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Blood Bank > Antigen Groups and Transfusion Reactions > Flashcards

Antigen Groups and Transfusion Reactions Flashcards

1
Q

Kell

A
  • IgG
  • Reacts with AHG
  • Enzymes have no effect
  • Causes: HTR, HDN
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2
Q

Duffy

A
  • IgG
  • Reacts with AHG
  • Destroyed by enzyme
  • Causes: HTR, HDN (expressed on cord cells)
  • Other: show dosage effect, glycoprotein is a receptor for P. vivax, the merozoites bind but cannot enter the cells
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3
Q

Kidd

A
  • IgG
  • Reacts with AHG
  • Enzymes enhance agglutination
  • Causes: HTR(delayed) and HDN
  • Other: show dosage effect, bind complement, deteriorate in storage
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4
Q

Lua

A
  • IgM
  • Reacts at room temp (4C)
  • Enzymes variable
  • Other: Not naturally occurring, not naturally significant
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5
Q

Lub

A
  • IgG
  • Reacts with AHG (37C)
  • Enzymes variable
  • Causes: HTR, HDN
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6
Q

Lewis

A
  • IgM
  • 4C (Cold reacting)
  • Enzymes cause enhanced agglutination
  • Other: produced by tissues and absorbed onto RBCs, not associated with HDFN
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7
Q

P

A
  • IgM
  • 4C
  • Other: Reacts at IS, 37C or AHG
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8
Q

M,N

A
  • IgM
  • Reacts at IS, 37C, or AHG
  • Destroyed by enzymes
  • Other: shows dosage effect; clinically significant if IgG
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9
Q

S,s

A
  • IgG
  • Reacts at 37C, with AHG
  • Enzymes are variable
  • Causes: HTR, HDN
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10
Q

Types of carrier molecules

A

Most Ag are carried on glycoproteins with a specificity to the Ag

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11
Q

MNS System

A

Most important transfusion Ag

  1. M/N on Glycophorin A
  2. S on Glycophorin B

M/S and N/s are usually found together

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12
Q

Anti-M

A

IAT if IS crossmatch is +

Will not react with enzyme treated cells, but can be enhanced by an acidified environ.

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13
Q

Anti-N

A

Seen in dialysis Pts with residual formaldehyde

Alters the N Ag in the Pt

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14
Q

Anti-Kell

A

Most Immunogenic after ABO and Rh

Can be “naturally occurring” after microbial infections, the IgMs clear after the infection

Other naturally occurring Ab are cold reactive with a negative IAT

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15
Q

I/i Ag

A
  1. Fetal cells express I antigen
  2. Adults express i Ag

Transition occurs by 18 mos

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16
Q

Anti-I

A

Usually an IgM cold-reactive Ab, found in 4C testing

Rarely found as an autoanti-I at 37C from complement binding at RT that carry over to IAT, these can cause Cold Agglutinin Syndrome:

  • May be helpful to use a monospecific IgG reagent
  • O cells run at RT and 4C can ID cold-agglutinins
  • Prewarming techniques can remove cold-agglutinins, but are usually not used
17
Q

Increase in Temp of 1C/chills

A
  • HTR
  • TACO
  • Bacterial Contamination
  • Febrile non-hemolytic transfusion reactions (FNHTR)
18
Q

Hypotension/Tachycardia

A
  • HTR
  • TACO
  • Anaphylaxis
  • Bacterial contamination
  • Air embolus
19
Q

Hypertensive changes

A
  • TACO
  • TRALI
20
Q

Pain/Anxiety

A
  • HTR
  • Febrile Rxn
  • Citrate Rxn
21
Q

Transfusion Reaction Procedural Steps

A
  1. Stop transfusion
  2. Review clerical info
  3. Check for hemolysis in pre/post transfusion samples
  4. Repeat ABO on post- DAT on post-, if +, DAT on most recent pre-

Further testing can include: compatibility testing, Ab screen on post-, eluate, bacteriologic studies, coag studies, plasma Hgb, bilirubin, urinalysis

22
Q

TRALI

A

Transfusion-Related Acute Lung Injury

Severe pulmonary issues within hours of transfusion, with fever

Donor anti-leukocyte Ab activate and aggregate WBCs, or transfusion of cytokines activates neutrophils in the lung present from an underlying condition

23
Q

TACO

A

Transfusion-Assoc. Circulatory Overload

Greatest at risk have underlying heart, lung, or kidney failure that make them intolerant of volume increase; those with massive transfusions, Peds, and severe anemia are also at risk

Show shortness of breath, coughing, elevated BP, low pulse rate, peripheral edema

Respond to diuretics (helps diagnose as well), ventilation/oxygen, slow transfusion of blood products helps prevent this

24
Q

Anaphylotoxins C5a/C3a

A

Promote release of serotonin/histamine from Mast Cells, causing smooth muscle contractions and bronchial/vascular dilation

Show hyptotension, chills, fever, back pain, shock, renal failure and death

25
Q

Intra/Extravascular Hemolysis

A

Both show hemoglobinemia, hemoglobinuria, increased plasma Hgb, low serum haptoglobin, increase indirect bilirubin

From non-ABO Ab-related hemolysis or a drop in Ab titer below detection level

26
Q

DHTR

A

Delayed Hemolytic Transfusion Reaction

Extravascular hemolysis weeks after transfusion

Usually require presensitization via transfusion, transplant, and pregnancy

Usually from Kidd, Duffy, Kell, and MNS

Chronically transfused Sickle Cell Pts may develop alloAb and risk DHTRs

27
Q

Transfusion Related Bacterial Infection

A

Sepsis, Fever, Hypotension

Immunosuppressed Pts may not show a febrile response

Can progress to DIC, renal failure, and death

Babesia microti has been implicated in a significant # of cases

If septic, they should be cultured and started on antibiotic therapy

28
Q

Allergic/Anaphylactic Rxns

A

Recipient IgE to soluble Ag in donor plasma, most commonly in plasma containing platelet products

Epinephrine will control the reaction while BP and volume are maintained, steroids may also help

29
Q

FNHTR

A

Cytokines released from WBC in storage cause inflame. in recipient

Treated/Prevented with antipyretics

30
Q

TAGVHD

A

Transmission Assoc. Graft-Versus-Host Disease

Non-specific symptoms within weeks of transfusion, will cause death

Immunosuppresed, those on chemotherapy, with congenital disorders, and newborns are at greatest risk

Donor T cells attack Pt cells

Use of irradiated units, and those tested for HLA compatibility

31
Q

Posttransfusion Purpura

A

Sudden onset of thrombocytopenia 1-2 weeks after transfusion from platelet-specific Ab in Pt from prior exposure

32
Q

HDFN Prenatal Evaluation

A

History of pregnancies/transfusions, screening at first prenatal visit for ABO/Rh/Ab screen, no maternal weak D testing needed

Screen should be with anti-IgG AHG and without enhancement via enzyme treated cells to detect only Ag assoc. with HDFN

33
Q

Ab titration in HDFN

A

To assess the relative strength of the Ab

Uses dilutions of maternal serum incubated at 37C with reagent RBCs with Ag against maternal Ab, and read at anti-IgG AHG phase

Procedure variations include: can be preformed in saline, gel cards, enhancement media, alter incubation times, and different Ag expressed on RBCs

Usually predictive in first affected pregnancy and not needed in any subsequent pregnancies

34
Q

Anti-Kell in HDFN

A

Suppress RBC production by encouraging phagocytosis before the cells produce hemoglobin, leading to anemia and hydrops without a significant titer

35
Q

Intrauterine Transfusions

A

Administered through the umbilical vein or peritoneal cavity, using fresh O units that are negative for maternal Ag, and irradiated to prevent TAGVHD

36
Q

False Negative in Direct Testing for D Ag

A

The cells are too coated in maternal Anti-D to agglutinate

37
Q

Quantification of Fetal-Maternal Hemorrhage

A

Screening Test is the rosette test

  • Maternal sample from 1hr after birth and mixed with Anti-D
  • Washed and indicator cells are added

Kleihauer-Betke (based on fetal Hgb resistance to elution from RBCs) acid elution or Flow Cytometry can also be used

38
Q

Previously Sensitized Women (D)

A

IgG with a titer lower than < 4, alloimmunization has IgM and a higher titer

39
Q

NAITP

A

Neonatal Thrombocytopetic Purpura Maternal IgG against fetal platelets, can be in first pregnancies, inter cranial hemorrhage can occur in utero/after delivery Irradiated, leucoreduced, CMV-seronegative, antigen negative platelets can be transfused to prevent hemorrhage

Blood Bank (11 decks)

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