Transfusion Medicine--Fung Flashcards

1
Q

What is blood banking?

A

The collection, processing, storage and distribution of whole blood and apheresis.
Occurs at a blood collection facility or blood center

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2
Q

What is apheresis?

A

derived blood and blood components

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3
Q

What is transfusion medicine?

A

Pretransfusion and compatibility testing, post-manufacture processing
Occurs predominantly at a hospital

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4
Q

What is a blood group? How many are there?

A

blood group: “an inherited character of the red cell surface detected by a specific alloantibody”
339 recognized ones

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5
Q

Give some proteins, glycoproteins, and glycolipids that are found as antigens on the surface of RBCs.

A
ABO
Rh (D)
Secretor (Se, se)
Lewis (Lea, Leb)
Kell (K, k)
Duffy (Fya, Fyb)
Kidd (Jka, Jkb)
I (I, i)
MNS
P
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6
Q

What are the basics of what you do when you type & cross match blood?

A

take a sample of blood
asking the Q: which antigens do these RBCs express?
add in test antibodies
watch for lattice formation & agglutination

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7
Q

What are the 3 phases of tube testing?

A

Immediate Spin
37dC phase: watch for agglutination at that temp
IAT phase

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8
Q

What do you usu find after the immediate spin?

A

usu find the IgM antibodies present in the blood. This is insignificant

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9
Q

What do you find in the IAT phase of tube testing?

A

at this phase you find RBCs coated with IgG or complement

these antibodies that are reactive are more likely significant

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10
Q

Describe DAT blood bank testing. Is this in vivo or vitro?

A

Direct Antiglobulin Test
in vivo: in the organism
tests whether the RBCs of the patient are sensitized to certain antibodies
**Wash away antibodies that are present.
**IgG antibodies added–see if they coat the RBCs
**AHG: antihuman globulin added to cause agglutination of RBCs bound to the IgG

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11
Q

Describe the IAT blood bank testing. Is this in vivo or vitro?

A

Indirect Antiglobulin Test
in vitro: on a slide
tests whether the serum of the pt has certain IgG antibodies
**Use fake RBCs
**Put them in patient serum
**Antibodies bind.
**AHG: antihuman globulin added to cause agglutination

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12
Q

What is the clinical significance of blood groups?

A

patients can get a hemolytic transfusion reaction

hemolytic disease of the newborn or fetus is also possible

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13
Q

Which are more significant antibodies: IgG or IgM?

A

IgG are more significant
warm reactive (37dC-temp of body)
require previous exposure
**IgM are naturally occurring & tend to be cold reactive
**ALso IGG can cross the placenta-significant for pregnancy

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14
Q

what are the Type I chains of the ABO blood system? Which gene modifies them?

A

glcyoproteins & glycolipids that are free floating in secretions & plasma
**found in saliva
Se gene modifies this to produce H antigen (substance)

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15
Q

What are the Type II chains of the ABO blood system? Which gene modifies them?

A

glycoprotein & glycolipids antigens that are bound to the RBC membrane
modified by H gene to produce H antigen (substance).
Further modified from there to A antigen or B antigen.

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16
Q

If the H antigen of Type II chains is not further modified…what is produced?

A

O antigen!

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17
Q

What determines a person’s genotype in terms of the ABO blood system?

A

3 codominant alleles on the long arm of chromosome 9

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18
Q

Aside from RBCs…where else are ABO antigens carried? Note: this is why it is important for organ transplants to be ABO compatible.

A
platelets
endothelium
kidney
heart
lung
bowel
pancreas
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19
Q

When do you first see ABO antigens on fetal RBCs? When do they reach adult levels?

A

First see: 6 weeks

Adult Levels: Age 4

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20
Q
Rank the following from most frequently seen to least frequently seen:
A Blood
AB Blood
O Blood
B Blood
Note: this holds true across races
A

O most common
A
B
AB

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21
Q

Which ethnicity has 79% Type O blood?

A

native americans

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22
Q

What is Bombay type blood? How do you deal with transfusions?

A
Oh
Lack of H, A, B antigens
No H or Se genes
can't be transfused!
Need to do autotransfusions
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23
Q

Why are we worried about patients having antibodies against transfused blood antigen?

A

b/c it can activate complement

can get an immediate intravascular hemolytic transfusion reaction

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24
Q

When do you start to see ABO antibodies form in a person? When do they reach adult levels?

A

Start: 4 yo

Adult Levels: 10 yo

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25
Q

Type A blood person has which antibodies?

A

Anti-B antibodies IgM
react strongly at body temp
these are clinically significant

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26
Q

Type B blood person has which antibodies?

A

Anti-A IgM antibodies
react strongly at body temp
these are clinically signficant

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27
Q

Group O blood people have which antibodies?

A

Anti-A & Anti-B IgG antibodies
react best at body temp
**can see mild hemolytic disease of the newborn with these O moms.
Note: IgGs can cross the placenta!

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28
Q

What is forward typing? Use Type B blood person as an example.

A

use person’s blood & fake serum w/ antibodies.
Check for antigen.
Here: you see B antigen. Binds Anti-B antibodies.

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29
Q

What is reverse typing? Use Type A blood person as an example.

A

Use person’s serum & antibodies & use fake cells.
Which antibodies does this patient have?
Anti-B antibodies.

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30
Q

What do you use reverse & forward typing for?

A

use to see which ABO group a patient falls into…both need to agree for you to be good.
use immediate spin to check.

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31
Q

What are the 2 genes involved in the Rh system?

A

RHD (D/nothing)

RHCE (C/c, E/e)

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32
Q

Which of the antigens involved in the Rh System makes the most antibodies?

A

D makes the most!

very immunogenic 80% of D-neg makes anti-D

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33
Q

What type of hemolytic transfusion reaction is involved w/ the Rh system?

A

extravascular hemolysis

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34
Q

Which causes a more severe reaction?
anti-D & anti-c
OR
anti-C & anti-D & anti-e

A

anti-D & anti-c HDFN is more severe

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35
Q

Describe the type of hemolytic disease for fetus involved in the Rh system.

A

not first pregnancy
D-neg mom w/ D+ baby
use RhIG (commercially prepared anti-D) to treat

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36
Q

When do you use RhiG?

A

D-neg females at 28 weeks gestation
D-neg females s birth
D-neg females w/ pregnancy complications or invasive procedure (like amniocentesis)

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37
Q

What are the contraindications for using RhIG?

A

D-neg female who already has anti-D
D+ females
D-neg mom with D-neg baby

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38
Q

When we are dealing with D+ whole blood…what is the dosing for RhIG?

A

on full dose vial (300 micrograms) per 30 mL

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39
Q

When we are dealing with D+ RBCs…what is the dosing for RhIG?

A

one full dose vial (300 micrograms) per 15 mL

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40
Q

What are ways to determine percentage of fetal-maternal hemorrhage?

A

Fetal blood screen; qualitative
Kleihauer-Betke; quantitative but poorly reproducible
Flow cytometry; quantitative and more accurate

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41
Q

If you know a person’s weight…how do you determine blood volume?

A

Blood Volume = Weight (kg) X 70 mL/kg

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42
Q

If you don’t know a person’s weight…what should you assume their blood volume is?

A

5L=5000mL

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43
Q

If you know the KB value…how do you determine the amount of baby blood in the mom?

A

KB% X blood volume=baby blood in mom

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44
Q

So…know we have the value for D+ baby blood. How do we determine the amount of RhIG units to give?

A

Baby Blood in Mom/30mL (for whole blood)=Y.X

X5 round up 2 units

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45
Q

Mom is 70 kg. KB=2%. How much RhIG should be given?

Mom is D neg & baby is D+

A
BV=70kg X 70mL/kg=4900 mL
0.02 X 4900 = 98 mL D+ baby blood
98/30=3.2
Round up once.
Give 4 units RhIG
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46
Q

What’s the deal with the LEwis system blood group?

A

consists of insignificant naturally occurring cold reacting igM antibodies

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47
Q

Secretors usu have which Lewis value?

A

Leb

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48
Q

Nonsecretors usu have which Lewis value?

A

Lea

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49
Q

What’s the deal with the MNS system blood group?

A

consists of IgM & IgG

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50
Q

Which antibodies to the MNS system are naturally occurring cold reacting IgM (insignificant)?

A

Anti-M & Anti-N

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51
Q

Which antibodies to the MNS system are significant, exposure requiring warm reacting IgG?

A

Anti-S
Anti-s
Anti-U

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52
Q

Which antibody that is a part of the MNS system could cause severe HDFN (dangerous for fetus!)?

A

Anti-M

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53
Q

What’s the deal with the I system?

A
antigens are built on 2 types of chains
simple chains (i) found in neonates
branched chains (I) found in adults
insignificant naturally occurring cold reacting IgM auto-antibody
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54
Q

What happens with auto-anti-I?

A

cold agglutinin disease

mycoplasma pneumonia infections

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55
Q

What happens with auto-anti-i?

A

infectious Mono

56
Q

What’s the deal with the P system?

A

P antigen is the parvovirus B19 receptor (think about for sickle cell patients)
pk antigen is receptor for various bacteria & toxins
insignificant naturally occurring cold reacting IgM

57
Q

What’s the deal with auto-anti-p?

A

paroxysmal cold hemoglobinuria

biphasic IgG autoantibody (binds cold & hemolyzes warm)

58
Q

What’s the Kidd system? Can it be dangerous?

A

Yes! Kidd kills!

Significant, exposure requiring, warm-reacting IgG (with IgM component)
Can fix complement with IgM component
Severe acute HTR possible
can be severe delayed hemolytic transfusion reaction that is intravascular. Intravascular is dangerous!
Mild HDFN possible.

59
Q

What is the kell blood group?

A

K antigen low frequency; k antigen high frequency (99.8%)

Severe acute or delayed, extravascular HTR
Severe HDFN
McLeod phenotype/ McLeod Syndrome

60
Q

What happens with anti-K?

A

Most common non-ABO antibody after anti-D
Significant, exposure requiring, warm-reacting IgG1
Most due to transfusion, not pregnancy

61
Q

What happens with anti-k?

A

Very uncommon due to high frequency antigen

62
Q

What happens in Mcleod phenotype/McLeod syndrome?

A

All Kell antigens decreased
Hemolytic anemias with acanthocytes, myopathy, ataxia, peripheral neuropathy, cardiomyopathy
X-linked chronic granulomatous disease

63
Q

What’s the deal with the Duffy Blood group? Which ethnicity is it common in?

A

Anti-Fya more common and significant than anti-Fyb
Significant, exposure requiring, warm-reacting IgG
Severe HTR, delayed and extravascular
Mild, but occasionally severe HDFN
Fy(a-b-) most common phenotype in African-Americans
Fy(a-b-) are resistant to Plasmodium vivax and P. knowlesi infection

64
Q

Once again, which phenotype is common in African Americans? What is the advantage of it?

A

Duffy A B-

Advantage: plasmodium vivax resistant

65
Q

What type of blood is donated? Who regulates it?

A

allogeneic whole blood donation

tightly regulated by FDA & AABB

66
Q

Blood donors are screened by what history features?

A

Name, address, DOB, previous deferrals, date of last donation
Sign, symptoms, risk factors for HIV
Medications

67
Q

Blood donors are screened by which physical criteria?

A

General appearance
Arm check
Weight, pulse, BP (common practice)

68
Q

What are some behaviors that keep you from being able to donate blood permanently?

A
high risk behaviors for AIDS: IV drug abusers, male-male sex, exposure to AIDS
receiving money for sex
use of transfusion clotting concentrates
growth hormone use from human source
use of insulin from bovine sources
use of medication teratogens: Tegison
69
Q

What are some medical conditions that will permanently defer you?

A
serologic positivity for HIV, HBV, HCV, HTLV
viral hepatitis after 11th birthday
hx of babesiosis or Chagas disease--attack RBCs
hypotension
weigh less than 80 lbs
dura mater graft
lymphoma or leukemia 
vCJD risk
70
Q

What will qualify you for 3 year deferral for giving blood?

A

Recovered from malaria
Immigrants from malaria endemic areas (5 years of living)
Medication teratogens: Soriatane

71
Q

What will qualify you for 1 year blood deferral?

A
Needle stick or other contact with blood
Sex with person with HIV or hepatitis
Sex with IVDA
Rape victims
Incarcerated >72 hrs.
Paying for sex
Allogeneic blood transfusion
Allogeneic transplant
Living with person with active hepatitis
Receiving HBIG
Tattoos/piercings
Travel to malaria endemic area
Syphilis or gonorrhea
Non-prophylactic  rabies vaccines
Travel to Iraq
72
Q

What are some other deferrals?

A
Pregnant: 6 wks. postpartum
Non-routine dental work: 72 hrs.
Immunizations: 2 or 4 week deferrals
Drugs:
Accutaine, finasteride: 30 days
Duasteride: 30 days
Aspirin: 48 hrs. (platelet function)
Plavix or Ticlid: 2 weeks (platelet function)
73
Q

How much blood is usu taken? What is tested?

A
500 mL taken
ABO & RH test
antibody screen
HTLV
West Nile Virus test
Chagas (anti-trypanosoma cruzi) testing
74
Q

What tests do they do for Serologic syphilis detection?

A

RPR/VDRL

FTA-ABS

75
Q

What tests do they do for hep B?

A

HBsAg
Anti-HBc
HBV NAT

76
Q

What tests do they do for Hep C?

A

Anti-HCV

HCV NAT

77
Q

What are these tests to do for HIV?

A

Anti-HIV1/2

HIV-1 NAT

78
Q

Which conditions do you have a low risk of contracting thru blood transfusions?

A

HIV-2
WNV
Syphilis

79
Q

What is the risk for getting HIV-1 from blood transfusion?

A

1 in 1.5 million

80
Q

What is the risk of getting Hep B from blood transfusion?

A

1 in 355 K

81
Q

What is the risk of getting Hep C from blood transfusion?

A

1 in 1.1 million

82
Q

What is the risk of getting a bacterial infection when you have a platelet transfusion? RBC transfusion?

A

Platelets: 1 in 75 K
RBC: 1 in 500K

83
Q

What are the restrictions for preoperative autologous blood donation?

A

less screening
AABB Standard: can’t give to other patients if unused
infectious disease screening required if it crosses to another facility
Note: this is donating blood to yourself!

84
Q

What is involved in testing the blood of a trauma recipient?

A

test the serum or plasma (red or lavender top) every 3 days & retain it for 7 days
Type & Screen
Type & Crossmatch

85
Q

What do you test with a type & screen?

A

Records check: Previous antibodies or compatibility problems
ABO/Rh testing
Antibody screen
Group O phenotyped RBCs
Antigens required by FDA: D, C, c, E, e, Fya, Fyb, Jka, Jkb, K, k, Lea, Leb, M, N, P1, S, s

86
Q

What is involved with a type & crossmatching?

A

Usually: recipient’s serum with donor RBCs

Less frequently: donor serum with recipient’s RBCs

87
Q

What does Fy mean? Jk mean?

A

Fy-Duffy

Jk-kidd

88
Q

After whole blood is taken from a donor. What is done? What is separated out?

A
Whole Blood
Soft Spin.
Platelet Rich Plasma + Packed RBCs
Hard Spin.
Platelet Concentrates + Fresh Frozen Plasma
89
Q

What is included in the fresh frozen plasma?

A

coagulation factors, fibrinogen, proteins

90
Q

What do you precipitate off of fresh frozen plasma?

A

Cryoprecipitate: includes fibrinogen + factor 8

Plasma derivates come from here too!

91
Q

How long do RBCs/WHole blood last when it has CPDA additive? How about when it has other additives? What temp must it be stored at?

A

CPDA: 35 days.
other Additives: 42 days
1-6 dC in a fridge

92
Q

What temp do frozen RBCs need to be kept at? How long do they last? When is this method of preservation required for a patient?

A

kept at -65dC
lasts 10 years
lasts 24 hrs after you thaw it
**good for patients with a rare blood phenotype–like bombay who need autologous donations

93
Q

How long do Washed RBCs last? What temp?

A

kept in fridge at 1-6 dC

lasts for 24 hrs

94
Q

How long do platelets last? What temp? What must be done to them?
WHat if they are pooled?

A

Last 5 days at 20-24 dC
**need to be gently agitated to prevent degranulation
Pooled (bad for disease risk): only last 4 hours

95
Q

How long does fresh frozen plasma last at the following temps?
-18dC:
-65dC:
1-6dC & then thawed:

A

-18dC: 1 year
-65 dC: 7 years
1-6dC after thawed: 24 hrs

96
Q

How long does cryoprecipitate last at the following temps:
-18 dC:
20-24dC after thaw:
Pooled:

A

-18dC: 1 year
20-24dC after thaw: 6 hours
Pooled: 4 hours bad for disease!

97
Q

If you have 1 bag of packed RBCs–about 250 mL…how much should the hct & hemoglobin increase? How many minutes after the transfusion should you test it?

A

Hct up 3%
Hgb up 1% g/dL
measure 15 minutes after transfusion

98
Q

What can you use to transfuse your RBCs with?

A

normal saline
ABO compatible plasma
5% albumin

99
Q

If you give someone platelets…how much should that raise their count? How long will it take? What testing do platelet transfusions require?

A

up 20-30K in 1 hour

don’t need to crossmatch or do ABO compatibility

100
Q

What is leukoreduction? When is it called for?

A

reducing the number of WBCs in a blood product
can do it prestorage, at the time of collection
can do it pre transfusion at the bedside
**perhaps good if the patient is immunocompromised

101
Q

What is washing? When might it be required?

A

this is where you remove 99% of the plasma

used in IgA deficiency–pts sometimes have anti-IgA. Need to get rid of the IGA in the donor blood!

102
Q

What does irradiation do to blood? When is it needed?

A

it prevents graft v. host disease in patients who are immunocompromised.
deactivates T lymphocytes
Donor WBCs could attack recipient cells.
Other indications:
intrauterine transfusion, neonatal transfusion
hematologic malignancies
granulocyte transfusions
receiving blood from first degree relative-even if ABO matched, may not be HLA matched

103
Q

What distinguishes an acute transfusion reaction from a delayed transfusion reaction?

A

timeframe!

acute: within 24 hours

104
Q

What’s the deal with the presentation of an acute transfusion reaction with fever?

A

acute hemolytic
febrile non-hemolytic
transfusion related sepsis
TRALI: transfusion associated lung injury

105
Q

What’s the deal with the presentation of an acute transfusion reaction w/o fever?

A

allergic
hypotensive
transfusion associated dyspnea
TACO: transfusion associated circulatory overload

106
Q

What’s the deal with a delayed transfusion reaction presenting with fever?

A

delayed hemolytic
TA-GVHD
graft v. host disease

107
Q

What’s the deal with a delayed transfusion reaction presenting w/o fever?

A

delayed serologic
post-transfusion purpura
iron overload

108
Q

What are the symptoms of acute hemolytic transfusion reactions that are immune-mediated?

A
ab pain, chest, flank or back pain
pain @ infusion site
feeling of impending doom
hemoglobinemia
hemoglobinuria
renal failure/shock
DIC
109
Q

What is the etiology of acute hemolytic transfusion reactions that are immune-mediated?

A

Type II hypersensitivity reaction

antibody-mediated IgG/IGM

110
Q

What are the symptoms of acute hemolytic transfusion reactions that are non-immune mediated?

A

asymptomatic hemoglobinuria

111
Q

What is the etiology of non-immune acute hemolytic transfusion reactions?

A

chemical or mechanical damage to blood product

112
Q

What causes intravascular acute hemolytic transfusion reactionS?

A

ABO incompatibility usu
ABO antibodies fix complement–rapid lysis!
other antibodies too…

113
Q

What causes extravascular acute hemolytic transfusion reactions?

A

usu less severe-lack of systemic complement & cytokine activation
Rh, Kell, Duffy antibodies

114
Q

What is the treatment for acute hemolytic transfusion reactions?

A

hydration

exchange transfusion!

115
Q

What are the steps involved in the transfusion reaction work up?

A
  1. Stop the transfusion!
  2. Clerical check
  3. Draw post-transfusion sample->compare to previous one, & look for hemoglo binemia
  4. DAT: see if RBCs are coated in IgG or complement
  5. Repeat ABO/Rh testing
116
Q

If you have a positive DAT…does that prove acute hemolytic transfusion reaction?

A

not necessarily

117
Q

What is the most frequently reported issue with transfusions? What is its etiology?

A

Febril non-hemolytic transfusion reactions
unexplained increase in temp by 1 dC
Etiology: increased pyrogenic substances from WBCs (secreted while in the storage bag). Recipient antibodies react

118
Q

What is the treatment for febrile non-hemolytic transfusion reaction?

A

antipyretics

demerol

119
Q

What is the only transfusion reaction in which you can start the transfusion again after the symptoms clear?

A

allergic reactions

120
Q

What are the symptoms of a mild allergic reaction to a transfusion?

A
Very common
Localized hives
Angioedema
Mild respiratory symptoms
Mild laryngeal edema
121
Q

What is the MOA for a mild allergic reaction?

A
Type I (IgE-mediated) hypersensitivity to transfused plasma proteins
Mast cell secretion of histamine and other mediators of allergic reactions
122
Q

What is the treatment & prevention for a mild allergic reaction to transfusions?

A

Diphenhydramine IV or oral (prevention)
Wash blood products
May restart transfusion after hives clear

123
Q

What are the symptoms for a moderate allergic reaction to transfusions?

A
Stridor
Hoarseness
Wheezing
Chest tightness
Dyspnea
124
Q

What is the MOA for a moderate allergic reaction to transfusions?

A
Type I (IgE-mediated) hypersensitivity to transfused plasma proteins
Mast cell secretion of histamine and other mediators of allergic reactions
125
Q

What is the treatment for allergic reactions to transfusions?

A

Diphenhydramine IV

Epinephrine

126
Q

What are the symptoms for a severe (anaphylactic) allergic reaction to a transfusion?

A
Uncommon
Anaphylaxis very early
Hypotension
Lower airway obstruction
Abdominal distress
Systemic crash
Urticaria
Puritis
127
Q

What is the MOA for a severe allergic reaction?

A

IgA deficient recipient with IgE anti-IgA
Haptoglobin deficiency
Latex drugs or foods in donor can lead to severe reactions in recipients

128
Q

What is the treatment for a severe allergic reaction to transfusions?

A

Washed blood products
IgA deficient blood products
Benadryl with corticosteroids
Epinephrine

129
Q

What’s the deal with delayed hemolytic transfusion reactions?

A

extravascular hemolysis

happens at least 24 hours after transfusion, but less than 28 days after

130
Q

What is the etiology for a delayed hemolytic transfusion reaction?

A

Anamnestic response
Antibody formed but fades over time
Anamnestic rapid production of IgG antibody
Typical for Kidd, Duffy and Kell antibodies
Primary response
Antibody is quickly formed and attacks still circulating transfused red cells

131
Q

What do you see in transfusion associated graft v. host disease?

A

attack on recipient cells by viable T lymphocytes in transfused blood product
Pt presents:
fever 7-10 days after transfusion
rash that spreads to extremities
mucositis, nausea/vomiting, watery diarrhea
hepatitis
pancytopenia

132
Q

What is the treatment to prevent TA-GVHD?

A

irradiate blood products

133
Q

What happens in transfusion associated sepsis?

A

Acute non-immune transfusion reaction
Due to bacteria in contaminated platelets (b/c they are kept at room temp) and RBCs
Staph, strep, Yersinia, bacillus, pseudomonas, E. coli

134
Q

What happens in patients who become hypotensive as a result of their transfusion?

A

Similar to severe allergic reaction but no skin symptoms, no GI or respiratory issues
>30mm Hg drop in systolic BP; diastolic ≤80mm Hg
Occurs <10 after stop
Associated with patients taking ACE inhibitors or receiving blood with negatively charged filters

135
Q

What is the deal with transfusion related acute lung injury?

A

1 cause of transfusion related fatality in US

New acute lung injury ≤6 hrs. post transfusion
Associated with platelets but also RBC/WB
Two proposed methods
Neutrophils produce toxic free radicals that damage endothelial cells
Donor anti-HLA or anti-neutrophil antibodies bind to recipient antigens and damage endothelial cells

136
Q

What’s the deal with transfusion associated circulatory overload (TACO)?

A

Acute onset of congestive heart failure as a direct result of blood transfusion

137
Q

What’s the deal with post-transfusion purpura?

A

Rare
Marked thrombocytopenia and increased risk of bleeding 10 days following transfusion
Due to antibody against a common platelet antigen
Anti-HPA-1A
PLA1 has a frequency of 98%