Blood Bank Polansky Review Flashcards
AABB criteria for whole blood donors
age allogenic
> 16 or allowed by state
Criteria for whole blood donors HGB/HCT allogenic
hgb >12.5g/dl
Hct >38%
Temperature of whole blood donation criteria allogenic
<99.5 f or 37.5c
Autologous whole blood donation requirements
age
hgb/hct
temperature
age determined by director
hgb >11g/dl
hct >33%
bacteremia is cause for deferral in temperature
aspirin deferral (if donor is sole source of platelets)
2 days
measels/rubeola, mumps, polio, yellow fever vaccine deferral
2 weeks
rubella, chicken pox (varicella zoster) vaccine deferral
4 weeks
pregnancy deferral
6 weeks
whole blood donation deferral
8 weeks
syphillis, gonorrhea, skin penetration, hepatitis contact, high risk HIV, Iraq travel…etc deferral
12 mos
malaria or endemic region deferral
3 years
permanent deferrals
parenteral drug use
CJD
GH treatment
hepatitis after 11yrs
Hep B
Chagas/bebesiosis
volume of blood collected routinely
450 - 500ml
Time of collection of whole blood
<10min, if >15-20min unit may not be suitable for prep of platelets or plasma
apheresis explanation
removal of 1 or more components of blood from donor and return of remainders to donor
advantages of apheresis
allows collection of larger volumes of specific components, reduces number of donors pt is exposed to
Donor testing required by AABB/FDA
Type ABO/Rh (weak D)
Ab Screen
Syphilis
Hep
HIV
HTLV
WNV
bacterial cultures
ACD-A anticoag
acid citrate dextrose
21 day life
chelates calcium, apheresis
CPD anticoag
citrate phosphate dextrose
21 days
higher pH , better 02 delivery
CP2D anticoag
citrate phos double dextrose
21 days
contains 100% more glucose than CPD
CPDA-1 anticoag
citrate phos dextrose w adenine
35 days
increases ATP, longer cell storage
additive solution purpose
consituents
lowers?
extends shelf life of rbcs to 42 days
glucose for energy, ATP
lowers viscosity
Examples of rbc additive solutions
AS-1, AS-3 AS-5
Open system
seal on unit is broken to attach external transfer bag, exposure to air poses bacterial contam
used w/in 24hr after opened, stored within 4 hr
closed system
sterilty maintained through satellite bags or device, welds tubing from one bag to another, no air exposure
no change in expiration
RBC storage temp
shelf life
indications
Hct
centrifuge to separate out WBC
store 1-6c
35 days in CPDA-1
inadequate tissue oxygenation
HCT >80%
how much does one unit of rbcs change HCT/HGB
1 unit increases Hgb 1g/dl
Hct 3%
Rbcs adenine, saline added storage
shelf
removal of most plasma
1-6c
42 days
mOST COMMONLY USED PRODUCT
frozen rbcs
storage
shelf
frozen in glycerol w/in 6 days
<65c after deglyc 1-6c
10yrs, after thaw 24hr
safe for IgA def patients, used to store rare cells
washed rbcs
storage
shelf
indications
washed with saline
1-6c
expires 24hr after wash
hxt of severe allergic rxn
not sub for wbc reduced rbcs
RBC leukoreduced
storage
shelf
indications
filtration/apheresis method
1-6c
history of febrile rxn
85% original rbcs must be retained
<5x10^6 wbc
irradiated rbcs
storage
shelf
indications
cGy irradiation
1-6c
origninal out date or 28 days from irradiation
immunodef,malignancy
prevention of GVH, kills donor t cells
FFP
storage
shelf
plasma sep from wb and frozen w/in 8 hr
frozen: <-18c
after thaw 1-6c
frozen: 12mos
thaw: 24hr
coag factor def, contains all coag factors
Cryoprecipitate
prep
storage
shelf
indications
thaw FFP at 1-6c, remove plasma, refreeze w/in 1hr
frozen: <-18c
after thaw: RT
frozen: 12mos
thaw: single unit 6hr, pool 6hr if sterile device (4hr regular)
factor I and vIII deficiencies
hemophilia A/VWD
Platelets
prep
strorage
shelf
centrifuge w/in 8hr
1st soft spin, (rich plasma) 2nd hard spin (separates plts)
20-24c
5 days from collection, after pooling 4hr
severe tp or abn plt function
Platelet component requirements
> 5.5 x 10^10 plts
ph >6.2
incs plts by 5000-10,000 in one unit
apheresis plt
storage temp
shelf life
plt count
20-24c
5 days with agitation
>3.0 x 10^11plts
Leukoreduced plt components
storage
shelf
indications
wbc removed,
20-24c
open system 4hr
apheresis 5 days
recurrent febrile rxn, decrease risk of CMV/HLA
prestorage pooled plts
prep
storage
shelf
ABO identical plts pooled in closed system
20-24c
5 days from collection
Leukoreduction purpose
wbc count
methods
to dec wbcs to dec febrile rxn, CMV, HLA
<5 x 10^6 wbcs
apheresis, filtration, filters
RBC storage lesion
INC: Lactic acid, Plasma K, Hgb, Aggregates
Decreased: ATP, 2,3BPG, pH, glucose, viable cells, labile coag factors
shift to the left of curve (inc oxy affinity, decreased oxy to tissues)
Primary response
stimulous
lag phase
ab
titer
1st exposure to ag
days to mos lag
IgM first, IgG after 2wk
titer is slow, peaks then declines
Secondary response (anamnestic)
stimulous
lag phase
ab
titer
subsequent ag exposure
lag phase hours
IgG first
titer rises faster and higher, stays elevated longer
Clin sign ab react at what temperature
37c
pH of most ab rxns
5.5-8.5
ionic strength
reducing ionic strength facilitates interaction of ab with ag (LISS)
optimum serum to cell ratio
80:1
what does reducing zeta potential do
allows rbcs to move closer together
Gel testing
more sensative than tube, rxn stable for 2-3days
AHG doesnt require washing or control cells
Type O frequencies
Whites
blacks
hispanic
asian
white 45%
black 49%
hispanic 57%
asian 40%
A frequency
w,b,h,a
40, 27, 31, 27
B frequencies
W,B,H,A
11, 19, 10, 25
AB frequency
W,B,H,A
4,4,2,7
Group O
ags on rbc
antibodies in serum
no ags on rbcs
Anti-A, Anti-B in serum
Group AB
ag on rbcs
ab in serum
A and B ag
no Anti-A or Anti-B
ABO discrepency
missing rxns
missing agglut in group O
inc reverse RT for 30 min
or 4c
Fisher race Rh ag
DCEce
Weiner Rh ag
Rh0
rh’
rh’’
hr’
hr’’
Rosenfield Rh ag
Rh1
Rh2
Rh3
Rh4..etc
Rh frequency
W/B
D
85% w
92% b
C frequency
68% w
27%B
E frequency
29% W
22% B
c frequency
80% w
96% b
e frequency
98% w
98% b
most common Rh genes
DCe, Dce, DcE, dce
r before h
BIG
rh’ = C
h before r
little
hr’ = c
R
presence of D
Rh1 = DCe
0
c+e
Dce
Rh0
Z or Y
C+E
rhy
dCE
rh typing
high protein Anti-D
pools of human sera
no anti-D
more false pos
rbcs w pos DAT
Low protein anti-D
monoclonal igM or igG
most used, lower rate of false pos with ig coated rbcs
False pos Rh typing
warm/cold auto
rouleax
poly rbcs
nonspec agglut
contamination
false negative rh type
no rgnt added
rbc suspension too heavy
resuspension too vigorous
contamination
blocking of ag sites by ab
Weak D testing
mother/infant being eval for RhIG
inc tubes at 37c for 15-60min through AHG
I system
adults
I, trace amounts of i
I system cord cells
trace I, lots of i
Naturally occuring antibodies
ABO, Lewis, P1, MN, Lua
Clinically significant antibodies
ABO, Rh, Kell, Duffy, KIdd, SsU
Warm antibodies
Rh, Kell, Duffy, Kidd
Cold Ab
M,N P1
Usually only react in AHG ab
Kell, Duffy, Kidd
can react in any phase of testing Ab
lewis
detection enhanced by enzyme treatment
Rh, Lewis, Kidd, P1
not detected with enzymes/destroyed
Duffy, M, N
enhanced by acidification
M
Shows dosage
Rh other than D
MNS
Duffy
Kidd
Binds complement
I, Kidd, Lewis
Causes in Vitro hemolysis
ABO, Lewis, kidd, Kell, P1
Labile in vivo and vitro
Kidd
Associated with PNH paroxymal nocturnal hemoglobinuria
Anti-P
Assoc w cold agg disease, Myco pneumoniae infections
Anti-I
assoc with infectious mono
Anti-i
Albumin
22% bovine, reduces zeta potential/net charge of rbcs, allows rbcs to get closer together
LISS
lowers ionic strength, ag/ab moves closer together more rapidly, reduces incubation time for IAT
PEG
increases Ab uptake, detects weak IgG abs
Enzymes
ficin and papain, reduce rbc surface charge by cleaving silaic molevules
M,N,S, Duffy destroyed
Polyspecific antihuman globulin serum
igG C3d
DAT
Monospecific antihuman globulin serum
IgG
routine compatibility/ID
clin sign ab detection
Anti-C3d or Anti-c3b-c3d
complement
immune hemolytic anemias
DAT antiglobulin test
in vivo sensitization of rbcs by ab
HDFN,tf rxn, AHA
IAT
in vitro sensitization of rbcs by ig
ab screen, xm, phenotype, weak D
same strength and 1 phase only
suggestive of single ab
all cells in AHG and autocontrol negative
multiple ab possible, ab to high frequency ag
all cells in AHG, autocontrol pos
warm autoab possible
all cells at 37c, neg AHGm autocontrol pos
Rouleaux
Anti-A1
cold ab
found only in A subgroups
agglut A1 and A1B but not A2 or O
Anti-I
cold ab
agg all adult cells except adult i, doesnt agg cord cells
Anti-i
agg cord cells more strongly than adult cells
Anti-H
most common in A1 and A1B, agg O most, A1B least
Compatibility testing
spec collected within 3 days
retain for 7 days after transfusion
antiglobulin xm
recipient serum and donor rbcs
if recipient has/had clin sign ab
IS XM
recipient serum/donor rbcs
no clin sign ab, detects ABO incomp, must be taken through AHG
what type of plasma can O person recieve
O, A, B , AB
Pretransfusion testing
what specimens need to be crossmatched?
which dont?
rbcs yes
plt/plasma/cryo no xm
Acute TFXN
hemolytic intravascular
fevers, chill, shock, DIC
backpain
immediate rbc destruction
dec Hgb/Hct haptoglobin
MOST SERIOUS, ABO incompatible
Febrile acute TFXM
inc temp >1c or 2c
anti-leukocyte wbc
common, multiple transfusion pt, or mult preg
give tylenol or aspirin
Allergic TFRXN
hives, wheezing
foreign plasma proteins
antihistamines
investigation not required
anaphylactic TFRXN
pulmonary edema, bronchospamsa
Anti-igA def recipient
dangerous, epi injection, washed products
TRALI
fever, chills, cough, dec BP,
WBC ag
most common cause of tf assoc death
reduced use of plasma from female donors
Sepsis rxn
dec Bp, cramps, DIC, fever, rigors, shock
bacteria
TACO
cough, cyanosis, pulmonary edema
too large volume at rapid rate
children, cardiac pt, elderly/anemia
Non immune hemolysis rxn
rbc destruction due to temp/medications
hemoglobinuria/emia
hypothermia rxn
cardiac arrythmia
rapid infusion of cold blood
use blood warmer
Delayed hemolytic rxn
fever, jaundice after
inc bili, DAT
dec hapto,hgb and hct
Kidd
TA-GVHD
rash, nausea, pancytopenia,
viable t lymphs attack recipient
irradiate components
iron overload
delayed transfusion rxn
diabetes, cirrhosis, cardiomyo
inc serum ferritin
repeated transfusion,m sickle cells or anemias
