Blood Groups pt1 - BB Flashcards by heather wade

What type of chains are Lewis Ags ?

Type 1

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What precursor gene(s) must you have to make Le(a)?

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What precursor gene(s) are needed to make Le(b)?

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What is the molecular form of Lewis ags on RBCs?

Glycolipid

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What is the molecular form of Lewis ags in saliva?

Glycoproteins

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Where are Lewis ags developed?

In the gut

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If a patient inherits Le, Se, and H, what Lewis antigens will they produce at birth, 10 days after birth, and at 5 years of age?

Birth: Le(a-b-)
10 days after birth: Le(a+b+)
5 years old: Le(a-b+)

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If a patient inherits Le, sese, and H, what Lewis antigens will they produce at birth, 10 days after birth, and at 5 years of age?

Birth: Le(a-b-)
10 days after birth: Le(a+b-)
5 years old: Le(a+b-)

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Which Le antigen is a receptor for H. pylori and norovirus?

Le(b)

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Which Lewis phenotype is more likely to develop E. coli and Candida infections?

Le(a-b-)

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How are Lewis Ags affected by enzyme/chemical treatment?

Enzyme enhanced

Chemically resistant

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What is the Lewis phenotype that will produce naturally occurring Lewis Abs?

Le(a-b-)

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What Ig class are Lewis Abs in?

IgM

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Why are Lewis Abs common in pregnant women?

Because Lewis Ags decrease during pregnancy

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Which Lewis Ab can react at 37C and cause HTRs (rare occurrance)?

Anti-Le(a)

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What is the most common Lewis phenotype?

Le(a-b+)

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What two genes code for the P1PK and GLOB blood group?

P1PK and P genes (different chromosomes)

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What is the common precursor for the P1PK and GLOB blood group?

Lactosylceramide

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What is the precursor for P1?

Paragloboside

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What kind of molecules are the antigens from the P1PK and GLOB blood group?

Glycosphingolipids

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What is the most common phenotype of the P1PK and GLOB blood group?

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Why does a person with a P1 phenotype show no Pk antigens?

They are covered up by P

They only show P and P1 ags

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What is the second most common phenotype from the P1PK and GLOB blood group? What antigens do they show?

P2, only P ags

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Which phenotype from the P1PK and GLOB blood group will have the most significant Ab in their serum? What is the Ab?

p(null), anti-PP1PK

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Where are P and PK antigens found?

RBCs, WBCs, and other tissues

Where are P1 antigens found?

On RBCs only

How are antigens in the P1PK and GLOB blood group affected by enzyme/chemical treatment?

Resistant

Fetal cells have P1 antigens at birth. T or F?

False, they first appear at approx. 6 months of age

What gene decreases P1 expression?

In(Lu)

What might cause P1 antigens to decrease on RBC's?

Pregnancy and storage

What soluble antigens can be used to neutralize anti-P1? Where are they found?

P1 and Pk; They are found in hydatid cyst fluid of dog tapeworms, pigeon poop, and bovine liver flukes

What is significant about the anti-PP1PK Ab?

It is usually IgG, naturally occurring, and can cause HDFN/HTR.

What is significant about the auto anti-P Ab?

It is a biphasic hemolysin, IgG, and can cause PCH (attaches at 4C and lysis cells with complement when at 37C)

What antibodies have the potential to cause early spontaneous abortion? Why does this occur?

anti-P and anti-PP1K (p null phenotype) because there is a high amount of P and Pk antigens in the placenta - mom can make Abs that attack the placenta

What individuals may have resistance to Human Parvovirus B19? Why?

People who lack P antigens (p and Pk people) because globoside is a receptor for the virus.

What enzyme is needed to convert linear i to branched I?

N-acetylglucosaminyltransferase

Which precursor can make i or I?

Paragloboside (P1 precursor)

What is the most common phenotype for Group I antigens at birth?

I-i+

What is the most common phenotype for Group I antigens in adulthood?

I+i-

What is the adult "null" phenotype for Group I?

I-i+

What kind of molecules are the I antigens?

Oligosaccharides (branched and unbranched)

How are the I/i antigens affected by chemical/enzyme treatment?

Both are resistant to chemical treatment; I is enzyme enhanced

How is I/i expression altered in the Bombay phenotype?

I is increased, since patients don't have A,B, or H it is more visible in reactions

When is increased i antigen seen?

On immature cells in disorders such as Thalassemia major, hypoplastic, sideroblastic, and megaloblastic anemias, acute leukemia, and chronic hemolytic states.

What might naturally occurring auto anti-I cause? Is it clinically significant?

It may cause cold agglutination which can mask clinically significant Abs, but is not clinically significant in vivo.

What might pathogenic auto anti-I cause? Is it clinically significant?

It is a cold hemagglutinin that may cause transient acute reactions in patients; it is also associated with the following disease: Mycoplasma pneumonia, HEMPAS (rare), or CHD.

How do you differentiate benign auto anti-I from pathogenic auto anti-I?

Pathogenic auto anti-I will titer higher than the benign Ab (greater than 1000)

What type of blood products should I-i+ adults receive? What harm could allo anti-I cause if the right blood product is not administered?

"Null" phenotype blood (I-); The Ab could cause a HTR, but not HDFN (IgM)

What might auto anti-i cause? Is it clinically significant?

Nothing that is clinically significant, may form secondary to disease

What are the most significant combined cold Abs?

anti-IH and anti-IP1

What cells will anti-IH be most reactive with and why?

The Ab will react mostly with adult cells that have lots of H antigen (O, A2, B, A1) because most adults express I.

What cells will anti-IP1 be most reactive with and why?

The Ab will react with most adult blood cells because most adults have I and P1.

What type of molecule are MNS antigens?

Sialoglycoproteins (SGPs)

What affect does sialic acid have on RBCs?

It increases the zeta potential - increases negative charge

Which glycophorin are MN antigens found on?

GPA

Which glycophorin are Ss antigens found on?

GPB (U is also there, close to the membrane)

Where is S/s located on GPB?

In the middle of the structure (not at the end like MN on GPA)

What prevents patients from making N Ab?

The N-like structure at the end of GPB

What is a U neg patient missing?

The entire GPB (no S/s)

What was the second blood group discovered? Why was it used for paternity testing?

MNS; The haplotypes have very strong linkage and little recombination

Are MNS antigens well developed at birth? If so, can they cause HDFN?

Yes; Yes

What is the immunogenicity of the MNS group in order?

M>S>s

What affect do chemical and enzyme treatment have on the MNS antigens (with the exception of U)?

MNS antigens are destroyed by enzymes and resistant to chemicals.

How is the U antigen affected by enzymes? Why?

It is resistant because it is so close to the cell membrane.

What is the most prevalent MNS phenotype in black and white people?

M+N+

What are the MNS null phenotypes (5)?

- Mg = no MN antigens (Mg ags instead) - En(a-) = No MN-SGP (GPA) - U- = no Ss-SGP (GPB) - MkMk = No GPA or GPB - Mur = hybrid gene; most common Ab behind anti-A,B in Hong Kong and Taiwan

Of the MNS group, what are the most significant Abs and why?

Anti-S, anti-s, and Anti-U, because they are all IgG

What is the significance of anti-M (IgM and IgG)?

Anti-M IgG can cause HDFN. | Anti-M IgM can put heart surgery patients at risk when their body temp is lowered (need M neg blood).

What kind of UTI might MN pos patients be more susceptible to?

Pyelonephritis causing E.coli infections (the antigens are receptors)

How does the U phenotype protect against malaria (P. falciparum)? What population has this phenotype?

MN and Ss-SGPs are alternative receptors for P. falciparum and allows the parasite to enter the RBCs. Only black people have anti-U.