Blood bank quiz 1

gene

segment of DNA that encodes for particular protein

Locus

loaction of gene on chromosome

allele

alternative forms of gene at specific locus

double dose

homozygous

single dose

heterozygous

hemizygous

only one copy of allele

linkage

physical association between two genes on same chromosome

linkage disequilibrium

specific combinations of alleles inherited together more frequently than expected by chance

hardy weinberg calculation

p² + 2pq + q² = 1

Most blood group antigens express what mode of inheritance

autosomal codominant

nucleic acid analysis

detection of genetic material

highly sensitive

protein analysis

detection of antibodies (fluid and solid phase)

fluid phases

sensitization: ab attach to ag on RBC

Agglutination: ab cross link RBC

prozone

ab excess

postzone

ag excess

What percentage of immunoglobulins are IgG

80%

What immunoglobulin lasts the longest?

IgG

What immunoglobulins can activate compliment

IgG and IgM

What immunoglobulin can cross the placenta

IgG

solid phase assay

ag/ab is immobilized on solid matrix and incubated

What immunoglobulin is most effective at activating complement?

IgM

What are molecular methods in transfusion medicine used for

Infectious disease testing and antigen typing

Which complement component is a strong opsonin

C3b

Why do we care about complement

Because it affects transfusion reactions

Where are ABO ag found

RBC, platelets, and many tissues

ABO inheritance type

Autosomal codominant, O gene is silent

When are antigens detectable in a human

5-6 weeks gestation

When are antibodies detectable in a human

3-6 months old

Group O antibodies

anti A, anti B, and anti AB

Group AB antibodies

none

H antigen

precursor for A and B antigens, has terminal fucose. found on type O people

A antigen

GALNAC added to terminal galactose of H antigen

B antigen

GAL added to terminal galactose of H antigen

H ag concentration on RBC surface (most to least)

O > A2 > B > A1 > A1B

Anti A and Anti B (Ig)

Predominantly IgM

Anti AB

Formed by group O people, IgG (Cross placenta)

Anti A1

Present in some A subgroup individuals

clinically significant if reactive at 37C

What percentage of group A individuals are A1?

80%

A2 group

20% of group A individuals are A2

• does not convert H to A antigen so RBCs don’t agglutinate with anti-A1

• Can produce anti-A1 in plasma (more common in A2B)

A3

Exhibits mixed field reactions

B(A) phenotype

Very rare, autosomal dominant

Weak expression of A antigen on group B cells

Acquired B phenotype

Temporary, seen in group A1 people. usually caused by infection with gastrointestinal bacteria

Forward typing

Patient RBCs and commercial antisera

Reverse typing

Commercial RBCs and patient plasma

Bombay phenotype

No ag on RBC. Also lack secretor gene

Have anti-A, anti-B and anti-H in plasma

Type as O

Most ABO ab are what class of immunoglobulin

IgM

What blood group is most likely to make anti-A1

A2B (A2 sometimes will)

Commercial antisera is used in which part of the blood typing assay?

forward typing

What antigen is the most immunogenic

D

What is the most common antigen in the Rh system

little e

D/d inheritance pattern

Autosomal dominant (little d means absence of D)

C/c and E/e inheritance pattern

Codominant

Which is the most uncommon antigen in the Rh system

big E

What is the most common Rh haplotype among black people?

Dce

What is the most common Rh haplotype among asian americans

DCe

(also white pop)

How does the C antigen affect the D antigen

The presence of C suppresses the number of D antigen sites

What is the most common Rh phenotype among black people

R₀r (Dce/dce)

What is the most common Rh phenotype among white people

R1r (DCe/dce)

Weak D (and is there risk of anti-D)

Reduced amount of D antigen expression

No risk of making anti D

Partial D (and is there risk of anti-D)

Missing portion of D antigen

Risk of making anti-D

DVI is most common phenotype

Rh null characteristic

Stomatocytes

(lack of all Rh ag)

Rh antibodies

Mainly IgG

Does the Rh system exhibit dosage

Yes

I system

i is precursor to I

(children will have i, adults will have I typically)

Auto anti-I

Common, IgM, usually cold reactant and related to cold agglutinin disease (I —> ice)

auto anti-i

uncommon, IgM, seen with IM

Allo anti-H

Seen in bombay, clinically significant

P1PK system P1 phenotype

Has P1 and P antigens, no Ab in serum, most common

P1Pk system P2 phenotype

P1 antibody in serum

P1pK system p phenotype

Very rare, no antigens, PP1PK ab in serum

Allo anti-PP1PK

Formed by those w p phenotype

Can cause hemolytic reactions

Lewis system phenotypes

Le(a+b-), Le(a-b+), Le(a-b-)

A and B not positive at same time

Lewis system antigens and synthesis

not synthesized by RBCs, found in plasma and on cells. requires lewis gene and secretor gene

Le^a

LE gene adds fucose to chain

Le^b

SE gene adds additional fucose to Le^a

Lewis expression in children

Ag is weak, valid phenotype not evident until 6yrs

HLA pattern of inheritance

autosomal codominant

25% chance of two siblings being HLA identical

Class I HLA ag

Heavy and light chains, found on all nucleated cells

Class II HLA ag

alpha and beta chain, found on leukocytes

RBC Bg antigens

Class I HLA antigens

Why do we do HLA typing

Transplants, forensic testing, relationship testing, disease association

U clinical significance (MNS)

A U- individual is also S- and s-

U is not destroyed with enzyme treatment