Blood Transfusion Flashcards

1
Q

At what age do detectable levels of Anti-B and Anti-A Abs begin?

A

6 months

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2
Q

Name the Antibodies that predominate in each blood type and why.

A
  1. IgM for A and B and AB blood types
  2. IgG for O type

RBCs have a physiologic gap between each other and the endothelial wall called the Zeta potential. This gap prevents contact between these components to prevent activation of complement proteins and an immune response. IgM is needed for A and B because those RBCs have larger sugars on the surface and need a the larger pentad IgM complex to prevent contact and maintain the Zeta potential. O does not need as much IgM because the sugars are small and only the Anti-A/anti-B antibodies (IgG) dominate the serum.

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3
Q

What two things are unique about the Anti-D antigen?

A

It is involved in Rh typing. Unlike Anti-A and Anti-B which are produced shortly after birth naturally, Anti-D is not produced (even in Rh- patients) until exposure to Rh+ blood occurs.

It also does not cause intravascular hemolysis like Anti-A and Anti-B antigens. Instead it acts like opsonization allowing phagocytes to engulf the RBCs causing Extravascular hemolysis.

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4
Q

Mechanism of Hemolytic Disease of the newborn (Erythroblastosis Fetalis).

A

Rh- mother is pregnant with Rh+ child. The child’s blood causes production of Anti-D Abs in the mother during delivery. During a second pregnancy, the Anti-D Abs have the ability to cross the placenta and if the child is Rh+ again it will cause hemolysis in the fetus.

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5
Q

Tx and mechanism of treatment to prevent Erythroblastosis fetalis.

A

Rhogam
-Protein very similar to Anti-D Abs that detects Rh+ fetal blood hopefully before the mother’s own immune system. This drug binds the fetus RBCs to “disguise” them from the mother’s immune system so that no “true” Anti-D Abs are formed. It cannot cross the placenta so it has no effect on the fetus.

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6
Q

Explain the two ABO typing blood tests.

A
  1. Forward: detects the actual antigens (sugars) on the RBC surface membrane.
  2. Reverse: detects the Anti-A, Anti-B or both Abs in the serum.

Tests are read as: w+ means no agglutination and the types are compatible

or 4+ meaning complete agglutination and the blood types are not compatible

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7
Q

What is the purpose for a crossmatch (compatibility) test?

A

Done after ABO and Rh testing is done. It’s a final test done before transfusion to look for any rare donor antigens that might cause an immune response in the recipient. These include:
Kell Antigen: causes a strong lethal response
Lewis Antigen: less severe response seen

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8
Q

Function of the Direct Coombs Test (Direct Antiglobulin Test).

A

Detects IgGs that might bind RBCs other than Anti-A or Anti-B. Used to rule out autoimmune hemolytic anemias.
(also picks up alloantibodies for incorrect infused blood but this is less common as blood tests are very conclusive preventing this from happening)

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9
Q

Main cause of complications with blood transfusions.

A

Human Error

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10
Q

Main infectious agent seen in blood transfusion errors.

A

Cytomegalovirus (CMV)

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11
Q

What occurs in an Acute Hemolytic Reaction due to transfusion error?

A

IgM or IgG binds RBC surface antigens activating the Classic Complement Cascade using Membrane Attack Complexes (MAC) to lyse cells.

May also illicit intrinsic clotting pathway response

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12
Q

Which two lab tests are very indicative of acute hemolysis?

A

Increased Lactate Dehydrogenase (LDH)

Low Serum Haptoglogin

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13
Q

What test will be positive during an acute hemolysis due to transfusion error?

A

Coombs Test

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14
Q

Major consequences of Acute hemolysis.

A

Shock (increased bradykinin)
Hyperkalemia (increase in serum K+ due to RBC lysis)
DIC
Death

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15
Q

Mechanism of Febrile, Non-hemolytic reaction of blood transfusions.

A

Everything with the RBCs is fine. A rare anti-leukocyte antibody exists in the recipient that acts against the WBC in the donor blood. This interaction causes pyrogen release Treatment is to stop the unit of blood.

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16
Q

How can you manage patients that need blood transfusions but have Febrile Non-hemolytic reactions?

A

Filter the WBCs from the donor blood. (Leukopore or Leukopoor blood). If a reaction is occurring use anti-febrile meds

17
Q

Mechanism of TRALI.

A

Transfusion-Related Acute Lung Injury.
Mechanism uncertain: possible alternate pathway activation of complement by donor Abs against recipient WBCs (mainly alveolar macrophages). This causes the cells to agglutinate and lodge in the alveolar tissue.

18
Q

Best management for TRALI.

A

High-dose steroids

19
Q

Mechanism of graft vs. host disease.

A

Donor lymphocytes attack recipient tissue (mainly skin, liver, bone marrow). The recipient usually has some underlying immune deficiency.

20
Q

Best way to prevent Graft vs. Host disease.

A

If the recipient has an underlying immune defiicenyc and the physician suspects G V H disease then the donor blood unit can be irradiated to inactivate the lymphocytes in it. Gamma radiation is used.