Transfusion Medicine DSA Flashcards

1
Q

In the RBC cell membrane, what are rhesus factors and the ABO system made of?

A

RF - proteins.

ABO - carbohydrates.

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2
Q

What is a primary vs. a secondary response in immunization to RBC antigens?

A

Primary: seen in the first immune exposure to a “foreign” protein antigen (noticed days or weeks after exposure).

Secondary: seen upon repeat exposure to a “foreign” protein antigen (noticed much quicker after sun exposure).

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3
Q

For most Blood Group Antigens, but not ABO, how does the composition of antibodies change after a primary vs. a secondary response?

A

Primary: high [IgM] with some formation of IgG after days or weeks.

Secondary: a transient rise in IgM and a sustaned increase in IgG is typical.

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4
Q

What 3 antigens are expressed in the ABO system?

What makes up O, A, B and AB blood types?

A

H, A, B (terminal sugar units).

O: H only.
A: H + A.
B: H + B.
AB: H + (A + B).

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5
Q

What is meant by the term “secretor”?

A

Someone who is capable of making ABO antigens in their secretions and plasma. About 80% of the population carries at least 1 allele called “Se”.

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6
Q

What is the significance of the Se allele?

A

It encodes an enzyme that allows that person to make the H antigen on long carbohydrate-rich chains (type 1 chains) found in secretions and plasma.

Once the H antigen is made, then the person can make either A or B (or both) on the type 1 chains.

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7
Q

How does leukemia alter the expression of ABO antigens?

A

It decreases the amount of ABO antigens.

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8
Q

What is “acquired B”?

A

It refers to intestinal obstruction leading to increased bowel permeability, causing an increase of bacterial polysaccharides into circulation absorbed by group A cells.

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9
Q

What is the Bombay phenotype?

What kind of blood must they receive?
Why?

A

Absence of H (Oh); RBC has no antigen.

May only receive Bombay blood.
These patients have anti-A, anti-B, anti-H and anti-A,B antibodies. The anti-H IgM binds complement and lyses cells.

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10
Q

What type of antibodies are produced against H?

A

IgM > IgG

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11
Q

What is the universal donor?

What is the universal recipient?

A

Donor: O

Recipient: AB

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12
Q

What is meant by the following Rh genes?

D
d
C/c
E/e

A

D: Rh factor or Rhesus Ag.
d: absence of D.
C/c: C and c are codominant.
E/e: E and e are codominant.

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13
Q

What is the main difference between Rh antibodies and ABO antibodies?

A

Rh antibodies are not naturally occurring, and exposure to the antigen is needed in pregnancy or transfusion.

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14
Q

RhoGAM is contraindicated in which patients?

A

Those who are Rh+.

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15
Q

What is “weak D”?

A

It is the most common immunogenicity. It is due to absence of the D antigen.
The recipient is D- (Rh-) and the donor is D+ (Rh+).

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16
Q

What is the significance of the Kell system?

What are the 2 most important antigens?

What antibodies are positive against it?
What 2 outcomes are possible?

A

It is the second most common immunogenicity (after D).

K = Kell (anti-K is more common)
k = Cellano

IgG and reaction at 37 deg.
Hemolytic disease of newborn, hemolytic transfusion reaction.

17
Q

What are the 2 most common antibodies in the Kidd system?

What is major outcome in patients with these antibodies?

What happens to the antibodies?

A

Anti-Jka and anti-Jkb (in low titer and weak avidity, thus they disappear rapidly).

3/4 of patients have delayed hemolytic transfusion reactions (IgG). Activates complement and causes rapid hemolysis.

Antibodies “disappear” and exhibit a dosage phenomenon in vitro.

18
Q

What are the 2 most important antigens in the Duffy system?

What phenotype is common in AAs?
Why is this significant?

What 2 outcomes are possible?

A

Fya (Duffy a) and Fyb (Duffy b).

Fy(a-,b-).
It is resistant to Plasmodium vivax infection.

IgG associated hemolytic disease of newborns and hemolytic transfusion reactions.

19
Q

What antigens are most important in the MNS system?

What antibodies are most common?

What is meant by the “dosage effect”?

A

M and N.
S and s.

Usually IgM.

Reaction is stronger with homozygous cells than heterozygous cells.

20
Q

What antibodies are seen in the Lewis system?

Where are they found? What is the significance of this?

A

IgM “warm” antibodies that are naturally occurring.

The Le antigen is found in secretions and plasma, then adsorbed onto the RBC membrane. This means that the patient must be a secretor and Hh genes.

21
Q

What is the most common complication of transfusion?

A

A febrile non-hemolytic reaction, which takes the form of fever and chills, sometimes with mild dyspnea, within 6 hrs. of transfusion of RBCs or platelets.

Symptoms are usually short-lived and respond to treatment.

22
Q

What causes a severe reaction from transfusions?

Which patients are they most likely to occur in?

A

Blood products containing certain antigens are given to previously sensitized recipients.

Patients with IgA deficiency - it is triggered by IgG antibodies that recognize IgA in the infused blood.

23
Q

What occurs in urticarial allergic reactions?

A

The presence of an allergen in the donated blood product is recognized by IgE antibodies in the recipient.

It tends to respond to antihistamines and does not require discontinuation of the transfusion.

24
Q

What causes acute hemolytic reactions after transfusions?

What are acute symptoms?
What are chronic symptoms?

What test is positive?

A

Preformed IgM against donor red cells that fix complement. It is usually due to an error in patient identification or tube labeling.

Fever, shaking, chills and flank pain occur rapidly.
DIC, shock, ARF and occasionally death.

Direct Coombs test is usually positive.

25
Q

What causes delayed hemolytic reactions occur with blood transfusions?

What test is positive?

A

Antibodies that recognize red cell antigens that the patient was previously sensitized to (prior infusions).

Direct Coombs test is positive.

26
Q

What is transfusion-related acute lung injury (TRALI)?

What antibodies are most associated with it?
Which patients are most likely to have these specific antibodies?

What products is it most likely to occur with?

What is the clinical presentation?

A

A severe, often fatal complication in which factors in transfused blood trigger activation of neutrophils in the lung microvasculature.

Antibodies binding MHC class I antigens.
Multiparous women (they don't generate antibodies against foreign MHC expressed by the fetus).

Products with high levels of donor antibodies like FFP and platelets.

Dramatic onset with sudden respiratory failure during or soon after transfusion. Fever, hypotension and hypoxemia may also ensue.