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