = 2+
A1 cells = 0
B cells = 4+

What type of ABO discrepancies is this?

A

Group II

Acquired B phenomenon

102
Q

Type of ABO discrepancies that is due to protein or plasma abnormalities resulting in ROULEAUX formation

A

Group III

103
Q

Type of ABO discrepancies that is due to miscellaneous problems

A

Group IV

104
Q

2nd most important blood groups system in terms of transfusion

A

Rh blood group

105
Q

blood group that is primarily the cause of HDFN and erythroblastosis fetalis

A

Rh blood group

106
Q

Well developed at birth causing HDN (if baby has Rh AG that mom lacks)

A

Rh antigen

107
Q

not soluble and not expressed on tissues

A

Rh antigen

108
Q

3 nomenclature of Rh antigen

A

fisher-race or DCE terminology
wiener or Rh-Hr terminology
Rosenfield and Coworkers or Alpha/Numeric Terminology

109
Q

Reacts optimally at 37 deg celsius or after antiglobulin testing

A

Rh antibodies

110
Q

Detects for the presence of D Ag on px’s RBC

A

Rh typing

111
Q

reagent used for Rh typing

A

anti-D and BSA (Bovine serum albumin; used as control)

112
Q

weakened form of the D antigen

A

Weak D (Du phenotype)

113
Q

done to confirm negative Rh typing results

A

Weak D testing

114
Q

Form of Indirect Antiglobulin Test

A

Weak D testing

115
Q

Spx used for Weak D testing

A

(-) result from the Rh typing

116
Q

Rgt for Weak D testing

A

AHG (Anti-human globulin)

117
Q

Not intrinsic to RBC; IgM in nature; Not clinically significant

A

Lewis Blood group

118
Q

Blood group Ag that deteriorates rapidly on storage

A

P1

119
Q

Ab that is associated with PCH (Paroxysmal Cold Hemoglobinuria)

A

Anti-P

120
Q

AKA Auto-Anti-P or Donath-Landsteiner Ab

A

Anti-P

121
Q

Antibody that is IgG Biphasic Hemolysin

A

Anti-P

122
Q

Binds complement to red cells at COLDER TEMPERATURE; Hemolyzes red cells at 37 deg celsius

A

IgG Biphasic Hemolysin

123
Q

Produced by individuals with p phenotype

A

Anti-Tj(a)

124
Q

Antibodies that is present in spontaneous abortions in early abortions

A

Anti-Tj(a)

125
Q

Associated with Infectious mononucleosis

A

Anti-i

126
Q

Associated with cold agglutinin disease & Mycoplasma pneumoniae

A

Anti-I

127
Q

Most common Ab seen in BB after ABO & Rh

A

Anti-K

128
Q

Ag that resist infection by P.vivax (humans) and P.knowlesi (monkeys(

A

Fy (a-b-)

129
Q

Abs that is notorious in BB due to its association to delayed hemolytic transfusion rxn

A

Kidd Abs

130
Q

Blood to given to the recipient came from the recipient himself

A

Autologous donation

131
Q

Hgb & Hct for Autologous donation should be at least

A 
Hgb = at least 11 g/dL
Hct = 33 %
132
Q

Detects unexpected Abs against RBC Ag

A

Antibody Screening

133
Q

Prevents coagulation by chelating calcium

A

Citrate

134
Q

Supports ATP generation

A

Dextrose (glucose)

135
Q

Substrate for ATP Synthesis

A

Adenine

136
Q

prevents excessive fall in pH during storage

A

Sodium biphosphate

137
Q

Shelf life for ACD

A

21 days

138
Q

Shelf life for CPD

A

21 days

139
Q

Shelf life for CPDA-1

A

35 days

140
Q

Shelf life for Adsol

A

42 days

141
Q

Used to salvage rare or type O units up to 3 days beyond expiration

A

PIPA (Phosphate-Inosine-Pyruvate-Adenine)

142
Q

Negative result effectively rules out presence of Autoantibody

A

Autocontrol

143
Q

Patient Serum + Donor Red Cells

A

Major Crossmatching

144
Q

Patient Red Cells + Donor Serum

A

Minor Crossmatching

145
Q

3 phases of Manual Crossmatching

A
  1. Immediate spin
  2. Incubation at 37 deg celsius
  3. AHG phase
146
Q

Hydatid cyst fluid
Pigeon droppings
Turtledove’s egg whites

A

Anti-P1

147
Q

Plasma or serum, secretor saliva

A

Anti-Lewis

148
Q

Removal of abs from SERUM

A

Adsorption

149
Q

Removal of abs bound to RED BLOOD CELLS

A

Elution

150
Q

Urine, guinea pig urine

A

Anti- Sd^a

151
Q

Rejuvination of a unit of RBC is used to

A

Restore 2,3-DPG, ATP to normal levels

152
Q

pH of platelets should be maintained at

A

6.2 or above

153
Q

blood component indicated for fibrinogen deficiencies

A

Cryoprecipitate AHF

154
Q

inhibits proliferation of T lymphocytes

A

Irradiation

155
Q

blood component that prevent HLA alloimmunization

A

PRBC-LR

Blood Bank (1 decks)

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