Podcast
Questions and Answers
In a scenario where a patient requires a blood transfusion, and their blood type is determined to be a weak A subgroup with a low number of A antigens, which antibody would be MOST effective in identifying the specific subgroup?
In a scenario where a patient requires a blood transfusion, and their blood type is determined to be a weak A subgroup with a low number of A antigens, which antibody would be MOST effective in identifying the specific subgroup?
- Anti-B antibody, as it cross-reacts with certain A subgroup antigens.
- Anti-A antibody, due to its high specificity for all A antigens.
- Anti-AB antibody, which can detect even low levels of A antigens on the RBCs. (correct)
- Rh antibody, as Rh factor is linked to A subgroup expression.
A researcher is investigating the expression levels of A antigens on red blood cells (RBCs) from different individuals. Based on the provided data, which of the following genotypes would MOST likely exhibit the LOWEST number of A antigens?
A researcher is investigating the expression levels of A antigens on red blood cells (RBCs) from different individuals. Based on the provided data, which of the following genotypes would MOST likely exhibit the LOWEST number of A antigens?
- A2B
- A3
- Ax (correct)
- A1
A medical technologist observes a mixed field agglutination reaction during blood typing. Which of the following BEST describes the underlying phenomenon causing this observation?
A medical technologist observes a mixed field agglutination reaction during blood typing. Which of the following BEST describes the underlying phenomenon causing this observation?
- The antigens on the RBCs have been degraded, leading to partial agglutination.
- A dual population of RBCs exists, where some agglutinate and others do not. (correct)
- All RBCs are uniformly agglutinated due to a high concentration of antibodies.
- The antibodies used are contaminated, causing non-specific agglutination.
A hematology lab is evaluating different A subgroups. If the lab technician loaded the samples in decreasing order of number of A antigens, which of the following represents the CORRECT order from MOST to LEAST?
A hematology lab is evaluating different A subgroups. If the lab technician loaded the samples in decreasing order of number of A antigens, which of the following represents the CORRECT order from MOST to LEAST?
In a serological study, red blood cells (RBCs) from different individuals are tested for the presence of A antigens. Based solely on the number of A antigens present, which of the following pairs of subgroups would be MOST easily distinguishable from each other?
In a serological study, red blood cells (RBCs) from different individuals are tested for the presence of A antigens. Based solely on the number of A antigens present, which of the following pairs of subgroups would be MOST easily distinguishable from each other?
In the context of weak A subgroups, what is the primary reason for strong agglutination reactions observed with Anti-H lectin?
In the context of weak A subgroups, what is the primary reason for strong agglutination reactions observed with Anti-H lectin?
Why might an $A_x$ donor's blood, when mistyped as group "O," cause a hemolytic transfusion reaction (HTR) in a group "O" recipient?
Why might an $A_x$ donor's blood, when mistyped as group "O," cause a hemolytic transfusion reaction (HTR) in a group "O" recipient?
What is the most significant challenge in identifying weak A subgroups, such as $A_x$, in routine blood typing?
What is the most significant challenge in identifying weak A subgroups, such as $A_x$, in routine blood typing?
In the context of blood transfusions, what is a potential consequence of not accurately identifying individuals with weak A subgroups?
In the context of blood transfusions, what is a potential consequence of not accurately identifying individuals with weak A subgroups?
What is the primary method for detecting weak A subgroups when standard serological tests yield inconclusive results?
What is the primary method for detecting weak A subgroups when standard serological tests yield inconclusive results?
How does the presence or absence of Anti-A1 antibodies in a patient's serum affect blood typing results and interpretations?
How does the presence or absence of Anti-A1 antibodies in a patient's serum affect blood typing results and interpretations?
What underlying genetic mechanism most likely contributes to the formation of a weak A subgroup phenotype?
What underlying genetic mechanism most likely contributes to the formation of a weak A subgroup phenotype?
How does the quantity of A antigens present on red blood cells in weak A subgroups compare to that of common A groups?
How does the quantity of A antigens present on red blood cells in weak A subgroups compare to that of common A groups?
How does the α-3-N-acetylgalactosaminyltransferase enzyme produced by the A1 gene differ from that produced by the A gene?
How does the α-3-N-acetylgalactosaminyltransferase enzyme produced by the A1 gene differ from that produced by the A gene?
What is the primary distinction regarding Anti-A1 antibody production between individuals with A1 and A blood types and individuals with A blood types?
What is the primary distinction regarding Anti-A1 antibody production between individuals with A1 and A blood types and individuals with A blood types?
Which antibodies are typically found in individuals with group O blood?
Which antibodies are typically found in individuals with group O blood?
What is the most accurate description of the reactivity of Anti-A,B antibodies compared to Anti-A and Anti-B antibodies?
What is the most accurate description of the reactivity of Anti-A,B antibodies compared to Anti-A and Anti-B antibodies?
Which characteristic is most distinctive of Anti-B antibodies compared to Anti-A antibodies regarding their immunoglobulin class?
Which characteristic is most distinctive of Anti-B antibodies compared to Anti-A antibodies regarding their immunoglobulin class?
What is the primary application of using plant lectin (Dolichos biflorus) in blood banking?
What is the primary application of using plant lectin (Dolichos biflorus) in blood banking?
Which of the following best describes the purpose of performing adsorption techniques in blood banking?
Which of the following best describes the purpose of performing adsorption techniques in blood banking?
In the context of blood group serology, how does the amount of inherited coding affect the efficiency of antigen conversion related A1 and A genes?
In the context of blood group serology, how does the amount of inherited coding affect the efficiency of antigen conversion related A1 and A genes?
In the context of blood banking, why is the differentiation between A1 and A2 phenotypes typically not performed routinely?
In the context of blood banking, why is the differentiation between A1 and A2 phenotypes typically not performed routinely?
A patient with blood type A exhibits a strong agglutination reaction with anti-A reagent but a negative reaction with Dolichos biflorus lectin. What is the MOST likely explanation for these findings?
A patient with blood type A exhibits a strong agglutination reaction with anti-A reagent but a negative reaction with Dolichos biflorus lectin. What is the MOST likely explanation for these findings?
A blood bank technologist observes agglutination during crossmatching at room temperature but not at 37°C. Which antibody is MOST likely responsible for this observation?
A blood bank technologist observes agglutination during crossmatching at room temperature but not at 37°C. Which antibody is MOST likely responsible for this observation?
A researcher is investigating the expression of A antigens on red blood cells. Which of the following is TRUE regarding the relative amounts of A antigen on A1 versus A2 red blood cells?
A researcher is investigating the expression of A antigens on red blood cells. Which of the following is TRUE regarding the relative amounts of A antigen on A1 versus A2 red blood cells?
What characteristic of Anti-A1 antibodies primarily contributes to their clinical insignificance?
What characteristic of Anti-A1 antibodies primarily contributes to their clinical insignificance?
How does the quantity of transferase enzymes affect the expression of A1 and A2 subgroups?
How does the quantity of transferase enzymes affect the expression of A1 and A2 subgroups?
In what scenario would adsorption techniques using red blood cells be MOST beneficial in resolving blood typing discrepancies?
In what scenario would adsorption techniques using red blood cells be MOST beneficial in resolving blood typing discrepancies?
Dolichos biflorus lectin is used to distinguish A1 and A2 phenotypes. What property of the lectin makes it suitable for this purpose?
Dolichos biflorus lectin is used to distinguish A1 and A2 phenotypes. What property of the lectin makes it suitable for this purpose?
In what manner in the branching of precursor substances different between A1 and A2 phenotypes?
In what manner in the branching of precursor substances different between A1 and A2 phenotypes?
A patient's red cells strongly react with anti-A, but the serum does not react with A1 cells at 37 degrees Celsius. The serum DOES react with A1 cells at room temperature, but there is no history of transfusion or pregnancy. What is the MOST likely cause for this?
A patient's red cells strongly react with anti-A, but the serum does not react with A1 cells at 37 degrees Celsius. The serum DOES react with A1 cells at room temperature, but there is no history of transfusion or pregnancy. What is the MOST likely cause for this?
What complication is most likely to arise due to the presence of anti-A1 antibodies in blood typing?
What complication is most likely to arise due to the presence of anti-A1 antibodies in blood typing?
How many antigen sites are present in A1 phenotype compared to the A2 phenotype?
How many antigen sites are present in A1 phenotype compared to the A2 phenotype?
Given that A2 individuals can produce anti-A1 antibodies, which of the following transfusion scenarios requires the MOST careful consideration?
Given that A2 individuals can produce anti-A1 antibodies, which of the following transfusion scenarios requires the MOST careful consideration?
In what clinical scenario would transfusion of A1 positive red cells to an A2 individual be considered acceptable?
In what clinical scenario would transfusion of A1 positive red cells to an A2 individual be considered acceptable?
What is the underlying cause for the difference in the number of antigen sites between A1 and A2 subgroups?
What is the underlying cause for the difference in the number of antigen sites between A1 and A2 subgroups?
Why is the qualitative differentiation of A subgroups based on antigen structure important in blood banking practices?
Why is the qualitative differentiation of A subgroups based on antigen structure important in blood banking practices?
In the context of blood typing, how does the presence of the linear A antigen in A1 individuals impact agglutination reactions when anti-A antibodies are introduced?
In the context of blood typing, how does the presence of the linear A antigen in A1 individuals impact agglutination reactions when anti-A antibodies are introduced?
Why does anti-A1 lectin (dolichos biflorus) yield a negative reaction with A2 red blood cells?
Why does anti-A1 lectin (dolichos biflorus) yield a negative reaction with A2 red blood cells?
What characteristic defines Weak A subgroups in terms of A antigen expression on red blood cells?
What characteristic defines Weak A subgroups in terms of A antigen expression on red blood cells?
How do Weak A subgroups typically react when tested with common anti-A antibody?
How do Weak A subgroups typically react when tested with common anti-A antibody?
How does the reaction of A2 individuals' red cells with anti-A compare to their reaction with anti-A1 lectin (dolichos biflorus)?
How does the reaction of A2 individuals' red cells with anti-A compare to their reaction with anti-A1 lectin (dolichos biflorus)?
What is the expected outcome when dolichos biflorus is used on Group A1 individuals' red cells and why?
What is the expected outcome when dolichos biflorus is used on Group A1 individuals' red cells and why?
For Weak A subgroups, what is the expected agglutination pattern when tested against human Anti-A,B?
For Weak A subgroups, what is the expected agglutination pattern when tested against human Anti-A,B?
How does the quantity of A antigen sites on red blood cells differ between A1, A2, and Weak A subgroups, and how does this difference affect agglutination with anti-A reagents?
How does the quantity of A antigen sites on red blood cells differ between A1, A2, and Weak A subgroups, and how does this difference affect agglutination with anti-A reagents?
How does the efficiency of transferase enzyme production in individuals with the A2 gene compare to those with the A1 gene, and what is the consequence of this difference on H antigen conversion?
How does the efficiency of transferase enzyme production in individuals with the A2 gene compare to those with the A1 gene, and what is the consequence of this difference on H antigen conversion?
What is the clinical significance of anti-A1 antibodies produced by A2 individuals, especially concerning their thermal reactivity and immunoglobulin class?
What is the clinical significance of anti-A1 antibodies produced by A2 individuals, especially concerning their thermal reactivity and immunoglobulin class?
During adsorption with A2 cells, what is the expected composition of antibodies in the remaining serum, and how is this serum then utilized?
During adsorption with A2 cells, what is the expected composition of antibodies in the remaining serum, and how is this serum then utilized?
In the adsorption method using serum from group B individuals lacking A antigens, what specific types of antibodies are expected to be present initially, and how does this influence the subsequent steps?
In the adsorption method using serum from group B individuals lacking A antigens, what specific types of antibodies are expected to be present initially, and how does this influence the subsequent steps?
Considering the limitations of the A2 gene in producing transferase enzymes and its impact on H antigen conversion, which transfusion scenario would be considered the safest regarding A subgroups?
Considering the limitations of the A2 gene in producing transferase enzymes and its impact on H antigen conversion, which transfusion scenario would be considered the safest regarding A subgroups?
How does the reactivity of human Anti-A,B differ from that of Anti-A and Anti-B regarding antigen site specificity?
How does the reactivity of human Anti-A,B differ from that of Anti-A and Anti-B regarding antigen site specificity?
What is the primary distinction between the A1 gene and the A gene concerning their function?
What is the primary distinction between the A1 gene and the A gene concerning their function?
In the context of blood banking, what is the MOST critical implication of an individual producing Anti-A1 antibodies?
In the context of blood banking, what is the MOST critical implication of an individual producing Anti-A1 antibodies?
What characteristic of Anti-B antibodies primarily contributes to cases of severe hemolytic transfusion reactions?
What characteristic of Anti-B antibodies primarily contributes to cases of severe hemolytic transfusion reactions?
How does the amount of inherited coding affect the efficiency of antigen conversion in A1 versus A subgroups?
How does the amount of inherited coding affect the efficiency of antigen conversion in A1 versus A subgroups?
Which of the following BEST describes the role of plant lectins, such as Dolichos biflorus, in differentiating A1 and A subgroups?
Which of the following BEST describes the role of plant lectins, such as Dolichos biflorus, in differentiating A1 and A subgroups?
When might adsorption techniques be MOST beneficial in resolving blood typing discrepancies related to A subgroups?
When might adsorption techniques be MOST beneficial in resolving blood typing discrepancies related to A subgroups?
What is the underlying reason for the varied expression of A antigens among A subgroups, such as A1 and A?
What is the underlying reason for the varied expression of A antigens among A subgroups, such as A1 and A?
If a weak A subgroup is mistyped as Group O and transfused into a Group O recipient, what is the MOST likely immunological consequence?
If a weak A subgroup is mistyped as Group O and transfused into a Group O recipient, what is the MOST likely immunological consequence?
What is the PRIMARY reason why weak A subgroups may not be detected by routine forward blood typing methods?
What is the PRIMARY reason why weak A subgroups may not be detected by routine forward blood typing methods?
Why do weak A subgroups typically exhibit strong agglutination reactions with anti-H lectin?
Why do weak A subgroups typically exhibit strong agglutination reactions with anti-H lectin?
Which methodological approach is MOST definitive for confirming the presence of a weak A subgroup when routine serological testing is inconclusive?
Which methodological approach is MOST definitive for confirming the presence of a weak A subgroup when routine serological testing is inconclusive?
What is the MOST direct genetic basis for the formation of weak A subgroups?
What is the MOST direct genetic basis for the formation of weak A subgroups?
In the context of transfusion medicine, what is the PRIMARY risk associated with failing to identify a patient with a weak A subgroup?
In the context of transfusion medicine, what is the PRIMARY risk associated with failing to identify a patient with a weak A subgroup?
What is the MOST reliable method for distinguishing $A_x$ red cells from Group O red cells in the laboratory?
What is the MOST reliable method for distinguishing $A_x$ red cells from Group O red cells in the laboratory?
An Ax individual's red cells are tested with anti-A reagent and show very weak or no agglutination. The serum is then tested and found to contain a strong anti-A1 antibody. If this individual requires a blood transfusion, which of the following blood groups would be MOST appropriate?
An Ax individual's red cells are tested with anti-A reagent and show very weak or no agglutination. The serum is then tested and found to contain a strong anti-A1 antibody. If this individual requires a blood transfusion, which of the following blood groups would be MOST appropriate?
How does the efficiency of the transferase enzyme produced by the A1 gene affect the conversion of H antigens, considering both linear and branched structures?
How does the efficiency of the transferase enzyme produced by the A1 gene affect the conversion of H antigens, considering both linear and branched structures?
In what way might the absence of A1 antigen influence the development of alloantibodies following exposure to A1 positive blood?
In what way might the absence of A1 antigen influence the development of alloantibodies following exposure to A1 positive blood?
How does the structural arrangement of A antigens (linear vs. branched) differ between A1 and A2 phenotypes, and how does this difference affect the number of available antigenic sites?
How does the structural arrangement of A antigens (linear vs. branched) differ between A1 and A2 phenotypes, and how does this difference affect the number of available antigenic sites?
What accounts for the inability of A1 individuals to produce anti-A1 antibodies, considering the presence of both A and A1 antigens on their red cells?
What accounts for the inability of A1 individuals to produce anti-A1 antibodies, considering the presence of both A and A1 antigens on their red cells?
What percentage range represents the likelihood of an A2 individual forming anti-A1 antibodies?
What percentage range represents the likelihood of an A2 individual forming anti-A1 antibodies?
An A2B individual has what likelihood of forming anti-A1 antibodies?
An A2B individual has what likelihood of forming anti-A1 antibodies?
What is the key distinction regarding antigen presentation between A1 and A2 red blood cells?
What is the key distinction regarding antigen presentation between A1 and A2 red blood cells?
How does the dual presence of A and A1 antigens on the red cell membrane of A1 individuals influence blood typing strategies and transfusion protocols?
How does the dual presence of A and A1 antigens on the red cell membrane of A1 individuals influence blood typing strategies and transfusion protocols?
Which of the following genetic scenarios would MOST likely result in the expression of an A2B phenotype?
Which of the following genetic scenarios would MOST likely result in the expression of an A2B phenotype?
In the context of ABO subgroups, what is the MOST critical implication of an A2 individual possessing naturally occurring anti-A1 antibodies?
In the context of ABO subgroups, what is the MOST critical implication of an A2 individual possessing naturally occurring anti-A1 antibodies?
How does the absence of the A1 antigen in A2 individuals MOST directly affect their ability to recognize different ABO antigens?
How does the absence of the A1 antigen in A2 individuals MOST directly affect their ability to recognize different ABO antigens?
What is the MOST likely outcome if an A2 individual, who has not been previously sensitized, is transfused with A1 red blood cells?
What is the MOST likely outcome if an A2 individual, who has not been previously sensitized, is transfused with A1 red blood cells?
Based solely on the information provided in the text, what is the MOST accurate characterization of anti-A1 antibodies in A2 individuals?
Based solely on the information provided in the text, what is the MOST accurate characterization of anti-A1 antibodies in A2 individuals?
How is the expression of A antigens on red cells in ABO subgroups described in the text, beyond simple presence or absence?
How is the expression of A antigens on red cells in ABO subgroups described in the text, beyond simple presence or absence?
In the context of A subgroups, how would a blood bank MOST effectively mitigate the risk of a transfusion reaction in an A2 individual requiring a red blood cell transfusion?
In the context of A subgroups, how would a blood bank MOST effectively mitigate the risk of a transfusion reaction in an A2 individual requiring a red blood cell transfusion?
If routine blood typing results are inconclusive for an individual, and there is suspicion of a weak A subgroup, which is the MOST appropriate next step in the laboratory investigation?
If routine blood typing results are inconclusive for an individual, and there is suspicion of a weak A subgroup, which is the MOST appropriate next step in the laboratory investigation?
In a scenario where both A1 and A2 individuals' red cells react positively with anti-A, what justifies the need for further testing using Dolichos biflorus?
In a scenario where both A1 and A2 individuals' red cells react positively with anti-A, what justifies the need for further testing using Dolichos biflorus?
An A subgroup exhibits weak agglutination with anti-A and varying degrees of agglutination with anti-A,B. Which follow-up test would be MOST effective in confirming a weak A subgroup and preventing potential transfusion complications?
An A subgroup exhibits weak agglutination with anti-A and varying degrees of agglutination with anti-A,B. Which follow-up test would be MOST effective in confirming a weak A subgroup and preventing potential transfusion complications?
In a mass casualty event, a blood bank faces a critical shortage of group O negative blood. If group O negative is unavailable, which of the following alternative blood types would be the SAFEST to transfuse to a recipient with a weak A subgroup, assuming crossmatch compatibility?
In a mass casualty event, a blood bank faces a critical shortage of group O negative blood. If group O negative is unavailable, which of the following alternative blood types would be the SAFEST to transfuse to a recipient with a weak A subgroup, assuming crossmatch compatibility?
A blood bank technologist encounters a sample with a weak reaction to anti-A and a negative reaction to anti-A1 lectin. To differentiate between an A2 phenotype with a weak A expression and an Ax subgroup, what additional serological test would provide the MOST conclusive differentiation?
A blood bank technologist encounters a sample with a weak reaction to anti-A and a negative reaction to anti-A1 lectin. To differentiate between an A2 phenotype with a weak A expression and an Ax subgroup, what additional serological test would provide the MOST conclusive differentiation?
In cases of weak A subgroups, what is the MOST reliable method for confirming the presence of the A gene when serological testing is inconclusive?
In cases of weak A subgroups, what is the MOST reliable method for confirming the presence of the A gene when serological testing is inconclusive?
An expectant mother is identified as having a weak A subgroup. What is the MOST critical consideration regarding potential hemolytic disease of the fetus and newborn (HDFN)?
An expectant mother is identified as having a weak A subgroup. What is the MOST critical consideration regarding potential hemolytic disease of the fetus and newborn (HDFN)?
A patient with a weak A subgroup requires a blood transfusion due to severe anemia. After receiving two units of correctly typed blood, the patient exhibits a decreased hemoglobin level and elevated bilirubin. What is the MOST likely cause of this adverse reaction?
A patient with a weak A subgroup requires a blood transfusion due to severe anemia. After receiving two units of correctly typed blood, the patient exhibits a decreased hemoglobin level and elevated bilirubin. What is the MOST likely cause of this adverse reaction?
A research laboratory is investigating the genetic basis of weak A subgroups. Which molecular mechanism is MOST likely responsible for the reduced expression of A antigens on red blood cells in these individuals?
A research laboratory is investigating the genetic basis of weak A subgroups. Which molecular mechanism is MOST likely responsible for the reduced expression of A antigens on red blood cells in these individuals?
Flashcards
A Antigen Quantity Order
A Antigen Quantity Order
The arrangement of A antigens from most to least abundant on red blood cells is: A1 > A2 > A3 > Ax > Ael.
A1 Antigen Count
A1 Antigen Count
A1 subgroup contains approximately 810,000 to 1,170,000 A antigens on each red blood cell.
A2 Antigen Count
A2 Antigen Count
A2 subgroup contains approximately 240,000 to 290,000 A antigens on each red blood cell.
A3 Subgroup Characteristics
A3 Subgroup Characteristics
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Mixed Field Agglutination (Mf)
Mixed Field Agglutination (Mf)
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A Phenotype Subgroups
A Phenotype Subgroups
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Quantitative Differentiation
Quantitative Differentiation
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Qualitative Differentiation
Qualitative Differentiation
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Antigen Sites: A1 vs. A2
Antigen Sites: A1 vs. A2
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Transferase Enzyme: A1 vs A2
Transferase Enzyme: A1 vs A2
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Branching: A1 vs. A2
Branching: A1 vs. A2
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Anti-A1 Antibody
Anti-A1 Antibody
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Anti-A1 Interference
Anti-A1 Interference
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A1 and A antigens
A1 and A antigens
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A1 Gene Function
A1 Gene Function
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A Gene Function
A Gene Function
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A1 Gene - Amount
A1 Gene - Amount
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A Gene - Amount
A Gene - Amount
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Anti-A1 Antibody Form
Anti-A1 Antibody Form
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Anti-A,B Reactivity
Anti-A,B Reactivity
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A1 Individuals and Anti-A
A1 Individuals and Anti-A
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A1 Individuals and Dolichos biflorus
A1 Individuals and Dolichos biflorus
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A2 Individuals and Anti-A
A2 Individuals and Anti-A
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A2 Individuals and Anti-A1 Lectin
A2 Individuals and Anti-A1 Lectin
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Weak A Subgroups Characteristic
Weak A Subgroups Characteristic
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Weak A Subgroups and Anti-A
Weak A Subgroups and Anti-A
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Weak A Subgroups and Anti-A,B
Weak A Subgroups and Anti-A,B
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A1 Antigen
A1 Antigen
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Identifying Weak A Antigens
Identifying Weak A Antigens
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AHTR Meaning
AHTR Meaning
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Anti-H Reactions
Anti-H Reactions
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Weak Agglutination
Weak Agglutination
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Ax Donor
Ax Donor
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Mistyping Risk
Mistyping Risk
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Anti-A1 Presence
Anti-A1 Presence
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Weak Transferase Enzyme
Weak Transferase Enzyme
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Agglutination Reaction (A1)
Agglutination Reaction (A1)
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Clinical Significance of Anti-A1 (IgM)
Clinical Significance of Anti-A1 (IgM)
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A2 Phenotype
A2 Phenotype
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Plant Lectins
Plant Lectins
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Dolichos biflorus
Dolichos biflorus
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A1 Group Characteristics
A1 Group Characteristics
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A2 Group Characteristics
A2 Group Characteristics
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A1/A2 Subtyping Importance
A1/A2 Subtyping Importance
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A Individuals Transfusion
A Individuals Transfusion
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A2 Gene and H Antigens
A2 Gene and H Antigens
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A2 and Anti-A1 Antibodies
A2 and Anti-A1 Antibodies
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Adsorption Method (Blood)
Adsorption Method (Blood)
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A2 Phenotype (Antigen Recognition)
A2 Phenotype (Antigen Recognition)
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A1 Gene Function (Enzyme Production)
A1 Gene Function (Enzyme Production)
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A1 Gene Conversion
A1 Gene Conversion
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A1 Individual Antigens
A1 Individual Antigens
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Anti-A1 Absence in A1 Individuals
Anti-A1 Absence in A1 Individuals
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Transferase
Transferase
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ABO Subgroups
ABO Subgroups
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Quantitative Antigen Differences
Quantitative Antigen Differences
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Qualitative Antigen Differences
Qualitative Antigen Differences
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A2 Individuals
A2 Individuals
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Anti-A1 Antibody Characteristics
Anti-A1 Antibody Characteristics
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A2B Individuals
A2B Individuals
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Anti-A1 Production in A2
Anti-A1 Production in A2
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A2 and A1 Transfusion Reaction
A2 and A1 Transfusion Reaction
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A1 Antigen Structure
A1 Antigen Structure
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A Antigen Structure
A Antigen Structure
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Human Anti-A,B Antibody
Human Anti-A,B Antibody
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A1 Gene Coding
A1 Gene Coding
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A Gene Coding
A Gene Coding
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A1 Antigen Type
A1 Antigen Type
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A2 and A1 Antigen
A2 and A1 Antigen
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Dolichos biflorus Reaction with A1
Dolichos biflorus Reaction with A1
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Agglutination Reaction
Agglutination Reaction
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Weak A Subgroups
Weak A Subgroups
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Weak A and Anti-A
Weak A and Anti-A
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Weak A and Anti-A,B
Weak A and Anti-A,B
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Study Notes
Okay, I have updated the study notes with the new information from the text provided. Here are the updated notes:
- ABO phenotypes are divided into categories also known as subgroups
ABO Subgroups
- The antigens differ in the amount expressed on the red cell membrane
- There is difference in the quality of the antigen
- Some subgroups are linear, and some are branched
A Subgroups: Quantitative and Qualitative Differences
- Von Dungern initiated research in 1911 to describe 2 antigens of the A phenotype
- This was based on reactions of group A red blood cells with the antibodies, anti-A and anti-A1
- The A phenotype has two subgroups: A1 and A2
- Quantitative differentiation is based on the number of antigens
- Qualitative differentiation is based on the structure of the antigen
Quantitative Differences between A1 and A2
- A1 has more antigen sites (810k-1.17M), while A2 has less (240k-290k)
- A1 has more transferase enzyme (alpha-3-n-acetyl-d-galactosamine transferases), while A2 has less
- A1 has more branching of precursor substances, while A2 has less (linear)
- The number of antigen sites in the RBC surface depends on the amount of transferase enzymes
- Gene A1 is much more capable of producing more transferase enzyme
- The enzyme for A1 and A2 is alpha-3-n-acetyl-d-galactosamine transferases
- Amount of enzyme produced depends on the gene, which attributes to the amount of A antigen present on the RBC membrane
- More enzymes = more H antigens placed with n-acetylgalactosamine sugar which will later on be converted to A1/A2 antigen
Qualitative Differences between A1 and A2
- In A subgroup, antigen is either in branched form or linear
- A1 individuals feature both linear and branched A antigens on the red cell, explaining why it has numerous antigens
- A2 has fewer antigen sites because of the lesser transferase enzymes produced
- A2 antigens are mostly linear, contributing to the reason why there are less antigens
Other Differences
- A2 individuals only have A antigen present on the red cell
- The absence of A1 antigen will prevent recognition of A1 antigens
- A2 individuals have the capability of producing anti-A1(only few)
- A2B individuals can receive the A gene and B gene from one parent, however, the A gene inherited is A2, meaning, linear A antigen will be present
- The Anti-A1 antibody is naturally occurring and is mostly in the form of IgM
- The Anti-A1 antibody is also clinically insignificant because unlike other ABO antibodies that can activate the complement at body temperature regardless of its IgG or IgM form, the anti-A1, despite being classified as IgM, is non-reactive at body temperature
- Thus, A2 individuals can receive red cells containing A1 antigen and the same goes for A2.
Important Note About Anti-A1
- Anti-A₁ is a naturally occurring IgM cold-reacting antibody and is unlikely to cause a transfusion reaction because it usually reacts only at temperatures well below 37°C
- It is considered clinically significant if it reactive at 37°C
- This antibody causes discrepancies between forward and reverse ABO testing and incompatibilities in crossmatches with A₁ or A₁B cells
Formation of A and A1 antigen
- Types of H antigen present on RBC Membrane: H1 and H2 (only A antigen is present)
- Also called linear H antigen
- H3 and H4 (both A₁ and A antigen are present)
- Also called branched antigen
- A₁ and A2 genes both code for the enzyme a-3-N-acetylgalactosaminyltransferase
- Transfers N-acetylgalactosamine sugar and converts both branched and linear H antigen
A1 and A2 GENE
- A1 GENE codes for higher amounts and more efficient production of transferase enzymes
- Converts both linear and branched H antigen (H1 to H4) to become A (linear) and A₁ antigen (branched)
- It is able to transform linear and branched antigen into A1 antigen
- Thus, in A1 individuals, they have two types of A antigens present on red cell membrane - A (linear) and A1 (branched) antigen
- A (linear) individuals are considered safe to be transfused with red cells that contain A1 antigen
- A2 GENE codes for lesser amounts and is less efficient in the production of transferase enzymes
- ONLY converts linear H antigens (H1 and H2) to become A antigen
- It is able to produce Anti-A1 antibodies (IgM form) and still is considered naturally occurring
- This type of antibodies is NOT REACTIVE at body temperature compared to ABO antibodies
- Activates the complement at 37 degree celsius/body temperature regardless of their form - may it be in IgG or IgM form
- It is not considered as clinically significant
Adsorption Method
- Adsorption makes use of serum from B individuals
- These individuals lack A antigens, so two types of antibodies are present (Anti A₁ and Anti A)
- Steps on performing the adsorption test:
- Add A2 cells on serum of B patients (px) so Anti A will be adsorbed: Left on the plasma is the Anti A₁
- Anti A1 will be added to the red cells of A, individuals
- Agglutination reaction indicates px has A₁ phenotype
- Adsorption is commonly done if patient (px) is A and finding out if the px is in A₁ or A2 phenotype
- Finding out if px is A₁ or A₂ is NOT ROUTINELY performed
Use Of Plant Lectin - Dolichos Biflorus
- Lectin has Anti A₁ specificity, thus, its reaction is like Anti A₁ antibody
- Lectins are seed extracts that agglutinate human cells with some degree of specificity
- The specificity of A₁ antigen is for Dolichos biflorus is for A₁ antigen
A Subgroups Reaction
- Group A₁ Individuals
- placing anti-A will cause an agglutination reaction
- using dolichos biflorus will produce a positive reaction
- Group A2Individuals
- placing anti-A on the red cells, will give a positive reaction, but anti-A₁ lectin will give a negative reaction because A₁ is lacking on the red cells
Weak A Subgroups
- Decreased number of A antigen sites per RBC = weak or no agglutination when tested with the common anti-A antibody
- Varying degrees of agglutination by human Anti-A,B
- Human Anti-A,B is an antibody from the plasma of the "O" individual in which they tend to have different antibodies present
- Tend to have both IgM and IgG form but Anti-B is more identified to be in IgG form
- Anti-AB will react on different antigenic sites than Anti-A/Anti-A/Anti-B
- Individuals wth A subgroups may produce anti-A in their serum, can have positive saliva studies, and have reactions that can test the transferase
- *Mf-mixed field agglutination reaction
Weak A Subgroup Identification
- Common anti-A antisera may appear to have no agglutination
Characteristics Weak A Subgroups
- strong agglutination = weak antigen
- low/ no agglutination= lot of unconverted weak antigens
- Common anti-sera used to identify A phenotype
- Anti A,B is efficient is detecting it
Characteristics weak A subgroups serum
- A3 & Aend: SOMETIMES produce anti -A1
- Ax always produces anti-A1
B Subgroups
- Subgroups are very rare and infrequent recognition is similar to the criteria of the subgroup A identification because of the reduced amount of antigens May demonstrate weak or no agglutination on RBCs with Anti-B reagent Subgroups are B3 mostly found in the lab
Clinical significance
- Mistypes as group O mistypes during donor testing if a weak A/B gets mistyped in the blood and gets used as someone else.
- Can also lead to a decreased survival of transfused cells
variations of HAntigen
- O>A2>B>A2B>A1>A1B is descending
- HAntigen has an inverse relation with BAg and AAg because H antigen gets taken away to form A and B
- Most HAg means low ABags and vice versa
####Lectins
- Help identify small amounts of AG present
- Lectins derived from plants specific antibodies
####Bombay Phenotype
- Must inherit H gene to express AB antigen
- Bombay is person with hh gene who have antiH
- Types as On serum and cell reactions will similar
####h-deficient phenotypes
- Anti-A. anti-B,Anti-A,B, Anti-H are the antibodies
- Can lead to Bombay another Bombay inididual
###Transfusions
- O in RBCs is an universal donor and can be transfused to any blood type.
- BUT needs to be transfused O in the red cell only because antibody is present
- However, AB in the PLASMA is the universal donor AB will also have antibody
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Description
ABO phenotypes are divided into subgroups based on differences in the amount and quality of antigens expressed on the red cell membrane. The A phenotype has two subgroups: A1 and A2. Quantitative differentiation is based on the number of antigens, while qualitative differentiation is based on the structure of the antigen.
