Lecture - Transfusion medicine (martin) Flashcards

1
Q

what does agglutination represent in blood typing

A

detecting presence of Ag corresponding to Anti-sera

ex. A+ pt

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2
Q

Forward/front typing

A

mix pt RBC w/ commercially made anti-sera

agglutination–> detecting presence of Ag corresponding to Anti-sera

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3
Q

if you have an A+ pt, what would you expect on their front/fwd typing to show?

A

would expect agglutination in anti-A, anti A,B, and Anti-D

neg on anti-B and D cont

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4
Q

Back/reverse typing

A

mix pt sera with commercially prepared cells

agglutination–> reveals presence of Ab to corresponding cells

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5
Q

if you have an A+ pt, what would you expect on their back/reverse typing to show?

A

+anti-B

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6
Q

Ab screen (Indirect antiglobulin test- IAT)

A

mix pt sera with screening cells

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7
Q

what does a + Ab screen result indicate?

A

detection of an immunoglobulin in pt sera against a foreign RBC antigen (pt must’ve been transfused at one point or exposed during a pregnancy)

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8
Q

if you are Rh+, what will you typically see when reacting your blood cells to anti-D sera

A

STRONG D expression response (one big agglutination)

can have WEAK D (Du)- weakly positive where may or may not be visible, might need to add reagent or incubation time for it to show up

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9
Q

if you are a weak D patient and you are donating blood, what are you considered as?

A

considered as Rh+ (bc have some form of D antigen there)

and a recipient could develop anti-D

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10
Q

if you are a weak D patient and you are receiving blood, what are you considered as?

A

some places may consider you as Rh- (espec in childbearing years), bc of possibility of developing anti_D

85% treat as Rh+ tho

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11
Q

ranked first in immunogenicity

A

Rhesus system (D)

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12
Q

ranked second in immunogenicity

A

Kell system

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13
Q

What dzs can the McLeod phenotype be associated with?

A

Chronic compensated hemolytic anemia

Chronic granulomatous dz

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14
Q

what would you see on peripheral blood smear in someone w/ chronic compensated hemolytic anemia

A

many acanthocytes (spur cells) - spiky, irregular cells close to normal size

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15
Q

special features of chronic granulomatous dz

A

lack Kx Ag on membrane of neutrophils and monocytes

deficiency of NADH-oxidase –> no H202 to destroy microbes (aka LOTS OF Infections)

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16
Q

What is impt to know about specimen collection

A

-specimen MUST be labeled at bedside (w/ time, date and initial of phlebotomist); permanent and unique ID of each pt

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17
Q

what is one of the biggest issues when have lethal transfusion rxns

A

misidentification

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18
Q

when a type and screen (T&S) is done, what is performed

A

only ABO, Rh, and Ab screen (no xmatch)

-usually when have surgical procedure or time needing blood

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19
Q

If have a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs…what do you do

A

Ab identification and look for units negative for that antigen that the alloantibody is against

then… Crossmatch (actually testing of pts serum compatibility w/ donor cells)

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20
Q

what does a positive Ab screen/indirect antiglobulin test (IAT)/indirect coombs detect

A

Ig in pts serum against Ag on RBCs (NOT pts RBCs)

Ab must NOT be bound to RBCs (either pts own RBCs or transfused RBCs) to enable detection

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21
Q

Direct vs. Indirect Coombs

A

Direct- Abs attached to own RBCs
[detect autoimmune hemolytic anemia and transfusion rxn workups]

Indirect- alloAbs in pts serums that will react to foreign RBCs’
[used prior to blood transfusion and in prenatal testing of pregnant women]

adding Coombs reagent (anti-human Igs) - makes it more visible to detection w/ test

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22
Q

what does an antibody work up screen for

A

UNEXPECTED allo-Abs

identify Ab in pt serum, not formed by pt (ex. maternal Ab in infant/fetal circulation)

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23
Q

antigen detection test

A

used after identifying Ab in pt serum

how: commercial anti-sera mixed w/ pt cells

confirmation pt +/- Ag on own cells
usually done in conjunction w/ Ag typing/screening donor cells for compatibility

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24
Q

Indirect Antiglobulin test/indirect coombs checks for what?

A

hemolysis + agglutination against “screening cells”

do at 3 diff phases (room temp, 37C, antihemoglobulin (AHG) )

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25
Q

@Room temp, IAT detects:

A

initial combination of pt sera w/ commercial suspension of RBCs

detect COLD Abs- IgM

(not rlly clinically significant)

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26
Q

@37 C, IAT detects:

A

“warm” Abs - Igm- IgG mixture + IgG

Warm Ab: Rh, Kell, Kidd, and Duffy

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27
Q

In the antihemoglobulin phase, IAT detects

A

“warm” Abs; IgG that coat the RBC membrane

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28
Q

when performing an IAT, what does adding a check cell (CC) do?

A

verify AHG was added and working

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29
Q

Rule out method

A

for every cell with negative rxn, go and cross out all the antigens that are positive on that cell

then find the only manufactured cell that is + for one antigen and negative in all the other cells

can take a while! why theres a delay typically; then have to antigen check them once find

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30
Q

what is an autoAb

A

Ab directed against individual own RBC ags

–> can cause RBC destruction

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31
Q

Autoimmune hemolytic anemia

A

when have intravascular hemolysis–> hemoglobinemia/uria

+/- anemia, incr reticulocytes, incr unconj bilirubin, decr haptoglobin

Confirm w/ DAT (coombs) and characterization of autoAbs as cold or warm reactive

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32
Q

what is the most common autoAb entity

A

cold autoantibodies (benign cold agglutinin) - 4 Celcius

IgM

usually low titer but often agglutinate at room temp; can activate complement in vitro

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33
Q

how can you get a false + rxn with cold autoAbs; how prevent this?

A

if self RBCs heavily coated w/ AB, may spontaneously agglutinate and cause a false +

Ab detection: can do a prewarm or autoabsorbed serum so cold Ab dont obscure alloAbs

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34
Q

when trying to test for compatibility of cold autoantibodies, what is most common and how do you do it?

A

auto-anti-I = MC (found on most donor units)

you also prewarm or use autoabsorption

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35
Q

What autoAbs react with an antihemoglobulin phase (autoimmune hemolytic anemia- AIHA)? what Ag group are they specific to?

A

warm Abs–> IgG

specific to Rh group Ags (high incidence)

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36
Q

how can the warm autoantibodies be induced?

A

idiopathic or SLE-assoc or drug-induced

need pt med hx and transfusion rxn

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37
Q

should you transfuse a patient with warm autoAbs

A

many patients dont require transfusions

can use steroids and splenectomy

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38
Q

Cold Agglutinin Dz

A

varies from none to life threatening hemolytic anemia (intravascular hemolysis- increases as pt is exposed to COLD and complement gets activated)

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39
Q

what should a person w/ cold agglutinin dz avoid?

A

COLD WEATHER (and walk in freezers lol)

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40
Q

infections assoc with cold agglutinin dz

A

mycoplasma pneumoniae pneumonia

or

infectious mononucleosis

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41
Q

how do you perform a crossmatch (compatibility testing)

A

first recheck the recipients ABO Rh type (forward and reverse typing + weak D)

if positive..AB ID

if negative (no unexpected antibodies)–>

CROSSMATCH:
utilizing pt sera and mixing it with donor RBC to make sure dont have any bad reactions and is compatible

detect agglutination: if no agglutination/hemolysis = COMPATIBLE

ex. donor PC A (compatible recipient = A and AB)

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42
Q

Adverse effects of transfusion include:

A

Shock, respiratory distress, fever, acute hemolyic or septic rxns, and TRALI

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43
Q

Mgmt of acute transfusion rxns

A
  1. STOP TRANSFUSION
  2. Keep IV open w/ 0.9% NaCl
  3. verify correct unit was given to correct pt
  4. notify attending physicians and blood bank

ADVERSE RXN: stop transfusion, report rxn to blood bank IMMEDIATELY, return bag w/ attached tubing, return all paperwork, send post-transfusional blood sample

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44
Q

Transfusion-related GVHD

A

infusion of immunocompetent donor lymphs to immunocompromised recipient

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45
Q

what is the circulatory overload transfusion rxn

A

either too large a volume or too fast infusion

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46
Q

when giving a pt a transfusion, how long should you monitor them for?

A

monitor pt closely during first 15 mins of transfusion and intermittently during transfusion

47
Q

most impt lab response to transfusion rxn

A

the first thing theyre going to do is check for identification errors (PROBS is a labeling error)

then.. Visual check, serologic test for incompatibility (ABO/Rh, gram stain + culture, H/H and urine for hemolysis, R/O TRALI)

48
Q

symptoms: Acute hemolytic transfusion rxn

A
HYPOtension
hemoglobinuria
DIC
flank pain or infusion site pain
\+DAT

also fever, chills, N/V, dyspnea, tachy

late complication: renal failure

49
Q

symptoms: Delayed hemolytic transfusion rxn

A

unexplained rise in unconj Hgb
drop in H/H
+DAT

other: unexpected anemia, fever, chills, jaundice, pain or dyspnea; increased LDH and bili, new RBC Ab

50
Q

symptoms: Febrile non-hemolytic transfusion rxn

A

fever
chills
HYPERtension

secondary sx: HA, N/V

not life threatening (but need to exclude other causes of fever)

51
Q

symptoms: Allergic transfusion rxn

A

urticarial rxn

pruritis, urticaria, erythema, and cutaneous flushing

laryngeal edema (upper airway)
bronchoconstriction (lower airway)
52
Q

symptoms: TRALI transfusion rxn

A

**NON-CARDIOGENIC pulmonary edema
assoc w/ passive transfer of donor granulocyte Abs

CXR: pulmonary edema (may persist >7 days)

lack of abnormal breath sounds
NO SIGNS OF CARDIAC FAILURE

presentation resembles ARDS

53
Q

symptoms: Septic transfusion rxn

A

fever
chills
rigors
shock

caused by contaminated blood component (platelets usually)

54
Q

what transfusion rxn presents within hours, within <24 hours, and >24 hours post-transfusion

A

within hrs: TRALI

<24 hrs: Acute hemolytic

> 24 hrs: Delayed hemolytic (usually <2 weeks, but can be >6 weeks)

55
Q

how do AHTRs happen

A

pre-existing natural IgM Abs induce complement-mediated intravascular hemolysis

+DAT

56
Q

what does mortality depend on in AHTRs?

A

depends on amount RBC transfused (less put in, less hemolysis, less likely mortality)

57
Q

DDx with AHTRs

A

AIHA, cold hemogglutinin dz, congenital hemolytic anemia, nonimmune hemolysis, hemoglobinopathies, polyagglutination, PNH, artificial heart valve

58
Q

Treatment and prevention of AHTRs

A

Tx: discontinue + verify ID; Mild- observe, severe- CV support, fluid resusc, pressor support; avoid fluid overload, maintain urine output

Prevention- proper ID of patient!!

59
Q

single most common cause of AHTRs

A

not proper identification of patient

60
Q

what kind of hemolytic rxn is DHTR?

A

extravascular hemolysis!!

61
Q

how do DHTRs happen

A

IgG from prior transfusion/exposure (Rh, Kell, Kidd)

+DAT

62
Q

what dz may DHTRs precipitate

A

Sickle Crisis in sickle pt

63
Q

DDx with DHTRs

A

same as AHTR, emphasis on occult infection, AIHA, cold hemogluttin dz

DIFFICULT DDX

64
Q

Treatment of DHTRs

A

Tx: most tolerate well, follow carefully; tx complications as needed
*IVIG- extravasc hemolysis *

Prevention: serologic detection of RBC Ab = key to prevention (select donor units neg for RBC ag)

65
Q

Febrile non-hemolytic transfusion rxns

A

rise in temp of 1C or greater (may be 30 mins to 1 hr post transfusion)

rxn is associated w/ acquired Ab to leukocyte ag in transfused pdts; attributed to pyrogenic cytokines in units during storage

66
Q

DDx of FNHTRs

A

hemolytic transfusion rxns, TRALi, bacterial contamination vs. dz or treatment related fever

67
Q

Tx and prevention of FNHTRs

A

Tx: +/- antipyretics (Acetaminophen); fever self limited (resolves in 2-3 hrs); if rigors- can give meperidine (caution bc its resp depressant)

Prevention: pre-medicate w/ antipyretic (if hx of previous febrile rxns)

  • pre-storage leukocyte reduction decreases cytokines
  • plasma reduction or wash pack cells (removing all plasma form pack cell unit)
68
Q

what should you not give a patient with suspected FNHTRs

A

NO ASPIRIN (due to effect on platelet function)

69
Q

Allergic (urticarial ) transfusion rnxs are associated w/

A

any type of blood component (assoc with amt of plasma transfused)

70
Q

if a pt has dyspnea after transfusion, what should you rule out if youre thinking it might be an allergic rxn

A

rule out TRALI syndrome and volume overload

71
Q

Tx and Prevention of allergic transf rxns

A

tx: intubate prn + O2 prn; IV antihistamine

prevention: usually cant ID Ag, thus unable to select Ag- products; (EXCEPT IGA deficiency)
* *premedicate w/ antihistamine to prevent mild allergic rxn**

72
Q

A pt comes in w/ either CV instability, hypotension, tachy, loss of consciousness, arrhythmia, shock, or cardiac arrest. what are they likely experiencing?

A

severe allergic (anaphylactic) transfusion rxn

73
Q

Tx + prevention of severe allergic (anaphylactic) transfusion rxn

A

Tx: what do for acute + epinephrine + diphenhydramine (Espec w/ cutaneous syx), aminophylline w/ bronchospasm

Prevention: IgA def pt dev anti-IgA, give IgA def pdts; washed pack cells (PC)
premedicate w/ antihistamine or steroids

74
Q

what transfusion products is TRALI seen on most?

A

FFP + Platelets (high level donor antibodies)

75
Q

How long does it take for noncardiogenic pulmonary edema to resolve

A

48-96 hrs from onset

76
Q

Tx and prevention of TRALI

A

Tx: antipyretics + fluid (fever + hypotension); supportive tx - O2 (ventilator)

Prevention: attributed to presence of Ab in plasma of the donor unit directed against HLA or granulocyte Ag on RECIPIENT leukos; also due to lipid inflammatory mediators

need to decrease lipid mediators by pre-storage leukocyte reduction or decreasing storage time (esp platelets)

77
Q

common bacterial organism contamination seen w/ transfusion

A

Yersinia enterocolitica + Pseudomonas - PC due to ability to grow at low temp and high iron environment

staph and strep (gm+ cocci) + salmonella, escherichia and serratia (gm - rods) in platelets

78
Q

Processing of blood donation

A

single donation (450-500 mL)–> centrifugation–> 3 components (200 mL RBC, 50 mL platelets, 200 mL plasma)

79
Q

components of RBCs

A

leuko reduced
washed RBCs
frozen RBCs (never thaw until certain needed)
Irradiated RBCs

80
Q

components or platelets

A

platelet concentration

81
Q

components of plasma

A

leukocytes/ granulocytes

FFP –> solvent –detergent treated plasma

cryoprecipitate

other: albumin, plasma protein fraction, plasma fraction concentration

82
Q

indication for RBCs in transfusion

A

increase oxygen carrying capacity (someone is hypoxic)

Hgb<7 g/dL or Hct <21% in otherwise healthy individual w/ acute anemia (bleeding)

Hgb 7-9 g/ dL in pt w/ CV or cerebrovascular risk factors

HbS 30-50% in Sickle Cel pts to prevent stroke

Must be careful to not give blood to a chronic anemia patient too quickly or may go into congestive heart failure

83
Q

indication + contraindication for packed RBCs in transfusion

A

I: symptomatic anemia (from increased loss, decreased survival or decr pdtion of RBCs); also increases oxygen carrying capacity (expected: 1-2 g/dL Hb; ~3% Hct per unit in 24 hr)

CI: volume expansion, coagulation deficiency or drug treatable anemia

84
Q

indication for frozen/deglyced RBCs

A

storage of rare or autologous units

HSN to plasma proteins

85
Q

indication for washed RBCs

A

recurrent severe allergic rxn to unwashed RBCs

86
Q

indication for irradiated RBCs

A

risk of GVHD in immunocompromised pts

87
Q

indication for leukocyte reduced RBCs

A

febrile rxns due to leukocyte antibodies

88
Q

storage of the RBC components

A

PRBC, irradiated, leukocyte reduced: 35 - 42 days

frozen: 10 yrs, 24 hrs post-thawing
washed: 24 hrs

89
Q

indication and contraindication for platelet transfusion

A

I: bleeding due to thrombocytopenia (decreased production, incr loss, sequestration, dilution, or abnormal platelet fxn) or prophylaxis in severe thrombocytopenia
(benefit: improved homeostasis)

CI: plasma coagulation deficit, clinic conditions associated w/ rapid platelet destruction (ITP or TTP)

90
Q

transfusion threshold of platelets

A

prophylaxis in ABSENCE of bleeding: <10,000 plts

if significant hemorrhage: <50,000 plts

risk of CNS bleed: < 100,000 plts

91
Q

“six pack”

A

pooled platelets; 6 single units of plts from whole blood pooled into a “single standard dose”
contents: 5.5x10^10 platelets

92
Q

what can you occasionally see with platelet transfusions; how treat?

A

bloody platelets

RBC contamination–> Rh exposure

may need to administer RHIG

93
Q

what is pharesis

A

single donor of platelets, automated cell separator is used

single unit aphereis platelet = ~same as 6 pooled single donor (same storage and infusion rate)

get decreased exposure to single donors; increased platelet retention

94
Q

what are irradiated platelets

A

gamma irradiation inactivates donor lymphs

this decreases risk of GVHD

leukocyte reduction filter is utilized during administration of platelets (leukocyte reduced platelets)

also same storage and transfusion rate as pooled plts)

95
Q

Indications and contraindications for FFP

A

I: deficiency of stable + labile plasma coagulation factors (w/ or w/out bleeding)

  • emergent reversal of WARFARIN
  • tx TTP

CI: volume expansion( USE ALBUMIN)

96
Q

what is in FFP

A

all coagulation factors + fibrionogen
(Very few RBC, WBC, or platelets)

1 unit shud increase factor level 20-30%
dose = 2 units/adult

storage for 1 yr at 18C

97
Q

What is a cryoprecipitate transfusion

A
fibrinogen 150-250 mg
factor 8 (80-120 units)
vwF replacement (40-60 units)

dosage: 10 bags/ dose; thaw at body temp (30-37)

98
Q

indication for cryoprecipitate transfusion

A

hemophlia A

vw Dz
factor Xlll deficiency
topical glue

threshold: fibrinogen<80 mg/dL w/ ongoing bleed

99
Q

Kleihauer-Betke test

A

measure fetal Hgb in moms circulation

standard method of quanitying fetal-maternal hemorrhage (via a standard blood smear)

100
Q

RhoGAM dosage

A

1 full dosse (300 mg) at 26-28 weeks gestation or within 72 hrs of delivering Rh+ infant

one full IM dose prevents alloimmunization of 15 mL of Rh+ RBCs or 30 mL of Whole Blood

IV: aliquots 8 hrs until full dose is reached

**IM and IV are not interchnageable

101
Q

Solvent Detergent treated plasma (SDP plasma)

A

pooled plasma from up to 2500 donors

inactivates enveloped viruses (HIV + HepB) using solvent detergent; not effective in those lacking lipid envelope

102
Q

Granulocytes (pheresis)

A

contents: lots of WBCs; some platelts and plasma

Indications: neutrophenia unresponsive to appropriate Antibiotics; must be ABO compatible

Hazards: allergic + febrile rxns (GVHD unless irradiated to inactivate lymphs)

103
Q

what is the most impt step in safe transfusion

A

CLERICAL VERIFICATION

104
Q

infusion time must be completed within how much time

A

4 hours

105
Q

unused units of blood must be returned within how much time

A

w/in 30 minutes of release from blood bank to not be discarded

106
Q

what is the size of the IV that must be used for blood infusion

A

18 gauge needle

107
Q

what can be transfused w/ blood

A

Only NORMAL saline

108
Q

when giving neonatal transfusion, what should you do

A

subdivide blood components–> quad pack (24 hr expiration on one removed; can get more than 1 transfusion out of one unit of blood w/out running out of 24 hr expiration date for others)

use sterile technique

15 mL/kg aliquot of PC

109
Q

Massive transfusion

A

transfusion that amts to FULL BLOOD volume within 24 hrs

10-12 units in an adult/day

assoc problems: coagulopathy, hypothermia, hypocalcemia

110
Q

what is the rule of thumb for massive transfusions

A

1 unit FFP per every 2-3 units of RBCs

not a substitute for coagulation parameters + pt condition

111
Q

when would you do a donor apheresis

A

stem cell collection for BM transplant

112
Q

when would you do a plasma exchange

A

TTP + HUS

113
Q

when would you do therapeutic plasma pharesis

A

hematological and neuro dz

114
Q

when would you do therapeutic RBC exchange

A
sickle cell (crisis or prevention)
fetal + neonatal HDN