ABO Blood Groups Pt 2 Flashcards
Relate secretor status to Bombay antigen expression in ABO and Lewis families
- Genes: hh, sese, unknown ABO, Le
- Ab: anti-A, anti-B, anti-H, anti-A,B
- Ag: Lewis a (Lea)
- Secretions: Lewis a
Relate secretor status to Parabombay antigen expression in ABO and Lewis families
- Genes: hh, SeSe, A or B
- Ab: anti-A or anti-B
- Ag: Lewis b (Leb), small amount of Lea, small amount of absorbed A or B
- Secretions: A or B
Describe how secretor status affects presentation of Lewis and ABH antigens on RBC and in secretions
- A secretor does not have to have H antigen (can be hh like Parabombay)
- Must be SeSe or Sese to be secretor bc need functional FUT2 to add terminal fucose to Type 1 precursor chain
- Must be LeLe or Lele bc need FUT3 to add non-terminal fucose, thus making Leb
- Only Leb can be secretor, not Lea, bc only it has the terminal fucose from FUT2
- Can express A or B and thus secret A or B
What is the clinical significance of Lewis Ab in patient plasma to ABO Ab in patients plasma?
Testing the Lewis Ab in patient plasma combined with testing the ABO Ab in patient plasma helps to get a more complete picture interpretation, such as if they’re Bombay, Parabombay, or a normal secretor
Is a person who has Lea on their RBCs secretor or non-secretor? Genotype?
- Non-secretor
- sese
Is a person who expresses Leb on their RBCs a secretor or non-secretor? Genotype?
- Secretor
- Sese or SeSe
How are secretions formed biochemically? Hint: Le(a-b+)
- FUT2 (Sese or SeSe) gene codes for fucosyl transferase that adds Fucose to Type 1 precursor chain
- FUT3 (Lele or LeLe) gene encodes for another transferase that adds fucose to the non-terminal end of the Ag in secretions only
- Leb formed!
How are non-secreted substances formed? Hint: Le(a-b-)
- FUT2 doesn’t add fucose to terminal sugar to make H-antigen but FUT3 still adds its non-terminal fucose to create Lea
- Expressed on RBCS that are non-secretors
Why do Leb positive pt not make anti-Lea?
Secretors make a little bit of Lea while mostly making Leb
Genotype for person with no lewis antigens (negative for FUT3)
lele
Can an lele person still secrete ABH antigens? Why or why not?
Yes, because different genes encode them
H/h = FUT1 gene (encodes H Ag)
Se/se = FUT2 gene
Le/le = FUT3 gene
AB = ABO gene
Alleles for FUT1 and protein the gene encodes
- H/h
- Fucose on terminal sugar of Type 2 precursor chain to make H antigen
Alleles for FUT2 and protein the gene encodes
- Se/se
- Fucose on terminal sugar of Type 1 precursor chain to make H antigen
Alleles for FUT3 and protein the gene encodes
- Le/le
- Lewis a (non-secretor) or Lewis b (secretor)
List the positive and negative controls for anti-A1 lectin
- Positive control: A1 cells
- Negative control: A2 cells (or B cells but non-specific to lectin function)
Name of guy who discovered ABO typing system
Landsteiner
T/F
ABO was the first genetic marker used in forensic and paternity testing
True
Discrepancy
When forward and reverse typing results don’t agree on the same blood type
What is the most common ABO discrepancy? How do you solve it?
Missing reactivity
Solve by cooling bc IgM Ab react best at cold temp
How do you solve a serological test where there’s too much reactivity?
- Warm the patient plasma (rvs)
- Wash patient RBCS (fwd)
- Test against O screen cells
What are A and B subgroups?
- Weak expressions of A or B Ag on patient RBCs
- Forward type
T/F
You can use B1 lectin to assess B subgroups
False, B1 lectin does not exist
T/F
You can use anti-A2 Ab to assess a patient’s A subgroup status
False, anti-A2 doesn’t exist
T/F
Weak expression of Ab has more to do with a pt’s immune status than their subgroup status
True
When should you consider the possible existence of a subgroup?
If there is extra Ab expression
When should you add anti-A1 lectin to patient RBCS?
When the pt has weak A expression
Want to see if they’re A2
When should you add A2 cells to patient plasma?
When the pt has an extra reaction with A1 cells (anti-A1 present in pt plasma even though anti-A Ab identified them as Type A or AB)
When should you add anti-A,B Ab to patient RBCS?
- When the patient has weak or missing reactions with anti-A or anti-B
- anti-A,B targets a broader spectrum of Ag sites that anti-A or anti-B may not catch
When should you add screen cells (Type O) with patient plasma?
- When the pt has extra Ab activity that may be related to A or B Ag
- Looking for Lewis Ag
When should you use patient cells against patient plasma?
When the pt has extra Ab activity that may be related to all other cells
?????
Which blood type is the universal RBC donor and why?
Type O because recipient won’t have Ab against it
Universal plasma recipient
Which ABO type is the universal plasma donor and why?
Type AB because it contains no antibodies against any of the other types
Universal RBC recipient
What % donors can give A plasma in trauma situation?
85%
Type AB plasma also okay bc universal plasma donor (no Ab made)
Describe naturally occurring antibodies
- Found in plasma of ppl who have not been previously exposed to RBCS through transfusion or pregnancy
- Formed early in life and may persist
- Usually IgM
- Questionable clinical significance
- May be non-specific or reactive to variety of immune stimuli
- e.g., anti-A, anti-B, anti-H
Choose the answer that is false about ABO Ab:
A. Fix complement
B. Cold reacting at room temp
C. IgG for most part
D. Strength of Ab decreases in some disease states and old age
C
The correct answer is IgM for most part
Describe immune-stimulated Ab
- Made by pt after exposure to RBCs via transfusion or pregnancy
- Formed later in life and may grow dormant/serologically undetectable
- Usually IgG
- Often indicates ability to have reaction if exposed again
- May be specific
- e.g., anti-D, anti-Lea
Draw Type 1 or Type 2 precursor chain
Draw H antigen
D
Draw Lewis b Ag
Draw Lewis a Ag
Draw A Ag
Draw B Ag
