Unit 4: Other Blood Groups Flashcards

1
Q

How is Lewis blood group system unique?

A

Lewis blood group system gets adsorbed onto the RBC membrane from plasma

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2
Q

Where are the lewis antigen located?

A

type 1 glycosphingolipids

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3
Q

Why are Lea and Leb not antithetical?

A

they don’t result from alternative alleles of a single gene

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4
Q

What is fucosyltransferase?

A

an enzyme that transfers a l-fuc sugar from GDP-fuc donor substrate to an acceptor

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5
Q

What produces lewis antigens?

A

tissue cells (plasma/body secretions)

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6
Q

Where is the Se gene located?

A

chromosome 19

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7
Q

What are the two genes of Se?

A

Se and se (absence)

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8
Q

Where does the Se gene add L-fuc?

A

to type 1 precursor chains (body fluids)

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9
Q

What do you require to have Lewis B?

A

a Secretor

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10
Q

In Le(a+b-) what genes are present? What is secreted?

A

Le and H genes, Le(a) antigen substance secreted

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11
Q

In Le(a-b+) what genes are present? What is secreted?

A

Le, H and Se genes, A, B, H, Le(b) and small amts of Le(a)

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12
Q

In Le(a-b-) what genes are present? What is secreted?

A

nothing, possibly have Se (must test)

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13
Q

If you have a weak secretor gene what occurs?

A

you will have more Le(a) because it makes less Le(b) and causes Le(a+b+)

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14
Q

Cord blood and RBCs of newborns type as Le___

A

Le(a-b-)

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15
Q

In newborn secretions, if they have Le gene, what do they have?

A

Le(a) in secretions (saliva)

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16
Q

At how many days old will Le be present on RBCs? What will show?

A

10 days, Le(a+b-)

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17
Q

After 10 days… what will newborns type as

A

Le(a+b+)

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18
Q

Why does Lw blood group substance transfusion rarely cause hemolysis of RBCs?

A

they bind to free-floating anti-Le(a or b) in plasma rather than ones attached to RBC membrane

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19
Q

What does Anti-Le(bH) react with?

A

group O Le(b+) and A2 Le(b+)

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20
Q

In the serum of Le(a-b-) secretors, what is found?

A

Anti-Le(a) and Anti-Le(b)

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21
Q

What are techniques to ID anti-Le’s?

A

neutralization of antibodies

enzyme-treated cells that enhance reactivity

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22
Q

Why don’t individuals who type Le(a-b+) make anti-Le(a)?

A

because they still have small amounts of Le(a)

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23
Q

Lewis system is known to be associated with…

A
peptic ulcers
ischemic heart disease
cancer
kidney transplant rejection
helicobacter pylori
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24
Q

Where are antigens M and N found?

A

glycophorin A

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25
Q

Where are the S antigens found?

A

Glycophorin B

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26
Q

What antibody is found frequently in human sera and agglutinates in saline?

A

Anti-M

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27
Q

Anti-M exhibits the _______ with the N antigen

A

dosage effect

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28
Q

Anti-M fails to react with….

A

enzyme-treated red cells (it gets destroyed)

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29
Q

What are not common antibodies that are usually IgG and immune in nature?

A

Anti-S and Anti-s

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30
Q

What antibody is rare and reacts with the cells of most people?

A

Anti-U

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31
Q

What phenotype produces Anti-U? Which population is it almost exclusively found?

A

S-s-U-

African American

32
Q

En(a-) phenotype results from…

A

gene deletion at GYA locus for glycophorin A

33
Q

What is the M(k) phenotype?

A

single near-complete deletion of both GYPA and GYPB so they will have no M, N or S

34
Q

Which enzyme(s) destroys only S & s?

A

chymotrypsin

35
Q

Which enzyme(s) destroys only M & N?

A

trypsin
ZZAP
DTT w/ papain or ficin
AET

36
Q

Which enzymes destroys all MNS?

A

ficin
papain
bromelin
pronase

37
Q

Where are P & Globoside blood groups found?

A

RBCs, lymphocytes, granulocytes and monocytes

38
Q

What is the common precursor for globoside?

A

lactosylceramide

39
Q

What are the antigens for the P & Glb blood group system?

A

P
P1
P(k)
Luke (LKE)

40
Q

What antigen is assigned to the Glb system?

A

P antigen

41
Q

How long could it take for P1PK to be fully expressed?

A

7 years

42
Q

What could inhibit the P1 antigen expression?

A

In(lu) gene

43
Q

Where is the P1 antigen found?

A

in individuals with a hydatid cyst infection

44
Q

Where does the P1 gene reside? Where does the P antigen (GLOB) reside ?

A

chromosome 22

chromosome 3

45
Q

What is known as the Donath-Landsteiner antibody?

A

(IgG) Anti-P

46
Q

Describe why Anti-P is a powerful biphasic hemolysin…

A

it attaches to red cells in the cold buy lyses them in warmer temps

47
Q

What are the diseases associated with the P1Pk and Glb blood group systems?

A
hydatid cyst infection
fascioliasis
adenocarcinoma
HTRs
HDNs
PCH
Tertiary syphilis
acute condition secondary to viral infection
shigella dysentery
E. coli-associated hemolytic uremic syndrome
UTIs
48
Q

What is the structure of i vs I?

A

i is linear and I is branched

49
Q

How are i and I antigens formed?

A

glycosyl transferases

50
Q

What is the principle of adsorption?

A

removes antibodies from serum by adding target antigen, it gets agglutinated and then removed by centrifugation

51
Q

What is human plt concentrates used for?

A

to adsorb Bg-like antibodies from serum

52
Q

What is RESt? What does it process?

A

ID’s cold-reacting autoantibodies, it processes I, H and IH-like structures

53
Q

How are autoantibodies removed?

A

adsorption techniques

54
Q

If reactivity occurs during autoadsorption…

A

autoantibody remains in serum and further adsorption is necessary

55
Q

Describe homologous adsorption…

A

patient is phenotyped, then phenotypically matched RBCs are used for the adsorption in place of autologous cells.

56
Q

What blood group systems are treated with enzymes to be negative for DAT?

A

duffy and MNS

57
Q

What is the most critical step in preparing the eluate?

A

original washing

58
Q

What are the enzymes used to separate specificities and allows for ID?

A

trypsin
ficin
bromelin

59
Q

What do enzymes remove on the RBC surface?

A

Sialic Acid residues or glycoproteins

60
Q

Enzymes may be used in place of which enhancement medias?

A

LISS/PEG

61
Q

What is the purpose of pretransfusion testing?

A

to reveal any possible incompatibility between a donor’s blood and the recipient’s blood

62
Q

What is the second purpose of pretransfusion testing?

A

to select blood products with acceptable survival rates

63
Q

What is the major cause of transfusion-associated fatalities?

A

clerical errors

64
Q

What percentage of the errors are misidentification?

A

47%

65
Q

What is the preferred specimen for transfusion services?

A

plasma (no waiting time to clot)

66
Q

What is the preferred specimen for complement ID since EDTA could neutralize complement?

A

serum

67
Q

What is the major difference between a T/S vs a T/C?

A

in a T/C, the donor RBC is mixed with recipient RBC

68
Q

What occurs in a T/S and T/C if you have a positive antibody screen?

A

identify the antibody, perform AHG Xmatch then set aside antigen-negative blood for patient

69
Q

What is the most common bacterial contaminant?

A

Yersinia enterocolitica

70
Q

What are the phases of cross-matching?

A

Immediate spin crossmatch
antiglobulin crossmatch
Weak D (once)

71
Q

What test is sufficient for a patient receiving large volumes of plasma?

A

immediate spin crossmatch

72
Q

What are the massive transfusion measurements?

A

8-10 RBC units/24 hours or 4-5 RBC units/1 hour

73
Q

How can complete coagulation be accelerated?

A

adding thrombin

74
Q

What is the purpose of the MSBOS?

A

to promote more efficient utilization of blood and establish realistic blood ordering levels

75
Q

What is required for issuance of blood/blood components?

A

After all pretransfusion testing
after all serological discrepancies resolved
a minimum of 2 patient identifiers
a written request