Mixed Flash Cards
(155 cards)
1
Q
5 types of Acute Immunologic Transfusion Reactions
A
Hemolytic, Intravascular Febrile Allergic Anaphylactic TRALI (Transfusion Related Acute Lung Injury)
2
Q
Cause of Hemolytic, Intravascular transfusion reaction
A
Immediate destruction of donor RBCs by recipient Ab
3
Q
Clinical Signs of Hemolytic, Intravascular transfusion rxn
A
Fever; chills; shock; renal failure; DIC; pain in the chest, back and flank
4
Q
Most serious Acute Immunologic Transfusion Reaction
A
Hemolytic, intravascular
5
Q
Usually due to transfusion of ABO-incompatible blood
A
Hemolytic, intravascular
6
Q
Laboratory findings in Hemolytic Intravascular Transfusion Reaction
A
HGB in urine & serum
Mixed-field DAT
decrease haptoglobin, hgb, hct
7
Q
Cause of febrile transfusion reaction
A
Anti-leukocytes Abs or cytokines
8
Q
Medicine that can be use to premedicate febrile transfusion reaction
A
Antipyretics (aspirin, acetaminophen)
9
Q
Clinical Signs of Febrile Transfusion Reaction
A
Increase greater than or equal to 1 degree Celsius during or after transfusion
10
Q
Cause of Allergic Acute Immunologic Transfusion Reaction
A
foreign plasma protein
11
Q
Treatment for Allergic Transfusion Reaction
A
Antihistamines
12
Q
Clinical Signs of Allergic Transfusion Reaction
A
Hives(urticaria), wheezing
13
Q
Cause of Anaphylactic Transfusion Reaction
A
Anti-IgA in IgA deficient recipient
14
Q
Rare but dangerous kind of transfusion reaction
A
Anaphylactic
15
Q
Clinical Signs of Anaphylactic transfusion reaction
A
Pulmonary edema, bronchospams
16
Q
Treatment for Anaphylactic transfusion reaction
A
Epinephrine
Transfuse with washed products
17
Q
Most common cause of tf-related deaths in U.S
A
TRALI (transfusion related acute lung injury)
18
Q
Cause of TRALI
A
Unknown. Possible donor Abs to WBC Ags
19
Q
Transfusion reaction that recommended the use of plasma from female donors to reduce this transfusion reaction fatalities
A
TRALI
20
Q
Clinical signs of TRALI
A
Fever; chills; coughing; respiratory distress; fluid in the lungs; decrease BP within 6 hrs of tf.
21
Q
4 types of Acute Nonimmunologic Transfusion reactions
A
Sepsis
TACO (Transfusion-associated circulatory overload)
Nonimmune hemolysis
Hypothermia
22
Q
Cause of TACO
A
too large a volume or too rapid rate of infusion
23
Q
Cause of Hypothermia (Acute nonimmunologic tf rxn)
A
Rapid infusion of large amounts of cold blood
24
Q
Cause of Nonimmune hemolysis (Acute nonimmunologic tf rxn)
A
Destruction of RBCs due to extremes of temp, addition of meds to unit
25
3 types of Delayed Immunologic Transfusion Reactions
Hemolytic, extravascular
Alloimmunization
TA-GVHD (Transfusion associated - Graft vs Host disease)
26
Type of Delayed nonimmunologic Transfusion reaction
Iron overload
27
Cause of Hemolytic, Extravascular ( Delayed transfusion reaction)
Donor RBCs sensitized by recipient IgG ab & removed from circulation
28
Laboratory findings in Hemolytic, Extravascular ( delayed tf rxn)
Increased Bili; Mixed-field DAT; decreased Haptoglobin; decrease Hgb & Hct; (+) antibody screening
29
Kidd Ab usually cause this type of delayed transfusion reaction
Hemolytic, extravascular
30
Cause of alloimmunization (delayed transfusion reaction)
Development of abs to foreign RBCs, WBCs, plt, plasma protein ff transfusion
31
Cause of TA-GVHD
Viable T lymphs in donor blood attack the recipient
32
Cause of Iron Overload (delayed nonimmunologic tf rxn)
Build up of iron in body
33
Composition of RhIG (Rh immune globulin)
Anti-D derived from pools of human plasma
34
RhIG means
Rh immune globulin
35
Purpose of RhIG
prevent immunization to D
36
Ag are on the
cells
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Ab are on the
serum
38
Substance recognized as foreign and react with a complementary antibody or cell receptor
Antigens
39
Immunoglobulin developed in response to the presence of antigens
Antibodies
40
Type of antibody that is from another species
Hetero/Xenoantibodies
41
Type of antibody that is from individuals of the same species
Alloantibodies
42
Body's own antigens
Autoantibodies
43
Discoved by Karl Landsteiner in 1900s
ABO Blood Group
44
Most significant for transfusion practice
ABO Blood Group
45
1st blood group discovered
ABO Blood Group
46
Landsteiner's Rules for the ABO Blood Group
1. A person doesn't have Ab to his own Ag
| 2. Each person has Ab to the Ag he lacks
47
Develops as early as the 37th day of fetal life
ABO Ag
48
expression is fully develope by 2 to 4 years of age and remains constant for life
ABO Ag
49
ABO Ag are controlled by
Secretor (Se) gene
50
Inherited Homozygous (SeSe) or Heterozygous (Sese) genotype
Secretors
51
Inherited the sese genotype
Non-secretors (no ABH substance in secretions)
52
What are the ABO Abs
Anti-A
Anti-B
Anti-A,B
53
Absent at birth and start to appear around 3-6 months
ABO Abs
54
Developed shortly after birth ff exposure to ABO-like Ags in the environment
Naturally occuring Abs
55
Optimal temp for reactivity of IgM
24 deg celsius or lower
56
Develop in response to exposure to ABO-incompatible RBCs
Immune type Ab
57
Antibody that can cross the placenta
IgG
58
Structure of IgG
monomer
59
Number of Ag-binding sites of IgG
2
60
Optimal temp for reactivity of IgG
37 deg celsius
61
Ab that reacts best in IAT
IgG
62
Ab that can cause HDFN
IgG
63
Structure of IgM
Pentamer
64
Number of Ag-binding sites of IgM
10
65
Detection of Ags on patient's RBCs with known antisera
Forward Blood Group Typing
66
Detection of ABO Abs in serum of patients with Known RBCs
Reverse Blood Group Typing
67
Type of Ag found in Blood type A person
A
68
Type of Ag found in Blood type B person
B
69
Type of Ag found in Blood type O person
H
70
Type of Ag found in Blood type AB person
A, B
71
Type of Ab found in Blood type A person
Anti-B
72
Type of Ab found in Blood type B person
Anti-A
73
Type of Ab found in Blood type O person
Anti-A, Anti-B
74
Type of Ab found in Blood type AB person
None
75
Cause by decreased amounts of Ag on RBCs
ABO subgroups
76
2 main A subgroups
A1, A2
77
Anti-A1 lectin
Dolichos Biflorus
78
6 types of Weak A Subgroups
A3, A(x), A (end), A(m), A(y), A(el)
79
Shows mixed field agglutination with Anti-A or anti-A, B reagents
A3 (Weak A Subgroup)
80
RBCs are not agglutinated by Anti-A rgt but agglutinate with most examples of Anti-A,B
Ax (Weak A Subgroup)
81
Also shows mixed field agglutination with Anti-A and anti-A,B but only a = 10% of RBCs agglutinate
A(end) (Weak A Subgroup)
82
RBCs are not agglutinated or only weakly agglutinated by anti-A or anti-A,B
A(m) (Weak A Subgroup)
83
RBCs are not agglutinated by anti-A or anti-A,B; with detectable amount of A glycosyltransferase
A(y) (Weak A Subgroup)
84
Very rare and less frequent ABO subgroup
B Subgroups
85
Anti-B lectin
Griffonia simpliciforia (prev. Banderiae simpliciforia)
86
4 types of B Subgroups
B3, Bx, Bm, B(el)
87
mixed field agglutination with anti-B and anti-A,B
B3 (Weak B Subgroup)
88
weak agglutination with anti-B and anti-A,B
Bx (Weak B Subgroup)
89
unagglutinated by anti-B or anti-A,B; B glycosyltransferase is present
Bm (Weak B subgroup)
90
RBCs are not agglutinated by anti-A or anti-A,B; no detectable amount of A glycosyltransferase
A(el) (Weak A Subgroup)
91
unagglutinated by anti-B or anti-A,B; no B glycosyltransferase is present
B(el) (Weak B subgroup)
92
Lacks the H gene (hh genotype)
Bombay phenotype
93
Absence of A,B and H Ag
Bombay phenotype
94
Can only be transfused with blood from another Bombay
Bombay phenotype
95
No reaction to Anti-H lectin
Bombay phenotype
96
Anti-H lectin
Ulex europaeus
97
Type of ABO discrepancies that is due to weakly or missing Abs
Group I
98
Anti-A = 0
Anti-B = 0
A1 cells = 0
B cells = 0
What type of ABO discrepancies is this?
Group I
99
Type of ABO discrepancies that is due to weakly reacting or missing Ag
Group II
100
Associated with diseases of the digestive tract (e.g., cancer of colon)
Acquired B phenomenon
101
Anti-A = 4+
Anti-B = 2+
A1 cells = 0
B cells = 4+
What type of ABO discrepancies is this?
Group II
| Acquired B phenomenon
102
Type of ABO discrepancies that is due to protein or plasma abnormalities resulting in ROULEAUX formation
Group III
103
Type of ABO discrepancies that is due to miscellaneous problems
Group IV
104
2nd most important blood groups system in terms of transfusion
Rh blood group
105
blood group that is primarily the cause of HDFN and erythroblastosis fetalis
Rh blood group
106
Well developed at birth causing HDN (if baby has Rh AG that mom lacks)
Rh antigen
107
not soluble and not expressed on tissues
Rh antigen
108
3 nomenclature of Rh antigen
fisher-race or DCE terminology
wiener or Rh-Hr terminology
Rosenfield and Coworkers or Alpha/Numeric Terminology
109
Reacts optimally at 37 deg celsius or after antiglobulin testing
Rh antibodies
110
Detects for the presence of D Ag on px's RBC
Rh typing
111
reagent used for Rh typing
anti-D and BSA (Bovine serum albumin; used as control)
112
weakened form of the D antigen
Weak D (Du phenotype)
113
done to confirm negative Rh typing results
Weak D testing
114
Form of Indirect Antiglobulin Test
Weak D testing
115
Spx used for Weak D testing
(-) result from the Rh typing
116
Rgt for Weak D testing
AHG (Anti-human globulin)
117
Not intrinsic to RBC; IgM in nature; Not clinically significant
Lewis Blood group
118
Blood group Ag that deteriorates rapidly on storage
P1
119
Ab that is associated with PCH (Paroxysmal Cold Hemoglobinuria)
Anti-P
120
AKA Auto-Anti-P or Donath-Landsteiner Ab
Anti-P
121
Antibody that is IgG Biphasic Hemolysin
Anti-P
122
Binds complement to red cells at COLDER TEMPERATURE; Hemolyzes red cells at 37 deg celsius
IgG Biphasic Hemolysin
123
Produced by individuals with p phenotype
Anti-Tj(a)
124
Antibodies that is present in spontaneous abortions in early abortions
Anti-Tj(a)
125
Associated with Infectious mononucleosis
Anti-i
126
Associated with cold agglutinin disease & Mycoplasma pneumoniae
Anti-I
127
Most common Ab seen in BB after ABO & Rh
Anti-K
128
Ag that resist infection by P.vivax (humans) and P.knowlesi (monkeys(
Fy (a-b-)
129
Abs that is notorious in BB due to its association to delayed hemolytic transfusion rxn
Kidd Abs
130
Blood to given to the recipient came from the recipient himself
Autologous donation
131
Hgb & Hct for Autologous donation should be at least
```
Hgb = at least 11 g/dL
Hct = 33 %
```
132
Detects unexpected Abs against RBC Ag
Antibody Screening
133
Prevents coagulation by chelating calcium
Citrate
134
Supports ATP generation
Dextrose (glucose)
135
Substrate for ATP Synthesis
Adenine
136
prevents excessive fall in pH during storage
Sodium biphosphate
137
Shelf life for ACD
21 days
138
Shelf life for CPD
21 days
139
Shelf life for CPDA-1
35 days
140
Shelf life for Adsol
42 days
141
Used to salvage rare or type O units up to 3 days beyond expiration
PIPA (Phosphate-Inosine-Pyruvate-Adenine)
142
Negative result effectively rules out presence of Autoantibody
Autocontrol
143
Patient Serum + Donor Red Cells
Major Crossmatching
144
Patient Red Cells + Donor Serum
Minor Crossmatching
145
3 phases of Manual Crossmatching
1. Immediate spin
2. Incubation at 37 deg celsius
3. AHG phase
146
Hydatid cyst fluid
Pigeon droppings
Turtledove’s egg whites
Anti-P1
147
Plasma or serum, secretor saliva
Anti-Lewis
148
Removal of abs from SERUM
Adsorption
149
Removal of abs bound to RED BLOOD CELLS
Elution
150
Urine, guinea pig urine
Anti- Sd^a
151
Rejuvination of a unit of RBC is used to
Restore 2,3-DPG, ATP to normal levels
152
pH of platelets should be maintained at
6.2 or above
153
blood component indicated for fibrinogen deficiencies
Cryoprecipitate AHF
154
inhibits proliferation of T lymphocytes
Irradiation
155
blood component that prevent HLA alloimmunization
PRBC-LR
