1. Who among the following was the first person to perform AB forward and reverse grouping?

● Pope Innocent VIl

● Landsteiner
● Bernstein
● Weiner
Karl Landsteiner:
• Discovered the first human blood group system → ABO
• First individual to perform forward and reverse grouping
• 1901: collected blood from himself 5 colleges and separated the cells and serum → mix each
sample with the serum

Pope Innocent VII

• First ever recorded to receive blood transfusion

Landsteiner’s Law
1. The antigen on the RBC determines the blood group
Ex.: Antigen A → Blood Group A
2. The corresponding antibody is never found in the individual’s serum
Ex.: Blood Type A → no Anti-A will be present
3. The opposite antibody is always present in the individual’s serum
Ex.: Blood Type A → Anti-B is present

ABO Blood Group System

• Only blood group system in which individual’s have antibody in their serum to the antigens
that are absent to their RBC
• Most important of all blood groups
• Incorrect ABO group transfusion remains the leading cause of death in HTR
• TRALI: most cause of death in the year 2009
• Both forward and reverse grouping must be done on all donor and patient
• ABO forward and reverse grouping is the most frequently performed test in the blood bank

ABO Blood Group Antibodies

• “naturally occurring” meaning, prior expose to antigens is not needed for production of
antibodies
• Predominantly IgM which activates complement and react at room temperature or even colder
• Produce strong direct agglutination
➢ If reactions are not strong, reagent mixture is not properly conducted
• Reactions during ABO testing
• Production: initiated at birth with very low titter
• Detectable titers: 3 to 6 months
➢ ABO testing before 3 to 6 months old is not considered valid because some of the
antibodies present may be from maternal IgG that has cross the placenta and only forward
grouping is performed
➢ In cases of geriatric patients, lower levels of anti-A and anti-B are produced thus, only
forward grouping is performed
• Peaks at: 5 to 10 years
• ABO antibodies can cause rapid intravascular hemolysis which may lead to death thus, results
must be thoroughly checked before releasing a blood bag

ABO Blood Group Antibodies

Blood Group Antibody Produced
A Anti-B
B Anti-A
AB none
O Anti-A, anti-B, Anti-AB

2. Which of the following is the peak of ABO antibody production?

 ● 2 to 4 years of age → peak of ABO antigen production
● 3 to 6 months → Antibodies are detectable
● None of the Choices
● 5 to 10 years of age

3. Which type of oligosaccharide chains is primarily associated with body secretions?

● Types 1 and 2
● Types 1 and 3
● Types 2 and 4
● Types 2 and 3

Types of Oligosaccharide chains: 1, 2, 3, 4

➢ Type 1 and 3: Bodily secretions
➢ Type 2 and 4: RBC membrane

Comparison of ABH Antigens on RBCs with A, B, and H Soluble Substances

ABH antigens on RBCs A, B, and H Soluble Substances
• RBC antigens can be glycolipids, • Secreted substances are
glycoproteins, glycosphingolipids glycoproteins
• RBC antigens are synthesized only • Secreted substances are primarily
on Type 2 chain synthesized on Type 2 chains
• Type 2 chain refers to a Beta-1,4 • Type 1 chains refers to a Beta-1,3
linkage linkage
• The enzymes produced by H antigen • The enzyme produced by Se gene
(-) the acts primarily on type 2 chains the preferably acts on type 1 chains
which are prevalent on the RBC in secretory tissues
membrane
Both produces alpha-2-L-fucosyltransferase

4. Which of the following shows the reactivity of anti-H antisera with ABO blood groups from least to
greatest amount of H antigen?
● None of the Choices
● O>A2>B>A2B>A1>A1B
● A1B
● A1B>A1>A2B>B>A2>0

ABH Antigens
O antigen: greatest source of H antigen
A1B: least source of H antigen because almost all H antigen is converted into A1 by placing the large
N-acetylgalactosamine sugar on the H substance
A1B and A1: H antigen is hidden and cannot be reacted with anti-H antisera
A2: only some of the H antigen is converted into A2 and the remaining will be detectable on the cells
● Greatest to Least: O>A2>B>A2B>A1>A1B
● Least to Greatest: A1B>A1>A2B>B>A2>0

5. Which of the following is the reactivity temperature of anti-H?

● None of the choices
● below room temperature
● 37C
● Below room temperature and 37C
Anti-H
• Naturally occurring IgM cold agglutinin that reacts best below room temperature
• Reacts mostly with cells of Group O individuals which has the greatest amount of H substance
and reacts least with A1B which contains the smallest amount of H substance
• An insignificant antibody in terms of transfusion purposes because it has no reactivity at body
temperature (37 C)

Rh Blood Group System

• Rh
▪ A specific red blood cell antigen → D antigen
▪ Complex blood group system currently composed of over 50 antigenic specificities
▪ 2nd most important blood group system in terms of transfusion
▪ Rh antigens are very immunogenic and reside on the glycoproteins

• Rh antibodies
▪ Produced only after exposure to foreign red blood cells
▪ Once present, they can produce:
1. HDFN
➢ Erythroblastosis Fetalis
2. HTR

Rh Reading and Reporting

• Rh positive: individual’s red blood cells possess one particular Rh antigen, the D antigen
• Rh negative: red blood cells lack the D antigen

Terminology:
1. Fisher-Race: DCE Terminology
2. Wiener: Rh-Hr Terminology
Note: Both Fisher-Race and Wiener are postulated base on genetic mechanism of Rh system

3. Rosenfield and Coworkers: Alphanumeric Terminology

➢ Base on the absence or presence of the Rh system
4. ISBT: Updated Numeric Terminology
➢ Combined efforts of ISBT party on the terminology of the red cell surface antigen

Fisher-Race: DCE Terminology

• They postulated that the antigens of the system were produced by 3 closely linked set of
alleles (D/d, C/c, E/e)
- each GENE was RESPONSIBLE for PRODUCING = 1 ANTIGEN on the RBC surface
- EACH ANTIGEN and CORRESPONDING GENE were given the SAME LETTER
designation
- Gene – LETTER is Italicized → (D/d, C/c, E/e)
- Antigen – LETTER is in STANDARD FORM → (D/d, C/c, E/e)
* They named the antigens of the system D, d, C, c, E, e
- “d” represents the absence of the D antigen. (REMEMBER there is NO “d” antigen it just
denotes absence of “D” antigen/ D negative / Rh-)
• Fisher-Race theory: Each person inherits a set of Rh genes from each parent (1 haplotype
from each parent)
- The combination of genes inherited from one parent is called a haplotype.
▪ Example: 1 Parent has GENES – D, C, e → HAPLOTYPE : DCe
▪ EXAMPLE: Mother = Haplotype: DCe + Father = Haplotype: DcE =
GENOTYPE: DCe/DcE
 • Rh genes are codominant
- Each inherited gene expresses its corresponding antigen on the RBC
• An individual’s Rh phenotype is reported as “DCE” rather than “CDE” – because the “C
“ALLELE is in between the “D” and “E”
o Other BOOKS still utilize CDE , so its still acceptable, but still RECOMMEND/BETTER
is DCE
o FISHER POSTULATED THAT THE C/c LOCUS LIES BETWEEN D/d & E/e LOCI
o
• The combination of maternal and paternal haplotypes determines one’s genotype and dictates
one’s phenotype.
o EXAMPLE: GENOTYPE: DCe/DcE → PHENOTYPE: Rh +

• Rare phenotypes that involve deletions is represented with a dash.

- Probable GENOTYPE of a person exhibiting DELETION PHENOTYPE: DC- or Dc- or D-
- a DELETION of Cc and Ee has not been reported
- EXAMPLE: GENOTYPE has ONLY “D” no “C” and “E” → written as D –

• Rhnull : Absence of Rh antigens on the RBC → ( - - - / - - - ) or ( - / - )

- Rh subscript null
* Rhmod phenotype: weakened antigen expression of all Rh antigen
- Placing parenthesis around (D), (C), and (e) indicates weakened antigen expression

Wiener: Rh-Hr Terminology

• Wiener - believed that there was one gene responsible for defining Rh that produced an
agglutinogen containing three Rh factors.
- this Rh GENE produced at least 3 FACTORS within an AGGLUTINOGEN
* AGGLUTINIGEN - Phenotypic expression of the haplotype
* BLOOD FACTORS (D,C,E) – is an antigen recognized by an antibody. Antibodies
can recognize single or multiple factors (antigens)

Rho – “ D “ - antigen
hr’ (hr prime) – “ c ”- antigen
hr”(hr double prime) – “ e “- antigen

Shorthand Symbol D C E c e Designation

R 1 + + 0 0 + R1
r ‘ 0 + 0 0 + r’
R 2 + - + + 0 R2
r “ 0 0 + + 0 r”
R z + + + 0 0 Rz
r y 0 + + 0 0 ry
R o + 0 0 + + Ro
r 0 0 0 + + r
(Harmening, D. (2019). Modern Blood Banking and Transfusion
Practices (7th ed.) F. A. Davis Company)

• The agglutinogen may be considered the phenotypic expression of the haplotype.

 • Each factor is an antigen recognized by an antibody.
• The original Wiener nomenclature named the five common Rh antigens as: Rho (D), rh’ (C),
rh” (E), hr’ (c), and hr” (e),
o but these terms are no longer used in favor of a modified form of Wiener notation.
• BLOOD FACTORS (1st used terminology of wiener)
- when referring to Rh antigens (or factors) in the Wiener nomenclature:
o C or c – single prime (‘)
o E or e – double prime (“)
o If r precedes h (ie., rh’ or rh”) - refers to C or E antigens respectively
o If h precedes r (ie., hr’ or hr”) - refers to c or e antigens respectively
o Rho – is equivalent to D
o No designation for the absence of D antigen
▪ Example: Rhohr’hr”=(Dce) ; Rhorh’rh”=(DCE) ; rh’hr’”=(dCE/CE)
Modified Wiener nomenclature:
- An AGGLLUTINOGEN is described by a LETTER and SYMBOL based on the factors
present
o Uppercase R- denotes the presence of the D antigen
o Lowercase r- indicates absence of the D antigen
o Presence of C antigen- indicated by a 1 or a single prime (‘)
o c antigen- implied when there is no 1 or single prime (‘)
o E antigen- indicated by a 2 or a double prime (“)
o e antigen- implied when no 2 or double prime (“)
o Subscript o – small letter c and e
o When both C and E are present- letters z or y is used ( Rz and ry )
o Examples:
▪ R1= DCe
▪ r’= dCe
▪ Ro= Dce
▪ Rz= DCE
▪ ry= CE
▪ r = dce
▪ r”=dcE
• Italics or superscripts are used when describing Rh genes in the Wiener nomenclature.
• Standard type is used to describe the gene product or agglutinogen ( ie., Rho, hr’, rh”)
• Subscripts are used with the uppercase R → ( Rz)
• Superscripts with the lowercase r → (ry)
• The genotype for the Rhnull that arises from an amorphic gene at both Rh loci is pronounced
“little r double bar”. →

Rosenfield and Coworkers: Alphanumeric Terminology

• System that assigns a number to each antigen of the Rh system in order of its discovery or
recognized relationship to the Rh system.
• It has no genetic basis, nor was it proposed based on a theory of Rh inheritance but simply
demonstrates the presence or absence of the antigen on the RBC.
• A minus (-) sign preceding a number designates ABSENCE of the antigen
• For the 5 major antigens:
o D= Rh1
o C= Rh2,
o E= Rh3
 o c= Rh4
o e= Rh5
o If an antigen has not been typed, its number will not appear in the sequence
• Example: For RBCs that type D-positive, C-positive, E-positive, c-negative, and e-negative,
(D+C+E+c-e-)
- the Rosenfield designation is: Rh: 1, 2, 3, –4, –5.
- If the sample was not tested for e, the designation would be Rh: 1, 2, 3, –4
• EXAMPLE 2: D+C-E-c+e+ = Rh: 1, -2, -3, 4, 5
• Its primary limiting factor is that there is a similar nomenclature for numerous other blood groups,
such as Kell, Duffy, Kidd, and more. Therefore, when using the Rosenfield nomenclature on the
computer, one must use both the alpha (Rh:) and the numeric (1, 2, –3, etc.) to denote a
phenotype.

International Society of Blood Transfusion Committee (ISTB) : Updated Numeric

Terminology
• The International Society of Blood Transfusion (ISBT) formed the Committee on Terminology
for Red Cell Surface Antigens.
• Its mandate is to establish a uniform nomenclature that is both eye- and machine- readable
and is in keeping with the genetic basis of blood groups. (NO GENETIC BASIS)
• Adopted a 6-digit number for each authenticated antigen belonging to a blood group system.
• First three numbers represent the system and the remaining three represents the
antigenic specificity
• EXAMPLE: ISBT = Rh
004 001 (D) = Rh1
• Number 004 was assigned to the Rh blood group system, and then each antigen assigned to
the Rh system was given a unique
number to complete the six-digit
computer number.
o D= ISBT 004001
o C= ISBT 004002
o E= ISBT 004003
o c= ISBT 004004
o e= ISBT 004005
6. Which of the following is the conversion of R2r Wiener to Fisher-Race?
● dCe/dce
● Dce/dce
● DcE/dce
● dcE/dcE

7. A medical technologist tested a blood sample for weak D and reacted as positive. What will be the
next thing to do?
● Confirm if true positive by further testing
● Report as positive
● Report as negative
● Repeat D testing

WEAK D: VARIATIONS OF D ANTIGEN EXPRESSION (Du)

• For many years, the generic term weak D was used to identify individuals whose D was not
detectable at immediate spin, without defining the nature of the weakened expression.. Weak
D types can be separated into three categories: position effect, quantitative, and partial-D
antigen (missing one or more alleles).
• RhD antigen was altered
• Categorized into different phenotypes defined as weakened D due to:

1. Position Effect: C in trans to D

• DUE to a POSITION EFFECT or GENE INTERACTION EFFECT
• The allele carrying the RHD is trans (opposite haplotype) to the allele carrying C
• Example: Dce/dCe
• This interference with D expression does not occur when the C gene is inherited in
the cis position to RHD, such as DCe/dce.

2. Weak D: Quantitative Changes Due to Fewer D Antigen Sites

 • Results from the inheritance of RHD gene that codes for the weakened expression of
the D antigen.
• D antigen → appear to be COMPLETE but FEWER in number
• MUTATIONS in the RHD gene
o Cause CHANGES in AMINO ACIDS present in the transmembrane
o Causing CONFORMATIONAL CHANGES in the PROTEIN
• Wagner, Gassner, and others described the classification of weak D RBCS based on
single nucleotide polymorphisms (SNP).23 Mutations for these weak D types occur
because SNP affects amino acid insertion of the protein on the RBC membrane.
When these changes occur, normal RhD antigen expression is altered because there
are fewer antigen sites overall.
➢ On molecular level there is mutation on the RhD gene causing changes in the
amino acids present in the transmembrane intercellular region of RhD protein
thus, conformational changes in the protein. The normal RhD expression will
be altered resulting to a fewer antigen on the overall side.
➢ Individuals with weak D will rarely make an antibody against D since the RhD
antigen are present as expected however, protein changes will still occur
inside the RBC.
➢ Changes in RhD gene causes altered expression and are categorized with
type 1 and 3 being the most common.

3. Partial D or D Mosaic
• D antigen expression can be weakened when 1 or more D epitopes within the entire
D protein is missing or altered.
• The D antigen is not complete because one or more epitopes are missing
• Wiener and Unger → postulated that the D antigen is made of antigenic subparts,
genetically determined, that could be absent in rare instances
• Tippett and Sanger → worked with RBCs and sera of partial D individuals, to
classify these antigens. BASED on TESTING anti-D sera from D-positive people
• Partial-D antigens can be classified on a molecular level and are attributed to hybrid
genes resulting from portions of the RHD gene being replaced by portions of the
RHCE gene.

4. Del
• Occurring in individuals whose RBCs possess an extremely low number of D antigen
sites that most reagent anti-D are unable to detect.
o Need to perform ADSOPRION and ELUTION → ONLY WAY TO DETECT
the D ANTIGEN
• This phenotype occurs most often in individuals of Southeast Asian descent,
occurring in up to 10-30% of that population. It is rare in Caucasians/WHITES.
• Del individuals of Southeast Asian descent have not been reported to make anti-D in
response to transfusion or pregnancy, but there have been a few instances of anti-D
production in Caucasian individuals.

8. Which of the following Rh typing reagents can be used to test cells that are already coated with IgG
antibody?
● High protein anti-D
● Saline anti-D and High protein anti-D
● None of the Choices
 ● Saline anti-D

Rh Typing Reagents:
• High-protein based
• Low-protein based
• Saline based
• Chemically modified
• Monoclonal
• Blends of monoclonal
Goal: use reagent anti-D that will allow for the typing of individual RBC as quickly as typing of
ABO antigens

Saline reactive reagents with IgM:

• First typing reagents available to test for the D antigen
• Advantage:
➢ Low-protein based
➢ Used to test cells that are already coated with IgG antibody
➢ Use for autoantibodies binding to their RBCs causing false positive result
• Primary Disadvantages:
➢ Limited availability
➢ Cost of production
➢ Lengthy incubation time
➢ It cannot be used for weak D typing

9. Which of the following will cause a false positive in Rh typing?

● Variant antigen
● Rpm too low
● Centrifugation too long → because instead of breaking the cell button upon centrifugation what will
happen is that the blood may adhere to the tube and may not be dislodge for checking
● Reagent deterioration

10. Which of the following may cause a false negative in Rh typing?

● Cold agglutinins
● Rouleaux
● Incorrect reagent selected
● Resuspension too vigorous → upon dislodging the centrifuge tube, do not resuspend too vigorously,
dislodge only until the formed button mixes to the solution because a true agglutination do not easily
break upon dislodging the solution present in the tube
 ❖ A1 population is > A2 individuals
❖ A = A1 ; A2 = A2

THE BOMBAY PHENOTYPE (Oh) or (H null) Phenotype

• First reported by Bhende in 1952 in Bombay, India.
 • Results from the inheritance of a double dose of the h Box 4. The Bombay Phenotype
gene, (Oh)
producing the very rare genotype hh. • hh genotype
o As a result, the ABO genes cannot be expressed
• No H antigens formed; therefore,
and ABH antigens cannot be formed, since there is
no
no H antigen made in the Bombay phenotype
A or B antigens formed
• The Bombay anti-H can often be potent and reacts
• Phenotypes as blood group O
strongly at 37 degrees celsius
• Anti-A, anti-B, anti-A,B, and anti-H
• The (Oh) Bombay phenotype is inherited as an
present in the serum
autosomal recessive trait.
• Can only be transfused with blood
• Since these RBCs lack normal ABH antigens, they fail
from another Bombay (Oh)
to react with anti-A, anti-B, and anti-H antisera.
• In RBC testing using anti-A and anti-B, the Bombay
(Harmening, D. (2019). Modern
would phenotype as an O blood group.
Blood Banking and Transfusion
o However, RBCs of the Bombay phenotype (Oh) do
not react with the anti-H lectin (Ulex europaeus), Practices (7th ed.) F. A. Davis
unlike those of the normal group O individual, Company)
which react strongly with anti-H lectin.
• Bombay serum contains anti-A, anti-B, anti-A, B, and anti-H.
• Transfusing normal group O blood (with the highest concentration of H antigen) to a Bombay
recipient (anti-H in the serum) would cause immediate cell lysis. Only blood from another
Bombay individual will be compatible and can be transfused to a Bombay recipient.
• ABH substance is also absent in the saliva of individuals with the Bombay phenotype.

General Characteristics of Bombay Oh (Hnull) Phenotypes

a) Absence of H, A, and B, antigens: no agglutination with anti-A, anti-B, or anti-H lectin
b) Presence of anti-A, anti-B, anti-A,B and a potent wide thermal range of anti-H in the serum
c) A, B, H non-secretor (no A, B, or H substances present in saliva)
d) Absence of a-2-L-fucosyltransferase (H enzyme) in serum and H antigen on red cells
e) Presence of A or B enzymes in serum (depending on ABO genotype) → cannot demonstrate
without H antigen
f) A recessive mode of inheritance (identical phenotypes in children but not in parents)
g) RBCs of the Bombay phenotype (Oh) will not react with the anti-H lectin (Ulex europaeus)

h) RBCs of the bombay phenotype (Oh) are compatible only with the serum from another
Bombay individual

The Para-Bombay Phenotypes

• Rare phenotypes in which the RBCs are completely devoid of H antigens or have small
amounts of H antigen present
• RBCs are completely devoid of H antigens or have small amounts of H antigen present.
• The genetic basis for the para-Bombays is a mutated FUT1 gene (H gene) with or without an
active FUT2 gene (Se gene) or a silenced FUT1 gene with an active FUT2 gene.

• Categories of H-deficient phenotypes:

1. Bombay Phenotype
o hh sese
o Antibodies in serum: Anti-A, anti-B, anti-H
o RBC H-Deficient
o Non-secretor
o Oh, OhA, OhB, OhAB
 2. RBC H-Partially Deficient
o Non-secretor
o Oh, Ah, Bh, ABh
o hh se
o Proposed genes inherited: A and/or B
3. Para-Bombay Phenotype
o Red cell H-deficient
o hh Se
o Secretor
o OhO, OhA, OhB, OhAB

Functional Roles of the Blood Group Systems:

Glycosyltransferases
✓ ABO, P1PK, Lewis, and H blood group systems
Structural relationship to Red Cell
✓ MNS, Diego, and Gerbich blood group systems
Transport Proteins (transports CO2 & NH4 & Proteins)
✓ Rh, Kidd, Diego, Colton, and Kx blood group systems
Complement Pathway Molecules
✓ Chido/Rodgers, Cromer, and Knops blood group systems
Adhesion Molecules
✓ Lutheran, Xg, Lansteiner-Wiener, and Indian blood group systems
Microbial Receptors
✓ MNS, Duffy, P, Lewis, and Cromer blood group systems
Biologic Receptors
✓ Duffy, Knops, and Indian blood group system
Note: many of these functional relationships have been predicted based on molecular
cloning studies and remain under investigation.

11. Which of the following is the location of Lewis antigens?

● None of the choices
● Type 1 glycosphingolipids and Type 2 glycosphingolipids
● Type 1 glycosphingolipids
● Type 2 glycosphingolipids

The Lewis Blood Group System

ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number (ability to
cause HDFN
& HDR)

LE 007 NO IgM 37oC RT → (IgM) Enhanced

(COLD)
RT or lower AHG→
(MOST) (SOME IgG )
-ANTI
HUMAN
 GLOBULIN
PHASE

(Blaney K.D. & Howard, P.R. (2008). Concepts of

immunohematology (2nd ed.). USA: Mosby)
➢ not intrinsic to the RBCs but are on type 1 glycosphingolipids
➢ passively adsorbed from the RBC membrane from the plasma
➢ It was named after one of the first individuals to make the antibody, reported by Mourant in
1946. → LEWIS
➢ The Lewis (Le, FUT3) gene is located on chromosome 19 (at 19p13.3).
➢ The Secretor (Se, FUT2) gene is located on chromosome 19 (at 19q13.3)
o LEWIS ANTIGEN – in contrast to OTHER BLOOD GROUP ANTIGEN → they are
MANUFACTURED by TISSUE CELLS and SECRETED to BODY FLUIDS
➢ There are two alleles at the Lewis locus, →Le and the amorph le,
and there are two alleles at the secretor locus,→ Se and the amorph se
➢ Le gene → must be present for a precursor substance to be converted to → Lea,
but the Se gene → must also be present for conversion to → Leb
o RESULTING TO 4 PHENOTYPES

Lewis Antigens: Lea and Leb

✓ Are not expressed on cord RBCs and are often diminished on the mother’s RBCs during
pregnancy.
✓ They are found on lymphocytes and platelets and on other tissues such as the pancreas,
stomach,
intestine, skeletal muscle, renal cortex, and adrenal glands.
✓ SOLUBLE ANTIGENS -. Found in SALIVA as GLYCOPROTEINS → SECRETOR GENE
✓ Lewis antigens are resistant to treatment with the enzymes ficin and papain, DTT
(Dithiothreitol) and glycine acid EDTA.
✓ Lewis antigens (Lea and Leb) are not intrinsic to RBCs but are on Type 1 glycosphingolipids that
are passively adsorbed onto the RBC
membrane from the plasma.
Lewis Antibodies: Anti- Lea and Anti- Leb
*Are IgM and have no clinical significance.
*Have not been implicated in HDFN → because the antibodies do not cross the placenta, and
the antigens are not well developed at birth → NO ANTIGEN – ANTIBODY REACTION → NO
HDFN
*It can bind complement → IgM ( NOTE: in OTHER BLOOD GROUP SYSTEM NOT ALL IgM
can BIND COMPLEMENT)
*The most commonly encountered of the Lewis

Table 1. Phenotypes of the Lewis System

ADULT PHENOTYPE PREVALENCE (%)
PHENOTYPE
Whites Blacks
Le (a+b-) 22 23
Le (a-b+) 72 55
 (MOST
COMMON)
Le (a-b-) 6 22
Le (a+b+) Rare Rare
(Harmening, D. (2019). Modern Blood Banking and Transfusion Practices (7th ed.) F. A.
Davis Company)
78% - 80% of the WHITE POPULATION are SECRETORS
20% are NON SECRETORS
IN TERMS of (Le (a-b-) individuals
80% are SECRETORS
20% are NON SECRETORS
NOTES:
➢ Le (a-b+) red cell phenotype → arises from the inheritance of Le, Se, and H gene.
o (Lea → Leb = Le (a-b+) – THUS A will be NEGATIVE because it CONVERTED TO B) →
presence of POSITIVE B comes about the
CONVERSION of A → THUS A will be NEGATIVE because it
CONVERTED TO B
➢ Lewis glycolipids → are not detectable in plasma → until about 10 days after birth.
➢ Cord blood and RBCs from newborn infant’s phenotype as Le (a-b-) → not expressed
during PREGNANCY → ONLY UPON BIRTH

➢ In children who inherit the both the Le and Se gene:

➢ Le(a-b-) at birth → Le (a+b-) after 10 days → Le (a+b+) →and finally Le (a-b+), the TRUE
Lewis phenotype, after about 6 years.
➢ In contrast, children who inherit Le and sese genes phenotype as:
➢ Le (a-b-) at birth → Le (a+b-) after 10 days → Le (a+b-) phenotype persists throughout
life → (b-) = w/o SECRETOR GENE
(sese)
• Individuals with lele genes phenotype as Le (a-b-) at birth and for the rest of their lives.

➢ Lewis antigens found in the secretions → are glycoproteins.

➢ Lewis antigens found in the plasma → are glycolipids.
➢ Red cells adsorb only glycolipids, not glycoproteins, onto membrane
➢ A person can be a non-secretor (sese) → and still secrete Lea into the body fluid

Table 2. Lewis Genes and Red Cell Phenotypes

GENES PRESENT ANTIGENS IN SECRETIONS RED CELL PHENOTYPE
Le sese H Lea Le (a+b-)
Le Se H Lea Leb H Le (a-b+)
lele sese H None Le (a-b-)
lele Se H H Le (a-b-)
Le sese hh Lea Le (a+b-)
Le Se hh Lea Le (a+b-)
lele sese hh None Le (a-b-)
lele Se hh None Le (a-b-)
(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)
Summary of Lewis Inheritance and Biochemistry Concepts
 • Lea and Leb are not alleles
• Le (a-b+) red cell phenotype → arises from the inheritance of an Le, Se and H gene
• Individuals who have a phenotype of Le (a+b-) → are not secretors with the exception of the
Bombay phenotype.
• A Bombay phenotype (hh) → cannot express the Leb antigen
• A person can be a nonsecretor (sese) → and still secrete Lea into body fluids
• Lewis antigens found in the secretions are glycoproteins
• Lewis antigens found in plasma are glycolipids
• Red cells adsorb only glycolipids, not glycoproteins, onto the membrane
• Adult red cells with a phenotype of Le (a+b+) → are very rare.

Note: The Leb antigen is the receptor for Helicobacter pylori, a gram-negative bacterium associated
with gastritis, PUD, gastric carcinoma, and the Norwalk virus.

Good To Know:
• Le gene codes for the L-fucosyltransferase which adds L-fucose to the Type 1 gene
• Needed for the expression of Lea and Leb secretor genes
• Lele genotype is more common among blacks than among whites and results in the Le (a-b-)
phenotype
• Lewis antigens are poorly expressed at birth
• Lewis antibodies are generally IgM made by Le (a-b-) individuals
• Lewis antibodies are frequently encountered in pregnant women
• Lewis antibodies are not considered significant for transfusion medicine

12. Who among the following was the first individual identified as having anti-PP1Pk antibody?
● Mrs. Jay a p individual with adenocarcinoma of the pancreas
● Mrs. Jay a p individual with adenocarcinoma of the stomach → anti-PP1Pk
● Mrs. Jay a p individual with breast cancer
● Mrs. Jay a p individual with bone cancer

Anti-PP1Pk
• Originally called anti-Tja. (T = tumor / j = Mrs. Jay / a = adenocarcinoma)
• It was first described in the serum of Mrs. Jay, → a “p” individual with adenocarcinoma of the
stomach.
• Tumor cells of Mrs. Jay carries the P system antigens and the antibody was credited to have a cytotoxic
effect that help to prevent the metastatic post surgery
• produced by p individuals early in life without RBC sensitization and reacts with all RBCs except those of
the p phenotype
• It has the potential to cause severe HTRs and HDFN. (CLINICALLY SIGNIFICANT)
• It is also associated with an increased incidence of spontaneous abortions in early pregnancy.
• Components: IgM and IgG
• React at wide thermal range and tendency to bind with complement
• Anti-PP1Pk has the potential to cause severe HTRs and HDFN
• The antibody is also associated with an increased of spontaneous abortions in early pregnancy → IgG
anti-P
➢ Multiple plasmapheresis reduces the antibodies to prevent abortion

Additionals:
The P Blood Group: P1PK and Globoside Systems and Related Antigens

P1 Antigen
ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number

P1PK 003 NO IgM RT RT Enhanced

(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)

P1 Antigen
ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number

GLOB 028 YES IgM and 37oC RT

IgG Enhanced
RT AHG
(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)

➢ Traditionally, the P blood group comprised the P, P1 and Pk abtigens and later, Luke (LKE).
➢ Currently, in ISBT nomenclature: ALL RELATED TO EACH OTHER
o P1 and Pk → are assigned to the P1Pk blood group system (003, P1PK)
o → is assigned to the globoside blood group system (028, symbol GLOB)
o LKE and PX2 → are assigned to the Globoside Collection (029, GLOB)
➢ Genetics:
o P1PK gene → is located at chromosome 22q11.2
o P gene → is located at chromosome 3q26.1
➢ Biochemistry: Biosynthetic Pathways of the P blood group antigens
o There are two distinct pathways → for the synthesis of the P blood group antigens. The
common precursor → is lactosylceramide (or Gb2, also known as ceramide dihexose or CDH).
→ The pathway on the figure’s left
➔ results in the formation of paragloboside and P1→ . Paragloboside → is also the type 2
precursor for ABH.
➔ The pathway shown on the figure’s right side → leads to the production of the globoside
series: Pk, P, and Luke (LKE).
➢ The P blood group was introduced in 1927 by Landsteiner and Levine in 1927
➢ Matson and coworkers: Pk
➢ P1, P, or Pk → may be found on RBCs, lymphocytes, granulocytes, and monocytes;
➢ P → can be found on platelets, epithelial cells, and fibroblasts.
➢ P and Pk → have also been found in plasma as glycosphingolipids and as glycoproteins in hydatid
cyst fluid.
➢ The antigens have not been identified in secretions.

The P1 Antigen
• Poorly expressed→ at birth and may take up to 7 years to be fully expressed → NO HDFN
 • It deteriorates rapidly on storage.
• Blacks → have stronger expression of P1 (SOLUBLE FORM – can be detected in PLASM and
HYDATID FLUID) → than whites
P Antibodies
• 2 Categories:
• Clinically insignificant
• Potently hemolytic
1. Anti-P1
• Common, naturally occurring IgM antibody in the sera of P- individuals. → develop anti-P1 if
transused with P+ blood
• Typically weak, cold reactive saline agglutinin → optimally reactive at 4oC and not seen in
routine testing.
• Associated with parasitic infections. → hydatid fluid
• Anti-P1→ in 2 P1 individuals → infected with Echinococcus granulosus tapeworms → led to
the identification of P1 and Pk substance in hydatid cyst fluid.
• Strong antibodies to P1 have also been found in patients with fascioliasis ( bovine liver fluke
disease) and in bird handlers.
3. Alloanti-P
• Rarely seen → But it is very significant in transfusion.
• IgG class anti-P → may occur and has been associated with habitual early abortion.
4. Autoanti-P Associated with Paroxysmal Cold Hemoglobinuria (PCH)
• Associated with the cold reactive IgG autoantibody in patients with PCH.
• The IgG autoantibody → in PCH is described as a biphasic hemolysin. (bi = 2 / phasic=
PHASES)
o Antibody binds to RBCs in the cold (Phase 1)
o Via complement activation, the coated RBCs lyse as they are warmed to 37 degrees
Celsius. (Phase 2)
• It typically does not react in routine test systems but is demonstrable only by the Donath-
Landsteiner Test.

• Luke (LKE) Antigen

✓ Described by Tippett and colleagues in 1965 → in the serum of a patient with Hodgkin’s
Lymphoma. (patient name = LUKE)
✓ Three phenotypes:
o 80% tested Luke+
o 14% Lule (w) - weak
o 2% Luke -
*All individuals with the p (Pnull)and Pk phenotype are Luke
p Phenotype (Pnull)
• Rare
• Slightly more common → in Japan, North Sweden, and in an Amish group in Ohio.

P BLOOD GROUP: PHENOTYPE, ANTIGENS, and ANTIBODIES

ANTIGENS POSSIBLE PREVALENCE (%)
PHENOTYPE
PRESENT ANTIBODIES Whites Blacks
P1 P1, P, Pk NONE 79 94
P2 P, Pk Anti-P1 21 6
P NONE Anti- PP1Pk Rare Rare
 P1k P1, Pk Anti-P Very Rare Very Rare
P2k Pk Anti-P, Anti-P1 Very Rare Very Rare

DISEASE ASSOCIATIONS
*Anti-P1: Parasitic Infections
*Anti-PP1Pk or anti-P: Early abortions
*Autoanti-P: PCH
*The P system antigens: receptors for P-fimbriated uropathogenic E.coli (causes UTI).
*The Pk antigen: receptor for shiga toxins, which cause shigella dysentery and E.coli -associated
HUS.
*P is the receptor of human parvovirus B19
Pk provides some protection against HIV infection of peripheral blood mononuclear cells.

13. Which of the following treatment shows resistance to l and i antigens?

I Ficin → enhance
Il. Papain → enhance
Ill. DTT → resistant
IV. Glycine-acid EDTA → resistant
● Three of these
● Two of these
● One of these
● Four of these

The I Blood Group System

ISBT ISBT Clinical Antibody Optimal Reaction Effect of

System System Significance Class Temperature Phase Enzymes
Symbol Number

I 027 NO IgM RT RT Enhanced

(Blaney K.D. & Howard, P.R. (2008). Concepts of

immunohematology (2nd ed.). USA: Mosby)
➢ Wiener and coworkers: I → for “Individuality “
➢ Marsh and Jenkins: reported finding anti-i
➢ I and i antigens → are found on the membranes of leukocytes and platelets in
addition to RBCs.
➢ I and i → have also been found in the plasma and serum of adults and newborns and
in saliva, human milk, amniotic fluid, urine, and ovarian cyst fluid.
➢ I and i antigens are not antithetical ; they have a reciprocal relationship.

The I and i Antigens:

• Both I and i → are high-prevalence antigens
• Infant RBCs → are rich in i;
o I → is almost undetectable.
o During the first 18 months of life,→ the quantity of “I” slowly decreases → as “ I
” increases until adult proportions are reached.
• Adult RBCs are rich in I.
 • INFANTS = “ i “ & small quantities of “ I ”
• ADULTS = “ I ”

Table 4. I and i Antigens

PHENOTYPE STRENGTH OF REACTIVITY WITH
Anti-I Anti-i Anti-IT
(T – TRANSITION)
Adult I Strong Weak Weak
Cord Weak Strong Strong
Adult i Weak Strong Weakest
(Harmening, D. (2019). Modern Blood Banking and y)
Transfusion Practices (7th ed.) F. A. Davis Compan

I Antibodies:
1. Anti-I
• It is a common autoantibody that can be found in virtually all sera.
• It is a typically a benign, weak naturally occurring, saline-reactive IgM autoallutinin
• Testing at 4oC and/or against enzyme treated RBCs may be required to detect
the reactivity.
• It is not associated with HDFN → because the antibody is IgM, and the I antigen
is poorly expressed on infant RBCs.

2. Autoanti-I
• Found in the serum of many normal healthy individuals and is benign → it is
not associated with in vivo RBC destruction.
• Weak, naturally occurring, saline reactive IgM agglutinin.
• The production of autoanti-I → may be stimulated by microorganisms carrying
I-like antigen on their surface.
• Associated with Mycoplasma pneumoniae infections (CLINICAL SIGNIFICANCE)
→ patients with Mycoplasma pneumoniae often develops STRONG
AGGLUTININS with “ I “ SPECIFICITY and can experience
a TRANSIENT episode of ACUTE ABRUPT HEMOLYSIS just as the
infection begin to RESOLVE.

3. Pathogenic autoanti-I
• Associated with Cold agglutinin syndrome (CAS)
• When peripheral circulation cools → in response to low ambient temperatures,
these antibodies attach in vivo and cause
* autoagglutination
* peripheral vascular occlusion (acrocyanosis) or hemolytic anemia.

4. Pathogenic anti-I
• Typically reacts with adult and cord RBCs equally well at room temperature
and at 4oC.
• a strong cold autoagglutinin that demonstrates high-titer reactivity at 4 C and reacts
over a wide thermal range (up to 30 C to 32 C)

5. Alloanti-I
 • Exists as an IgM and IgG antibody → in the serum of most individuals with the
adult “ i ” phenotype.

6. Anti-i
• a rare IgM agglutinin that reacts optimally at 4 C potent examples may be associated
with infections
• Alloanti-i: never been described
• Autoanti-i
o Potent examples are associated with Infectious mononucleosis (IM)
(Epstein Barr virus infections) and some lymphoproliferative disorders.
• IgG Anti-i have also been described and have been associated with HDFN.

The IT Antigen and Antibody

• Reacts Strongly with CORD RBCs, Weakly with NORMAL ADULT RBCs and
MOST WEAKLY with ADULT i RBCs.
• The agglutinin→ recognizes a transition state of “ I “ into “ I “ and designated
the specificity IT (T for “Transition”).
• Examples of IgM and IgG anti-I reacting→ preferentially at 37oC →h ave also
been found in patients with WAIHA, with a special association with Hodgkin’s
disease.

14. Which of the following treatment destroys M and N antigens?

I. Ficin
Il Papain
Ill. DTT
IV. AET
● Two of these
● One of these
● Three of these
● All of these

The MNS Blood Group System

M and N Antigens → ANTITHETICAL ANTIGENS – coded by DIFFERENT ALLES of a SINGLE

GENE
ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number

MNS 002 NO IgM 37oC RT; AHG Destroyed

(SOME)
(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)

S and s Antigens
ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number
 SsU 002 YES IgG 37oC AHG Variable
(HDFN
&HTR)
(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)
➢ MN → destroyed by Ficin, Papain, DTT, AET, bromelain, trypsin, Zzap butnot affected
by DTT alone, 2-aminobenzothiobronium bromide and etc. it requires other enzymes to be
destroyed
➢ located on the outer M of the GPA
➢ Anti-M and anti-N are cold reactive saline agglutinins that do not bind complement or
react with enzyme treated cells
➢ 46 antigens have been included in the MNS system
➢ Landsteiner and Levine: anti-M and anti-N
➢ Walsh and Montgomery: discovered S (its antithetical partner “s” was
discovered in 1951)
➢ U (for “Universal” distribution), an antibody to a high-prevalence antigen, was
named by Wiener. (ORIGINALLY = MNSsU)
➢ Demonstrates “Dosage Effect” → DOUBLE M (MM) GENOTYPE – reacts
STRONGLY than SINGLE M GENOTYPE → depends on the target antigen present on
the target RBC

Glycophorin A (GPA): M and N Antigens

• The major RBC sialic-rich glycoprotein (sialoglycoprotein, SGP)
• GPA → consists of 131 amino acids, with 72 outside the cell membrane.
• M and N antigens → are antithetical → and differ in their amino acids at positions 1 and
5
M: Serine, Serine, Threonine, Threonine, Glycine
1 2 3 4 5
N: Leucine, Serine, Threonine, Threonine, Glutamic acid
• The antigens are well developed at birth.

Glycophorin B (GPB): S, s and U Antigens

• GPB → consists of 72 amino acids, with 43 outside the cell membrane.
• S and s antigens differ at position 29:
o S antigen → has Methionine
o s antigen → has Threonine
• The U antigen is located near the membrane and is always present when S or s is
inherited.
• The antigens are well developed at birth.
• S and s antigens are less easily degraded by enzymes because the antigens are located
farther down the glycoprotein.
• Anti-S and anti-s are IgG antibodies, reactive at 37 C and the antiglobulin phase. They may
bind complement and have been associated with HDFN and HTRs.
• The S-s-U phenotype is found in blacks
• Anti-U is usually an IgG antibody and has been associated with HTRs and HDFN

Anti-M
 • MORE COMMON in CHILDREN than Adults
• Particularly COMMON in PATIENTS with BACTERIAL INFECTIONS
• They do not bind complement→ regardless of their immunoglobulin class, and they do
not react with enzyme treated RBCs.
• It rarely causes HTRs, decreased red cell survival, or HDFN.
Anti-N
• Examples of N-like antibody have been found more frequently in dialysis patients
exposed to formaldehyde-sterilized dialyzer membranes.
Anti-S, Anti-s, and Anti-U
• Clinically significant IgG antibodies→ that can cause decreased red cell survival and
HDFN.
• They may bind complement, and they have been implicated in severe HTRs with
hemoglobinuria.
U phenotype
• Typically IgG
• Has been reported to cause severe and fatal HTRs and HDFN.
• RBCs usually type S-s-U-
o these individuals can make anti-U in response to transfusion or pregnancy.
• U antigen→ is resistant to enzyme treatment.
GPAM
• may serve as the receptor → by which certain pyelo-nephrogenic strains of E.coli→
gain entry to the urinary tract.
• The malaria parasite Plasmodium falciparum → appears to use alternative receptors,
including GPA and GPB for cell invasion.

15. Which of the following antibodies are associated with severe HTRs?
● Anti-K
● Anti-Kpa
● Anti-Jsb
● Anti-Jsa

The Kell and Kx Blood Group System

Kell
ISBT ISBT Clinical Antibody Optimal Reaction Effect of
System System Significance Class Temperature Phase Enzymes
Symbol Number

KEL 006 YES IgG 37oC AHG No effect

(HDFN
&HTR)
(Blaney K.D. & Howard, P.R. (2008). Concepts of immunohematology (2nd ed.). USA:
Mosby)

➢ The Kell blood group system → consists of 32 high-prevalence and low-prevalence

antigens.
➢ Anti-K was identified in 1964 in the serum of Mrs. Kelleher.
➢ The associated antigen Kx → is the only antigen in the Kx system, ISBT number 019
and symbol XK.
 ➢ Kell blood group antigens are found ONLY on RBCs.
➢ The associated Xk protein → is found in erythroid tissues and in other tissues, such
as brain, lymphoid organs, heart, and skeletal muscle.
➢ The K antigen can be detected on fetal RBCs as early as 10 weeks and is well
developed at birth. → HDFN
➢ The k antigen has been detected at 7 weeks.
➢ Other antigens: Kpa, Kpb, and Kpc, Jsa and Jsb Antigens
➢ The antigens are not denatured by enzymes ficin and papain → but are destroyed by
trypsin and chymotrypsin when combined. Thiol- reducing agents→ such as 100 to 200
mM DTT, 2-mercaptoethanol (2-ME), AET, and ZZAP→ destroy Kell antigens → but not
Kx. Glycine-acid EDTA → also destroys Kell antigens.
➢ IgG in nature which is reactive at AHG phase
➢ k antigen is high prevalence

K and k Antigens
• Excluding ABO,→ K is rated second only to D in immunogenicity.
- Most anti-K appears to be induced by pregnancy and transfusion.
Anti-K
• Outside the ABO and Rh antibodies, → anti-K is the most common antibody seen in
the blood bank.
• The antibody is usually made in response to antigen exposure through pregnancy and
transfusion and can persist
for many years. It has been associated with HTRs and HDFN.
• The most reliable method of detection is the IAT (INDIRECT ANTIGLOBULIN TEST)
• Antibodies usually do not bind the complement.
• Depressed reactivity of anti-K is observed in some LISS reagents.

Kell ANTIBODIES
Antibodies to Kpa, Jsa and Other Low-Prevalence Kell Antigens
• Antibodies to the low-prevalence Kell antigens are rare → because so few people are
exposed to these antigens.
• The serologic characteristics and clinical significance of these antibodies parallel
anti-K.
Antibodies to k, Kpb, Jsb, and Other High-Prevalence Kell Antigens
• Antibodies to high-prevalence Kell system antigens are rare → because so few people lack
these antigens.
• They also parallel anti-K in serologic characteristics and clinical significance.

The Kx Antigen
• Kx is present on all RBCs → except those of the rare McLeod phenotype.
• Ko and Kmod phenotype RBCs have increased Kx antigen.
• Red cells with normal Kell phenotypes carry trace amounts of Kx antigen.
• NOTE: Kell ANTIGEN & Kx ANTIGEN are INVERSLY PROPORTIONAL
The Ko Phenotype and Anti-Ku (K5)
• Ko RBCs lack expression of all Kell antigens.
• Immunized individuals with the Ko phenotype → typically make an antibody called anti-
Ku (K5) → that recognizes the “Universal” Kell antigen (Ku) - present on all RBCs
except Ko.
 • Anti-Ku has caused both HDFN and HTRs.
The McLeod Phenotype
• It is very rare and is seen almost exclusively in males as a result of the X
chromosome-borne gene.
• Decrease Kell system antigen expression
• Clinical manifestations: abnormal RBC morphology, compensated haemolytic anaemia
and neurologic and muscular abnormalities, X-linked chronic granulomatous disease
• McLeod phenotype RBCs → Lack Kx and another high-prevalence antigen, Km, and
have marked depression of all Kell antigens.
• Significant proportions of the RBC in individuals with the McLeod phenotype → are
acanthocytic →with decreased deformability and reduced in vivo survival.
• Individuals with the said phenotype have a chronic but well compensated hemolytic
anemia characterized by reticulocytosis, bilirubinemia, splenomegaly, and reduced
serum haptoglobin test.
• It is associated with Chronic Granulomatous Disease (CGD).
• CGD is characterized → by the inability of phagocytes to make NADH oxidase, - an
enzyme important in generating H2O2, which is used to kill ingested bacteria.
• Not all males with the McLeod phenotype have CGD, nor do all patients with CGD
have the McLeod phenotype.

McLeod Syndrome
• McLeod individuals → develop a slow, progressive form of muscular dystrophy between
ages 40 to 50 years and
cardiomegaly (leading to cardiomyopathy) as well as elevated serum creatinine
phosphokinase levels of the MM
type (cardiac/skeletal muscle) and carbonic anhydrase III levels.

16. Which of the following Kidd phenotype has also been identified in Filipinos?
● Jk (a+b-)
● Jk (a-b+)
● Jk (a+b+)
● Jk (a-b-)

The Kidd Blood Group System

ISBT ISBT Clinical Antibody Optimal Reaction Effect of

System System Significance Class Temperature Phase Enzymes
Symbol Number

JK 009 YES IgG 37oC AHG Enhanced

(HDFN
&HTR)
(Blaney K.D. & Howard, P.R. (2008). Concepts of
immunohematology (2nd ed.). USA: Mosby)
➢ In 1951, Allen and colleagues reported finding an antibody in the serum of Mrs. Kidd,
→ whose infant had HDFN.
➢ Jka and Jkb
-commonly found on RBCs of most individuals.
 ➢ Jka and Jkb antigens → are well developed on the RBCs of neonates.
Jka has been detected on fetal RBCs as early as 11 weeks;
Jkb has been detected at 7 weeks.
➢ Jk allele or null phenotype → is a silent allele that produces neither Jka nor Jkb
antigens nor Jk3; it is a common allele in Polynesians, Filipinos, and Chinese
; the JkJk genotype → results in a Jk (a-b-) phenotype.
; most abundant among Polynesians
; also reported among Fresh, English and British
➢ Jk (a-b-) phenotype can also be derived by the action of a dominant suppressor
gene, “ In (Jk) “ – for “Inhibitor”.
➢ Anti-Jk3 → has been associated with severe immediate and delayed HTRs and with
mild HDFN.

Anti-Jka and Anti-Jkb

• Kidd antibodies have a notorious reputation in the blood bank.
• They demonstrate dosage are often weak, and are found in combination with other
antibodies, all of which make them difficult to detect.
• Agglutination reactions are best observed by the IAT
• Antibody reactivity can also be enhanced →
(1) LISS (LOW IONIS SALINE SOLUTION) or PEG (POLYETHYLENE GLYCOL) →
(promote IgG ATTACHMENT) ,
(2) by using 4 drops of serum instead of 2 (to increase antibody-to-antigen ratio) or
(3) by using enzymes such as ficin or papain.
• The antibodies are produced in response to antigen exposure through transfusion or
pregnancy.
• The antibodies do not store well; antibody reactivity quickly declines in vitro and the
difficulty in detecting Kidd antibodies are reasons why they are common cause of
HTRs, → especially of the delayed type.

Kidd Blood Group System:

• May bind complement and are made in response to foreign RBC exposure during pregnancy or
transfusion
• Kidd system antibodies are a common cause of delayed HTRs
• Kidd system antibody reactivity is enhanced with enzymes LISS, and PEG
• Demonstrate a dosage effect, often weak and are often found in combination with other
antibodies
• IgG and react at AHG phase of testing

Table 7. Characteristics of Antibodies in the Kell, Duffy, and Kidd Blood Group Systems
CHARACTERISTIC KELL SYSTEM DUFFY SYSTEM KIDD SYSTEM

Red cell stimulated YES YES YES; weak antibody

IgG YES YES YES
Reactive with AHG YES YES YES
Effect of Enzymes NO EFFECT NO REACTIVITY ENHANCED
Clinical YES YES YES
Significance
 Unique Features Anti-K most Fy (a-b-) resist Bind complement
common infection by Common cause of
Anti-Jsb more P. knowlesi and P. Delayed HTRs.
common in blacks vivax
Anti- Kpb more
common in whites

(Blaney K.D. & Howard, P.R. (2008). Concepts of

immunohematology (2nd ed.). USA: Mosby)

17. Which of the following antigens is found in Tamm Horsfall glycoprotein?

● Ata
● Jra
● Vel
● Sda

Sda Antigen:
• High prevalence carbohydrate antigen named for Sid
• His RBCs has been used for many years as a panel donor and they reacted strongly with
examples of a new antibody
• The soluble form of Sda is Tamm-Horsfall glycoprotein found in urine
• The antigen is not expressed on RBCs of newborns but is in their saliva, urine, and meconium

18. Which of the following structure carries the LW antigens?

● None of the Choices
● ERMAP
● AE1
● ICAM-4

ICAM-4 (LW-016)
• A member of the immunoglobulin superfamily
• LW gene ICAM4 is located on chromosome 19 at position 19p
• Part of the Band 3 microcomplex

ERMAP
• (Sciana) SC gene ERMAP is located on chromosome 1 at position 1p
• Product of the gene is a protein called erythroid membrane associated protein (ERMAP)
• RBC adhesion protein

AE1:
• Carried on band 3 which is a major integral RBC membrane glycoprotein with 1 million copies in
RBC; seen on Diego antigens
• Band 3 is also known as the red blood cell anion exchanger (AE1) or solute carrier family-4
anion exchanger, member (SLC4A1)

Note: 1940, Landsteiner and Weiner reported that an antibody produce in rabbit after injection with
RBCs of the rhesus monkeys reacted with 85% of Human RBCs which is called, anti-Rh
19. Which of the following is the swollen form of chromatin in cells and is also considered to be more
active in the synthesis of RNA for transcription?
● Euchromatin
● Achromatin
● None of the choices
● Heterochromatin

Staining Patterns:
➢ Heterochromatin: stains as dark bands
➢ Achromatin: stains as light bands and consist of highly condensed regions that are usually not
transcriptionally active
➢ Euchromatin: is the swollen form of chromatin in cells, which is considered to be more active in
the synthesis of RNA for transcription

Note: the nucleus of the cell contains the genetic material which is important for replication and is of
highly organized in structure.

20. Who among the following individuals developed a mathematical formula that allowed the study of
Mendelian inheritance in great detail?
● Hardy and Weinberg
● Weinberg
● Mendel
● Mendel and Landsteiner
● Hardy

Hardy: a British mathematician

Weinberg: German physician

p = gene frequency of the dominant

allele
q = gene frequency of the recessive
allele
21. Which of the following trait is carried by either parent or both parents but is not generally seen at
the phenotypic level unless both parents carry the trait?
● Recessive ● Amorph
● Genotype ● Phenotyp
● Autosomal

• Autosomal Recessive - trait is expressed only when an individual is HOMOZYGOUS for the Allele and
inherited the recessive allele from both parents.
• Phenotype – Includes an ENZYME to control a BLOOD GROUP ANTIGEN
o Checked through: Length of the long bones of the skeleton, Ratio of Muscle Fibers, Levels of
Hormones produced and obvious traits such as Eye, Hair, Skin Color

22. It is a gene that does not produce any obvious, easily detectable traits.
● Recessive ● Phenotype
● Amorph ● Genotype
● Autosomal
23. According to AABB Standards, which of the following is an example of an indefinite deferral?
● Dexter, who lived in England for 6 months in 1981
● Benjamin, who had admitted having a sexual contact with a prostitute 3 days ago
● Cielo, who took tegison 2 weeks ago
● Bernadatte, who took Plavix 3 days ago

• Indefinite deferral – donors are unable to donate blood for a UNSPECIFIED period of time, due to current
regulatory requirements in each country
o Cannot donate blood until current regulation changes
o Dura mater transplant or pituitary growth hormone from a Human Cadaver
• Temporary deferral – Donor is not able to donate blood for a LIMITED period of time
• Permanent deferral – Donor can never be eligible to donate blood for someone else

Creutzfeldt-Jakob Disease (1980-1996)

- Prion Disease
- Transmissible Spongiform
Encephalopathy

- VARIANT ONLY (blood

relative of diagnosed
person)
- but if were to be
DIAGNOSED it would be a
PERMANENT DEFERRAL
24. Which of the following medications has a 3-year deferral?
● Soriatane ● Tegison
● Avodart ● Dutasteride

• Avodart = Dutasteride → 6 MONTHS

• Tegison → PERMANENT

25. How many days will be the deferral period for a platelet donor who took Plavix?
● 14 days – from last dose ● 5 days
● 2 days ● 7 days
• Plavix or Ticlid – medication that can decrease the chance of Heart Attack or stroke at risk of this
conditions → can affect PLATELETS but will not inhibit the WHOLE BLOOD DONATION (no
deferral)
•
26. What is the deferral period for a person who received a skin graft?
● 12 months ● 3 years
● Permanent ● 6 months

27. Which of the following containers is required if platelets are going to be prepared?
● Single container with in-line filter ● Collection container with diversion
● Single container pouch
● None of the choices
• Container with diversion pouch- this system will allow diversion of the first 30-45 mL of blood being
collected into the pouch at the collection tubing instead of the collection blood bag
o DIVERSION POUCH (1st) → before main Blood bag because this will reduce Bacterial
Contamination
o Bacteria from the skin will be diverted unto the pouch instead of the main blood bag
o Blood from the diversion bag can be used for laboratory test / screening

• Single container with in-line filter

- Filter – removes clots and small clamps of platelet; also filters White blood cells (WBC) during
collection and storage
- Utilized for LEUKO-REDUCED BLOOD COMPONENT

28. When an anticoagulant-preservative is present, the minimum hematocrit in whole blood units is
usually around
● 36% ● 34%
● 35% ● 33%

• Whole blood collection – most commonly collected then separated into components
o Rarely transfused directly – due to the different components (can cause OVERLOAD) it
has and it is only given to those who has SEVERE BLOOD LOSS
o SEVERE HEMORRHAGES such as those resulting in trauma may benefit from fresh
whole blood when platelets are not available
29. Which of the following is the most common cause of deferral during a physical examination of a
blood donor?
● Pulse ● Blood pressure
● Temperature ● Hemoglobin

• 1st Hemoglobin → Blood pressure → Pulse → others

• High Blood pressure – leading cause of Heart attack (some researches shows that regular blood
donation can be beneficial) → may also help regular blood flow and reduce arterial blockages
• Hemoglobin → > 12.5 g/dL (>38%) is the cut-off (MOST COMMON DEFERRAL)

30. Which of the following components should not be prepared from Whole blood labeled as low-
volume units?
I. RBCS IlI. FFP
I. Platelets IV. Cryoprecipitate
● Three of these ● One of these
● Two of these ● All of these

• RBC’s – labeled as low – volume units are made able for transfusion when:
o 300- 404 mL of whole blood in 450 mL bag
o 333- 449 mL of whole blood in 500 mL bag

31. How many hours can FFP be prepared after Whole Blood collection?
● within 12 hours ● within 4 hours
● within 8 hours ● within 6 hours

• Plasma must be FROZEN within 8 hours or 24 hours depending on which Frozen plasma product you
are going to do.
o FFP – 8 hours → CRYOPRECIPITATE and CRYOPOOR PLASMA
o PF24 – 24 hours or liquid plasma
o ACD – 6 Hours
32. Hartzell wants to donate blood but she only weighs 45 kgs. How many ml of blood can she donate?
● 405 mL ● 420 mL
● 375 mL ● 400 mL
• Maximum blood to collect 10.5 mL/kg
- 10.5 mL/kg x 45 kg = 405 mL

33. Which of the following should be the flow rate when blood components are to be transfused
rapidly?
● 15 to 25 mL/ second ● None of the choices
● 10 to 25 mL/ second→ 600 – 1500 mL/min ● 5 to 15 mL/second
• Intravenous Catheter size ranges used for cellular transfusion of blood components is 14- 22 gauge.
o 18-20 gauge → General Adult Population, provide adequate flow rates without excessive
discomfort to the patient
o 22-24 gauge → Infant / Toddler, requires transfusion through a syringe

• RAPID INFUSION – the use of PRESSURE INFUSION, the Large bore Administration Tubing, the 8 French-
intravenous catheter → can decrease the transfusion time without Inducing any Hemolysis.
o Use specific tubing’s with its appropriate filter
• Rapid Infusion rates → can also introduce HYPOTHERMIA
• Multiple Units are infused in Tubing the FLOW RATE may DECAREASE appreciately

34. Which of the following is the shelf life of packed RBs with CP2D anticoagulant?
● 42 days ● 15 days
● 35 days ● 21 days
 • ACD-A → Apheresis Components

35. What is the storage temperature of platelets collected via apheresis?

● 37 C with agitation ● 2-4C
● 20-24 C with agitation ● 20-24 C without agitation

• Agitation → facilitate OXYGEN transfer into the Platelet bag → Oxygen consumption of platelets
o OXYGEN – maintenance of Platelet pH → which is a Key Parameter in maintaining the
VIABILITY of platelet in vivo when stored into 20-22 C
• Platelet Storage Lesion → loss of platelet QUALITY during storage
o During storage a varying degree of platelet activation releasing some intracellular granules
and decline in ATP & ADP
o Through storage → Oxygen tension can sink → causing Increase Glycolysis rate of the
platelets to compensate in the decrease of ATP regeneration from the Oxidative metabolism
→ can also increase Lactic acid (need Buffer) → Fall in pH
• Buffer: Bicarbonate (HCO3)

36. When will be the expiration date of a unit of packed RBC irradiated July 4, 2021?
● July 30, 2021 ● August 1, 2021
● July 31, 2021 ● August 2, 2021
 • packed RBC irradiated → EXPIRATION: 28 days from irradiation or original outdate
• which is SOONER from date of irradiation and original outdate will be FOLLOWED

• Expiration of Granulocyte and Platelets are not impacted by the Irradiation upon irradiating it early
• Irradiated Blood Product USE: Immunocompromised and Immunosuppressed → so that the T-
Lymphocyte will not engraft and attack the host tissues
• Irradiation of Blood Components (RBC, platelets, Granulocytes) → indicated to prevent Transfusion
Associated Graft vs Host disease:
o Immunocompromised receiving a Bone marrow or Stem cell transplant
o Fetus undergoing an intrauterine transfusion
o Transfusion of component collected from Blood Relative
o HLA match Donor
• Gamma Irradiation
o 25 Gy done in the central portion of Blood Unit
o 15 Gy Any part of the Blood Unit
• Achieved through any Radioactive source such as:
o CECIUM 137
o COBALT 60
o X- RAY

37. A unit of cryoprecipitate is thawed at 8:00 AM, what time will be its expiry?
● 1:00 PM ● 2:00 PM
● 12:00 PM ● 6:00 PM

• CRYOPRECIPITATE: thawed quickly @ 30- 37C after is stored @ room temperature 22-24 C until
used
• The pre-storage pooled cryoprecipitate and single units of cryoprecipitate must be transfused with
6 hours
o Pooled Cryoprecipitate (Open System) → 4 hours
• Indication:
o Factor 13 deficiency as a source of Fibrinogen for Hypofibrinogenemia
o as a secondary line of treatment for Classic Hemophilia
o Von willebrand disease
• Not be used to treat Hemophilia A or Von willebrand disease, if VIRUS inactivated or recombinant
factor preparations are available

38. Which of the following is the shelf-life of irradiated platelets?

● 36 hours ● 24 hours
● 72 hours ● 120 hours
* Irradiation has no effect in the shelf life of irradiated platelets, which is sooner will be used as outdate
39. Which of the following is the storage temperature of Normal Serum Albumin?
● 3-6 C ● 2-10 C
● 2-4 C ● 1-6 C

• 25% Normal Serum Albumin is

CONTRAINDICATED in patients
who are Dehydrated unless
followed by Crystalloid infusion for
volume Expansion

40. Which of the following is the shelf life of irradiated granulocytes?

● 3 days
● 2 days
● 24 hours
● 5 days

41. Which of the following methods are used for RBC leukoreduction?
I. In line filter that can be attached to the whole blood unit and filtered via gravity, plasma and RBCs
can then be prepared.
II. Plasma is initially removed from the whole blood unit and then packed cells are passed through an
inline reduction filter
lII. A sterile docking device can be used to attach a leukocyte reduction filter to a unit of RBCs which is
allowed to flow via gravity
● One of these ● None of these
● Two of these ● Three of these

• LEUKOCYTE-REDUCED RBCs
o Average unit of leukocyte reduced RBCs contain <5x106 leukocytes
o After Leukocyte reduction with these filters, most leukocyte count are <1x10 6
o Donor leukocytes may cause Febrile non-hemolytic transfusion reaction, transfusion
associated graft vs host disease, transfusion related immune suppression/ transfusion
induced immunomodulation.
o HLA is responsible for HLA alloimmunization. Abs also harbor CMV→ thus Leukocyte
reduction.
o
42. Which of the following is the FDA and AABB recommended minimum dose of gamma irradiation for
RBCs?
● 35 Gy
 ● 20 Gy ● 30 Gy

• 25 Gy on the central portion of the blood unit

WHY IS GAMMA IRRADIATION DONE?
- To reduce any substances that can cause transfusion reaction to immunocompromised px.
• 15 Gy- delivered to any part of the unit
• Irradiation may be achieved by using either a radioactive source (cesium-137 or cobalt-60) or X-ray.
- Radiochromic film label affixed on the component before placing on the metal canister- Used to determine
complete irradiation. Darkening of the film= complete irradiation
- Irradiation equipment require annual and semi-annual dose delivery using an outside source.
- Detection device is wil be sent through an irradiation cycle and the minimum and maximum dose will be
determined.
- As the irradiator decays, the time for exposure should be prolonged.
- 28 DAYS- LOST LIFE FOR IRRADIATED RBCs

● 25 Gy

43. The preparation of platelets from Platelet Rich Plasma consists of which of the following?
● Hard spin ● Soft spin then hard spin
● Hard spin then soft spin ● Soft spin

• Soft spin of WB = platelet rich plasma → hard spin PRP = plasma from PRP
**Plasma can be removed from the platelet pellet → held undisturbed for 30-60 minutes before
being resuspended.

44. Plasma units prepared from buffy-coat depleted units have approximately how many mL more
plasma than plasma prepared by the PRP method?
● 35-40 mL ● 45 mL
● 40-70 mL ● 41 mL

• Plasma units prepared from buffy-coat depleted units have approximately 41 mL more plasma
than plasma prepared by the PRP method

45. How many viable lymphocytes is present in thawed FFP prepared from the soft spin method?
● None of the choices ● 0.04 to 3.6 X 10^6 and 0.47 to 45.4 X 10^6
● 0.04 to 3.6 X 10^6 ● 0.47 to 45.4 X 10^6

• Hard spin: 0.47 to 45.4x106

• Soft spin: 0.04 to 3.6 X 106
• Second spin method: 0.4-37.2x106

46. Which of the following component is processed into derivatives such as albumin and/or
immunoglobulins?
● Recovered Plasma
 ● Platelet Rich Plasma ● Platelet Poor Plasma

• Recovered plasma = converted plasma and liquid plasma to an unlicensed component

- Shipped into a fractionator and processed into derivatives.
- How to ship→ the lab must have a supply agreement with the manufacturer
- Has no expiration date- thus records are retained indefinitely
- Storage condition are from the one who fractioned it
- FFP used as a human plasma or for fractionation in Europe must comply to the requirements of
European pharmacopeia guidelines

● FFP
47. Which of the following ways are used to prepare cryoprecipitated AHF products prior to
transfusion?
I. Single units can be stored for 6 hours after thawing
II. Units pooled using a "close" system can be stored for 4 hours after thawing
Ill. Units pooled by an "open" system either before storage or after thawing can be stored for 6 hours after
thawing or post-thaw pooling.
• Single units can be stored for 6 hours after thawing
- >6 hours- expired na ang cryoprecipitate
• CLOSED SYSTEM- ONLY 1 single product from donor using 1 tubing, it can be stored for 6 hours after thawing
• Pooled- from multiple blood bags then combined
• OPEN SYSTEM- Units pooled from open system can be stored for 4 hours after thawing

● None of the choices ● All of these

● Two of the ● One of these

48. According to AABB standards, at least how many days old are the RBC units to be issued for
neonatal or pediatric transfusions?
● < 6 to 7 days ● None of the choices
● < 3-5 days ● < 7 to 10 days
- Some prefer those without additive solutions
- Depends on local practice

49. Which of the following component was introduced to increase the viral safety of plasma?
● Quarantine FFP and Quarantine ● None of the choices
cryoprecipitate ● Quarantine cryoprecipitate
● Quarantine FFP

• Quarantine FFP
o Introduced to INCREASE VIRAL SAFETY of PLASMA
- Council of Europe notes that quarantine FFP can be released from quarantine after the donor returns to
the blood center and has repeatedly negative test result for:
▪ Hepa B and C, HIV-1 and 2 beyond a minimum quarantine period that is greater than
the diagnostic window period for viral infection, typically 6 months
▪ With the use of nucleic acid test for the window period of FFP can be reduced

50. Which of the following are used for pathogen reduction of plasma?
I. Methylene blue
Il. Psoralen
Ill. Riboflavin
IV. Solvent/detergent treatments
● Two of these ● All of these
● One of these ● Three of these

• pathogen reduction of plasma

o Methylene blue- added to thawed FFP followed by inactivation using white light→ methylene
blue is removed by filter→ Plasma can be frozen
o Psoralen (amotosalen)→ removed from plasma via adsorption device→ frozen at -18C
o Riboflavin
o Solvent/ detergent treatments
- Used to inactivate microbial agents for pathogen reduction

51. According to AABB standards, thawing of cryoprecipitate is to be performed at what

temperature?
● 2-6C ● 1-6C
● 2-4C ● None of the choices
• Cryoprecipitate can be stored for 36 months at <-25
• -18 to -25C= 3 months
• FFP- thawed at 30-37C

52. Which of the following cryoprotective agents is most commonly used for cryopreservation of
platelets?
● HES ● Glycerol
● Glycerol and DMSO ● DMSO

Cryopreservation - Not usually used

• 2-6% Dimethyl sulfoxide (DMSO) – Commonly used for cryopreservative for platelets
- for autologous platelet transfusion
- for patients who are refractory to allogenic platelets
o Cryopreserved platelets can be preserved for 2 years→ after thawing platelet recovery site can
be 75%
• Glycerol- most commonly used for RBC cryopreserve
- Added in either high or low concentrations to RBCs within 6 days of collection
• Hydroxyethyl starch (HES)- common sedimenting agent. Causes RBCs to aggregate→ complete
sedimentation. Protects RBC by forming a glassy shell. Used in reducing red cell content. Starch/
gelatin/dextran/ polygelin.

53. Which of the following are the major indications for Whole Blood transfusion?
I. Symptomatic anemia with large volume deficit
II. Severe chronic anemia
IIl only
● None of the choices
 ● Iand Il ● I only
• Symptomatic anemia with large volume deficit
- Use of WB is not common because of transfusion overload
- Use of WB: Increase oxygen carting ability. Increase blood volume. For infectious diseases: hemolytic/
septic/ toxic/ allergic reactions. Iron overload, TACO, TRALI, TRGVHD.
• DO NOT use WB with people with Severe Chronic anemia. They do have low RBC BUT it is compensated
with increase in blood volume (plasma)- only PRBC→ WB to them will lead to pulmonary edema and heart
failure

54. Which of the following are the indications for platelet transfusion?
I. Thrombocytosis with bleeding or invasive
Procedure → THROMBOCYTOPENIA
II. Chemotherapy for malignancy
III. DIC
IV. Massive transfusion
● Two of these ● Three of these
● All of these ● One of these
• Chemotherapy for malignancy (<5,000-10,000 platelets/uL)
• DIC (platelets are destroyed <50,000/uL)
• Massive transfusion (rapid consumption of platelets for hemostasis, dilution of platelets by
resucitation of fluids and RBC transfusion; 50,000-100,000/uL)
• Thrombocytopenia not cytosis

**Platelet is used for the primary hemostatic plug and maintenance of hemostasis

55. Leukocyte-reduced RBs must contain how many remaining leukocytes are in the BC unit?
● 3X 10^11 ● 5 X10^11
● 5X 10^6 ● 3 X 10^ 6

• Leukocyte-reduced RBs must contain < 5 x 10^6 leukocytes to avoid any Febrile non-transfusion
reaction, Transfusion related graft vs host disease & Transfusion related Immune suppression /
transfusion induced immunomodulation

56. Immune globulin is prepared primarily from which of the following immunoglobulin?
● IgA
 ● lgG ● IgM

• IgG
o Immune globulin from pooled plasma are primarily IgG
o Small amounts of IgM and IgA may be present
o 2 administration methods:
▪ 1. Given via intramuscular- You cannot use intramuscular products to vascular because it
may cause problems.
▪ 2. Intravascular- Intravascular products naman should be administered slowly to lessen
risk of reaxn. Used increasingly in therapy of autoimmunediseases: myasthenia gravis,
autoimmune thrombocytosis
o Used for patients with congenital hypogammaglobulinemia and for patients exposed to
Hepa A and measles
o Hyperimmune globulins are available to treat viruses i.e. Hepa B, varicella zoster, rabies, mumps
and others.
▪ Produced from the plasma of donors who have Ab titers against the virus. Dose is from the
ano of manufacturer.
▪ Will cause: PASSIVE IMMUNITY, so it must be accompanied with active immunization.

● lgD

57. All of the following are the responsibilities of a medical technologist during a transfusion reaction,
EXCEPT
● Report findings to the transfusion service ● Perform primary testing on pest reaction sample
physician ● Generate a final transfusion report including
● Perform additional testing as per transfusion interpretation of the transfusion reaction and
service physician orders recommendations for future transfusions

58. Which of the following correctly defines acute hemolytic transfusion reaction?
● Transfusion reaction in which signs and symptoms present within 12 hours of transfusion
● Transfusion reaction in which signs and symptoms present after 12 hours of transfusion
● Transfusion reaction in which signs and symptoms present within 24 hours of transfusion
 ● Transfusion reaction in which signs and symptoms present after 24 hours of transfusion

• Transfution rxn in w/c s/s present within 24 hours of transfusion

- HTR- Rapid destruction of RBCs due to Ab mediated incompatibility

- acute hemolytic transfusion reaction – defined as the combination of the signs and
symptoms which are associated with biochemical evidence of haemolysis and serologic
evidence of RBC incompatibility that occurs within/ during 24 hours after/of transfusion

59. Which of the following transfusion reaction presents with body temperatures usually 2C or more
above normal and rigors that can be accompanied by hypotension?
● TACO ● TAS
● FNHTR ● TAGVHD

• Transfusion Associated Sepsis→ s/s: rigors; fevers and tachycardia

o Other s/s: shock, low back pain, DIC, inc or dec in systolic pressure
o Platelets are associated with the highest risk of sepsis and fatality→ Why? Because sepsis
due to sepsis can occur hours after the transfusion

60. Which of the following transfusion reactions can be treated with subcutaneous epinephrine?
● TAS ● TRALI
● Severe allergic reaction ● TACO

• Transfusion associated Circulatory Overload (TACO)- adverse reaction characterized by acute respiratory
distress acquired from pulmonary edeme caused by intravascular volume because of Rapid transfusion/
increased blood volume.
- s/s: seen within 2 hours after transfusion but they take up to 6 hours to be seen
- 2nd most common reason for death of HTR by FDA

• TRALI- also with acute respiratory distress BUT it is caused by adverse effects of transfusion. No Diagnostic
test for TRALI.
o Diagnosis is primarily made up according to the clinical criteria that support the diagnosis and
exclusion of other possible causes of acute lung injury