Type&Screen Flashcards
IgG
Monomer Most common Abs Cross placenta Bind complement Leads to phagocytosis 4 subclasses: IgG1-4 IgG1: Fixed complement, 23 days, bind macrophage via Fc IgG3: Fixed complement, 8 days, bind macrophage via Fc
Complement pathway
- Classic: via C1, triggered by IgM, IgG
- Alternative: low grade, constant, via C3. Normal: inactive bound C3 via DAF (CD55). Abnormal: Paroxymal Nocturnal Hemoglobinuria
- Lectin: via sugar, no need C1
Landsteiner’s law
Have antigen, shouldn’t have antibody
Define “naturally occurring”
- Immune exposure to the environment (bacteria, pollen)
- Not require exposure to blood transfusion
- Noticeable 3-6 months
Isoagglutination
IgM, IgG, IgA
Cause hemolysis by fixing complement
At RT (due to IgM)
Where ABO?
RBC, WBC, PLT
endothelium
epithelium
secretion
How much blood can cause an acute hemolytic transfusion reaction
10mL
Anti-A,B
Produced by group O –> react A or B cells
Mostly IgG –> cross placenta
Cause ABO HDFN (Hemolytic Disease Fetus & Newborn)
ABO genetic
H, h: chromosome 19
A,B,O: chromosome 9
* O = amorph: enzyme produced has no function
Precursor chains
Type 1: 1-3 terminal galactose & N-acetylglucosamine
Secretion & Plasma
Type 2: 1-4 terminal galactose & N-acetylglucosamine
RBC & tissue
H-antigen
HH or Hh
a-2-L-fucosyltransferase: bring L-fucose to terminal galactose
Amount of H: O>A2>B>A2B>A1>A1B
A-antigen
AO, AA, AB
a-3-N-acetyl-D-galactoseamyltransferase: bring N-acetyl-D-galactosamine to terminal Galactose
Requires L-fucose
B-antigen
BO, BB, AB
a-3-D-galactosyltransferase: bring D-galactose to terminal galactose
Requires L-fucose
Bombay
Lack of H antigen –> hh –> Denote: Oh
Plasma contains all types of Abs: anti-A, anti-B, anti-A,B, anti-H
Cause AHTR
Able to pass on A and B genes
ABO in newborns
- Weak expression –> no isoagglutination until 4 months –> No reverse test
- Maternal Abs can cross and attach to baby’s RBC –> no severe as weak ABO
FWD testing
- Antigen?: Pt’s RBC + known Abs
- Routinely test with monoclonal IgM (anti-A, anti-B, anti-D)
- AB group requires control to R/O autoagglutination (Control: neg)
RVS testing
- Antibody (IgM)? Pt’s plasma + pool A1/B
- Routinely test with A1 cells, B cells
- Perform at Immediate Spin
- No test for D
Gel card
FWD: Pt’s RBC + gel with Ab –> Trapped: Pos/Pellet: Neg
RVS: Pt’s plasma + cells –> Trapped: Pos/Pellet: Neg
Mix field: May been seen in FWB when pt had a transfusion in the past.
Pro: stable vs Cons: spin 10min
Stage of Agglutination
- Sensitization: Ab & Ag mix and bind
- Lattice formation: Abs cross-linking and bind multiple cells
Happen at the same time: IgM
Happen at different times: IgG
Potentiators
Time, Temp, Medium, Conc, pH, enzymes
Prozone
Too much plasma –> excess abs
Postzone
Too less plasma –> excess antigen
Zeta potential
Negative charge surrounding RBC to keep them away from each other
Enhancement
Standard: 37C, 30-60min Decrease zeta potential by - LISS: 0.2% saline --> 37C, 5-15 min - Albumin: 22% --> 37C, 15-60 min Dry out RBC: PEG --> bring cells closer --> 37C, 10-30 min
Gel card pro & cons
Pro: smaller, no washing, clear, stable, can be automated
Cons: Expensive
Solid-phase pro & cons
Pro: reduce volume, increase sensitivity, less skilled
Cons: Expensive, reagent expired, learning curve (?)
Direct Antiglobulin Test
Does pt have Ab and/or Complement stuck on RBC/
In vivo
Pt’s RBC + AHG
Indirect Antiglobunlin Test
Does pt have Ab that could bind RBC?
In vitro only
Pt’s plasma + Known screening cells
IgD
Found on B cells (play role in B cell development)
Low level in serum
IgE
Allergic reaction
Can cause allergic transfusion rxn. Med is ok
IgA
Found in milk and secretion
Monomer or Dimer
IgA deficiency can develop anti-IgA –> Anaphylatic reaction
IgM
Pentamer (J chain)
First Abs made when exposure
Fixes complements
React at cold temp.
Haplotype
Group of genes inherited together due to close physical location
E.g: DCEce, MNSs
Rare blood tend to run in families
