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Misc BOC Questions > Blood Groups pt1 - BB > Flashcards

Blood Groups pt1 - BB Flashcards

1
Q

What type of chains are Lewis Ags ?

A

Type 1

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2
Q

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

A

Le

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3
Q

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

A

Se

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4
Q

What is the molecular form of Lewis ags on RBCs?

A

Glycolipid

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5
Q

What is the molecular form of Lewis ags in saliva?

A

Glycoproteins

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6
Q

Where are Lewis ags developed?

A

In the gut

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7
Q

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?

A

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

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8
Q

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?

A

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

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9
Q

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

A

Le(b)

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10
Q

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

A

Le(a-b-)

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11
Q

How are Lewis Ags affected by enzyme/chemical treatment?

A

Enzyme enhanced

Chemically resistant

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12
Q

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

A

Le(a-b-)

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13
Q

What Ig class are Lewis Abs in?

A

IgM

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14
Q

Why are Lewis Abs common in pregnant women?

A

Because Lewis Ags decrease during pregnancy

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15
Q

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

A

Anti-Le(a)

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16
Q

What is the most common Lewis phenotype?

A

Le(a-b+)

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17
Q

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

A

P1PK and P genes (different chromosomes)

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18
Q

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

A

Lactosylceramide

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19
Q

What is the precursor for P1?

A

Paragloboside

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20
Q

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

A

Glycosphingolipids

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21
Q

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

A

P1

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22
Q

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

A

They are covered up by P

They only show P and P1 ags

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23
Q

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

A

P2, only P ags

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24
Q

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

A

p(null), anti-PP1PK

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25
Q

Where are P and PK antigens found?

A

RBCs, WBCs, and other tissues

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26
Q

Where are P1 antigens found?

A

On RBCs only

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27
Q

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

A

Resistant

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28
Q

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

A

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

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29
Q

What gene decreases P1 expression?

A

In(Lu)

30
Q

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

A

Pregnancy and storage

31
Q

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

A

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

32
Q

What is significant about the anti-PP1PK Ab?

A

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

33
Q

What is significant about the auto anti-P Ab?

A

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

34
Q

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

A

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

35
Q

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

A

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

36
Q

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

A

N-acetylglucosaminyltransferase

37
Q

Which precursor can make i or I?

A

Paragloboside (P1 precursor)

38
Q

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

A

I-i+

39
Q

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

A

I+i-

40
Q

What is the adult “null” phenotype for Group I?

A

I-i+

41
Q

What kind of molecules are the I antigens?

A

Oligosaccharides (branched and unbranched)

42
Q

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

A

Both are resistant to chemical treatment; I is enzyme enhanced

43
Q

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

A

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

44
Q

When is increased i antigen seen?

A

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

45
Q

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

A

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

46
Q

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

A

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.

47
Q

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

A

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

48
Q

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?

A

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

49
Q

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

A

Nothing that is clinically significant, may form secondary to disease

50
Q

What are the most significant combined cold Abs?

A

anti-IH and anti-IP1

51
Q

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

A

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

52
Q

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

A

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

53
Q

What type of molecule are MNS antigens?

A

Sialoglycoproteins (SGPs)

54
Q

What affect does sialic acid have on RBCs?

A

It increases the zeta potential - increases negative charge

55
Q

Which glycophorin are MN antigens found on?

A

GPA

56
Q

Which glycophorin are Ss antigens found on?

A

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

57
Q

Where is S/s located on GPB?

A

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

58
Q

What prevents patients from making N Ab?

A

The N-like structure at the end of GPB

59
Q

What is a U neg patient missing?

A

The entire GPB (no S/s)

60
Q

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

A

MNS; The haplotypes have very strong linkage and little recombination

61
Q

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

A

Yes; Yes

62
Q

What is the immunogenicity of the MNS group in order?

A

M>S>s

63
Q

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

A

MNS antigens are destroyed by enzymes and resistant to chemicals.

64
Q

How is the U antigen affected by enzymes? Why?

A

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

65
Q

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

A

M+N+

66
Q

What are the MNS null phenotypes (5)?

A
  • 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
67
Q

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

A

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

68
Q

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

A

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).

69
Q

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

A

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

70
Q

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

A

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

Misc BOC Questions (3 decks)

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