ABO AND CARBO BLOOD GROUP SYSTEM Flashcards
Which terminal protein of the ABO oligosaccharide chain MUST be present and is the required precursor for the biosynthetic expression of A and B antigens? A. N-acetylgalactosamine B. Fucose C. Galactose D. N-acetylglucoseamine
B. Fucose
This is the H antigen (ABO precursor)
A - added to form A antigen
C - added to form B antigen
D - this is part of the carb chain that the H antigen is formed on
What is the enzyme responsible for the biosynthesis of A and B antigens?
Glucosyltransferase
A1 and A2 can be distinguished from each other by serologic testing. Which of the ff is true?
A. A2 cells agglutinates with both Dolichus biflorus lectin and Anti-H lectin Ulex europaeus
B. A1 cells agglutinates with Dolichus biflorus lectin, but not A2. A2 cells agglutinate with Anti-H lectin Ulex europaeus
C. A1 cells agglutinates with both Dolichus biflorus lectin, but not with Anti-H lectin Ulex europaeus
D. A2 agglutinate with both Dolichus biflorus lectin but NOT with Anti-H lectin Ulex europaeus
B. A1 cells agglutinates with Dolichus biflorus lectin, but not A2. A2 cells agglutinate with Anti-H lectin Ulex europaeus
Dolichos acts as Anti-A1, A2 cells have more H antigen than A1
______ is an ABO phenotype that occurs when an ABO gene encoding ann ABO glycosyltransferase can use both A and B specific nucleotide sugars in a more equal way than B(A) or A(B) phenotype
Cis AB
Which of the ff is true about ABO antibodies?
A. Majority of Anti-A and -B from group O idividual are of IgG isotypes
B. Anti-A and -B are generally of IgM isotype
C. Anti-A and/or -B is clinically significant and causesABO HDFN
D. Anti-A1 is mostly IgG, and is considered clinically significant
A. Majority of Anti-A and -B from group O idividual are of IgG isotypes
B- in group A or B individuals,
C- RHD HDFN is more problematic; ABO is mostly of IgM and cannot cross the placenta
D - they are usually IgM, reacts at room temperature and mostly clinically insignificant
Which of the ff requires the routine completion of reverse or serum group typing?
A. Typing infants 4 months and younger
B. ABO typing donors at the time of donation
C. Confirmation testing of labeled previously typed donor red cells
D. None of the above
B. ABO typing donors at the time of donation
A and B does not require backtyping
Which of the ff causes an ABO discrepancy resulting in problems in red cell testing/ front typing?
A. A group A pt transfused with group O platelets
B. Fibrin clots in plasma or incompletely clotted serum
C. Neutralization of Anti-A and Anti-B typing reagents by high concentrations of A or B blood group substance in serum resulting in unexpected negative reaction with serum or plasma suspended red cells
D. Cold allo or auto antibodies that are reactive with corresponding antigen positive reverse grouping cell
C. Neutralization of Anti-A and Anti-B typing reagents by high concentrations of A or B blood group substance in serum resulting in unexpected negative reaction with serum or plasma suspended red cells
- remember that A, B, H antigens may exist in secretions (like Lewis ag)
A- causes unexpected passively acquired Anti-A (from plt unit) in pt’s plasma (reverse typing prob)
B - these can be mistaken as red cell agglutinates when performin reverse typing
D - Ex. A1 red cell reagen is positive for M antigen and wil react if pt has anti-M in serum (reverse typing prob)
What should be the appropriate next step in resolving ABO discrepancies in patient’s with suspected B(A), acquired B or A(B) phenotype?
A. Repeat the test with the same sample and reagents to exclude the possibility of technical error
B. Retest patient sample using different monoclonal and polyclonal reagents
C. Enhance ag-ab binding by incubating red cells at 4C or use enzyme treated red cells
D. Wash the red cells then repeat testing sing same reagents
B. Retest patient sample using different monoclonal and polyclonal reagents
A - this is always the first step, esp if encountered for the first time
C - do this ig there is weak/ missing ABO ag or ab
Which of the ff would resolve an ABO discrepancy where red cells are unexpectedly agglutinationg due to IgM isoantibodies?
A. Wash red cells with warm saline
B. Perform saline replacement
C. Test red cells using Dolichos biflorous
D. Incubate red cells with dithiothreitol or 2-aminoethylisothiouronium bromide
D. Incubate red cells with dithiothreitol or 2-aminoethylisothiouronium bromide
-reduces disulfide bonds on IgM molecules = decreases polyvalency and ability to agglutinate red cells
A - if caused by cold auto
B - if rouleaux formation is observed in reverse typing
C - if anti-A1 is suspected to be causing discrepancy
What is the correct order of the ABO blood group with the highest to least amount of H antigen expression? A. O > A1 > B > A2B > A2 > A1B B. O > A2 > B > A2B > A1 > A1B C. O > A1 >A1B > B > A2B > A2 D. O> A2 > A1 > B > A2B > A1B
B. O>A2>B>A2B>A1>A1B
H expression is highest ub group O individuals. H is converted to A and B antigens in group A and B individuals
Which of the ff can serologically confirm if a patient has a bombay phenotype (Oh)?
A. Type patient using anti-H and for Le(b) since bombay phenotype individuals have high expression of H antigens in their red cells and typically type as Le(b-)
B. Check their clinical history for leukocyte adhesion defeciency type 2 (LAD2)
C. Type patient for the H antigen and Le(b) antigen; patient should test negative for both
D. Type patient for the H antigen and demonstrate the presence of strong anti- H in serum that reacts with O cells but not with O(h) cellsk
D. Type patient for the H antigen and demonstrate the presence of strong anti- H in serum that reacts with O cells but not with O(h) cells
- H antien should be lacking; anti-H should show strong reactivity with O(h) cells
Which possible phenotype can an individual with probable genotype of (Lele, sese) have? A. Le (a+b+) B. Le (a-b+) C. Le (a+b-) D. Le (a-b-)
C. Le (a+b-)
Le = FUT3 gene = can synthesize Le(a) se = FUT2 gene lacking/non functional = Le(b) not synthesized, no H type 1 chain precursor made
Which possible phenotype can an individual with probable genotype of (lele, Sese) have? A. Le (a+b+) B. Le (a-b+) C. Le (a+b-) D. Le (a-b-)
D. Le (a-b-)
le = FUT3 gene lacking/nonfuctional = Le(a) not synthesized Sese = one functional FUT2 gene = can synthesize H type 1 = ABH antigens only WITHOUT Le gene
Which antigens is/are present in the secretion in individuals with probable genotype of LeLe, Sese? A. Le(a), Le(b), ABH antigens B. Le(a) and Le(b) only C. H antigens only D. Le(a) only
A. Le(a), Le(b), ABH antigens
Le = Functional FUT3 gene = Le(a) synthesized Sese = one functional FUT2 gene = can synthesize H type 1 = ABH and Le(b) antigens
Which antigens is/are present in the secretion in individuals with probable genotype of lele, Sese? A. Le(a), Le(b), ABH antigens B. Le(a) and Le(b) only C. H antigens only D. Le(a) only
C. H antigens only
le= FUT3 gene lacking/nonfunctional = Le(a) not synthesized Sese = one functional FUT2 gene = can synthesize H type 1 chain and type 1 precursor BUT without FUT3 = cannot make A and B antigens
Which of the following is NOT true about the Lewis blood group system?
A. Lewis antigns are synthesized by the erythroid cells
B. Lewis antigens are decreased on stored red cells
C. The gastrointestinal tract is thought to be the primary source of Lewis glycolipid in plasma
D. Pregnant females can transiently type as Le(a-b-) due to increase in circulating plasma volume
A. Lewis antigens are synthesized by the erythroid cells
- they are passively adsorbed in red cell membranes
B- typing should be done ASAP on fresh units
C- it is rich lewis glycolipid and glycoprotein
Which of hte ff combination of genes are responsible for the formation of Lewis antigens? A. FUT1 AND FUT2 B. FUT1 AND FUT3 C. FUT2 AND FUT3 D. FUT2 AND FUT4
C. FUT2 AND FUT3
- secretor gene and lewis gene enzyme; enzymes encoded by these genes fucosylate type 1 H chains
Which of the ff is true about the biosynthesis of Lewis antigens?
A. FUT2 and FUT3 preferentially fucosylate H type 2 chain susbtrate
B. The Lewis enzyme synthesizes Le(b) from Le(a) by adding a second fucose to the N-acetylglucosamine type 1 chain precursor
C. FUT3 encodes an enzyme that adds a second fucose to H type 1 chain to form Le(a) antigen
D. Majority of individuals with both Lewis and secretor gene have Le(a-,b+) phenotype
D. Majority of individuals with both Lewis and secretor gene have Le(a-,b+) phenotype
- true. Instead of Le(a+b+) which is rare, type 1 H chain is favored over Le(a) formation so most of the antigens in secretion are Le(b+), and less of Le(a+) giving the phenotype Le(a-b+)
A - they fucosylate type 1 H chain
B - this is the synthesis of Le(a)
C - this describes synthesis of Le(b); for Le(a), a fucose is added into the N-acetylglucosamine (H type 1 precursor)
True/false - Le(a+b+) is the most common Lewis phenotype. These individuals have both functional FUT3 and FUT2 genes.
False
- Le(a-,b+ is the most common phenotype); Le(a+b+) is a rare phenotype due to the inheritance of weak secretor gene ; common in east asia
Which of the ff is true about the allo-H antibody?
A. Predominantly IgG and is considered clinically significant
B. Reacts with both O and O(h) red cells
C. Antibody isotype can react in both lower and at body temperature
D. Anti - H in both para and bombay phenotype may demonstrate similar titers
C. Antibody isotype can react in both lower and at body temperature
- IgM isotype with broad thermal range
A - they are usually IgMs
B - O = rich in H ag; O(h) = lacks H ag
D - Para has lower titers; less prone to direct lysis
True/false - auto anti- HI are usually clinically significant and patients transfused with group O has lower in-vivo survival of donor cells
False
They are clinically insignifican; group O cells have high in-vivo survival
