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NURS 5315 (Advanced Pathophysiology) WEEK 3 ORGAN TRANSPLANT UNIVERSITY OF TEXAS AT ARLINGTON

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NURS 5315 (Advanced Pathophysiology) WEEK 3 ORGAN TRANSPLANT UNIVERSITY OF TEXAS AT ARLINGTON

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NURS 5315 (Advanced Pathophysiology)
WEEK 3 ORGAN TRANSPLANT UNIVERSITY
OF TEXAS AT ARLINGTON

, 1


N5315 Advanced Pathophysiology
Solid Organ Transplant Rejection
Transplantation is an important part of medical and nursing practice today; however, just like many things in medical and nursing
science, it is not without complications. Individuals are required to take many medications (with significant side effects) post-
transplantation to suppress their natural immune response in an attempt to prevent rejection. Additionally, they have to take
medications to prevent infections. Often individuals have issues with some degree of rejection and opportunistic infections. Because
of their suppressed immune systems, they are susceptible to an array of opportunistic bacterial, viral and fungal infections.

Organ transplants occur for the heart, lungs, small intestine, pancreas, liver, kidneys, cornea, cartilage, and bone marrow. Bone
marrow is not considered a solid organ and the process of rejection is slightly different than with solid organ transplants. The rejection
in a bone marrow transplant recipient is termed graft versus host disease. The target of rejection is the recipient’s own cells. Any cell
with HLA is a target. In comparison, in solid organ transplantation, the target of the rejection is only the transplanted organ. The
process of rejection is basically an immune response to the transplanted organ and is most commonly T-cell mediated.

Human leukocyte antigen (HLA) system is made up of proteins called HLA antigens. The histocompatibility genes are responsible for
the coding of these proteins and are located on chromosome 6. The location of the histocompatibility genes is known as the major
histocompatibility complex. HLA, as mentioned, is the targeted response for transplant organ rejection. Tissue typing occurs prior to
most transplants to identify the HLA of both the recipient and the donor to match them as closely as possible to decrease the risk of
rejection. Class I antigens are HLA-A, HLA-B, HLA-C and are found in most human cells. They are primarily responsible for organ
rejection. Class II antigens are found on macrophages, dendritic cells, Langerhans cells, B cells and T cells. Some diseases such as
ankylosing spondylitis are associated with the presence of a specific HLA antigen. Persons with HLA-B27 antigen are at an increased
risk of developing ankylosing spondylitis.

Graft rejection is classified as hyperacute, acute, or chronic. Hyperacute rejection occurs immediately when circulation to the graft is
restored. The organ turns white instead of pink. It is uncommon. This type of rejection may occur if the person has had a previous
transplant or blood transfusion which contained platelets or white blood cells with foreign HLA. Acute rejection occurs days to
months after the transplantation and is a cell mediated immune response. Chronic rejection occurs months to years after the transplant
is completed. It is characterized by a slow, weak cell mediated immune response.

The concept map shows the steps of rejection. Once the organ is transplanted the antigen presenting cells (macrophages) present the
antigen, in this case HLA, from the transplanted organ to both CD4 cells and CD8 cells. This triggers the T-cell proliferation. T-cells

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