Patho Assg Md 1wk2 Discussion
Explain why you think the patient presented the symptoms described.
The patient suffers from rheumatoid arthritis and the medications include naproxen and methotrexate. Both medications inhibit the immune response to avoid the immune system from destroying their own body (Burmester & Pope, 2017). Prednisone improves the effects of methotrexate when both drugs are administered together. The weakened immune system did not destroy the infectious fungi that caused the infection. Chills, fever, weakness, and hemoptysis are signs and symptoms of respiratory and blood infections.Patho Assg Md 1wk2 Discussion
Identify the genes that may be associated with the development of the disease.
Invasive aspergillosis is an infection caused by the inhalation of Aspergillus fungus. In an immunosuppressed individual, the immune system is unable to kill the fungus upon inhalation, and the fungus induces a fatal infection known as invasive aspergillosis. It is mainly a lung infection that extends to other areas of the body (Firestein & Mclness, 2017). Mannose-binding lectin (MBL)2, chemokine ligand 10 (C-X-C10), toll-like receptors, plasminogen, and pulmonary surfactant protein A (SPA-2) are genes linked with the origin and development of this illness. These genes are involved with the body’s immune structure.
Explain the process of immunosuppression and the effect it has on body systems.
Immunosuppression is the inhibition of the body’s immune system. This suppression is accomplished pharmacologically to deter the rejection of grafting organs by the immune system or to prevent attacks by the body’s immune system on the body itself, for example in the case of cancer treatment or rheumatoid arthritis. Any pathological agents, including viruses or tumors, can also inhibit the body’s immune system (Venet et al., 2017). Antimetabolites including methotrexate is an immunosuppressive compound that interrupts the metabolic processes of immune cells, inhibits the dissemination of immune cells, and causes the death of immune cells by apoptosis. Some drugs inhibit the metabolism of purine and prevent the division of lymphoid cells. Any highly specialized medications only block T-cell multiplication. These medications inhibit the action of inosine monophosphate dehydrogenase (IMPDH) enzyme, contributing to the termination of replication and development of T-cells and death from apoptosis.
When a person undergoes immunosuppressive treatment or whose immune system is compromised for some cause (rheumatoid arthritis), they are considered to have been immunosuppressed (Venet et al., 2017). The body will almost always reject the new organ after a transplant, due to the protein membrane of its cells differing from that of the original organ. As a result, the immune system identifies the new tissue as “hateful” and seeks to kill it by targeting it with leukocytes, leading to tissue death. Immunosuppressants are introduced to obstruct this response.Patho Assg Md 1wk2 Discussion
Immunosuppressive drugs inhibit the release of cytokines by the lymphocyte. Due to the blocking of these signals, lymphocytes are not activated, leading to no or very weak immune response. Immunosuppression, if severe, does not impact the body’s other organs. However, if immunosuppression is not severe, it may also have a harmful effect on other problems. For instance, non-specific immunosuppressive drugs inhibit the spread and replication of bone tissue.
Burmester, G. R., & Pope, J. E. (2017). Novel treatment strategies in rheumatoid arthritis. The Lancet, 389(10086), 2338-2348.
Firestein, G. S., & McInnes, I. B. (2017). Immunopathogenesis of rheumatoid arthritis. Immunity, 46(2), 183-196.
Venet, F., Rimmele, T., & Monneret, G. (2018). Management of sepsis-induced immunosuppression. Critical Care Clinics, 34(1), 97-106.Patho Assg Md 1wk2 Discussion