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*MHD Exam 6 > Transfusion > Flashcards

Transfusion Flashcards

1
Q

What is the main clinical use of plasma and PCC (Prothrombin Complex Concentrate)?

A
  • Immediate reversal of warfarin (if bleeding occurs)
  • If patients have a supratherapeutic INR before surgery
  • Global coagulopathy (bleeding) - used to incr. factors II, VII, IX, X, protein C, protein S (Vitamin K-dependent)
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2
Q

What is the main clinical use of cryoprecipitate?

A

fibrinogen deficiency (can also be used for FVIII deficiency, but not as common anymore because we have purified FVIII concentrate)

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3
Q

Blood group antigens on the surface of RBCs are defined serologically by:

A

an antibody

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4
Q

What is the difference between autoantibodies and alloantibodies?

A
  • autoantibodies are directed against host antigens

- alloantibodies are directed against donor antigens

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5
Q

What is the difference between alloantibodies and isohemagglutinins?

A

alloantibodies are formed after antigen exposure, whereas isohemagglutinins are formed before antigen exposure

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6
Q

The complement system consists of proteins that augment the effects of antibodies through:

A
  • cell lysis
  • generation of mediators that participate in inflammation and attract neutrophils
  • opsonization (enhancement of phagocytosis)
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7
Q

What are the main carb vs. protein surface antigens we are concerned about?

A
  • carb: ABO

- protein: Rh (mostly D)

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8
Q

The Group O RBC phenotype results from:

A

mutated ABO gene (no A or B antigen expression)

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9
Q

What is the A antigen composed of?

A

H antigen + N-acetylgalactosamine

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10
Q

What is the B antigen composed of?

A

H antigen + D-galactose

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11
Q

What is the base unit of the blood antigens?

A

ceramide

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12
Q

Alloantibodies require exposure to…

A

antigen on donor RBCs (pregnancy, transfusion, transplantation)

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13
Q

Which type of immunoglobulin are anti-A and anti-B isohemagglutinins?

A

IgM (however, group O individuals make anti-A and B IgG, which can cross the placenta)

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14
Q

Do isohemagglutinins and/or alloantibodies activate complement?

A

isohemagglutinins do, while alloantibodies usually do not

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15
Q

What are the 2 isohemagglutinins present in humans?

A

anti-A and anti-B

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16
Q

How are isohemagglutinins made?

A

They are naturally occurring and made against bacteria that share polysaccharide epitopes (like GI bacteria).

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17
Q

What are autoantibodies directed against? Do they cause hemolysis?

A
  • directed against non-specific RBC membrane antigens

- usually do not cause hemolysis (some can though)

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18
Q

What is the main clinical indication of a RBC transfusion?

A

symptomatic anemia

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19
Q

True or false: blood for transfusions is FDA regulated.

A

true

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20
Q

What is the set of processes that must occur for a safe blood transfusion?

A

good clinical indication to transfuse –> pre-transfusion testing –> issue unit –> administer at bedside –> monitor and evaluate –> intended clinical outcome

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21
Q

What is forward vs. reverse typing for determining the blood type of a specimen?

A
  • Forward: typing of patient’s RBCs with reagent antisera (adding anti-A, anti-B, and anti-D –> agglutination = presence of antigen)
  • Reverse: typing of patient’s isoagglutinins (serum) with reagent RBCs (A cells and B cells)
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22
Q

When there are unexpected alloantibodies in a patient’s serum, what does this indicate?

A

The patient had prior exposure to another person’s RBCs. These patients lack the corresponding antigen, and RBC destruction can happen in 10-14 days (slow extravascular hemolysis).

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23
Q

What are the different transfusion reactions?

A
  • allergic/anaphylactic
  • acute hemolytic
  • febrile nonhemolytic
  • transfusion-related acute lung injury (TRALI)
  • transfusion-associated circulatory overload (TACO)
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24
Q

Acute hemolytic transfusion reactions are typically mediated by which type of antibody?

A

IgM

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25
Q

What are the acute transfusion reactions that are immune mediated?

A

hemolytic, febrile non-hemolytic, allergic/anaphylactic, TRALI

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26
Q

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

A

hemolytic (due to physical/chemical insult), hypocalcemia, air embolus, TACO, hypothermia, transfusion transmitted infection

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27
Q

How long after transfusion do acute vs. delayed transfusion reactions precipitate?

A
  • Acute: <24 hrs

- Delayed: >24 hrs

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28
Q

What are the immune vs. non-immune delayed transfusion reactions?

A
  • Immune: hemolytic (anamnestic response), graft vs. host disease, post-transfusion purpura
  • Non-immune: iron overload, transfusion transmitted infection
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29
Q

Signs and symptoms of acute hemolytic transfusion reaction?

A
  • free Hb in serum and urine
  • fever, hypotension, shock
  • pain along infusion site
  • patient anxiety
  • coagulopathy progressing to DIC
  • renal failure w/ oliguria or anuria
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30
Q

What is the mechanism of acute hemolytic transfusion rxn?

A

pre-formed Abs (recipient) bind donor RBCs –> complement activation –> MAC –> intravascular red cell lysis

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31
Q

Cause of allergic transfusion reaction?

A

recipient Abs (IgE) against donor plasma proteins leading to mast cell degranulation and histamine release

32
Q

Signs and symptoms of allergic transfusion reaction?

A

rash, itching, and hives within minutes of transfusion

33
Q

Can you re-start the blood transfusion after a patient’s allergic transfusion reaction has subsided?

A

Yes! If symptoms resolve (w/ anti-histamines and steroids), you may slowly restart the unit. You CANNOT do this with an anaphylactic transfusion reaction.

34
Q

What are the signs and symptoms of anaphylactic transfusion reaction?

A

hypotension leading to shock, difficulty breathing and bronchospasm leading to cyanosis, N/V/D (all sudden onset)

35
Q

Cause of anaphylactic transfusion reaction?

A

recipient (IgA deficient) makes anti-IgA Abs against donor IgA

36
Q

Cause of febrile non-hemolytic transfusion reactions?

A
  • cytokines accumulated in donor plasma

- recipient Abs against donor leukocyte antigens

37
Q

What is the leading cause of transfusion-related mortality?

A

TRALI

38
Q

Cause of TRALI?

A

donor HLA antibodies against recipient WBCs –> complement activation –> leukocytes aggregate/adhere to capillary epithelium in lungs and cause damage

39
Q

The majority of fatalities in TRALI are linked to:

A

female donors with history of pregnancy who have anti-HLA Abs (greater risk w/ high plasma volume components)

40
Q

What are the main signs/symptoms of TRALI?

A
  • acute onset of respiratory distress
  • hypoxemia (O2 sat <90% on room air)
  • hypotension
  • bilateral infiltrates on CXR

*all within 6 hrs of transfusion

41
Q

How might a blood transfusion cause hypocalcemia?

A

blood is stored in preservatives with citrate, and citrate binds calcium

42
Q

Cause of TACO?

A

rapid increase in blood volume in a patient with compromised cardiac function

43
Q

Signs and symptoms of TACO?

A
  • acute respiratory distress
  • HTN
  • elevated BNP
  • elevated CVP
  • evidence of left HF
  • evidence of (+) fluid balance
  • pulmonary edema
44
Q

Best way to prevent TACO?

A

slow down transfusion rate

45
Q

What are the differences in radiographic findings between TRALI and TACO?

A

TRALI- bilateral pulmonary infiltrates

TACO- pulmonary edema

46
Q

Transfusion-transmitted bacterial infections are most often seen with _______ transfusions.

A

platelet (platelets are stored at room temp, therefore bacteria are more likely to grow)

47
Q

Symptoms of transfusion-transmitted bacterial infection?

A
  • rapid onset of fever chills, hypotension, muscle pain
  • N/V/D
  • shock, hemoglobinuria, renal failure, DIC
48
Q

What are the immediate steps when dealing with any type of transfusion reaction?

A

1) Stop transfusion
2) Keep line open with saline
3) Notify blood bank and attending physician

49
Q

When a patient has a transfusion reaction, what is done after sending patient samples back to the blood bank?

A

Comparison of pre- and post-transfusion patient samples…
-clerical check (was there an error?)
-visual check of serum for hemolysis
-RBC/ABO/Rh typing
-DAT
(may also check bilirubin, LDH, haptoglobin, and blood culture)

50
Q

What is one of the leading causes of preventable transfusion-related deaths in the U.S.?

A

patient misidentification

51
Q

What is the purpose of giving Rhogam to pregnant mothers?

A

Rhogam prevents B-cell activation and memory cell formation against the fetus’ Rh(+) antigens, thus preventing hemolytic disease of the newborn.

52
Q

What is the most common cause of HDN vs. what causes the most severe form of HDN?

A
  • ABO most common cause (usually a group O mother who makes IgG that can cross placenta)
  • RhD causes most severe form (most immunogenic)
53
Q

What are the classic clinical findings associated with HDN?

A
  • hemolysis (leading to anemia and jaundice)
  • hyperbilirubinemia
  • “erythroblastosis fetalis”
  • “hydrops fetalis”
54
Q

What is the critical antibody titer level when assessing fetal risk with HDN?

A

levels of 1:16 or higher

55
Q

How is middle cerebral artery used to assess fetal risk associated with HDN?

A

It is an indirect and non-invasive assessment looking at flow rate (higher flow=greater degree of anemia).

56
Q

What are the 2 types of transfusion to treat HDN?

A
  • Intrauterine (simple) - corrects fetal anemia
  • Neonatal (exchange) - used to reduce bilirubin, remove Ab-coated RBCs, and replace w/ antigen-neg RBCs (after baby is born)
57
Q

What exactly is Rhogam?

A

concentrate of IgG anti-D, developed from pools of human plasma; it binds RhD antigen, preventing B-cell activation and memory B-cell formation

58
Q

Who is Rhogam given to?

A
  • RhD negative pregnant women
  • RhD negative women of child-bearing age
  • At 28 wks gestation and within 72 hrs postpartum, or following abortion, trauma, or blood transfusion
59
Q

What is autoimmune hemolytic anemia (AIHA)?

A

It happens when a person has autoantibodies against RBC antigens. Most are not clinically significant but may cause crossmatch incompatibility with RBC units. Some cause hemolysis, and this risk increases with each decade of life.

60
Q

What are the causes of autoimmune hemolytic anemia?

A
  • autoimmune disorders
  • malignancies (CLL, lymphoma)
  • idiopathic
61
Q

Autoimmune hemolytic anemia (AIHA) plus immune thrombocytopenic purpura (ITP) is known as what?

A

Evans syndrome

62
Q

What is the difference b/t warm autoimmune HA and cold agglutinin disease?

A
  • Warm: predominantly IgG with Ab-Ag rxn @ 37 deg C; caused by autoimmune diseases and lymphoid malignancies
  • Cold: predominantly IgM with Ab-Ag rxn @ 25 deg C or colder; caused by infection (mycoplasma or mono) and lymphoid malignancies
63
Q

How is hemolysis cleared in warm autoimmune HA vs. cold agglutinin disease?

A
  • Warm: extravascular (Fc receptors in spleen and liver)

- Cold: extravascular (C3 receptors in liver)

64
Q

Describe DAT findings in warm autoimmune HA vs. cold agglutinin disease.

A

Both will result in (+) DAT result, but cold agglutinin disease will be positive for complement only.

65
Q

What are isohemagglutinins?

A

substances that agglutinate the red blood cells of others of the same species (anti-A and anti-B isohemagglutinins in human blood)

66
Q

Alloantibodies are mostly which type?

A

IgG

67
Q

What happens during the crossmatch process of pre-transfusion testing?

A

ABO-compatible donor RBC unit selected –> recipient plasma mixed and centrifuged w/ sample of donor RBCs –> if no hemolysis or agglutination observed, donor RBC unit issued

68
Q

What is a direct vs. indirect antiglobulin test looking at?

A
  • Direct: using patient’s RBCs and adding anti-IgG reagent to detect antibodies on surface of RBC
  • Indirect: using patient’s serum and adding anti-IgG reagent to detect antibodies in patient’s serum
69
Q

What is the rationale for screening unexpected, clinically significant allantibodies?

A

While unexpected alloantibodies usually do not bind complement, they have the potential to shorten the anticipated survival of transfused RBCs (slow extravascular hemolysis with destruction of RBCs in 10-14 days).

70
Q

What are the more serious symptoms of transfusion-transmitted bacterial infection?

A

shock, renal failure, DIC

71
Q

What are the steps that should be followed from transfusion-transmitted bacterial infection?

A
  1. Stop transfusion immediately!
  2. Microbio workup on remaining blood in unit and pt’s blood sample
  3. Antibiotic treatment
72
Q

What is the most common virus that can be transmitted via transfusion?

A

Hepatitis B (although overall incidence of this is very low compared to bacterial causes)

73
Q

What are some of the risks associated with HDN?

A
  • Fetomaternal hemorrhage (FMH) may occur as early as 8 weeks
  • FMH more likely as pregnancy progresses
74
Q

How can ABO blood groups cause HDN, and how common is this?

A

Group O individuals may make IgG that can cross the placenta. If a group O mother has anti-A and anti-B isohemagglutinins crossing the placenta, these can attack the baby’s RBCs. This happens in 15% of pregnancies.

75
Q

Why does hyperbilirubinemia occur in HDN?

A

Hemolysis of fetus’ RBCs –> heme broken down into bilirubin –> mother’s liver conjugates bilirubin

76
Q

True or false: HDN is treated with transfusion.

A

True! It can either be intrauterine (simple) transfusion or neonatal (exchange) transfusion. Neonatal transfusion reduces bilirubin levels, removes antibody-coated RBCs, and replaces with antigen-negative RBCs.

*MHD Exam 6 (20 decks)

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