Bbguy

Front 1

which products are leukoreduced

Back 1

whole blood, platelets, rbss

Front 2

what does leukoreduction mean

Back 2

reducing the majority of wbcs from blood products

Front 3

what are the deleterious effects of wbcs in blood

Back 3

1. wbcs deteriorate while sitting in bag leading to cytokine release and febrile transfusion reactions (esp in plts)
2. wbcs present foreign HLA antigens to host
3. some viruses live in wbcs

Front 4

why do we care about the production of HLA antibodies from a transfusion reaction

Back 4

- causes future problems:
with platelet refractoriness
future febrile reactions
issues with transplants

Front 5

what HLA antigen class is the big problem on wbcs in transfusions

Back 5

HLA II on wbcs presents to HLA1 to form anti-HLA1 antibodies (on plts) or anti plt ab

Front 6

what viruses can live in wbcs (thus increasing risk of transfusing virus if no leukoreduction)

Back 6

CMV
HTLV1 and 2
EBV

Front 7

what are some of the ways we leukoreduce

Back 7

filters on dialysis/apheresis machines
separate by centrifugation to isolate desired product

Front 8

when should one leukoreduce

Back 8

ideally before 5 days

Front 9

indications for leukoreduction

Back 9

-prevent febrile reactions in those with hx
- prevent HLA immunization for those getting plts with heme malignancies
- prevent CMV in immunocomprised recipients

Front 10

weird complication from leukoreduction

Back 10

some patients on ACE inhibitors can get hypotension with leukoreduced products

Front 11

is leukocyte reduction the same as irradiation

Back 11

no

Front 12

which is better to prevent GVHD leukocyte reduction or irradiation

Back 12

irradiation virtually eliminates risk for GVHD; LR only reduces risk

Front 13

can granulocytes be irradiated

Back 13

yes, but not leukoreduced

Front 14

which filters better (for leukoreduction) cold or room temp rbcs

Back 14

cold rbcs are better for filtering

Front 15

in what patients are you most likely to get filter failures in terms of leukoreducing

Back 15

sickle cell patients

Front 16

only indication for irradiated blood products

Back 16

to eliminate transfusion associated GVHD

Front 17

what organs are most affected by transfusion associated GVHD

Back 17

skin, liver, GI tract, mucosal membranes and bone marrow

Front 18

clinical course of transfusion associated GVHD

Back 18

rapid, can be fatal within 1 month from overwhelming infection

Front 19

1 clinical manifestation of transfusion associated GVHD

Back 19

rash on palms and soles

Front 20

what does bone marrow look like in transfusion associated GVHD

Back 20

hypocellular and fibrotic

Front 21

when does transfusion associated GVHD reaction occur

Back 21

2-30 days (usually 10 or so); delayed febrile

Front 22

what cell type in the product causes transfusion associated GVHD

Back 22

donor T lymphocytes (CD4, CD8 and NK)

Front 23

can transfusion associated GVHD occur in an immunocompetent recipient and if so, how

Back 23

one way HLA match:

donor shares HLA with half of recipients tissue. Donor's T cells target the foreign half; the recipients own counter-attack T cells only see self-HLA and don't counterattack

Front 24

common sources of irradiation

Back 24

gamma irradiators
xray irradiators
linear accelerators (used for radiation therapy

Front 25

how much irradiation to give

Back 25

25 Gray to center of bag; 50 Gray max, 15 gray min (at periphery)

Front 26

indications for treatment with irradiated blood products (8)

Back 26

T cell defects (acquired/congenital)
intrauterine pregnancies/premies
HLA matched products, family member donors
hematopoietic stem cell transplants
those with Hodgkins (and other heme malign) - some solid (like neuroblastoma)
if on fludarabine
fresh whole blood
cardiac patients

Front 27

what products are always irradiated

Back 27

granulocytes

Front 28

who doesn't need to be irradiated

Back 28

solid organ transplant patients (even though being treated)
HIV
small volume transfusions to neonates
if previously frozen

Front 29

disadvantages of irradiating

Back 29

K goes up, hgb goes up (maybe wash for neonates)

Front 30

how long can you store irradiated products

Back 30

28 days

Front 31

which moms need prophylactic RhIG

Back 31

D neg moms (they can form anti D's if a D+ fetus)

Front 32

what is the risk that a D- mom can form antibodies with the first pregnancy

Back 32

20% (occurs at delivery); standard is to give one vial at 28 weeks (risk goes from 16% to 1%) and then after (within 72 hours ideally)

Front 33

what is a "vial" of rhogam

Back 33

one standard dose of antiD antibodies (300ug or 1500 IU) sufficient to protect against 30 ml of D+ blood (or 15 ml rbcs)

Front 34

so, do you give one vial post delivery or more than one

Back 34

based on fetal bleed screen (if neg - just one vial; if pos, do a quantitative test to determine how much to give)

Front 35

how doesa fetal bleed screen work

Back 35

put rbcs (baby and mom) on a slide, add anti D, add indicator to agglutinate and form rosettes against those bound with anti D; count rosettes
positive test: 3 or more/10 hpf

Front 36

methods for a quantitative test to determine how much rhogam is needed for maternal-fetal bleed in a D- mom

Back 36

- Kleihaur-Betke
- flow

Front 37

how does the Kleihaur-Betke method work and how from there can you determine how much rhogam to give

Back 37

HgF is acid resistant, HgA is not; flood blood smear with acid; count 2000 cells, percent that are "bright" is the percent of fetal cells; multiple that percent by 5000 ml (presumed mom blood volume) and get amount of fetal blood mom was exposed to - divide that by 30 ml (for one vial of rhogam) and that will give you how many vials to give with the addition of a "safety factor" (rounding up) (fudge factor is if fraction is <0.5 round up one vial, if .5 to .9 round up two vials) e.g. 2.2 give 3 vials but if 2.5 give 4 vials

Front 38

if get weight instead of assuming blood volume, how would you calculate it

Back 38

weight (in Kg) * 70

Front 39

what should make you think of a transfusion reaction (6)

Back 39

fever/chills, circulatory/pulmonary issues, "doom", skin changes, pain, coag/bleeding issues

Front 40

transfusion reactions that present quickly with fever (4)

Back 40

acute hemolytic, febrile non-hemolytic, transfusion-related sepsis, TRALI

Front 41

transfusion reactions that present delayed but with fever (2)

Back 41

delayed hemolytic, transfusion associated GVHD

Front 42

transfusion reactions that present quickly without fever (5)

Back 42

allergic, hypotensive, transfusion-related dyspnea, TACO, acute pain

Front 43

transfusion reactions the present delayed and without fever

Back 43

delayed serologic, post-transfusion purpura, iron overload

Front 44

what is meant by an "acute" transfusion reaction

Back 44

during the transfusion to the next 24 hours

Front 45

what is the time frame for a delayed transfusion reaction

Back 45

greater than 24 hours, can be up to weeks later

Front 46

what are some of the first steps in how respond to a possible transfusion reaction

Back 46

1. stop transfusion
2. perform clerical check
3. draw post transfusion sample

Front 47

what are the three tests you would immediately perform on a post transfusion sample to work up for a possible transfusion reaction

Back 47

1. hemoglobinemia
2. DAT
3. ABO/Rh repeat testing
if all negative, have ruled out acute hemolytic transfusion reaction

Front 48

how does the test for hemoglobinemia work

Back 48

collect blood in an EDTA tube, centrifuge, if as little as 2-5 ml of hemolyzed blood, will detect that as off color in supernatant

Front 49

is the hemoglobinemia test sensitive, specific both or neither

Back 49

very sensitive - not specific;
can have "positives" with bad sticks, nonimmune hemolysis and G6PD
can have false negatives if delay in blood draw

Front 50

what is a DAT test

Back 50

direct antibody test
looking for in vivo coating of antibodies/complement on rbcs (IgG and C3d)
so, have coated rbcs, add an antiIgG or anti-C3d that agglutinates the coated rbcs

Front 51

what antibodies can classically coat an rbc without in vivo agglutination

Back 51

IgG that is nonABO

Front 52

what is the first question you should ask if you get a positive DAT

Back 52

what was the pretransfusion DAT - if there was one, maybe not the problem, if there wasn't one, get busy!!

Front 53

if early reponse tests (DAT, ABO/rh repeat testing, and hemoglobinemia tests) show something of concern, what tests could you then consider (2nd tier testing; 6)

Back 53

haptoglobin, bilirubin, LDH, urine hemoglobin, crossmatch, eluate

Front 54

what is the function of haptoglobin

Back 54

to bind free hemoglobin (decreased when free hemoglobin is running around - aka acute hemolytic transfusion reaction)

Front 55

what happens to bilirubin (conjugated or unconjugated) in acute hemolytic transfusion reactions

Back 55

they go up fast (as breakdown product of hemoglobin) but also go down fast -
historically, thought indirect (unconjugated) was intravascular and direct (conjugated) was extravascular

Front 56

which is the possible sign of a transfusion reaction: hematuria or hemaglobinuria

Back 56

hemaglobinuria

Front 57

on a peripheral smear, what would you see in an intravascular hemolytic reaction

Back 57

schistocytes (classic example ABO incompatibility)

Front 58

on a peripheral smear, what would you see in an extravascular hemolytic reaction

Back 58

spherocytes (classic example IgG that bind rbcs but don't fix complement)

Front 59

what would you do if you specifically suspected a septic trx reaction (ex. high fever >102 or severe rigors)

Back 59

culture everything :)

Front 60

what would you do if you specifically suspected a respiratory type trx reaction

Back 60

CXR, BNP (to rule out affect of circulatory overload)

Front 61

what would you do if you specifically suspected an allergic type trx reaction

Back 61

if severe only, consider IgA

Front 62

most common cause of acute hemolytic transfusion reactions and frequency

Back 62

clerical errors (60%)

Front 63

most sensitive clinical symptom of an acute hemolytic transfusion reaction

Back 63

fever/chills (80% present with this alone) - time frame - a lot within first 15 minutes; peak of curve (representing distribution of those getting fever) is at 70 minutes - btw, this is why you are to transfuse slowly

Front 64

how long before hemoglobulinemia due to acute hemolytic transfusion reactions goes away

Back 64

matter of hours

Front 65

how long before hemoglobulinuria due to acute hemolytic transfusion reactions goes away

Back 65

gone in a day

Front 66

what could result in a false negative DAT in an acute hemolytic transfusion reaction

Back 66

wait too long before do DAT, the offending rbcs are destroyed

Front 67

name two useful tests to rule in DIC

Back 67

d-dimers, fibrin split products

Front 68

which antibody type fixes complement better IgM or IgG

Back 68

IgM

Front 69

name some of the chemokines/cytokines released during an acute hemolytic transfusion reactions

Back 69

C3a/C5a
TNFalpha (fever producing)
IL1b (fp), IL6 (f) and IL8
bradykinin

Front 70

how does an acute hemolytic transfusion reaction affect coagulation/cause DIC (3)

Back 70

Ag-Ab complexes trigger Factor X11 down intrinsic pathway
cytokines/TNF triggers TF down extrinsic pathway
also fibrinolysis is triggered too

Front 71

vasodilation in an acute hemolytic transfusion reaction is caused by what (2)

Back 71

nitric oxide
bradykinin

Front 72

renal damage in an acute hemolytic transfusion reaction is caused by what (2)

Back 72

- renal vasoconstriction (compensating for systemic hypotension)
- microthrombi
leads to ATN

Front 73

what is a febrile nonhemolytic transfusion reaction

Back 73

UNEXPLAINED 1C (2F) elevation of temperature, diagnosis by exclusion

caused by: wbc-derived cytokines (ex. TNFa, IL1a, IL6) or plt-derived sCD40L

Front 74

where do most febrile nonhemolytic transfusion reactions occur

Back 74

often in PLT products (which contain plts and unhappy wbcs)- so cytokines, etc in bag that is given to recipient

If from rbcs, usu. recipient Ab or wbcs cause problem against wbcs in donor

Front 75

if very early fever in transfusion reaction, what should you think of

Back 75

septic

Front 76

what will prevent a febrile nonhemolytic transfusion reaction

Back 76

prestorage leukoreduction (esp needed as prestorage in plt products)

Front 77

what is the number one infectious risk from transfusions

Back 77

transfusion-related sepsis

Front 78

what products (plts vs rbcs) have what kind of bugs

Back 78

plts - skin contaminants (gram positive cocci) and rarely gram neg rods (those cause fatalities)
rbcs - skin contaminants (staph epidermidis)
- Gram neg rods (yersinia, e coli, enterobacter, serratia, pseudomonas) - YEEPS!
subclinical sepsis in donor

Front 79

what do yersinia, e coli, enterobacter, serratia, pseudomonas have in common

Back 79

like cold temps, like iron-rich environment; also capable of releasing endotoxins

Front 80

number one infectious cause of FATALITIES in transfusion reactions

Back 80

babesia (protozoan parasite)

Front 81

what is the "endotoxin effect" in a transfusion-related septic event

Back 81

rapid onset of super high fever, rigors, shock, dic
abdominal complaints

Front 82

what are the three causes of an acute crash in a transfusion

Back 82

-sepsis
- anaphylaxis (really rare)
- acute hemolytic reaction

Front 83

what color does a bacterial contaminated blood unit turn

Back 83

darker/purple

Front 84

if going to culture to evaluate for a bacterial contaminated blood unit, where do you get the source material

Back 84

from the bag (not from the segments outside the bag)

Front 85

do leukoreduction filters have any affect in filtering out bacterial contamination in a blood unit

Back 85

actually, yes, shown with Yersinia

Front 86

what's the shelf-life for plts

Back 86

5 days

Front 87

**most common cause of transfusion related fatality

Back 87

TRALI

Front 88

blood product specific source of TRALI

Back 88

historically thought of as a FFP issue, but can happen in any type of blood product

Front 89

define TRALI

Back 89

new acute lung injury (ALI) less than 6 hours after transfusion
and no other known risk factors for pulmonary edema

Front 90

define ALI (in context of TRALI)

Back 90

hypoxemia (o2 sat<90% as one measure) and bilateral CXR infiltrates

Front 91

symptom sequence for TRALI

Back 91

fever (not as fast as septic but generally sooner than febrile, nonhemolytic) chills, Hypertension followed by hypotension

Front 92

name two mechanisms to get TRALI

Back 92

1. donor antibody mediated (donor antibody - HLA or neutrophil antibodies - attacks PMNs, lead to pulmonary endothelial damage in part through ROS)
2. two event pathway - preexisting condition in recipient followed by biologic response modifiers (sCD40L) or Ab that promote damage

Front 93

which donors are most likely to cause TRALI

Back 93

donors who have been transfused or pregnant

Front 94

percent fatalities and percent recovery from TRALI

Back 94

fatalaties 5-25%
recovery 80%

Front 95

allergic transfusion reactions are mediated by what Ig subtype

Back 95

IgE

Front 96

only transfusion reaction in which you might consider restarting the transfusion

Back 96

mild allergic reaction (if hives/angioedema clears with benadryl/treatment)

Front 97

what clinical sx is almost always present in allergic reactions from transfusions

Back 97

skin findings

Front 98

which antibody is pentameric

Back 98

IgM

Front 99

which antibody is classically a dimer

Back 99

IgG

Front 100

which antibody has two dimers coupled by a secretory molecule

Back 100

IgA

Front 101

what underlying problem should you think of when you hear about severe allergic reactions in the setting of transfusion reactions

Back 101

though not frequent, think of IgA deficiency - patients with IgA deficiencies can develop an IgE-mediated anti IgA, which when transfused can have a reaction to the IgA in the donor blood

Front 102

when you test for antiIgA in the lab what are you testing for

Back 102

you are looking for an IgG anti IgA not an IgE anti IgA

Front 103

a relatively common cause of allergic reactions in transfusion reactions in Asians

Back 103

haptoglobin deficiency

Front 104

how to rule out IgA deficiency as a cause of allergic reaction in transfusion reaction

Back 104

on pretransfusion sample, do an IgA level; if super low, then do an antiIgA

Front 105

what can you do if you determine IgA deficiency as the cause of allergic transfusion reaction

Back 105

use IgA deficient donors; wash rbcs (and to a lesser extent) plts

Front 106

cause of acute hypotensive transfusion reaction

Back 106

bradykinin (from those on ACE inhibitors or from some LR filters)

Front 107

what is transfusion associated dyspnea

Back 107

diagnosis of exclusion (ie not TRALI, TACO or allergy)

Front 108

what is TACO

Back 108

transfusion associated circulatory overload: acute CHF due to transfusion

Front 109

symptoms of TACO

Back 109

- typical CHF (JVD, dyspnea, hypertension, hypoxia)
- CXR: bibasilar infiltrates with enlarged cardiac silhoutte

Front 110

ways to clinically distinguish between TACO vs. TRALI (5)

Back 110

- diuretics work in TACO
- hypotension eventually in TRALI
- fever in TRALI
- CXR: cardiac silohoutte in TACO
- BNP up in TACO

Front 111

what is the cause of delayed hemolytic reactions

Back 111

an anamnestic response of antibodies initially too low to detect that come flying back on exposure - most common with Kidd, Kell, Duffy

Front 112

where do most delayed hemolytic transfusion reactions occur

Back 112

extravascular except kidd which can often occur intravascularly

Front 113

two useful lab findings in those with delayed hemolytic transfusion reactions

Back 113

- icteric serum
- mixed field (some agglutination but not entirely on gel) DAT

Front 114

what must be absent in delayed serologic transfusion reactions

Back 114

hemolysis

Front 115

clinical course for transfusion-associated GVHD

Back 115

nearly always fatal

Front 116

common clinical sx for transfusion associated GVHD

Back 116

- rash, mucositis, hepatitis, bone marrow failure
on average 7-10 days post transfusion

Front 117

prevention of transfusion associated GVHD

Back 117

irradiation (so esp important in those immunosuppressed/leukopenic)

Front 118

should frozen blood products receive irradiation (if clinically indicated)

Back 118

usu not cuz the freezing process kills the wbcs in the bag, except if cryopreserved (in glycerol) where usually the wbcs persist

Front 119

maximum number of days post irradiation for a blood product

Back 119

28 days (or regular expiration date - whichever first)

Front 120

presentation of post-transfusion purpura

Back 120

severe thrombocytopenia (<10K) and wet purpura (oozing from mucosal surfaces)

Front 121

what is post-transfusion purpura

Back 121

antibody mediated destruction of platelets ~ 10 days post transfusion

Front 122

mortality rates for post-transfusion purpura

Back 122

up to 12%, intracranial bleeds

Front 123

who gets post-transfusion purpura

Back 123

females 5:1 males; mostly multips - patients who lack HPA-1a are the most common to get this

Front 124

why does post-transfusion purpura occur

Back 124

most commonly recipient has previously developed an HPA-1A antibody that then targets the transfused plt with that antigen and strangely this goes on to target their own plts as well (hence why such severe thrombocytopenia)

Front 125

treatment for post-transfusion purpura

Back 125

ivig or if failure plasma exchange

Front 126

what are the three phases of test tube testing for agglutination

Back 126

1. immediate spin (serum + rbcs together in tube, centrifuge for 15 second, examine)
2. 37 C (serum+rbcs inclubate at 37C) length of time dependent (LISS, PEG/alb or none)
3. IAT (above, wash, add AHG, cenrifuge and examine)

Front 127

list times for 37C test tube agglutination study depending on presence or absence of potentiators present

Back 127

LISS- 10-15 min
alb/PEG 15-30 min
none 30-60 min

Front 128

what does IAT look for

Back 128

ability of antibodies (in vitro) to identify ags on rbcs. use AHG to agglutinate since many ab (e.g. IgG) won't efficiently agglutinate rbcs

Front 129

what does DAT look for

Back 129

presence of antbodies in vivo that recognized ags on rbcs. Use AHG to help agglutinate since many ab (eg IgG) won't efficiently agglutinate rbcs

Front 130

where does dosage matter most

Back 130

Kidd, duffy, Rh and MNS systems

Front 131

why are ficin and papain useful in blood group testing

Back 131

they can enhance, decrease or not affect ab-ag binding - thus enabling us to classify the different types of ags on rbcs

Front 132

what are the four members of the ABO family

Back 132

ABO blood group, Lewis, I/i, P blood groups

Front 133

what are the three blood groups/blood group families that are enhanced by enzymes

Back 133

1. abo family (includes abo, lewis, I/i and P)
2. Rh
3. Kidd

Front 134

what are the three blood groups that are decreased by enzymes

Back 134

1. MNS
2. Duffy
3. Lutheran

Front 135

what are the three blood groups that are not affected by enzymes

Back 135

1. Kell
2. Diego
3. Colton

Front 136

what are neutralizing substances in study of agglutination in blood bank

Back 136

premix with neutralizing substances reducing the strength of the antibody (blocks binding sites) to lessen ab-ag reaction

Front 137

neutralizing substance for ABo family

Back 137

saliva (secretor)

Front 138

neutralizing substance for lewis

Back 138

saliva (secretor for Leb)

Front 139

neutralizing substance for P1

Back 139

hydatid cyst fluid, pigeon egg fluid

Front 140

neutralizing substance for Sda

Back 140

urine

Front 141

neutralizing substance for chido, rodgers

Back 141

serum

Front 142

what are lectins and what are their utility

Back 142

seed derived products that act like antibodies (and can be very specific); useful in polyagglutination studies

Front 143

specificity of lectin: dolichos biflorus

Back 143

A1

Front 144

specificity of lectin: Ulex europaeus

Back 144

H

Front 145

specificity of lectin: vicia graminea

Back 145

N

Front 146

specificity of lectin: arachis hypogea

Back 146

T

Front 147

specificity of lectin: glycine max

Back 147

T, Tn

Front 148

specificity of lectin: salvia

Back 148

Tn

Front 149

what is the definition of a blood group antigen

Back 149

present on rbcs and targeted by an alloantibody

Front 150

fx of warm reactive antibodies (4)

Back 150

1. often IgG
2. require exposure
3. cause HTR, HDN
4. significant clinically

Front 151

fx of cold reactive antibodies (4)

Back 151

1. often IgM
2. naturally occurring
3. don't usually cause HTR/HDN
4. usually not significant clinically

Front 152

is ABO a cold reactive or warm reactive ab

Back 152

interestingly, best as cold reactive and a lot of ABO is IgM but obviously very clinically significant

Front 153

describe a type 1 chain in the ABO system

Back 153

one of two chains upon which the H antigen can be built: composed of a
Gal----GalNAc-----R (bound by beta1-3) between gal-galnac; R group is predominantly glycoprotein, in secretions

Front 154

describe a type 2 chain in the ABO system

Back 154

one of two chains upon which the H antigen can be built: composed of a
Gal----GalNAc-----R (bound by beta1-4) between gal-galnac; R group is predominantly glycolipids, on rbcs

Front 155

what is a secretor

Back 155

80% of us: we have the Se gene (encodes for FUT2); someone who can make H antigen on type I chains

Front 156

what does FUT2 do

Back 156

makes H antigen: FUT2 adds a fucose to the terminal gal in TYPE I chains (chains that are mostly in secretions)

Front 157

what does the H gene encode

Back 157

the H gene encodes FUT1

Front 158

what does FUT1 do

Back 158

makes H antigen on TYPE 2 chains by adding fucose to terminal gal (recall type 2 chains are found predominantly on rbcs)

Front 159

what does the A gene encode for

Back 159

GalNAc transferase; adds a galNAc to terminal gal on H antigen, making A antigen

Front 160

what does the B gene encode for

Back 160

gal transferase; adds a gal to terminal gal on H antigen- making B antigen

Front 161

what chains do the gene products of A and B genes operateon

Back 161

both type 1 and type 2

Front 162

order the following ags based of amount of H antigen expressed:
O, B, A1, A2, A2B, A1B

Back 162

O>A2B>B>A2B>A1>A1B

Front 163

Where are the A, B, O genes and what does O gene do

Back 163

czome 9; O gene does nothing

Front 164

when do ABO antigens appear in newborn

Back 164

6 weeks

Front 165

when do ABO antigens achieve adult levels

Back 165

4 years

Front 166

when do ABO antibodies appear

Back 166

4 months

Front 167

when do ABO antibodies reach adult levels

Back 167

10 years

Front 168

what type antibodies are anti A and anti B

Back 168

IgM (hence don't cross placenta)

Front 169

what type of antibodies can a blood group O person have that is different from type A and type B people

Back 169

it is thought that blood group O people develop anti A and anti B antibodies that are IgG
In addition, a unique anti-AB are formed that are IgG
these all can cross placenta and cause problems in utero

Front 170

order of A, B, O and AB blood types across all races

Back 170

O>A>B>AB

Front 171

will ulex europeaus only react against O blood type

Back 171

no, it's reacting to the H antigen. Thus, A1B will react less than A2

Front 172

what is the most common cause of HDFN

Back 172

blood type O mom with IgG antibodies against baby with A, B or AB; mild form

Front 173

what blood group antigens does a type A individual have

Back 173

A, H

Front 174

which is more frequent A1 or A2

Back 174

A1 (80%); A2 (20%)

Front 175

which has more A antigen on its surface A1 or A2

Back 175

A1 has 5x more than A2

Front 176

what is important about distinguishing between A1 and A2

Back 176

1. understand relative amount of H/strength of A expression
2. slight biochemical differences in the A2 strand
3. some of A2 population (esp A2B) can form AntiA1 ab

Front 177

who is the universal recipient and why

Back 177

AB, no antibodies to A, B or H

Front 178

what is forward grouping and what's another name

Back 178

cell testing; patients rbc against lab's antibodies

Front 179

what is reverse grouping and what's another name (2)

Back 179

backtyping/serum testing; patients serum agains lab's rbcs

Front 180

what is an acquired B phenotype

Back 180

look like reacting to AntiB on forward testing (wk reaction with B) but no obvious B expression of reverse testing

Front 181

what population can acquired B phenotype happen in

Back 181

A1 individuals

Front 182

how does acquired B phenotype develop

Back 182

gram neg bugs (from sepsis, colon ca, obstruction) come into contact with A antigen and chew off an Acetyl group off of GalNAC to make GalN; then reagent antiB will think it's B and react

Front 183

ways to resolve acquired B phenotype in lab

Back 183

1. acidify serum
2. autoincubate (mix own antib with antib)
3. monoclonal Ab that don't recognize the acquired B

Front 184

what is the bombay phenotype (Oh)

Back 184

no Se or H genes so no A, B or H antigens; strong antiA, strong AntiB and strong AntiH

Front 185

what is the genotype of bombay phenotype (Oh)

Back 185

hh,sese

Front 186

lab findings for bombay phenotype

Back 186

O forward, O reverse, screen +

Front 187

what is parabombay phenotype

Back 187

essentially same as bombay phenotype except have Se gene and thus make some H antigen in their secretions and a little in their plasma

Front 188

what does the Le gene encode and what does it do

Back 188

Le gene encodes FUT3 that adds a fucose to subterminal GalNAc on TYPE 1 CHAINS only. This make an antigen known as Le a (that is without Se gene)

Front 189

if Le gene and Se gene what do you get

Back 189

Le b: this is two fucose molecules (one on terminal gal and one on subterminal GalNAc)

Front 190

what options (3) can you get if se gene and le gene act on type 1 chains

Back 190

HLe b, ALe b, B le b

Front 191

why do type I chains matter in the blood if they are generally in secretions

Back 191

b/c free type I chains can float in plasma and adsorb onto rbcs (le b does this much better than le a - which is in low quantity anyway) so adults tend to look le a-b+

Front 192

what are the three possibilities for lewis antigen expression in relative order

Back 192

le (a-b+), le (a+b+) le (a- b-) - though infrequent the last one can have significance (>20%) of blacks

Front 193

are lewis antigens significant or no

Back 193

generally not too significant, IgM, seen mainly in Le (a-b-)

Front 194

funny thing about lewis system and pregnancy

Back 194

antigens can decrease during pregnancy and person can convert to le(a-b-)

Front 195

two bugs that interact with le blood system

Back 195

norwalk and E coli UTIs

Front 196

what chain(s) does the I system work on

Back 196

type II chains

Front 197

what does anti I react to, how about anti i

Back 197

anti I: 3D structure of branching type II chains
anti i: 3D structure of relatively simple type II chains

Front 198

who has "big I" antigens, who has "little i" antigen

Back 198

big I - big people
little i - little people

Front 199

Auto anti I are found in what diseases (2)

Back 199

1. mycoplasma pneumonia (esp older adults)
2. cold agglutinin disease

Front 200

auto anti i are found in what disease (1)

Back 200

infectious mono

Front 201

what is the antigen in the P system

Back 201

P1 (modified by P and Pk)

Front 202

most people are P1 - what does this mean

Back 202

P+P1+Pk-

Front 203

significance of antiPP1Pk (in contrast to antiP1)

Back 203

antiPP1Pk can cause HDFN, HTRs
antiP1 - IgM, not so significant

Front 204

p is receptor for what bug

Back 204

parvovirus

Front 205

in what population would you see an increase in antiP1

Back 205

bird handlers (neutralization with pigeon eggs...)

Front 206

what is paroxysmal cold hemaglutinuria and what are its associations

Back 206

biphasic IgG (donath landsteiner biphasic hemolysin) that reacts against P
associated with: syphilis, viral infections in kids

Front 207

what are the five antigens in the Rh system

Back 207

D, C, E, c, e (no little d that just means not big D)

Front 208

what are the two genes that dictate the rh antigen system

Back 208

RHD and RHCE

Front 209

what is little d

Back 209

mutated or deleted D

Front 210

of R1, R2, RO, Rz, r', r", r, ry, which has big D

Back 210

R1, R2, RO, Rz,

Front 211

of R1, R2, RO, Rz, r', r", r, ry, which has little D

Back 211

r', r", r, ry,

Front 212

of R1, R2, RO, Rz, r', r", r, ry, which has big C

Back 212

R1, Rz, r', ry

Front 213

of R1, R2, RO, Rz, r', r", r, ry, which has little c

Back 213

R2, RO, r", r

Front 214

of R1, R2, RO, Rz, r', r", r, ry, which has big E

Back 214

R2, Rz, r", ry

Front 215

of R1, R2, RO, Rz, r', r", r, ry, which has little e

Back 215

R1, RO, r', r

Front 216

what are the big four Rh antigens that occur in our population most often

Back 216

R1, R2, RO and r

Front 217

frequency of big four rh antigens in blacks and whites

Back 217

whites: R1, r, R2, Ro
blacks: Ro, r, R1, R2

Front 218

are rh antibodies igm or igG

Back 218

warm requiring IgG

Front 219

what is the most immunogenic nonABO antigen

Back 219

Rh

Front 220

where do HTRs occur in Rh reactions

Back 220

extravascular, prototypical for HDFN (for antiD and antic)

Front 221

why are whites usually little d

Back 221

deletions from big D

Front 222

why are blacks often little d

Back 222

they have a pseudogene in its place

Front 223

why are asians often little d

Back 223

have big D but inactive protein product

Front 224

what is a weak D phenotype

Back 224

people in whom antibodies coat rbcs but need AHG to cause agglutination (IAT); caused by deletions,cis/trans etc; IAT required for D- donors and d- babies with d- moms (to make sure they are not actually D+ not reacting- b/c don't want to give D+ blood to D- person)

Front 225

what is partial D

Back 225

missing certain epitopes on D antigen on exterior part

Front 226

how can partial D cause problems

Back 226

if exposed to D positive blood, you may develop Ab against the portion of the D antigen that you lack
call them d-

Front 227

do partial D moms need Rhogam

Back 227

yes!

Front 228

in the kidd system, which antigen (of two) is more common

Back 228

Jka>jkb (unusual)

Front 229

are Kidd antibodies IgG, IgM or both

Back 229

mostly IgG, exposure requiring but some IgM (as fix complement)

Front 230

two famous things about Kidd

Back 230

1. marked dosage effect
2. variable expression over time (cause delayed HTRs often)***

Front 231

where are MNS antigens found

Back 231

On glycoproteins named
glycophorin A
glycophorin B

Front 232

what MNS antigens are found on glycophorin A

Back 232

M and N (equal frequencies in population)

Front 233

what MNS antigens are found on glycophorin B

Back 233

S,s, U (find s more than S in population)

Front 234

what is the difference between M and N antigens

Back 234

the last five aa on the glycophorin A molecules (specifically the last and the fifth to last)

Front 235

where is the U antigen found

Back 235

on glycophorin B - whether S or s "universal"

Front 236

what is the difference between glycophorin B molecules that are S vs. s

Back 236

one a.a.difference between the two

Front 237

what MNS pattern can you find in some small percent (2%) of blacks but not at all in whites

Back 237

S-s-U- (they completely lack glycophorin B)

Front 238

compare and contrast anti M/N antibodies within AntiS,s,U antibodies

Back 238

antiM/N: naturally occurring, cold IgM, "insignificant", dose effect
antiS,s,U: exposure requiring, warm IgG, significant, minimal dose effect

Front 239

what are the two antigens for the duffy system

Back 239

Fya, Fyb

Front 240

what is the phenotype for the duffy system for 2/3rd of blacks and why

Back 240

Fya- Fyb- they have an FyFy genotype and no duffy genes at all

Front 241

what is the Duffy system antibodies: IgG or IgM

Back 241

warm, IgG and, like Kidd in many ways (dose effect, variable expression, delayed HTRs) but lower severity than kidd

Front 242

what is Duffy receptor a natural receptor for

Back 242

P. vivax

Front 243

what do those who are Fya-b- have resistance to

Back 243

malaria from P. vivax and P. knowlesi

Front 244

what are the two main ag of the lutheran system

Back 244

Lu a and Lu b (b is high frequency)

Front 245

what destroys Lu antigens

Back 245

many enzymes and DTT

Front 246

are Lutheran igG or IgM

Back 246

mostly IgG except Lu a - despite this only mild HTRs and no HDFN

Front 247

what are the two major antigens of the Kell system

Back 247

K (K1, Kell) and k (K2) (k more frequent)

Front 248

what is the second most common immunogenic antigen outside of the ABO blood group

Back 248

Kell

Front 249

what kind of antibody is K1

Back 249

warm, exposure requiring IgG, severe HTRs, HFDN

Front 250

is K1 hemolytic

Back 250

not really; the antibody binds precursor rbcs and prevents them from forming mature rbcs

Front 251

what does kell null mean and why do they matter

Back 251

Kell antigens are missing; Kx (nearby antigen on rbcs) is increased; anti-Ku develops (u for universal) and need to have blood from other kell null individuals

Front 252

what is the McLeod phenotype/syndrome

Back 252

absence of Kx antigen, decrease in Kell antigens resulting in membrane instability with acanthocyte formation (acanthocytic hemolytic anemia)

Front 253

what is the McLeod phenotype associated with

Back 253

x linked Chronic Granulomatous disease (lack of NADPH oxidase, infection with oxidase positive organisms like Staph)

Front 254

where are the Diego antigens found

Back 254

Band 3 (HCO3/Cl exchanger)

Front 255

what are the two sets of antigens in the Diego system

Back 255

Dia/b (b high frequency)
wra/b (b high frequency)

Front 256

do Di a/b antibodies matter clinically

Back 256

cause severe HDFN but not so much HTR

Front 257

Do wra/wrb antibodies matter clinically

Back 257

Wra - naturally occurring but can cause HTRS and HDFN
Wrb- common autoantibody

Front 258

which is higher frequency in the Colton system

Back 258

Co a is higher (like ~100%) compared to Co b (10%)

Front 259

are Colton antibodies IgG or IgM

Back 259

mostly IgG, not common abs, can cause HDFN

Front 260

what is the Dombrock system

Back 260

composed of multiple antigens with Do a/Do b being the most common, can cause some HTRs but not HDFN (acute and delayed)

Front 261

what is the Yt system

Back 261

Cartwright (found on acetylcholinesterase in CNS but also rbcs)
Yta is very high frequency (>99%) can cause HTRs
Ytb lower frequency (<10%) - usu not significant

Front 262

what is the Xg system

Back 262

on x czome;
on all panels but doesn't cause problems

Front 263

what is Vel

Back 263

rare ab; but anti-Vel can cause big problems, not part of system, mix of IgG and IgM; can look weak but cause big problems,

Front 264

if vel negative person, do what

Back 264

give vel neg blood

Front 265

what are the two endpoints you look for in a crossmatch

Back 265

hemolysis or agglutination

Front 266

with hemolysis, what is often happening molecularly and what antibody type mediates this

Back 266

complement is being fixed and this is often IgM mediated

Front 267

classification of cold reactive antibodies (2 fx and 6 examples)

Back 267

- often IgM
- often reacting against CHO antigens
- eg. include entire ABO family (ABO, Le, I, P) and M, N

Front 268

classification of warm reactive antibodies (2 fx and 4 examples)

Back 268

- IgG
-often reacting against protein antigens
- e.g. Rh, K, Jk, Fy

Front 269

what are the two end points for evaluation of compatibility

Back 269

agglutination, hemolysis

Front 270

what are five factors that can alter antibody-antigen reactions

Back 270

1. change temperature
2. centrifugation to overcome size differences between rbc and antibodies
3. electric issues - use LISS to minimize charge repulsion
4. alter pH (7.0 seems to optimize many reactions)
5. change relative concentrations (usually two drops serum with one drop of 2-5% rbcs but can change that)

Front 271

cold reactive abs usually are what type and react to what type of antigen. Name six examples of cold reactive abs in the blood group systems

Back 271

- IgM; react to CHO antigens
examples: all of ABO family (ABO, Lewis, P and I), M and N

Front 272

warm reactive abs usually are what type and react to what type of antigen.

Back 272

- IgG, react to protein antigens
examples:Rh, K, Jk and Fy

Front 273

what charge do rbcs tend to have and why

Back 273

neg; due to sialic acid residues

Front 274

how far can an IgG molecule reach

Back 274

14 nm

Front 275

how far can an IgM molecule reach

Back 275

30 nm

Front 276

what is the zeta potential of an rbc

Back 276

distance rbcs stay from one another due to charge repulsion; 14 nm

Front 277

why is a pH of 7.0 optimal for ab-ag interaction on rbcs

Back 277

b/c at 7.0, rbcs have a negative charge and antibodies have a positive charge

Front 278

what is the problem with too low a pH

Back 278

dissociation of ab-ag interaction - by lowering the pH, you can actually elute the ab off the rbcs

Front 279

what is the prozone effect in antibody-antigen interaction

Back 279

too much Ab so covering rbcs and limit their ability to interact with each other (aka agglutinate)

Front 280

when are potentiators added and name 4 examples of potentiators

Back 280

after immediate spin, prior to 37C to enhance Ab-ag binding.
examples: LISS, PEG (decrease ionic cloud by moving out H2O), albumin (reduces zeta), proteolytic enzymes (last not routinely used)

Front 281

what is the drawback of PEG and how do you try to get around it

Back 281

can cause nonspecific agglutination; must wash before IAT and consider not at 37C

Front 282

without a potentiator how long do you incubate at 37C

Back 282

30-60 min

Front 283

with albumin, how long do you incubate at 37C

Back 283

15-30 min

Front 284

with LISS, how long do you incubate at 37C

Back 284

10-15 min

Front 285

with PEG< how long do you incubate at 37C

Back 285

15 min...?

Front 286

in test tube agglutination studies, what does a turbid background mean

Back 286

no or little agglutination (0-1+)

Front 287

in test tube agglutination studies, what does a pellet mean

Back 287

4+ agglutination

Front 288

what is in the gel for gel agglutination studies and how do they work

Back 288

anti IgG designed to grab onto IgG-coated rbcs as they go by - the distance of how far the go in the tube is related to how coated they are (if really coated rbcs won't make it far through the tube). the negative rbcs make it to the bottoms

Front 289

how does the sensitivity of gel testing compare to LISS and PEG potentiation

Back 289

better than LISS; about the same as PEG

Front 290

what is on the bottom of a solid phase testing microwell

Back 290

lysed "donor" rbcs so that splayed across the well is rbc antigens

Front 291

how does solid phase testing work

Back 291

lysed donor rbcs/rbc antigens, patient serum (with antibodies). then add "indicator rbc bound to IgG" - like of like IAT but the AHG is replaced by AHG bound to rbc.

Front 292

what does a positive look like on solid phase testing

Back 292

carpet across well; if negative, pellet in center

Front 293

which type of compatibility testing can be automated

Back 293

gel and solid phase

Front 294

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is best known for: cold autoantibody enhancement

Back 294

Tube LISS

Front 295

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is best known for: warm autoantibody enhancement

Back 295

tube PEG (though gel and SP are pretty good at this)

Front 296

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is the less sensitive

Back 296

tube LISS (the others are roughly equal sensitivity

Front 297

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is best known for: having stable reactions (ones that can stick around so the supervisor can review)

Back 297

Gel and solid phase

Front 298

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is best known for: being expensive

Back 298

gel and solid phase

Front 299

in comparing Tube LISS, Tube PEG, Gel and solid phase testing, which is best known for: being able to be automated

Back 299

gel and solid phase

Front 300

name three AHGs you might use in the lab and what they might mean (2)

Back 300

-polyspecific antiIgG, anti C3d
- anti-IgG - pretty good at just recognizing IgG
-anti-C3b or C3d - id's complement fixation (and hence pretty good at detecting IgM which fixes complement

Front 301

what is another name for check cells

Back 301

coombs control

Front 302

what are check cells

Back 302

positive control to make sure AHG is there and working (esp needed when a wash step is present

Front 303

what type of testing doesn't necessary require check cells

Back 303

gel testing

Front 304

what does prewarming do to alter compatibility testing

Back 304

reduces cold auto and alloantibodies; not to be used proactively but as confirmation of an identified reaction

Front 305

what is adsorption and what are the two types

Back 305

a way to remove an antibody by preincubating the sample with antigen-positive rbcs
autoadsorption (incubate with patient's blood; way to unmask important antibodies by removing "predominant" autoantibody)
alloadsorption (more directed type specific rbcs to pull out antibodies to individual antigens to unmask others

Front 306

what are three examples of how to elute an antibody

Back 306

heat, cold or chemical (glycine)

Front 307

how can elution be used

Back 307

by eluting abs off of the rbc, you can create mixture of antibodies that you can then challenge

Front 308

name four reagents that can be used to alter rbc ag expression

Back 308

DTT and 2ME, ZZAP,chlorquine

Front 309

what rbc ag does DTT affect

Back 309

K, Lu, Do, Yt, LW deactivated/destroys
deactivates IgM

Front 310

what does 2ME do

Back 310

deactivates IgM

Front 311

what is ZZAP

Back 311

proteolytic enzyme and DDT action

Front 312

what does chloroquine do

Back 312

strips IgG from DAT+cells (does also remove Bg antigens from rbcs)

Front 313

for confirmation of ABO blood type/rh from blood center unit, what is necessary

Back 313

1. forward confirmation of ABO blood type (unit's rbcs with reagent antibodies)
2. Rh D negatives only (weak D not required)

Front 314

name 2 preanalytical controls on blood sample acquisition

Back 314

- labeling by bedside
- two identifiers

Front 315

what is the q3 day rule and who, possibly, could deviate from that

Back 315

day 0 is day of draw, then days 1, 2, 3
technically only required for someone pregnant or transfused within last three months but most BB just make it simple and apply it to everyone

Front 316

how long required to keep sample post transfusion

Back 316

7 days

Front 317

what type of tubes are acceptable for compatibility testing

Back 317

red (serum) or lavendar (plasma)

Front 318

what type of tube is preferable for blood collection for solid phase and gel and why

Back 318

plasma (lavendar); b/c not fully clotted blood can result in debris that interfers

Front 319

what is a disadvantage to using a lavendar top tube in blood compatibility testing

Back 319

the EDTA in a purple top can interfere with complement-dependent antigens

Front 320

what are two fx you might see in a specimen collected for blood compatibility testing that would make you "reject" the sample

Back 320

- hemolysis
- lipemia

Front 321

what is required to test the PATIENT sample in blood bank

Back 321

1. ABO - forward and reverse
2. Rh - IS (polyclonal/monoclonal anti D)
3. antibody screen (see separate flashcard

Front 322

how should partial D's be classified in patients, in donors? how should weak D's be classified in patients, in donors?

Back 322

- partial D - should be (in recipient) called D neg
- weak D should be (in recipient) be called D pos

In donors, weak or partial D should be D pos

Front 323

in an ab screen as a component of compatibility testing, when does the antibody detection need to be read

Back 323

so, three phases - IS, 37 and IAT, must be read after AHG, at least (and with Gel or SP, this is all you are reading at)

Front 324

when should cross check with patient records be performed and what is required in that check

Back 324

immediately after testing patient sample and before cross-match
- check previous ABO/rh testing of at least last 12 months (1/3 significant antibodies disappear in one year; 1/2 significant antibodies disappear in 10 years)

Front 325

in component selection, what is required for whole blood

Back 325

ABO identical to recipient

Front 326

in component selection, what is required for rbcs

Back 326

ABO identical to recipient's plasma

Front 327

in component selection, what is required for granulocytes

Back 327

ABO identical to recipient's plasma

Front 328

in component selection, what is required for FFP

Back 328

ABO identical to recipient's rbcs

Front 329

in component selection, what is required for platelets

Back 329

some say anything goes: preference: ABO compatability preferred, esp if thinking about giving O to nonO patients, esp if young)

Front 330

in component selection, what is required for cryo

Back 330

anything goes

Front 331

in component selection, what is required for rh

Back 331

if premenopausal female: D neg (unless emergency)

Front 332

can you give D neg males D+ blood

Back 332

in trauma setting, absolutely! postmenopausal women too UNLESS HAVE D ANTIBODY