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blood banking > exam 1 > Flashcards

exam 1 Flashcards

1
Q

allele

A

one of two or more different genes that may occupy a specific locus on a chromosome

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2
Q

amorph (silent allele)

A

a gene that does not appear to produce a detectable antigen

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3
Q

phenotype

A

the outward expression of genes

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4
Q

genotype

A

an individuals actual genetic makeup

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5
Q

heterozygous

A

possessing different alleles at a given gene locus

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6
Q

locus

A

the site of a gene on a chromosome

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7
Q

homozygous

A

posessing a pair of identical alleles

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8
Q

dominant

A

a trait or characteristic that will be expressed in an off spring even though it is carried on only one of the homologous chromosomes

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9
Q

recessive

A

a type of gene that in the presence of its dominant allele does not express itself; expression occurs when inherited in the homozygous state

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10
Q

co-dominant (egalitarian)

A

a pair of genes in which neither is dominant over the other; they are both expressed

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11
Q

zeta potential

A

the net negative charge surrounding RBC’s causing them to repel one another

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12
Q

how does the addition of albumin to RBC effect the zeta potential?

A

works by reducing zeta potential and dispersing the charges allowing RBC to approach each other so that IgG can cross link between RBC (increased chance of agglutination)

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13
Q

IgG

A

-only Ig that cross placena (CS)
-not found in nature (pregnancies of transfusions)
-likes 37C (CS)
-needs AHG for detection
Rh, Kell, Duffy, Kidd, Ss,
D, C, E, e, c, k, Fy, Jk, S, s, LeA, LeB

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14
Q

IgM

A
  • largest “j” chain
  • 1st Ab to appear
  • found naturally
  • not clinically significant
  • ABH, Hh, Ii, Lewis, MN, P, IS phase
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15
Q

what is LISS

A

low salt media

decreases ionic strength of rxc media to reduce zeta potential

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16
Q

what are the proteolytic enzymes?

A

ficin
papain
trypsin
bromelin

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17
Q

how do the proteolytic enzymes work?

A

reduce zeta potential by removing some glycoproteins from RBC surface to make RBC more hydrophobic (more access for binding)

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18
Q

proteolytic enzymes increase reactivity for what systems

A 
Rh,
Kidd
P
Lewis
I antigens
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19
Q

proteolytic enzymes decrease or destroy reactivity for what systems?

A

duffy
M
N
S antigens

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20
Q

AGT/coombs is useful for detecting what?

A

IgG

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21
Q

DAT (direct antiglobulin test)

A

-in vivo(inside body)
-detects Ab/complement attached to RBC in vivo
useful for detecting HDN, HTR, and AIHA

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22
Q

IAT

A

in vitro
useful for compatibility testing, Ab screening, RBC phenotyping, titers
detects Ab/complement attached to RBC in vitro

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23
Q

anti-human globulin

A

obtained from immunized NON-human species bound to human globulins IgG and/or complement

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24
Q

why is AHG used?

A

used in DAT and IAT testing because the AHG will bind to IgG or complement showing the Ab-Ag rxc that usually goes undetected because of IgG’s size in comparison to IgM

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25
Q

alloantibodies

A

after exposure to genetically different antigens from same species

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26
Q

auto antibodies

A

produced to self antigens (autoimmune)

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27
Q

genotype

A

2 letters, what is inherited by both parents

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28
Q

phenotype

A

1 letter what is expressed by individual

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29
Q

dosage

A

a phenomenon whereby an antibody reacts more strongly without a RBC carrying a homozygous inheritance than with a heterozygous inheritance of an antigen

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30
Q

where is dosage shown?

A

kidd system

Rh system with C,c,E,e

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31
Q

what is the system in which the Ab are consistently and predictably present in serum of normal individuals whose RBC lack the Ag

A

ABO

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32
Q

what are the genotypes of the phenotype A

A

AA

AO

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33
Q

what are the genotypes of the phenotype B

A

BB

BO

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34
Q

what is the genotype of the phenotype O

A

OO

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35
Q

what gene is needed for the expression of ABO genes?

A

H gene

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36
Q

how does the H substance work?

A

the H gene secretes H substance that converted by A or B gene into A or B antigens

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37
Q

what ABO gene has the most H antigens on its surface?

A

O, because the O gene is a silent allele and doesn’t alter the H substance

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38
Q

type 1 precursor chain

A

1,3 linkage

found in plasma

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39
Q

type 2 precursor chain

A

1,4 linkage

found on RBC

40
Q

what is the order of H antigen present on cells from most to least?

A

O>A2>B>A2B>A1>A1B

41
Q

how is the A antigen made?

A

1) add H substance (fucose) to precursor

2) add immunodominant sugar N-Acetylgalactosamine

42
Q

how is the B antigen made?

A

1) add H substance (fucose) to precursor

2) add immunodominant sugar D- galactose

43
Q

what is the genotype of bombay individual?

A

hh

44
Q

what is the phenotype of bombaby individual?

A

O

45
Q

what are bombay individuals unable to produce?

A

H substance

46
Q

How does the inability to produce a certain substance affect the bombay individuals?

A

they can inherit A or B genes but because they lack the H substance they cannot make A or B antigens

47
Q

what antibodies are found in the serum of bombay individuals?

A

anti-A
anti-B
anti-H

48
Q

where are soluble Ag’s found?

A

body secretions

sweat, saliva, etc

49
Q

where do secretors secrete their soluble ag

A

body secretions

50
Q

what can nonsecretors secrete?

A

A,B, or H

51
Q

can bombay patients also be secretors/

A

yes, they will secrete H and whichever ABO suppressed gene they possess

52
Q

what test is used to detect ABH substances in saliva?

A

neutralization tests

53
Q

forward typing

A

patients RBC are added to antisera anti-A and anti- B to test for presence/absence of Antigens

54
Q

reverse typing

A

patient serum is added to A1 and B cells to test for presence/absence of antibodies

55
Q

landsteiners rule

A

antibodies are present in plasma only when the corresponding antigen is not present on the RBC

56
Q

anti-A1

A

produced by some subgroups of A ( A2 and A2B)
Ig class: M
low temp. range
HDNB: no
no extravascular hemolysis and rare intravascular hemolysis

57
Q

anti-A1 lectin

A

prepared from seeds of dolichos biflorus
identifies A1 subgroup
necessary when working with A2 or A2B because serum contains anti-A1

58
Q

anti-H (autoAb)

A

low thermal range
seldomly clinically sig.
naturally occuring in A1 and A1B

59
Q

anti-H (alloAb)

A 
occurs as IgG or IgM in bombay patients
CS: YES
Ab class: G or M
thermal: high range
HDNB: yes
both E and I transfusion reactions
60
Q

anti-H lectin

A

prepared from ulex europaeus

used in secretor testing

61
Q

anti- A,B in O serum

A

cannot be seperated into A or B
cross reacts with both A and B antigens
agglutinates RBC subgroups especially Ax

62
Q

Lewis group system

A

only blood group not manufactured by the RBC

63
Q

where is the lewis group manufactured?

A

tissue cells and secreted into body fluids as soluble Ag

Ag then absorbed onto RBC so not intrinsic part of RBC

64
Q

what are the antigens of the lewis system?

A

LeA

LeB

65
Q

what are the precursor chain for LeA?

A

type I chain with an added fucose

66
Q

what are the precursor chains for LeB?

A

Type I H chain add fucose (to be LeB individual must have inherited secretor gene)

67
Q

what is the phenotype of an individual who is both lewis and a secretor?

A

Le ( a-b+)

68
Q

what is the phenotype of an individual who is NOT secretor with lewis gene

A

Le (a+b-)

69
Q

why is the lewis antibody seldom clinically significant?

A
  • soluble LeA and LeB anitgen present in donor plasma neutralize recipients antibodies
  • lewis antigens rapidly elute from donor RBC which are transformed to recipients lewis phenotype
70
Q

what is the lewis system enhanced by?

A

enzymes

71
Q

what are the reasons the lewis system does not cause HDFN

A
  • LeA and LeB antigens are not well developed at birth

- anti-LeA and anti-LeB are IgM and cannot cross placenta

72
Q

dd

A

this does not mean recessive for D gene

this shows absence of D gene

73
Q

does anti-D occur naturally?

A

no, only occurs resulting from transfusions or pregnancies (immunization)

74
Q

T OR F

immunogenecity of D is greater than all other RBC antigens studied

A

true

75
Q

fisher-race theory

A

3 closely linked genes inherited from each parent

76
Q

wiener theory

A

1 Rh gene inherited from each parent

77
Q

D+w

A

weak form of D Ag

78
Q

how is D+w demonstrated?

A

IAT
anti-D
anti-D will be positive and the Rh control will be negative

79
Q

Rhnull

A

individual who express no Rh Ag on RBC characterized by hemolytic anemia

80
Q

Rhmod

A

lack most their Rh Ag expressions characterized by hemolytic anemia

81
Q

what is the significance of D+w in donors?

A
  • weak D blood given to Rh = patients may ellicit immune response to D
  • weak D cells may suffer accelerated destruction in recipient serum that already contains anti-D (severe HTR)
82
Q

HDFN

A

the destruction of the RBC of a fetus and neonate by Abs produced by the mother

83
Q

what are the two most common causes of HDFN

A

ABO incompatibility

Rh Antigen

84
Q

kernicterus

A

infiltration of the brain and spinal cord with unconjugated billi causes permanent damage to the CNS

85
Q

Rh HDFN general characteristics

A

mother Rh =

fetus Rh +

86
Q

what happens in the second pregnancy of a rh = mother and rh + fetus?

A

at 28 weeks and onward the secondary response to pregnancy stimulates the Ab created from the first pregnancy into high titers.
IgG crosses placenta combines with fetal Rh+ cells and starts destruction

87
Q

ABO HDFN general characteristics

A

independent of Rh factor
anti-A,B most potent
diagnosis made when infants blood is DAT + and anit-A or B can be eluted from affected RBC

88
Q

what pregnancies are affected by ABO HDFN?

A

first pregnancies and onward

89
Q

what ABO blood group is the mother usually in ABO HDFN?

A

group O becuase they have naturally occuring IgG and IgM anti-A anti-B and anti-A,B

90
Q

RHIG candidates upon testing

initial visist

A

Ab screen for unexpected IgG Abs

  • anti-D is identified = no RHIG candidate
  • anti-D is negative = RHIG at 28 weeks
91
Q

RHIG candidates upon testing

follow up visit:

A

if Rh is negative repeat Ab screen

  • Ab screen is = : give RHIG at 28 weeks
  • Ab screen is + because of anti-D: no RHIG possible HDFN
  • Ab screen is + because of something unrelated : RHIG at 28 weeks
92
Q

RHIG candidates upon testing:

at delivery

A
  • D = with history of alloanti-D: suspect HDFN test cord blood no RHIG
  • D = with NO history of alloanti-D: candidate RHIG
  • cord blood rh = : no RHIG
  • cord blood rh +: screen for FMH and calculate doses RHIG
93
Q

when are intrauterine transfusions neccessary?

A
  • MCA-PSV indicates anemia
  • fetal hydrops are noted on ultrasound (accumulation of fluid in 2 or more fetal compartments)
  • cordocentesis blood sample has Hgb level <10g/dl
  • amniotic fluid results are high
94
Q

intrauterine transfusions general

A

access umbilical vein and inject donor cells directly
goal- maintain fetal hgb above 10g/dl
once performed repeated every 2-4 weeks until delivery

95
Q

why would a DAT be performed on cord blood postnatally?

A

a + test confirms that infants RBC have absorbed maternal Ab (HDN)

96
Q

RHIG or RHOGAM general

A

RHIG sensitizes infants Rh+ RBC within maternal circulation and are cleared by spleen and lymph nodes

prevents mother’s immune system to feel the need to react

97
Q

candidates of RHIG

A
  • rh = moms with no detectable anti-D in serum and have Rh+ infants
  • any rh = woman who has had miscarriage, abortion, 1st trimester amnio, trauma, ectopic pregnancy, etc unless father or fetus are known to be rh =
  • rh = women within child-bearing age who have to receive blood products containing rh + cells

blood banking (4 decks)

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