Martin: Transfusion Medicine Flashcards
RBC membrane contains what?
- Proteins: Rh antigens
- Carbs: ABO system
What are the primary and secondary response to immunization to RBC antigens?
In other words, how do we develop antibodies to antigens that we DON’T have?
1. Primary response: Occurs after 1st immune exposure to a “foreign” protein Ag (days or weeks after exposure)
2. Secondary (anamnestic) response: occurs upon a repeat exposure to a “foreign” protein Ag (noticed much quicker after such exposure); For example, during a transfusion.
For most Blood Group Antigens, but not ABO, what type of AB develop during a primary and secondary response?
- Primary response = a sustained high concentration of IgM + Ab and some IgG after days or weeks
- Secondary response = transient rise in IgM and a sustained IgG
What antigens make up ABO system?
- 1. H
- 2. A
- 3. B
What antigens make up the following blood types:
- O blood
- A blood
- B blood
- AB blood
- 1. O blood = H Ag only
- 2. A blood = H + A
- 3. B blood = H + B
- 4. AB blood = H + (A+B)
What is a secretor, in blood bank terms?
Someone with “Se” allele, which allows them to make ABO antigens in their secretions and plasma.
Roughly 80% of the population carries at least one allele called “Se.”
What is this allele?
“Se” => produces H antigen on “type 1 chains” (long carb-rich chains).
- Once the H antigen is made, then the person can make either A or B antigens (or both) on the type 1 chains
What is the MC type of blood?
Least common?
- Most common: Type O (45%)
- Least common: AB
Antigens & Antibodies in person with Type O blood.
- Antigens = H
- Antibodies =
- Anti-A
- Anti- B
- Anti- AB
Antigens & Antibodies in person with Type A blood.
- Antigens = H + A
- Antibodies = Anti-B
Antigens & Antibodies in person with Type B blood.
- Antigens = H + B
- Antibodies = Anti-A
Antigens & Antibodies in person with Type AB blood.
- Antigens = H/A/B
- Antibodies = None
What are Subtypes of
What are the 2 steps in Blood Typing?
- “Front/forward typing” = determines which antigens are on the patient’s RBC by mixing patients blood with anti-A/B/D antibodies
-
“Back/reverse typing” = test for isohemagglutinins (antibodies against ABO antigens they do NOT have), like Anti-A/anti-B.
- Serum or plasma that was separated from the pts RBC is mixed with two different red cells from the laboratory (A and B cells)
ABO subtypes exist and pose what problem?
Can cause compatability issues when transfusing a patient.
What disease can alter expression of ABO antigens on the RBC?
- 1. Leukemia = ↓ Ag
- 2. “Acquired B” = Intestinal obst → ↑ bowel permeability, bacterial
polysaccharides into circulation abs = orbed by grp A cells
- 2. Gastric or pancreatic cancer = bld grp specific soluble substances (BGSS) in serum neutralizes antisera used in forward grouping.
What is Bombay phenotype?
What is the problem with this phenotype?
- Rare blood type (Oh/ h/h) where patient lacks H antigen. Thus, RBC has NO antigens.
- Antibodies: anti-A, Anti-B, Anti-AB and Anti-H Ab.
- Problem
- Can donate to ANYONE
- Can ONLY receive Bombay blood.
What happens when a patient with Bombay phenotype receives a blood transfusion?
Anti-H IgM Ab (more common than IgG) activates compliment system => intravascular hemolysis of RBC => acute hemolytic transfusion reaction.
What is a complication in mothers with Bombay phenotype?
Hemolytic disease of the newborn can occur (Oh, h/h)
Type O blood can donate blood to who?
All types.
Type A blood can donate blood to who?
- Type A
- Type AB
Type B blood can donate blood to who?
- Type B
- Type AB
Type AB blood can donate blood to who?
- Type AB
What is the Rh (Rhesus) System?
NOT naturally-occuring antibodies made d/t exposure of a antigen during pregnancy or transfusion. 5 most important antigens are
- D (Rhesus factor/Ag)
- “d”= absence of D
- C = co-dominant with c
- E = co-dominant with e
- Rh (+) =
- Rh (-) =
What is the most common?
- Rh (+) = has D antigen* (MC)
- Rh (-) = lacks D antigen
- Do Rh (-) people develop anti-D Ab?
- If so, what type of Ig are they?
- What problem can develop if Ab develop?
- Antibodies only develop if pt is exposed to D+ RBC, like in transfusions and during pregnancy if mom is D- and baby is D+ (hence, NOT naturally occuring Ab)
- IgG anti-D Ab
- IgG anti-D Ab can cross placenta and Newborn Hemolytic Disease (Hydrops fatalis):
- Occurs if mom is Rh(-) and bb is Rh(+) or if dad and bb are both (Rh+):
- 1st pregnancy: Mom is exposed to Rh(+)/D+ RBC when baby is delivered and develops IgG anti-D Ab.
- 2nd pregnancy: IgG anti-D Ab => cross placenta => attack bbs RBC if the 2nd bb is also Rh(+)/D+.
Test to determine if mom has anti-D IgG Ab?
Indirect Coombs Test:
- Mix moms serum + D+ RBC
-
(+) = mom has anti-D+ IgG aB
- RBC will agglutinate
-
(-) = mom does NOT have anti-D IgG aB
- RBC do NOT agglutinate
What is RhoGAM?
What findings will be seen after administration?
RhoGAM = anti-D Ig medication that prevents Rh immunization in pregnancy or obstretrical complication, a condition where Rh(-) mom develops Ab after exposed to Rh(+) blood.
Transatory increase of passively transferred Ab in the patients blood will cause positive serology testings results.
- What are other antigens on the RBC?
- When are they tested for?
- How do AB against these antigens develop?
- Kell, Duffy, Kidd, MNS, Lewis, MNS
- Only tested when patient has ABNL screening tested
- Ab only develop during pregnancy or transfusion (thus, NOT natural. ONLY natural are A/B antibodies)
- What is the Kell antigens on the surface of RBC?
- What is their importance?
- Most common phenotype?
- Antigens =
- 1. K = kell
- 2. k= cellano
- 2nd in immunogenicity (2nd most targeted antigens, D).
- MC phenotype = kk (91%)
What alloantibodies develop to Kell antigens?
When does this cause a problem?
Anti-K IgG alloantibody.
- No Kell antigen => Anti-K IgG AB develop during transfusion/pregnancy with blood containing that antigen.
- Can cause
- 1. HDN
- 2. Hemolytic transfusion rxn
Kell system McLeod phenotype is associated with what diseases (2)?
- Chronic compensated hemolytic anemia = presence of acanthocytes on blood smear.
- Chronic granulomatous disease (CGD) = Lack K Ag on neutrophil/monocytes membrane => deficiency of NADH-oxidase => no H2O2 to destroy microbes = > increase risk of bacterial infections.
What are the Duffy Antigens?
Duffy glycoprotein = receptor for malarial parasite Plasmodium vivax.
Antigens =
- Fya = Duffy(a)
- Fyb = Duffy (b)
What is the MC Duffy phenotype in African-Americans?
What does this imply?
Fy (a-,b-) = resistant to Plasmodium vivax infection
What antibodies are produced against Duffy antigens?
What problems can they cause?
IgG => cause HDN & hemolytic transfusion rxn
What are the MNS antigens?
- Antibodies?
- Exhibits what effect?
- 4 important antigens: M, N, S and s
- Antibodies: Anti-M IgM antibodies, but non-hemolytic
- Dosage effect = react more strongly with homozygous cell, than hetero
- What are Kidd antigens?
- What antibodies develop to antigens?
- What problems does it cause?
- Antibodies exhibit ____ phenomenon.
- Antigens = Jka/Kidd (a) and Jkb/Kidd (b)
- Antibodies = anti-Jka IgG ab and anti-Jkb IgG ab = common, but low titers and weak, so they disappear quickly.
- Causes
-
Delayed Hemolytic Transfusion reactions: (+) compliment => rapid hemolysis. Then, Ab disappear and reappear when transfusion with Kidd
4. Dosage phenomenon