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Blood Transfusion Reaction

Zuhal

Full Member
Dec 29, 2012
247
4
Thompson
  1. Medical Student
    Hi guys
    I'm having difficulties differentiating between febrile nonhemolytic transfusion rxn and extravascular hemolysis in acute hemolytic transfusion rxns. they're both type II hypersensitivity rxns and both involve the pt having prior exposure to some foreign antigen (and making antibodies against it). is it just a difference of symptomology?
    Tried goljan, wasn't helpful this time :(
    Thanks
     
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    Zuhal

    Full Member
    Dec 29, 2012
    247
    4
    Thompson
    1. Medical Student
      ok so please correct me if my understanding is wrong:

      In nonhemolytic, you have antibodies from the host against the donor's MHC I located on WBCs? (I don't even know why wbc are involved here but it wouldn't make sense if we say against RBC because they don't even have an MHC). and the symptoms are minor

      in hemolytic intravascular: you're a type A and we transfuse you with a type B so you naturally have antibodies against B and the hemolysis of those RBC happens intravascullarly.
      in extravascular, i'm totally confused...is it just that it happens in the spleen where macrophages digest the cells? or is there more to it?

      Thanks for your replies btw!
       

      Ycut

      Full Member
      Oct 20, 2012
      101
      1
      1. Non-Student
        ok so please correct me if my understanding is wrong:

        In nonhemolytic, you have antibodies from the host against the donor's MHC I located on WBCs? (I don't even know why wbc are involved here but it wouldn't make sense if we say against RBC because they don't even have an MHC). and the symptoms are minor

        in hemolytic intravascular: you're a type A and we transfuse you with a type B so you naturally have antibodies against B and the hemolysis of those RBC happens intravascullarly.
        in extravascular, i'm totally confused...is it just that it happens in the spleen where macrophages digest the cells? or is there more to it?

        Thanks for your replies btw!

        In non hemolytic as the name denotes there is no hemolysis (rbc s lack HLA antigens and therefore are not involved) Other elements which come with transfused blood such as lymphocytes, platelets etc having HLA on surface can induce type 2 hypersensitivity in host and thats the reason for this

        Extravascular hemolysis occurs in spleen where defective or opsonized rbc are phagocytosed by macrophages, degraded and remaining heme transformed into bilirubin which is released into circulation and transported to live for glucuronidation
         

        Zuhal

        Full Member
        Dec 29, 2012
        247
        4
        Thompson
        1. Medical Student
          In non hemolytic as the name denotes there is no hemolysis (rbc s lack HLA antigens and therefore are not involved) Other elements which come with transfused blood such as lymphocytes, platelets etc having HLA on surface can induce type 2 hypersensitivity in host and thats the reason for this

          Extravascular hemolysis occurs in spleen where defective or opsonized rbc are phagocytosed by macrophages, degraded and remaining heme transformed into bilirubin which is released into circulation and transported to live for glucuronidation

          Great! Thank you so much, that clears up a lot of things! I have one more question: in a chronic transplant rejection the MOA in FA is a little confusing. So the grafted CD8 cells are recognized as self by recipient's CD8 cells. so no problem there. But the grafted tissue presents an antigen on their MHCI that the recipient's CD8 cells recognize as foreign. Is that the general idea?

          Also, according to goljan, someone with DiGeorge will have a danger of GVH reaction...Is that because they've never "seen" or been exposed to T cells before? Would you expect the same thing in someone with AIDS/SCID?
          Sorry those are just a few questions bothering me lately! I appreciate your help!
           

          Ycut

          Full Member
          Oct 20, 2012
          101
          1
          1. Non-Student
            Great! Thank you so much, that clears up a lot of things! I have one more question: in a chronic transplant rejection the MOA in FA is a little confusing. So the grafted CD8 cells are recognized as self by recipient's CD8 cells. so no problem there. But the grafted tissue presents an antigen on their MHCI that the recipient's CD8 cells recognize as foreign. Is that the general idea?

            Also, according to goljan, someone with DiGeorge will have a danger of GVH reaction...Is that because they've never "seen" or been exposed to T cells before? Would you expect the same thing in someone with AIDS/SCID?
            Sorry those are just a few questions bothering me lately! I appreciate your help!

            In chronic graft rejection self CD8 cells recognize foreign MHC1 molecules as self+antigen and attack together with antibodies-this process is irreversible and not controlled anymore by immunosuppressives
            In contrast acute graft rejection is recognition of foreign MHC1 as non self and proliferation of CD8 cells against those nonself MHC1 molecules which is controlled by immunosuppression (not allowing reactive clones to proliferate, but eventually the whole immune system recognize the foreign MHC1 molecules as self + antigen and thats the transition from acute to chronic irreversible rejection)

            In digeorge syndrome u got no T cells and due to this there is possibility for foreign T cells(CD8+CD4) in transplanted tissue to proliferate
            immunity can not efficiently clear them

            I think whatever decreases Tcell response can predispose to graft vs host disease (when sufficient amounts of immunocompetent cells are transplanted)
             

            Zuhal

            Full Member
            Dec 29, 2012
            247
            4
            Thompson
            1. Medical Student
              I think whatever decreases Tcell response can predispose to graft vs host disease (when sufficient amounts of immunocompetent cells are transplanted)

              Thanks for your answer! About your last statement,if someone gets a bone marrow transplant i can understand how the new donor cells start attacking the body because they don't recognize it but what I don't get is why is it that thats specifically true for those who are IC? These ppl don't even have any T/B cells to fight off in the first place? Am I missing something here?
               

              Ycut

              Full Member
              Oct 20, 2012
              101
              1
              1. Non-Student
                Thanks for your answer! About your last statement,if someone gets a bone marrow transplant i can understand how the new donor cells start attacking the body because they don't recognize it but what I don't get is why is it that thats specifically true for those who are IC? These ppl don't even have any T/B cells to fight off in the first place? Am I missing something here?


                Yep immunocompromised individuals are at risk
                If person has weak Immunity he is more prone to develop grafts immune response when transplanted tissues have high numbers of Tcells (bone marrow or liver)
                 

                yankees527

                Full Member
                5+ Year Member
                Aug 5, 2013
                674
                466
                1. Medical Student
                  BUMP

                  So First Aid seems to be behind on this:Febrile nonhemolytic reactions are supposedly from accumulated cytokines in the donor product

                  Uptodate says alot about this mechanism being best supported:

                  "FNHTRs are commonly caused by cytokines that are generated and accumulate during the storage of blood components. Implicated cytokines include interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-alpha (TNFα)."

                  This is in contrast to FA which states it is from antibodies against donor HLA and WBCs (although this is given one line as an"alternate mechanism proposed" on uptodate)

                  Just thought us test takers would want to be aware of this!
                   
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