L36: Transfusion Reactions, Pt. 1

Question 1

Type 1 chains for blood groups

Answer 1

Antigens in secretions and plasma

Have secretor gene Se

Galactose connected to N-acetylglucosamine via 1, 3 linkage

Question 2

Type 2 chains for blood groups

Answer 2

Antigens expressed on red cells

Galactose and N-acetylglucosamine attached via 1, 4 linkage

Question 3

H antigen

Answer 3

Core blood group (galactose and the N-acetylglucosamine) with fucose attached to the galactose

Acts as a basis for which A and B expression is built on

Question 4

A antigen

Answer 4

N-acetylgalactose is added galactose of H antigen

Question 5

B antigen

Answer 5

Galactose is added to galactose of H antigen

Question 6

Bombay phenotype

Answer 6

Absence of H antigen

hh on Type 2 chain

No fucose is available, so H antigen doesn’t form

In absence of H, there is no A or B antigens

If you type them, they look like O but react to any blood group you give them since they have anti-H

Only accept blood from other Bombay phenotypes

Question 7

Para Bombay phenotype

Answer 7

Similar to Bombay phenotype except it has secretor gene

Has Se gene, so H, A, B or AB antigens are found in the secretions and plasma (Type 1 chain)

Expression of A or B depends on the inheritance of the pt

Antibody response that the pt makes can be mild or strong

Based on the reactivity of that antibody that they make, have to decide if you they can receive other compatible blood or only Bombay phenotype blood

Question 8

Why is there no anti-A or anti-B at birth?

Answer 8

When baby is born, immune system hasn’t yet been exposed to bacteria which looks like A or B antigen so they can then start make naturally occuring antibodies

If reverse group is done, where there should be anti-B or anti-A, it is very weak or not present

If antibody is foundi the plasma, it is IgG passed from mother

Immune response is not developed until they start getting exposed to certain bacteria, flora from the gut

Question 9

What chromosome is ABO on?

Answer 9

Chromosome 9

Question 10

What chromosome is H antigen on?

Answer 10

Chromosome 19

Question 11

Why is ABO expression on cord cells weak?

Answer 11

Due to immature type 2 chain precursors

Question 12

When do embryos start to express ABO antigen?

Answer 12

Weak expression of ABO antigen on RBC of embryos at 5 - 6 weeks

Question 13

At what age is ABO antigen developed? At what age is there an adult level?

Answer 13

3 - 6 months will have antigen developed

5 - 10 years will have adult level

Question 14

What is the front and back type of type A?

Answer 14

Front: A antigen
Back: anti-B Ig

Question 15

Fisher-Race system

Answer 15

DCE or CDE

Five major antigens: D, C, E, c, e

Whites: R1 (CDe) > r (cde) > R2 (cDE) > R0 (cDe)

Blacks: R0 (cDe) > r > R1 > R2

Question 16

What antigen is most important in RH blood group?

Answer 16

D antigen

Rh+ means D+

Rh- means D-

Question 17

Weak D

Answer 17

Quantitative defect in D antigen (less D than normal)

D antigen is normally formed

Weak D requires IAT (indirect antiglobilin test) to detect D presence

Won’t make anti-D since D is present, just at lower levels

Question 18

Partial D

Answer 18

Qualitative D antigen defect (abnormal forms, missing parts of the antigen)

Will produce anti-D if they are exposed to D+ blood

Question 19

Why are weak D and partial D important in labor and delivery?

Answer 19

Whether they are candidate for Rhogam to protect fetus from hemolytic disease of newborn

If they are partial D, should be treated as Rh- pt and be given Rhogam

Can do genotyping to see if they are partial D

Question 20

Stomacytic anemia

Answer 20

Absence of all Rh antigens

Question 21

Differentiate b/w IgG and IgM

Answer 21

IgG: reacts best at body temps; has to be very high titer since not very strong; most hemolysis will be extravacular (macrophage-mediated) which is not as severe as intravascular since no complement activation takes place; crosses placenta; hemolytic disease of the newborn is IgG mediated

IgM; cold-reacting antibody usually; if it reacts at body temp, it becomes very important; can cause acute hemolytic transfusion reactions and intravascular hemolysis and can be fatal

Question 22

Agglutination

Answer 22

RBC antigen (donor red cell) + RBC antibody (pt serum/plasma) = agglutination

Question 23

Indirect Coombs test

Answer 23

Antibody (from pt’s serum) + antigen → antigen and antibody reaction takes place (no visible agglutination since it is not strong enough) → add anti-human antibody → forms a lattice and there is visible agglutination

Question 24

Direct coombs test

Answer 24

Detects antibodies coating patient RBC in vivo

Important test in hemolytic disease or RBC destruction

RBCs with IgG bound to membrane → add anti-human globulin → visible agglutination

Question 25

What does hemolytic disease of fetus and newborn cause?

Answer 25

Anemia

Erythroblastosis

Hydrops: edema bc of anemia

Rising bilirubin (kernicterus) which crosses the blood-brain barrier and becomes very toxic

Question 26

Rhogam

Answer 26

Rh immune globulin prohylaxis

Given at 28 weeks and also post-deliver or following invasive procedure or bleeding during pregnancy

Question 27

Rosette test

Answer 27

Qualitative

Mother’s RBCs, treated with anti-D, binds to fetal Rh positive RBC wash and add RH positive RBC

Rh positive RBC forms a rosette around the fetal RBC bound with anti-D

Question 28

Kleihauer betke test

Answer 28

Quantitative

Acid denaturation of adult hemoglobin (Hgb A)

Hgb F is not susceptible to acid denaturation

Look at percent of cells that were not subject to acid denaturation and thus calculate how much fetal D this pt had

Blood volume x %fetal cells/30 mL = RhIG dose in vials

Add extra vial to be safe

Question 29

I and i group

Answer 29

Children with i and adults with I

Anti-I associated w/ Cold Hemagluttin Disease (CHAD) and Mycoplasma Pneumonia

Anti-i associated in infectious mononucleosis

Question 30

P blood group

Answer 30

Anti-P1 associated w/ Paroxysmal cold hemoglobinuria (PCH), Hydatid cyst and in bird handlers (exposed to P antigens when they handle birds and make anti-P)

Question 31

Lewis System, Type 1 chain

Answer 31

With Se gene in presence of 1H, makes Leb

Leb is receptors to Helicobacter pylori

Question 32

Anti-M and anti-N

Answer 32

Cold reacting

Cold IgM

Becomes significant if reactive at body temp.

Question 33

Anti-S, anti-s, anti-U

Answer 33

Will cause hemolytic disease of the newborn and hemolytic transfusion reaction

Warm IgG

Question 34

Kell system

Answer 34

There is an association of Kell system w/ Kx antigen
If they are missing, have McLeod syndrome
Also causes X-linked chronic granulomatous disease

Kell antibodies, in addition to causing hemolytic disease of fetus/newborn, also suppress erythropoiesis; so, they both cause hemolysis and suppress erythropoiesis; pts have very severe hemolytic disease of newborn since double problem

Question 35

Duffy system

Answer 35

Fy (a-b-) is most common Fy phenotype in African-Americans; this is protective against malaria

Higher incidence of prostate cancer in africans

Question 36

Kidd

Answer 36

Kidd antigens cause animistic reactions

Kidd antibodies: over course of time, completely dissapears; if pt comes in and does antibody screening, it shows negative; if you give A or B type blood, will have an immediate animistic reaction; reaction will include IgG and IgM antibodies; causes severe intravascular hemolysis

Jka and Jkb are also urea transporters; they are resistant to hemolysis if you add dextrose; bc it doesn’t transport urea, it is resistant to osmotic hemolysis