BBGuy & Notes Flashcards
What is the “sensitization” phase of agglutination, and how do enhancement media facilitate it?
Coating of red cells by antibody.
LISS: Decreases zeta-potential, enhances COLD Ab
PEG: Excludes H2O, enhances WARM Ab
What is the “lattice/bridging” phase of agglutination?
When antibodies and RBCs crosslink to actually agglutinate. IgM is better at this than IgG due to size.
Describe the process of the IS phase and 37C phase. Include incubations.
IS: 1 drop 2-5% RBCs, 2 drops serum, spin 15-30sec.
37C: Same ratio, with 10-15min for LISS, 15-30min for PEG/albumin, 30-60min for no potentiation.
What is the most sensitive system for tube testing?
PEG (similar to gel testing)
How are the results of solid-phase red-cell adherence testing interpreted?
Indicator RBCs coated with IgG are used to attach to test RBCs. A tight button is negative, a spread “carpet” is positive.
Distinguish between the antiglobulins used in antiglobulin testing.
Anti-IgG: Used for PEG, gel, and solid phase tests. Detects IgG-coated red cells.
Anti-C3b/d: Detects complement components, most useful in IgM and cold-agglutinin.
Polyspecific: Both. Usually the first choice.
What is the role of a check cell?
A positive control used after a negative DAT/IAT tube test to ensure functioning of AHG reagent.
What blood group systems demonstrate dosage effect?
Rh
Duffy
Kidd
MNS
(Kell, but this will rarely be observed)
What blood groups are enhanced by enzyme treatment?
ABO-related
Rh
Kidd
What blood groups are diminished by enzyme treatment?
Duffy
MNS
Lutheran
What are some sources of neutralizing substances for:
- ABO
- Lewis
- P1
- Sda
- Chido, Rodgers
1, 2. Saliva of secretors
- Hydatic cyst fluid, pigeon egg-whites
- Human urine
- Human serum
Recall 6 lectins and their antigen specificity.
Dolichos biflorus - A1 Ulex europeaus - H Vicia graminea - N Arachis hypogea - T Glycine max - T, Tn Salvia - Tn
Distinguish between Type 1 and Type 2 chains. What acts on each?
Type 1: Free-floating antigens, secreted. Acted upon by FUT2 (Se) to make Type 1H antigen
Type 2: Bound antigens. Acted upon by FUT1 (H) to make Type 2H antigen
How common are the FUT1 and FUT2 genes? What are the consequences of lacking each?
FUT1 is ubiquitous; absence results in Bombay phenotype.
FUT2 expressed in 80%; absence results in non-secretor phenotype.
What is the terminal sugar in group A sugars? Group B?
A: N-acetylgalactosamine
B: Galactose
Recite the blood groups (incl. subgroups) by level of H expression.
O > A2 > B > A2B > A1 > A1B
Trace the expression of ABO antigens in gestation and childhood.
ABO antigens first appear at 6wks gestation, but don’t reach adult levels until age 4.
Trace the expression of ABO antibodies in gestation and childhood.
Begin to appear at 4mo age, reach adult levels by age 10, then fall off with advanced age.
What are the three types of ABO antibodies?
Anti-A or -B IgM expressed by B/A
Anti-A or -B IgG expressed by O
Anti-A,B IgG expressed by O
How do ABO group frequencies differ by race?
Whites have relatively more A-groups. Blacks and Asians have relatively more B-groups. Native Americans are largely just O-group
How often do A2 or A2B patients produce Anti-A1?
1-8% of A2 and 25% of A2B will form Anti-A1.
What is B(A) phenotype?
Group B patients with weak A activity; an inherited condition that looks like the opposite of acquired B.
What is the difference between LeA and LeB?
LeB is the product made when Se acts before Le(FUT3). It is generally more abundant than LeA in secretors.
What is the racial makeup of Lewis antigens?
Black patients are more likely to be Le/FUT3 negative than white patients.
What are the infectious associations of the Lewis system?
H. Pylori and Norwalkvirus attach via Leb antigen. Le(a-b-) patients are at increased risk for Candida and E. Coli infections.
What are the I antigens?
Built on type 2 chains, expression of big-I increases with age (except in some asians, “i-adult”).
What are the classic associations of:
- Auto-anti-I
- Auto-anti-i
- i-adult phenotype
- Cold agglutinin disease, mycoplasma pneumoniae infection.
- Infectious mononucleosis
- Cataracts, HEMPAS
What diseases are associated with the P-system?
P antigen is a parvovirus receptor.
Anti-P antibodies are associated with paroxysmal cold hemoglobinuria (biphasic IgG binds in cold, lyses in warm; “Donath-Landsteiner”)
Recall three basic rules of Wiener haplotype prevalence.
- R1 always comes before R2
- r is always #2
- R0 is #1 in blacks, #4 in whites
What are the big four Wiener haplotypes in whites and blacks?
White: R1 > r > R2 > R0
Black: R0 > r > R1 > R2
How do different races mechanistically lose the D-antigen?
Caucasians: Deletion of RHD gene
Africans: Point mutations of RHD gene (“pseudogene”)
Asians: Inactive RHD gene
Summarize weak D phenotype.
D is present in very low level, requiring AHG/IAT testing to detect (test negative in IS). To avoid alloimmunizing a D-negative patient, test all donors and D-negative babies in AHG.
Summarize partial D phenotype.
Various epitopes of D antigen are missing. These patients may type as D but can still form Anti-D. May be hard to detect; try to give partial D mothers RhoGAM.
What is “D-E-L”?
In a third of D-negative asians, tiny amounts of D can actually still be found (different than weak D, as can only be detected on elution of reagent anti-D?)
What is the “G” Rh antigen?
An antigen that is present when either C or D are present. Suspect when a D-negative patient forms an anti-D when not obviously exposed to D.
What is the “f” Rh antigen?
Present when RHce is inherited (r and R0). Anti-f can be seen togther with anti-c or anti-e.
